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THE
Hlower Ueterinary Library
FOUNDED BY
ROSWELL P. FLOWER
for the use of the
N. Y. STATE VETERINARY COLLEGE
1897
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This book was digitized by Microsoft Corporation in
cooperation with Cornell University Libraries, 2007.
You may use and print this copy in limited quantity
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for revenue-generating or other commercial purposes.
CLINICAL DIAGNOSIS.
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CLINICAL DIAGNOSIS:
THE
BACTERIOLOGICAL, CHEMICAL, AND MICROSCOPICAL
EVIDENCE OF DISEASE.
BY
Dr. RUDOLF v. JAKSCH,
PROFESSOR OF SPECIAL PATHOLOGY AND THERAPEUTICS, AND DIRECTOR OF THE
MEDICAL CLINIC, IN THE GERMAN UNIVERSITY OF PRAGUE.
Granslated from the Third German Edition anv Enlarged by
JAMES CAGNEY, M.A., M.D.
MEMBER OF THE ROYAL COLLEGE OF PHYSICIANS OF LONDON ;
PHYSICIAN TO THE HOSPITAL FOR EPILEPSY AND PARALYSIS, REGENT’S PARK;
LATE DEMONSTRATOR OF ANATOMY, ST. MARY’S HOSPITAL MEDICAL SCHOOL,
With Mumerous Fllustrations (partly in Colours).
LONDON:
CHARLES GRIFFIN AND COMPANY, Limitep.
PHILADELPHIA : J. B. LIPPINCOTT COMPANY.
1893.
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Vorrede zur 2. englischen Ausgabe.
Die Edition einer 2. englischen Auflage dieses Buches, 2
Jahre nach dem Erscheinen der 1. Auflage, zeigt, dass es dem
Werke gelungen ist, auch in englischen Kreisen sich Freunde zu
erwerben. Indem ich dies mit Genugthuung feststelle, dringt
es mich, den Wunsch hinzufiigen, dass auch diese 2. Edition
bei den englischen Collegen dieselbe giinstige Beurtheilung finden
mége !
Herrn Dr. James Cagney sage ich fiir seine Miihewaltung
besten Dank.
Pror. R. v. JAKSCH.
PRAG, tm Oktober, 1892.
In the Second Edition of this book, as in the First, I have
endeavoured to adhere closely to the German text. The changes
are chiefly of form and arrangement, with here and there others
that have been made after consulting the original authorities. I
am indebted to Prof. v. Jaksch for his cordial co-operation. For
the new matter, which is in every case enclosed within square
brackets, I am alone responsible. It includes, however, a part
of that which was contributed by Prof. Stirling as an Appendix
to the First Edition. I have again to express my acknowledg-
ments to the publishers (Messrs. Griffin) for the assistance which
they have given me in putting the book through the press.
JAMES CAGNEY.
WIMPOLE STREET, November 1892.
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TABLE OF CONTENTS.
CHAPTER I.
THE BLOOD.
I. CoLour of THE BLoop
II. Reaction
III. Sprciric GRAVITY
IV. ae IN THE FORMED eee OF THE Engen
. Oligocythemia
(a. ) Thoma-Zeiss apparatus for counting blood-cor rpuseles
(b.) Gowers’ hemacytometer :
(c.) Bizzozero’s chromocytometer
(d.) V. Fleischl’s hamometer
é.) Hénocque’s heematoscope
(f.) Hedin’s hematocrite
. Leucocytosis
. Leukeemia ‘
. Anemia infantum pseudo- leukzemica
Melanzmia
. Microcytheemia
. Poikilocytosis
. Changes in the formed elements of the blood in chlorosis
! Changes in the formed elements of the blood in pernicious
anemia :
. Changes in the for med elements of the blood with haemorrhage
and the infectious fevers (secondary anzemia)
O ON ANEW YN
=
°
V. THe PaRAsiTEs oF THE BLoop
A, Vegetable Parasites :
Method of examining the blood for micro-organisms
1. Bacillus of anthrax ;
Spirillum of relapsing fever
Bacillus of tubercle
Bacillus of glanders
Bacillus of typhoid fever
Streptococci.
Micro-organisms of the blood in ‘hy drophobia
Bacillus of tetanus : : ;
BL. A ee Parasites Gane
ne oa ,
. Parasites of feran ague .
2. Parasites of quartan ague
. Parasites of acyclical and anomalous forms of ague
i Methods of examining the blood for the parasites
of malaria . : : :
pet Gena
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vili CONTENTS.
a a mes .
. Distoma heamatoninan
2. Filaria sanguinis hominis .
VI. Tue CHEmicaL CHANGES IN THE BLoop
1. Colouring-matter of the blood
1. Blood changes in dyspnoea
Blood changes in carbonic oxide poisoning
Blood changes in poisoning with sulphuretted hydr ogen
Blood changes i in prussic acid poisoning :
. Blood changes in poisoning with chlorate of potash
Blood changes in Dee with nitrobenzol
; Hemoglobinzmia :
Recognition of changes in the colouring- matter of the
blood : : :
. Proteids .
. Urea”. ;
: Dine acid and xanthin substances .
. Uric acid
2. Xanthin bases
. Carbohydrates (melithemia)
I. Grape-sugar
2. Glycogen
Ba: ellulose
. Organic acids (lipacideemvia)
. Lipemia ‘
. Cholemia
. Ureemia .
. Ammonizemia
. Acetonzemia
. Changes in the salts of the blood
CN AW Os
fw N
Wn
N= OW ON O
HOH
CHAPTER IL.
THE BUCCAL SECRETION.
I. Nakep-EyE APPEARANCES OF THE SALIVA
II. MrcroscopicaL APPEARANCES
1. Salivary corpuscles
2. Red blood-corpuscles
3. Epithelium
4. Fungi
III. CuHrmican Consumonton OF THE Bea AL SECRETION
IV. Constitution or MoRBID SALIVA IN GENERAL
V. THE SULPHOCYANIDE OF THE SALIVA
VI. Tuer Sativa In Spectan DIsEASES
1. Catarrhal stomatitis : : :
2. Other forms of stomatitis (mercurial, scorbutic, &c.)
3. Thrush . : , : :
VII. Deposit on TEEtH
VIII. Coatine oF tHE TonNGUE
IX. ee OF THE TONSILS
LU and diphtheritic Poneillitie
. Pharyngomycosis leptothricia
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CONTENTS. 1x
CHAPTER III.
THE NASAL SECRETION.
PAGE
I. Nakep-Eye and MicroscopicaAL CHARACTERS—CHEMICAL Con-
STITUTION : ‘ : : : : . 90
I]. THE SECRETION IN AFFECTIONS OF THE N ASAL ee ITIES, . . 90
CHAPTER IV.
‘THE SPUTUM.
I. NakED-Eyr CHARACTERS OF THE SPUTUM. 4 : : os
Il. MicroscoptcaL EXAMINATION OF THE SPUTUM. ; : . 94
1. White blood-corpuscles . ; 3 ; : : : > Ol
2. Red blood-corpuscles . : : : : ; : od)
3. Epithelium . : : : : : ; 5 : s 15
4. Elastic fibres s : 3 : : ; : Oy
5. Spirals . : ; : ; : : : : OS
6. Fibrinous coagula . : : : ‘ : : , . 100
7. Connective tissue . : 2 : e ; : . 100
8. Corpora amylacea . : ; : ; : : : . 101
9. ee : : : : é J s ; : Lon
. Fungi. : ; ; : : ! LOM
(a.) Non- pathogenic ‘ . : : . oe
1. Moulds : , : : 3 : Loe,
2. Yeasts : : : ; : : > nes)
Bs Sou aes : : ; : : Los)
. Sarcina pulmonis . : : : OR
2. Leptothrix . ; ; : . 103
3. Bacilli and Micrococei : 3 > Koss)
(b.) Pathogenic . : : : : O38}
1. Tuberele-bacillus . : , a 103)
Detection of tuberele-bacillus . . . 104
2. Pneumonia-microbes . : : : PLOT,
3. Actinomyces : : : ! ; OO)
2. Infusoria : ; : 3 : : : A . 109
Vermes . : 2 5 3 z : ‘ : . 10
TO. prea : : : 4 : : . 110
1. Charcot-Ley den cry stals : : ’ : ; . 10
2. Hematoidin crystals. : s : : : ey
3. Cholesterin crystals 2 . : : 5 Serta
4. Fat-crystals (margarine needles) : : : : 5 We)
5. Tyrosin crystals. : : : : : >
6. Oxalate of lime. : } : : ; : Li
7. Triple phosphate . E : } : : : unS
Ill. Carmican EXAMINATION : : ; 3 \ : : ua
1. Proteids and allied substances ; : : : 3 rts
2. Volatile fatty acids es : : : ; 1}
3. Glycogen : 4 ; ; ; : ; ; : . II4
o Ferment é : i : : : : . iid
5. Inorganic constituents : : : : : ; peel)
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CONTENTS.
IV. THr CHARACTER AND CONSTITUTION OF THE SPUTUM IN THE
PrIncrpAL DISEASES OF THE LUNGS AND BRONCHI
MV ee of the bronchi
. Acute bronchitis
. Chronic bronchitis and bronchiectasis
A Putrid bronchitis
4. Plastic bronchitis
2 ee of the lung tissue
. Tuberculosis
(a.) Miliary tuberculosis :
(b.) Acute tubercular infiltration .
(c.) Chronic pulmonary tuberculosis
0 MHI OMNI bv
. Chronic (non-tubercular) inflammation of the lung
. Croupous pneumonia :
. Pulmonary abscess
Gangrene of lung .
. Pulmonary edema
. Hemoptysis .
. Hemorrhagic infarction
. Pneumoconiosis
(a.) Anthracosis of the lung
(b.) Siderosis pulmonum
(c.) Mason’s lung
CHAPTER V.
THE GASTRIC JUICE AND VOMIT.
I. EXAMINATION OF THE GASTRIC JUICE
1. Naked-eye characters
2, Formed elements .
3. To obtain the gastric juice
4. Chemical constituents of the gastric juice
1. Pepsin .
(a.) Detection
(b.) Estimation
. Acids
Q NX
. Milk-curdling ferment ;
(a.) Acidity
(6.) Hydrochloric acid :
Als eee of Free Hydr ochloric cia}
2,
2
. Mohi’s tests
Aniline-dye tests
(a.) Methyl-aniline v iolet reaction
(b.) Tropeolin
(c.) Fuchsin .
(d.) Emerald-green
e.) Congo-red
(f.) Phloro- glucin and vanillin
(q.) Benzo-purpurin :
Uffelmann’s tests
a Ultramarine and zine sulphide :
B. Quantitative Estimation of Free Hydrochloric
Acid : : : :
1. Leo’s method
2. Sjoqvist’s method.
3. V. Jaksch’s modification of Sjoavist’s
method .
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NWNHNNYNNNNNNNNN LN
ODCOONN DADDAUIUN Ss
CONTENTS.
3. Acids (continued)—
B. Quantitative Estimation (continued)—
4. A. Braun’s method
5. Hoffman’s method
C. The Quantity of Hydrochloric “Acid ‘Physiolo i
cally Active in the Gastric Juice, and tts
Diagnostic Import
). Organic Acids of the Gastric Juice
1. Lactic acid
(a.) Qualitative tests
(6.) Quantitative estimation
2. Butyric and acetic acids
(a.) Qualitative tests
(b.) Quantitative estimation
4. Proteids
5. Urea
6. Ammonia.
7. Carbohydrates é
5. Estimation of the rate of absorption of the gastric contents .
6. To determine the contractile activity of the stomach
7. Asummary of the chemical examination of the gastric con-
tents
Il. Tae Inrestinan Jvurce
. Naked-eye characters
. Formed elements .
. To obtain the intestinal juice
4. Chemical constitution of the intestinal j juice
III. ExaMINnavtion oF THE VOMIT
1. Moulds .
2. Yeasts
3. Fission-fungi
Acute gastritis
Chronic gastritis .
Chronic ulcer of the stomach
Carcinoma of the stomach
Dilatation of the stomach
Parasitic affections of the stomach
. Croup and diphtheria .
. Fecal substances in the vomit
Pus :
. Animal parasites :
: Cee of the vomit in poisoning
. Poisoning with acids
(a.) Detection of sulphuric acid .
(b.) Detection of nitric acid
(c.) Detection of oxalic acid
. Poisoning with alkalies .
3. Poisoning with metals and metalloids
(a.) Poisoning with salts of lead .
(b.) Poisoning with salts of mercury
(c.) Poisoning with salts of copper
(d.) Arsenic poisoning :
(e.) Phosphorus poisoning .
4. Poisoning with alkaloids
(a.) Morphia poisoning
(6.) Poisoning with nicotin
(¢.) Poisoning with atropin
(d.) Poisoning with ptomaines and toxalbumins.
wn
OS ORCo SOS Oa
N
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X1l CONTENTS.
. Poisoning with ethylic alcohol
. Poisoning with chloroform
3 Poisoning with carbolic acid .
Poisoning with nitrobenzol and aniline
: Poisoning with prussic acid .
0 ON Dur
CHAPTER VI.
THE FACES.
I. Naxep-EvYE CHARACTERS OF THE Fa&cES .
II. MicroscopicaL CHARACTERS OF THE FACES
1. Constituents derived from the food
(a.) Vegetable cells
(b.) Muscle fibres
(c.) Elastic fibres
(d.) Areolar tissue
(¢.) Fat. :
(f.) Starch granules :
(g.) Coagulated proteids
a Hepacd elements derived from the intestinal tract
. Red blood-corpuscles
2. Leucocytes
3. Epithelium
4. Detritus
3. Parasites f . ;
A, Veg eae Parasites
. Non-pathogenic fungi
1. Moulds
2. Yeasts :
Fission-fungi .
_ Pathogenic fungi
. Cholera-bacillus
2. Bacillus of cholera nostras
Spirillum of cheese
3. Bacillus of typhoid fever
4. Tubercle-bacillus
B. Animal Parasites .
1. Protozoa.
1. Rhizopoda
(a.) Monadines
(b.) Ameeba coli
2. Sporozoa .
Ba Se
. Cercomonas intestinalis
Trichomonas intestinalis .
Paramecium coli
AW NA
. Vermes
Chass i Plntodes
(a.) Cestodes
1. Teenia saginata .
. Teenia solium
. Tenia nana
. Tenia flav opunetata .
. Tenia cucumerina .
. Bothriocephalus latus
OmbwWhy
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3-
CONTENTS.
B. Animal Parasites (continued)—
Crass I. Platodes (continwed)—
(b.) Trematodes :
1. Distoma hepaticum :
2. Distoma lanceolatum
3. Distoma Rathonisi
ie II. Annelides
. Order Nematodes qommce w Bre
(a.) eons Ascarides
_ Ascaris lumbricoides
2. Ascaris mystax
3. Oxyuris vermicularis
(f.) Family Strongylides.
Anchylostoma duodenale
(y.) Family Trichotrachelides
1. Trichocephalus dispar
2. Trichina spiralis
(6.) Rhabdonema strongyloides
Insects .
4. Crystals
4
OO SYDNEY H
. Charcot- Mevden eee
Heematoidin crystals
Cholesterin
Fat crystals
Oxalate of lime
Carbonate of lime .
. Sulphate of calcium
. Phosphate of lime .
. Triple phosphate .
. Sulphide of bismuth crystals
I1I. CurmicaL EXAMINATION OF THE FacEs
A. Organic Substances
4
Il.
12.
113}:
ODM W YN A
90 ON
. Mucin
. Albumin
. Peptone
Urea
. Carbohydr ates
Acids
(a.) Bile acids.
(B.) Volatile fatty acids
Phenol . ; ;
. Indol and skatol .
. Cholesterin, fats, and non- volatile « organic acids
] Sepa as matters ;
_ Urobilin.
. Blood colouring- matter
Bile pigment .
Taegan gases
Ptomaines
Ferments
B. Inorganic Substances
IV. EXAMINATION OF THE MECONIUM .
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xiv CONTENTS.
YV. CHARACTER OF THE FXCES IN CERTAIN INTESTINAL AFFECTIONS .
. Acute intestinal catarrh
. Chronic intestinal catarrh
Ulcerative enteritis
Typhoid fever
. Dysentery
Cholera
Hemorrhagic stools
. Acholic stools
COI DEW NA
CHAPTER VII.
EXAMINATION OF THE URINE.
I. Nakep-Eyr InspEcTION OF THE URINE
Quantity
Specific gravity
Colour .
Reaction
BYP om
IJ. MicroscoricaL EXAMINATION OF THE URINE
. Cellular constituents (organised sediments) of ihe urine
1. Red blood-corpuscles :
. Leucocytes
. Epithelium
Casts
. Spermatozoa . :
. Fragments of tumours
: pe
1. Fungi
(a.) Non- pathogenic
(b.) Pathogenic
. Infusoria
. Vermes .
1. Distoma haematobium
2. Filaria sanguinis hominis
3. Echinococci
4. Eustrongylus gigas
5. Ascarides
. Crystalline and amorphous deposits (ongiganisell rekmeney
A, Sediments from Acid Urine
(a.) Be ystalline deposits
. Uric acid.
Oxalate of lime
Bilirubin and hematoidin
. Triple phosphate :
Basic phosphate of magnesia
Neutral phosphate of lime
Calcium sulphate
. Hippuric acid .
. Cystin
Xanthin . :
. Tyrosin and leucin .
. Soaps of lime and magnesia
NAW ON
GN
a
PASO SY OMEY YS
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G2 Ga Ga G2 G2 G2 G2 G2 Go Ga G Od Ga NY
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CONTENTS.
(b.) Amorphous deposits
Urates
_ Oxalate of lime
. Calcium sulphate
. Brown and yellow concretions
eel atiee
4
WEN
B. Seuirnents from Alkaline Urine.
(a.) Crystalline deposits
. Triple ee
. Indigo :
: Urate of ammonia
. Phosphate of Aenea
. Cholesterin
m
wWeEwWhd
>
(b.) Amorphous deposits
. Urate of ammonia .
. Basic phosphatic earths
. Carbonates of the alkaline earths
. Carbonate of lime
. Indigo
WMEwnN
3. Urinary pemore ore ,
4. Foreign bodies in the urine .
III. CaHremican EXAMINATION OF THE URINE
A, Organic Substances
I. eects
. Albuminuria .
(a.) Renal albuminuria
(b.) Accidental albuminuria
Determination of albumin (serum- albumin) .
(a.) Detection ; :
(B.) Estimation .
Peptonuria :
. Albumosuria .
Globulinuria .
Fibrinuria
. Heematuria
. Hemoglobinuria
. Mucinuria
ON ANEW N
2. Carbohydrates
Aun &
21s cosuria
a.) Physiological glycosuria
(>) Pathological glycosuria
(a.) Transitory glycosuria
(.) Persistent glycosuria ;
Determination of grape-sugar
(a.) Detection ;
(B.) Estimation .
Leevulosuria :
Lactosuria
Dextrin .
Animal gum
. Choluria
. Urobilinuria .
Heemato-porphyrinuria .
. Ather-sulphuric acids and their derivatives (indigo- blue,
skatol, phenol, parakresol, pyrocatechin, hydro-
chinon) and the aromatic oxyacids :
Ph
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Xvl
ae
8.
9.
Io.
Il.
12.
13.
14.
15.
16.
Nei
18.
19.
20.
Que
CONTENTS.
(a.) Indicanuria . :
Detection of indican .
Estimation
(b.) Skatoxyl-sulphuric atid :
(c.) Parakresol-, phenol-zther sulphuric acid
Detection of ether-sulphuric acids
Estimation of eether-sulphuric acids .
Estimation of phenols 3
(d.) Pyrocatechin .
(e.) Hydrochinon . f
(f.) The aromatic oxyacids .
Detection .
Estimation
Alkaptonuria
Inosituria
Melanuria
Acetonuria
Diaceturia
Lipaciduria
Lipuria .
Chyluria
Oxaluria
Cystinuria
Uric acid diathesis
Urea
Kreatinin
Ptomaines (putrefaction bases)
Ferments of the urine
B. Inorganic Substances
=
ON Qu BW WV
. Chlorides
. Sulphates
. Phosphates
. Carbonates
_ Nitrates and nitrites
. Sulphuretted hydrogen (hy drothionuria)
. Peroxide of hy: drogen é
. Gases of the urine .
IV. CHARACTERS OF THE URINE IN DISEASE
. The urine in febrile states d
‘The urine in disorders of the circulation (congestion) :
3. The urine in diseases of the urinary organs .
1. Renal affections
Vor Ey yp
(a.) Acute nephritis
(b.) Chronic nephritis
(c.) Contracted kidney
(d.) Amyloid kidney
(e.) Ureemia
Pyelitis calculosa .
Cystitis .
Tuberculosis of urinary organs
. Calculus and tumours of the bladdex
Catarrhal urethritis
. Gonorrheeal urethritis
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G2 Go
ae
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WOW OOOIWO YN NWN
OWND HHH OUO
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CONTENTS. xvii
PAGE
4. The urine in diseases of the alimentary canal : meses
5. The urine in hepatic affections . : : : ; . 335
6. The urine in diabetes mellitus. : : : j £336
7. The urine in diabetes insipidus . : : : : Peso 7
8. The urine in anemia . : : : ; 3 7.
g. The urine of toxic states 2 : : } y esgo
1. Poisoning with acids. , : : : : . 338
Dp Poisoning with alkalies . : : F : Esso
3. Poisoning with metals and metalloids . : ; . 338
(a.) Lead salts. : : : A : : . 338
(b.) Salts of mercury . 3 ; : : : . 338
(c.) Salts of copper. : é : ; : » 339
(d.) Arsenic : : ; : p ; : . 340
(¢.)) Phosphorus . : ; : s i ; . 340
4. Poisoning with alkaloids : : ! ; é 340
5. Poisoning with ethylic alcohol . : : : . 341
6. Poisoning with chloroform , : : ; : . 341
7. Poisoning with carbolic acid . : : . 341
8. Poisoning with nitro-benzol and aniline : é - 342
9. Poisoning with carbonic oxide gas : : . 342
VY. Tae Detection or Certain DRUGS IN THE URINE. ; - 343
1. Iodoform and salts of iodine and bromine . : : . 343
2. Salicylates . 343
3. Quinine, kairin, antipyrin, thallin, antifebrin, and phenacetin 344
4. Chrysophanic acid : : : : ; « 345
5. Santonin ; : : : : 3 ; : - 346
6, Tannin. : : : . : : 4 2 : . 346
7. Naphthalin . : : : : : : y ‘ . 346
8. Copaiba balsam. : : : : ; : s . 346
CHAPTER VIII.
INVESTIGATION OF EXUDATIONS, TRANSUDATIONS,
AND CYSTIC FLUIDS.
A. Exudations . bhi : : : : ; : : meg 47,
1. Purulent exudations ; : : : : 3 5 aly
I. Naxep-Eye APPEARANCES . : : 3 A aed7,
II. MrcroscoricAL CHARACTERS : » 348
. White and red blood- sree id ee eliiren . 348
5, Fungi. : : : : : ; . 348
I. ‘Mieroeocei : : : : : : . 348
2. Tubercle-bacillus . : ; : ; - 349
3. Bacillus of syphilis . : : ’ : - 349
4. Actinomyces . : 2 : é ess
5. Bacillus of glanders ; : : ; ees 5
6. Bacillus of anthrax . : : : : 5a
7. Bacillus of leprosy . : . : : Begs
8. Bacillus of tetanus . ; : : : 55
g. Bacillus of influenza ; : . : . 356
b
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XVIil CONTENTS.
3. Protozoa
4. Vermes .
5. rae :
. Cholesterin er ystals
2. Heematoidin
3. Fat needles
4. Triple phosphate cr ystals
III. CapmicaLt ExaMINATION OF Pus
Sero-purulent exudations
Putrid exudations
Hemorrhagic exudations
Serous exudations
Chylous exudations
DALEY
B. Transudations
C. Contents of Cysts .
1. Hydatid cysts
2. Ovarian cysts
3. Cystic kidney
4. Pancreatic cysts
D. Secretions from Fistule
CHAPTER IX.
THE SECRETIONS OF THE GENITAL ORGANS.
I. Tue Seminan Fivuip
1: Naked-eye appearances of fhe semen
2, Microscopical examination of the semen
3. Chemical examination of the semen
II. SkcRETIONS OF THE SEXUAL ORGANS OF THE FEMALE .
1. Mammary secretion (the milk)
2. Vaginal secretion . ‘
3. The uterine secretions .
1. Menstruation
2. The lochia
CHAPTER X.
METHODS OF BACTERIOLOGICAL RESEARCH.
I. Tur Microscope . : F
IJ. Tort Detection or Micro- Ones ISMS
III, Cuntivation or Micro-OrRGANISMS
A. Methods of Sterilisation
Sterilisation of instruments, fluids, and nutrient substances
B. Nutrient Substances :
1. Nutrient fluids
2. Solid nutrient substances
1. Blood serum .
2. R. Koch’s nutrient gelatine
3. Agar-agar
4. Potato
Stained nutrient substances
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CONTENTS.
C. Preparation of Koch’s Pure Cultivations
1. Plate cultivations .
2. Cultivation by deep inoculation
3. Cultivations on glass slides .
4. Cultivations in hanging drops
5. Cultivation by exclusion of air
IV. THE TRANSMISSION oF PuRE CULTIVATIONS TO ANIMALS
(a.) By the lungs
(6.) In the food .
(c.) By cutaneous inoculation
(d.) By subcutaneous inoculation and injection.
Y. ScHEME OF A BACTERIOLOGICAL INVESTIGATION
BIBLIOGRAPHY
INDEX
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385
388
388
388
388
389
389
389
389
389
599
301
441
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I
I
I
I
I
I
I
2
2
2
LIST OF ILLUSTRATIONS.
IG.
1. Blood-plates from normal blood
2, Capillary tube :
3-5. Thoma-Zeiss apparatus for eames cea caramels
5 Gowers’ apparatus
7-10. Bizzozero’s chromo- eytometer
I. Von Fleischl’s hemometer
2-14. Hénocque’s hematoscope
5. Hedin’s hematocrite
6. Leukemic blood
7. Eosinophil cells . :
8. Blood in anemia infantum faeeude: Henleemien :
9. Melanzmic blood
0. Poikilocytosis
1. Blood in neGiee nee
2. Anthrax-bacilli from rabbit’s iricedl
23. Anthrax-bacilli from human blood
24. Spirilla of relapsing fever (Koch)
25. Tubercle-bacilli in blood
26. Bacilli of glanders in human blood :
27, 28, 29. Parasite of tertian ague (Golgi and others)
30. Parasite of quartan ague ((olg?)
31. Parasites of acyclical intermittent fever (C ella and Man One tn)
32. Parasites in Roman fever (Celli and Guarnieri)
33, 34. Blood in tertian ague
35. Distoma hematobium
2
36. Filaria sanguinis hominis lens Brol Lonckari)
37. Spectrum of oxyhemoglobin
38. Spectrum of reduced hemoglobin
39. Spectrum of hematin in alkaline solution
40. Spectrum of reduced hematin .
41. Teichmann’s hemin crystals
42. Spectrum of methemoglobin ;
43. Spectrum of carbonic oxide hemoglobin .
44. Hering’s spectroscope
45. Buccal secretion
46. Saliva of thrush
47. Leptothrix buccalis
48. Nasal mucus : F
5
5
49. Epithelium, recone nna poole of he eaten
o. Elastic fibres in the sputum
I, 52. Spirals from the sputum
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51; 52
54, 56
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30
34
35
36
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43
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47
52
2
53
58
59
60
60
60
61,
61
62
63,
66.
80,
85
86
go
95.
97
98, 99
XXI1 LIST OF ILLUSTRATIONS.
rma, PAGE
53, 54. Fibrinous coagula from a case of pneumonia . i : ; . 100
55. Fibrinous coagula from a case of plastic bronchitis . ‘ : . 101
56, 57. Moulds from the sputum in pulmonary abscess : : ; . 102
58. Tubercle-bacilli from sputum . : : : : ; : ‘ . 106
59. Tubercle-bacilli, stained . : : : : : : : : . 108
60. Pneumonia-cocci . : : : . 108
61. Echinococcus hooklets dl mombratie of hydatid an ; , : . 109
62. Charcot-Leyden crystals . : : ; : : ‘ : : LLL
63. Microbe of pneumonia . : : : : ; . : : . 120
64. Collective view of vomited matter . : : 5 : : . 145
65. Mucous cylinder from feces . : 4 ‘ : ; ; : . 165
66. Collective view of the feces . : : : : : ; ‘ LOT,
67. Degenerated intestinal epithelium . ; : 2 ; : ; . 168
68. Bacilli from the feces. . . : ely 2
69. Nothnagel’s clostridia and stunted bacilli ‘ow the core : : 72)
70. Koch’s comma-bacillus . : ° : : ; ‘ : 74:
71. Finkler-Prior bacillus of cholera SORES, ; 3 : : : Eel 7i7)
72. Bacilliof typhoid . : ; j ‘ : : : , lS)
73. Organisms in stools. : ; : : ; : , ; : . 180
74. Cercomonads from the stools . s : : : ‘ ; ; . 181
75. Tenia saginata . ‘ : : 4 é 5 : , : aS
76. Tenia solium . : 5 , : : : : : : : ELS
77. Tenianana . 2 : : ; : : ; : : ; . 184
78. Tenia cucumerina . 3 j : : : 3 ; , : . 185
79. Bothriocephalus latus. : ; 2 3 : : : ; . 186
80. Distoma hepaticum : : : ; : ; : : : Sy,
81. Distoma lanceolatum . : ‘ : e : : : : . 188
82. Ascaris lumbricoides : : : : : : : 3 : . 189
83. Ascaris mystax : : : : : : : : : ; . 189
84. Oxyuris vermicularis . , : ; : : ; : : - 190
85. Anchylostoma duodenale . : : : ; : : F . 191
86. Trichocephalus dispar. : ’ ; ; : 2 : : . 192
87. Trichine . : : : : : , : : : ; . 193
88. Anguillula perce : : ; : : ; : : . . 194
89. Hematoidin crystals 7 : : ; ; : ; : 5 . 196
go. Acholic stools : : : ; , : : : ‘ . 196
gt. Sulphide of bismuth erates i 7 . 3 : ! : : . 198
92. Stenbeck’s sedimentator . : : ; c ; : : 3 . 218
93. Urinary epithelium . ; : : : 3 ; ; ; : 222,
94. Cast of urates . ; : : . : I : : : : 225
95. Epithelium cast e : 3 3 : : : : : . 226
96. Cast of shrunken blood- Corpuecles ; : : : : : i . 226
97. Cast formed of leucocytes 5 4 : 6 5 A ‘ . 226
98. Casts formed of leucocytes and Serene ; ; : : : . 226
gg. Granular cast in chronic nephritis . ; : ; . : . Suez 277)
1oo. Granular cast in acute nephritis . A A : ; , 5 . 227
1o1. Granular cast in chronic nephritis : 4 : 3 , ; . 228
102. Waxy casts. : : 5 : : : : : : 5 . 229
103. Granular and fatty casts : ; ; : : : : : . 230
104. Hyaline casts . ; : ; ; : ¢ : I A é . 230
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105.
106.
107.
108.
109.
110.
III.
112.
113.
114.
ne
116.
117.
118.
119.
. Soaps of lime and magnesia
121.
122.
T2e5
124.
1255
126.
127.
128.
129.
130.
131.
1ig2)
Tee.
134.
135.
136.
137.
138.
139.
140.
I4l.
142.
143.
144.
145.
146.
147.
148.
149.
LIST OF ILLUSTRATIONS.
Cylindroids from the urine
Micrococcus ures :
Sediment from fermenting diabetrd urine
Tubercle-bacilli from urinary sediment .
Distoma hematobium in sediment . :
Uric acid crystals from urine in congestion from sinphysema
Uric acid crystals from urine in congestion from heart-disease
Oxalates of urine from sediment in cystitis and pyelonephritis
Triple phosphate crystals from the sediment in chlorosis
Basic phosphate of magnesia .
Neutral phosphate of lime from the urine of liner meatinaits
Calcium sulphate
Crystals of hippuric acid :
Crystals after the use of benzoic acid in a case of Fhonmation
Tyrosin, leucin, and cystin
Triple phosphate crystals
Indigo crystals
Urate of ammonia
Cholesterin crystals
Carbonate of lime
Esbach’s albuminimeter .
Phenyl-glucosazon crystals
Flask for estimation of sugar by fermentation
Lippich’s polarimeter ; ,
Spectrum of urobilin in acid urine
Spectrum of urobilin in alkaline urine
Ludwig’s filter
Hiifner’s apparatus
Gonococci of urethritis
Gonococci (two days after infection)
Cocci from an empyema
Actinomyces granules
Actinomyces from pleural cavity
Actinomyces from peritoneum
Preparation from same case as last, cei
Bacillus of tetanus .
Pus from putrid empyema
Contents of an ovarian cyst
Microscopical appearance of human semen
Colostrum , , 0 : . : : , 0
Vaginal secretion in cancer
Microscope (made by Reichert)
Abbe’s condenser 4
The same, showing the collecting Pen of fentes
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CIA DEIR I,
THE BLOOD.
Every change in the quantity or the quality of the blood itself is apt to
be attended with serious disturbance of the system; further, the blood is
the carrier and distributer through the body of nearly all the poisons,
organic and inorganic, which act upon the latter. From this it follows
that the physiology and pathology of the blood represent a mass of
knowledge, at once immense and various. It is not our purpose, here,
however, to treat these subjects exhaustively, but merely to select from
them certain well-established facts which bear upon disease, and to point
out the way in which they may help in its diagnosis.
I. COLOUR.—Arterial and venous blood differ considerably as to
colour in health, the former being scarlet, and the latter a bluish red.
The distinction, however, belongs not to the fluid part of the blood, or
plasma, but to the colouring-matter, or hemoglobin, contained in the
red corpuscles, and it depends upon the chemical constitution of the
corpuscles, which, changing colour themselves, determine the tint of the
whole mass of the blood.
Thus, when the blood is rich in oxygen, the amount of hemoglobin
is increased, and the fluid is proportionately bright red. Again, where,
as is always the case with venous blood, oxygen is deficient, or where,
from physiological or pathological causes, arterial blood contains but
little oxyhemoglobin, the colour is darker, and this in a degree corre-
sponding to the condition which underlies it. In certain morbid states,
however, the blood may assume a brighter tint than that of healthy
arterial blood. In carbonic oxide poisoning, for instance, it is of a
bright cherry colour (see p. 63). [Venous blood, which appears dark
red by reflected light, is green by transmitted light. It is therefore
said to be dichroic. Arterial blood is monochroic.1]* The blood which
is taken from the finger for the purpose of microscopical examination by
means of a slight puncture is usually venous in character.
* The Numbers refer to the Bibliography at the end of the volume.
A
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dS
THE BLOOD.
Il. THE REACTION of healthy blood, like that of nearly all the
tissue fluids, is alkaline. [It is due to the presence of disodic phos-
phate, Na,HPO,, and bicarbonate of soda.] Still, this reaction is lable
to considerable variation under certain conditions of health as well as
in disease.
The alkalinity of the blood diminishes when it has been with-
drawn from the influence of living blood-vessels. Hence we find
that an acid reaction is one of the phenomena of coagulation, and
that this becomes more pronounced the longer the blood is allowed
to stand. [The change depends upon the formation of an acid derived,
probably, from the decomposition of the colouring-matter of the red
corpuscles. |
To test the reaction of the blood, Liebreich ? employs plates of plaster
of Paris or clay soaked in neutral litmus solution. A few drops of the
blood to be examined are placed upon this, and washed off again with
water.* If the blood was alkaline, the spot upon which it has fallen
exhibits a blue, but if acid, a red colour.
For the same purpose Zuntz® uses glazed litmus paper soaked in a
solution of common salt or sulphate of soda; this he dips several times
in the blood to be tested, and again washes in the salt solution. The
same thing may be done by allowing a drop of the blood to fall on the
litmus paper, and then quickly washing it off again, as in Liebreich’s
method.
For the comparative estimation of the alkalinity of the blood in
animals, Lassar* has devised a process, which, however, cannot be
applied to the case of human beings, where the requisite quantity of
blood is not available. On the other hand, the plan which Landois°
recommends is very suitable for clinical purposes.
The author has obtained useful results in a large series of observations
by proceeding according to the following method (a modification of that
of Landois), for the quantitative estimation of the alkalinity of the
blood :—
A mixture is made of a concentrated solution of sulphate of soda with
1/100 and 1/tooo normal solution of tartaric acid (I.) in various propor-
tions ; and in this way a series of test-fluids is obtained, the members
of which contain varying quantities of acid to the cubic centimetre. +
* [The reaction of the blood with ordinary litmus paper is obscured by the red
colour of the fluid, and the various expedients for its determination are directed to
overcome this difficulty.]
+ The fluids are prepared thus: 7.5 grms. of pure tartaric acid are dissolved
in a litre of water, and a normal solution (1/10 of the acid) results. By appro-
priate dilution of this, the other normal solutions (1/100 and 1/1000) may be
obtained.®
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DETERMINATION OF ALKALINITY. 3
Experience shows that eighteen such test-solutions of varying acidity
are needed. And of these :—
I. contains in 1 ce, 0.9 ce, of 1/100 normal solution of acid and o.1 ce.
a
. °
Wit, 5 inI cc. 0,8cc. of 1/100 _,, ae of 02, /3 4
and so on, 23
- 2 n
IX, “3 in Ice, 0.1 cc, of 1/100 ——4, 2 a 99 | oH
dG 35 in I ce. 0.9 ce, of 1/1000 ,, ie ” oI ,, 2 2
and so on, Se
> , f a
XIV. SS in I cc. 0.5 ce. of 1/1000 ,, 5 “4 ONG 3 =
and so on, gn
XVIII. 7 in I ce. 0.1 ce, of 1/1000 ,, a - 0.9) 55 =
The experiment is conducted in the following manner :—The proper
quantities of the acid and sulphate of soda solutions are placed in a
series of watch-glasses, by means of a pipette graduated in o.1 cc.,*
and a number of strips of very sensitive blue and red litmus paper are
prepared. The blood is usually taken by means of cupping-glasses from
the patient’s back, and before it coagulates, 0.1 ce. of the blood is added
to each ec. of the fluids described above, well mixed in each case, and the
resulting mixtures tested with the litmus papers until one is found to
exhibit a neutral reaction, 7.2, leaving the red and blue litmus paper
unchanged. This will show what quantity of the acid is required to
neutralise o.1 cc. of the blood in question. In order to arrive at an
accurate result, it is necessary to proceed very quickly, and as a rule it
may be laid down that not more than 14 minutes should be allowed to
elapse between the taking of the blood and the conclusion of the experi-
ment, having regard to the rapid diminution of alkalinity after the blood
is withdrawn from the living vessels.
For the sake of clearness the following example may be taken :—
In the case of a man who suffered from tuberculosis and tabes dorsalis, it was
found that 0.4 cc. of 1/100 normal tartaric acid solution was required to neutralise
0.1 cc. of blood.
1 cc. of 1/100 normal solution of the acid corresponds to 0.0004 grm. NaOH.
OI » 95 ” c6 mi 0.00004 ,, 5
0.4 " in 68 9 » 0.00016 ,, 3
The alkalinity of the blood may, therefore, be expressed by 0.00016 grm. NaOH
for 0.1 cc., or .160 grm. NaOH for 100 ce.
Haycraft and Williamson’s Method.
[The method recently introduced by Haycraft and Williamson’ is very suitable
for clinical purposes, since by its means the alkalinity of the blood may be deter-
mined quantitatively from a single drop of the fluid.
A number of red litmus papers is prepared, containing varying quantities of
oxalic or some other acid. One of these is such as is found by experiment barely
to give a reaction with normal blood, and this is made the basis of a series of test
* For this purpose also the automatic pipettes (see p. 19) containing 0.1 cc. will
serve yery well.
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4 THE BLOOD.
papers answering to different degrees of alkalinity. The strength of each is esti-
mated by means of a solution of caustic potash of known concentration. The
papers are glazed, and dipped for a second or two in liquid paraftin and then
dried. In conducting the experiment a drop of blood is drawn from the finger
(previously well cleansed) and placed upon a paper of medium strength. There
it is allowed to rest for ten seconds. Sufficient of the plasma has then soaked in.
The blood is washed off, and the reaction, if any, is at once apparent. Should
this be so, a paper containing more acid is employed ; but if there be no reaction,
a weaker oneis taken. Suppose, now, it is found that the blood will give a reac-
tion with the sixth and not with the seventh paper, the former is then taken as
the expression of its alkalinity. But it is known that an = solution of an alkali
will give the same reaction, therefore the alkalinity of the blood will be =
“‘This is perhaps not absolutely true, for probably the blood plasma does not
percolate so readily into the litmus paper as does a watery solution of an alkali.
In this case, however, the error will be uniform,” and will not vitiate the con-
clusion in a series of comparative investigations. *]
It is true, as H. Meyer ® has shown, that the results to be obtained in
this way are open to error. This, indeed, we should expect, since the
final reaction varies in each specimen with the colour of the blood and
the quantity of CO, which it contains. The method has been described
here, faulty and unsatisfactory as it is, because by means of it certain
information has been obtained as to the character of the blood in
disease.?
The author’s experiments! have led him to the conclusion that the
alkalinity of 100 cc. of healthy human blood corresponds to 260-300
mgrms. of NaOH. Canard, who adopts a similar method, gives the
equivalent as 203-276 mgrms. NaOH ; while Mya and Tassinari,!2 from
experiments upon blood drawn from the veins, quote very much higher
figures (516 mgrms.) The alkalinity of the blood is often diminished
in fever. The author has invariably found it reduced considerably in
uremia, as well as in certain toxic states, as carbonic oxide poisoning.
[It is also reduced in persistent vomiting.] In organic disease of the
liver, leukemia, pernicious anemia, and diabetes, the author has found
such a diminution as was capable of being expressed in figures, and in
this (the condition of the blood in chlorosis alone excepted) he is borne
out by the researches of Girdber.15 His conclusions have also been con-
firmed by Pedper 14 and Rumpf. The results obtained by Kraus 16 with
another method are substantially the same. AJemperer!” has proceeded
also on the principle of estimating the proportion of CO,. He has found
that the diminished alkalinity of the blood in fever is not affected by
* [I am indebted to the courtesy of Dr. J. B. Haycraft for a personal communica-
tion on the subject discussed in the text. He informs me that he has already derived
important clinical inferences from the application of his method. By means of it he
has ascertained that the reaction of the blood in different conditions may vary as
widely as that of the urine.—(ED.)]
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SPECIFIC GRAVITY OF THE BLOOD. 5
the administration of anti-pyretic remedies. Cantani 8 is of opinion
that the blood in cholera may exhibit an acid reaction even during life.
Kraus’ Method.
The blood is taken by a lancet, and its content of carbonic acid determined by
weighing. This method is probably accurate ; but from the quantity of blood
which it demands, and the inexpediency of employing the lancet for clinical pur-
poses, it is not to be preferred to the other methods, which in general have yielded
the same results.
III. SPECIFIC GRAVITY OF THE BLOOD.—The specific gravity
of healthy human blood has been stated at 1.045-1.075 by Landois,!
and 1.035-1.068 by Lloyd Jones.2° It is usually lower in women than
in men; and the last-mentioned authority has shown that it is highest
at birth, falls gradually during the first few years of life, and reaches
its lowest point in man at 35-45 years of age. [It is diminished by
hunger, in pregnancy, by the ingestion of solid or liquid food, or by
gentle exercise.?1]
To estimate the specific gravity of the blood, Roy's method may be
adopted. ' This requires a series of test-tubes, holding a mixture of
glycerine and water in different proportions, so that the sp. gr. of these
shall range between 1.040 and 1.080. The test-tubes should have a
diameter of 4 cm. and should hold from 80-100 ce.
The proceeding is as follows :**—A drop of blood is drawn from the
finger by pricking it with an aseptic needle ; a capillary tube of glass,
bent at a right angle, and connected by a caoutchouc tube with the nozzle
of a Pravaz syringe is now taken, and the free pointed end of the tube is
placed in the centre of the exuding blood, some of which is drawn into
the tube by a slight movement of the piston. By gentle pressure on the
piston of the syringe a drop of blood is expelled into the middle of the
fluid in one of the test-tubes. There the blood will rise or sink according
to the density of the glycerine mixture, and successive trials are made
until a fluid is found in which the blood remains suspended. The
density of this fluid is that of the blood. The glycerine mixtures may
be preserved for future use by the addition of a little thymol, but their
sp. gr. must be verified before each investigation. [English observers
generally dispense with the syringe and employ the right-angled glass-
tube, which is pointed at one extremity and expanded at the other, where
it is closed by a caoutchouc cap, and by means of this the blood is drawn
in and again expressed in the test fluid. For purposes of comparison
the blood should be examined in the morning, and always at the same
hour, since Lloyd Jones®* has shown that its sp. gr. undergoes diurnal
variations, dependent probably upon the ingestion of food. Again, in
removing the blood for examination, it is important to avoid pressure on
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6 THE BLOOD.
the part from which blood is withdrawn (as by squeezing, or the applica-
tion of a ligature), since the sp. gr. is altered by such expedients. }
Hammerschiag’s?* method, and that of Schmaltz?® and Peiper,?® who
make use of a capillary pycnometer, seem to have no advantage over
that described here.
[Instead of glycerine Landois employs solutions of sulphate of soda
for the test fluids. The process is in other respects the same as Roy’s.””
Monckton Copeman?’ and Sherrington have investigated the sp. gr. of
the blood by a method founded on that of Roy. To prevent decomposi-
tion of the test fluids and consequent change in their density they are
derived from a stock fluid of glycerine and water saturated with boro-
elyceride and sulphate of magnesium, with a small quantity—1 in 1000
—of corrosive sublimate. Such a fluid will remain serviceable for more
than three years.] (See note on p. 78.)
Examination of the blood in the author’s clinic has shown that
intestinal hemorrhage, severe anemia, and prostration, are attended
with a fall in specific gravity. Siegl and Schmaltz have found that the
specific gravity varies with the proportion of hemoglobin, but not with
the total number of cellular elements. Hence it follows that a diminu-
tion in the number of red corpuscles may be inferred from a fall in
sp. gr., and the comparatively easy investigation of the latter may be
made in practice to replace the estimation of hemoglobin, which can be
effected only by the use of costly instruments.
IV. CHANGES IN THE FORMED ELEMENTS OF THE BLOOD.—
The blood contains red and white corpuscles, and recent observations
(Bizzozero) have shown the presence in it of a third class of formed
elements,—the blood-tablets (or blood-plates). The existence of these
bodies is now beyond dispute. To make them apparent in fresh blood,
it is necessary to fix the latter by the addition of some preserving fluid,
such as Hayem’s * solution, when it may be examined directly with an
oil-immersion lens and a narrow diaphragm.
The constitution of Hayen’s solution is as follows :—
1 grm. of chloride of sodium, 5 grms. of sodic sulphate, 0.5 germ. corrosive
sublimate, and 200 grms. distilled water.
The preparation will then show the bodies in question as minute
objects with a diameter less than half that of the red blood-corpuscles,
scattered singly, or in groups in the field. In the present state of our
knowledge, they possess no diagnostic importance. [They are supposed
to be most abundantly present in the blood of persons suffering from
chronic diseases ; and are said to increase in number during pregnancy
(Halla), in conditions of regeneration (Afanassiew), in febrile anemia
(Fusari), and to diminish in fever.?°]
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OLIGOCYTHAMIA. a
The physiology of the red and white blood-corpuscles is sufficiently
set forth in the Text-books of that science.
Pathologically, the corpuscles exhibit changes as to quantity and
character which are of the utmost importance in diagnosis. These
changes seldom occur separately, but are usually combinéd,—although
alterations of the structwre of the corpuscles may be more pronounced
in some cases, of their number in others. We shall consider :
1. The diminution in the number of the cellular elements of the
blood (oligocythcemia).
2. The increase in the number of the cellular constituents. An
absolute increase of this kind has not yet been proved to occur, but
a relative preponderance of white corpuscles is often met with. This
happens normally during digestion (physiological leucocytosis),—as a
Fia. 1.—Blood-plates from normal blood. (The blood had been fixed with Hayem’s solution.
Eye-piece III, objective Zeiss j,, homogeneous immersion).
transient phenomenon in a number of morbid states (pathological leu-
cocytosis), and as a persistent condition (/eukwmia).
3. Changes in the form of the blood-corpuscles (potkilocytosis, micro-
cythemia).
1. Oligocythemia.—Vierordt has computed that in health the
number of red blood-corpuscles is five millions in a man, and 44 millions
in a woman to the cubic millimetre of blood.* °° In disease the number
may diminish temporarily or permanently to two millions, or even sink
as low as 360,000 per cubic millimetre. Such a condition may occur as
a consequence of hemorrhage, whether of a traumatic origin, or due to
morbid changes in the blood-vessels, as when intestinal bleeding takes
place in typhoid fever. As a permanent state, it may be a phenomenon
of any disease which is attended with deficient regeneration of the blood.
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8 THE BLOOD.
[The number of the red corpuscles is lessened in chronic lead-poison-
ing, miasmatic conditions, and in syphilis. ]
Diagnosis of Oligocythemia.—The methods and apparatus employed
by physiologists to estimate a diminution of the red blood-corpuscles are
very many ; but of these a large number are useless for clinical purposes,
inasmuch as they require too great quantities of blood to work upon.
The apparatus which will serve our purpose is of two classes. One
is used to count the actual number of blood-corpuscles in a specimen
of blood ; the other, by estimating the quantity of hemoglobin present,
enables us to draw an inference as to changes in the blood. Both
methods have their advantages and supplement each other, since a
diminution in the hemoglobin is usually proportionate to a diminution
in the red corpuscles; thus, oligochromemia and oligocythemia mostly
occur together. Quite recently also, it has been found possible to take
account of the bulk of the red corpuscles (see p. 25), a point of some
value clinically.
When the oligocythemia is very pronounced, a glance through the
microscope will suffice to recognise it; and so with oldgochromemia—
diminution of hemoglobin—a little practice will enable us to detect it
by a simple examination of the blood in a very thin layer without the
addition of any fluid. To effect this, the end of the finger should be
washed in plain water, and pricked, and the first drops of blood allowed
to flow off. A glass slide should then be allowed to touch the summit
of the drop of blood on the skin without coming in contact with the
finger, quickly withdrawn, and a cover-glass placed over it.
In this way such impurities as epithelium, &c., are avoided.
The use of carbolic acid, ether, or alcohol, to wash the skin, is not to be
recommended, since these bodies are likely to produce changes in the appearance
of the corpuscles. When the object of the examination is the detection of micro-
organisms in the blood, the utmost care must be taken in cleansing the skin (see
p. 40).
Proceeding in this way in a case of oligocythemia, when the slide
is placed under the microscope, a marked diminution in the number of
blood-corpuscles will be noticed. The red corpuscles will also in most
cases be paler than normal ; their usual bi-concave shape less marked ;
they are somewhat flattened, and they tend less to run into rouleaux or
assume stellate forms. At the same time, they may be seen to have
undergone peculiar changes of shape (potkzlocytosis).
For many purposes it is well to fix the blood with some preserving
fluid before examination. A solution of common salt (0.8-1.0 per
cent.) or of sulphate of magnesium (5 per cent.) may be used (Gidiber).
Hayem’s or Pacini’s solution may be employed. Hayem’s has been
already described.
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ENUMERATION OF BLOOD-CORPUSCLES. 9
Pacini's solution is prepared thus :—A mixture is made of 1 part corrosive sub-
limate, 2 parts common salt, 13 parts glycerine, and 113 parts distilled water, and
the fluid is allowed to stand for at least two months. When about to be used, a
portion is diluted with three times its bulk of distilled water, and filtered through
blotting-paper.*#
When it is a question of a lesser degree of
oligocythemia, this proceeding will not suffice, and
we must have resort to special means of estimating
the precise number of the corpuscles or the relative
quantity of hemoglobin present. In recent times
a great many instruments have been constructed
with the firstnamed object—as those of Quinche,
Malassez, Hayem, Gowers, and Thoma and Zeiss.
The principle on which all these are constructed is
the same. A known quantity of blood is mixed in
definite proportion with some indifferent fluid (3
per cent. salt solution, &c.), a portion of the mix-
ture is placed upon a hollow slide of known con-
tents and graduated surface, and then the cor-
puscles are counted with the aid of the microscope.
(a.) The Thoma-Zeiss Apparatus for Counting
Blood-Corpuscles.—The simplest and best of these
instruments is that of Thoma and Zeiss. It con-
sists of a capillary tube of glass about ro centi-
metres long, expanding in its upper third to a bulb,
in which lies a small glass ball. The lower end of
the tube is furnished with a scale, graduated in
parts, numbered o.1, 0.5, 1, up to ror (fig. 2). With
this instrument is used a counting-chamber in-
vented by Abbe *® and Zeiss. This is a glass recep-
tacle cemented upon a glass slide (fig. 3); it is
exactly 0.1 mm. in depth, and its floor is marked
out into microscopic squares (fig. 4). The space
overlying each square = 1/4000 mm?* and the
squares are portioned out in groups of 16 by plainer yye, 2.—capillary Tube
7 Thoma-Zeiss Apparatus
s (fig. s). ( pp
line (fig 5) 5 tor Counting the Blood
Application of the Process.—A puncture is made Corpuscles).
in the tip of the finger, and in doing this the
precautions already indicated are taken. Blood from the summit of the
exuding drop is then sucked into the tube until it reaches the mark .5
or 1. The point of the tube is wiped, and a 3 per cent. solution of
common salt sucked in until the fluid has risen to the point marked rot.
* Mm ? = cubic millimetre.
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10 THE BLOOD.
For'some years the author has used Hayem’s fluid in this experiment
(see p. 6). Daland*” and Sadler *® prefer a 24 per cent. solution of
bichromate of potash. The contents of the tube are then thoroughly
mixed, and the column of fluid in the capillary tube is removed by
blowing into the tube, as the blood would not mix with the solution
of common salt. To neglect this precaution, therefore, would vitiate
the experiment.
The capillary tube must be carefully cleaned after use, by washing it with
distilled water, then with alcohol, and finally with zther, and a brisk current of
air blown through it. For the latter purpose Béhm’s air-pump is very suitable.
RW Quy WW a
Fic, 5.—Thoma-Zeiss Apparatus for Counting Blood-Corpuscles.
The hollow cell of the slide is next filled with the mixed blood-
and-salt-solution, care being taken to guard against the admission
of air-bubbles, and the cover-glass is accurately adjusted in such a
manner that Newton’s colour-rings are produced. The preparation
is left to stand for some minutes, so as to allow of an intimate ad-
mixture of its parts, after which it is placed under the microscope,
and looked at with a power of 30-70 diameters, when it will be seen
whether any air-bubbles or foreign bodies are present in it, and
whether the corpuscles are pretty evenly distributed through the fluid.
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ENUMERATION OF BLOOD-CORPUSCLES. IT
The latter are then counted under a high power. In doing this, the
number present in sixteen squares is counted, and from this the average
is estimated. The greater the number of the squares taken, the more
accurate will be the result attained. To count the corpuscles contained
in sixteen squares, Lyon and Thoma *® made the following suggestions :
The space overlying a vertical series of four of the squares is taken
as that the contents of which are to be estimated together. All the
cells which cover or impinge upon the upper boundary of the rectangle
formed by these four squares are to be reckoned, and that whether the
cells themselves are situated within or without the boundary-line in
question. So also are those which touch upon the line bounding the
field of four-squares on one (left) of its sides, and all that are entirely
included within its limits without being anywhere in contact with the
boundary.
The object-glass used in this investigation should be Ze7ss, C or D ;
Hartnack, 6; or Reichert, 7.
The estimation of the total number of corpuscles is conducted as
follows :—If the blood in the tube reached to the point 0.5, its propor-
tion in the mixed solution will be 1:200; if to the point 1.0, 1: 100.
Multiply the number of corpuscles counted in all the squares by 4000
aon being the cubic contents overlying a square), and the result by
100 or 200, according to the degree of dilution. Then divide the pro-
duct by the number of squares taken, and the result gives the number
of blood-corpuscles contained in a cubic millimetre of blood.
To estimate the number of white corpuscles in a specimen of blood,
Thoma * dilutes the latter with water containing one-third per cent.
glacial acetic acid in the proportion of 1:10. In this way the red cor-
puscles are destroyed, and the white alone remain in the field of vision.
In mixing the fluids, the same observer employs a mixing-glass speci-
ally devised by Zeiss for the purpose. The process may also be carried
out thus :—By means of a pipette of 1 ce. contents, and accurately
graduated in o.1 ec. units, 0.9 cc. of the acetic acid solution is measured
out into a watch-glass ; with another pipette holding exactly 0.1 cc., the
blood is added to this and the two well mixed. A drop of the mixture
is placed within the counting-chamber of the cytometer prepared as
before ; and now, since the number of corpuscles is relatively fewer,
the entire field, and not its marked-out divisions, is taken as the basis of
calculation, greater accuracy being so obtained. To the same end, a
lower power will be used, so as just to bring the marks in the floor of
the chamber clearly into view. Before beginning to count the corpus-
cles, however, it will be well to focus with the fine adjustment of the
microscope, and to make sure that the cells have all settled.
The cubie contents of that part of the chamber which corresponds
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12 THE BLOOD.
to the field of vision can be ascertained in the following way :—The
divisions of the chamber which appear in the field are first counted.
Each of these measures 4, mm. across (v. supra. the area= zo5 MM.”,
the cubic contents = z7455 mm.?). The diameter of the field, therefore,
is 4, mm. multiplied by the number of divisions which it contains.
Thus, for instance, if ten of the divisions are seen, the diameter of the
field =10 x A mm. or 39, and the radius=}?$ mm. The area of the
field, therefore = 7 (2°)? mm.®, and if the chamber is 0.100 mm. in depth,
its cubic contents=o.1 x (42)? = cubic mm. Hence we obtain the
following formula : *—
10xZ
UxQ
where M =the number of divisions under the microscope, Z = the
number of cells counted, Q=the cubic contents of the field (Q=o.1 =
R?, where R=the radius of the field in mm.), and where the blood is
diluted in the proportion of 1:10. The formula will give us the number
of cells contained in a cubic millimetre of undiluted blood. Where the
degree of dilution is 1 in 10, and where, as is usually convenient, 16
squares are taken, from the general formula results the following :—
10,000 x Z
314 2
or, if the degree of dilution be 1 in 20, the squares 16—
20,000 x Z
=e
z.e., the number of white corpuscles in 16 squares (Z) multiplied by
to,ooo for the 1 in ro solution, by 20,000 for the 1 in 20 solution, and
divided by 314, gives the number of white corpuscles in a cubic milli-
metre of blood.
When there is a very great increase in the number of leucocytes, as
in leukemia, their number can be estimated in the same manner as that
of the red corpuscles, and the relative proportion of the two can be de-
termined at the same time with sufficient accuracy, if only an adequate
number of squares is taken into account. Great assistance in such
experiments may be derived from the use of a 3 per cent. salt solution
coloured with gentian violet, in which the leucocytes are stained, and
become readily discernible from the red blood-corpuscles, which are
usually somewhat paler than normal. Yoison*#! employs for the pur-
pose a staining fluid of the following composition :—
Distilled water. , , 5 2 . 7 160 cc.
Glycerine r ; ‘ i : , : 4 30 cc.
Sulphate of soda . ; : : : : : 8 grms.
Chloride of sodium : : : P : : I erm.
Methyl-violet ; A : 3 : : - 0.025 grm.
7=3.1416. mm,?=square millimetre. mm.?=cubic millimetre.
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GOWER'S HAMACYTOMETER. 13.
For the same purpose, Mayet 42 recommends that the blood be mixed
with perosmic acid, glycerine, and water, which is said to confer upon
the coloured blood-corpuscles a beautiful red tint, whilst the white cor-
puscles remain unaffected by it.
[(b.) Gowers’ Hemacytometer.*—This instrument is the most commonly used
for clinical purposes in this country. ‘The hemacytometer (fig. 6) consists of :
(1.) A small pipette, which, when filled to the mark on its stem, holds exactly 995
cubic millimetres. It is furnished with an india-rubber tube and mouth-piece to
facilitate filling and emptying. (2.) A capillary tube marked to contain exactly
5 cubic millimetres, with india-rubber tube for filling, &c. (3.) Asmall glass jarin
which the dilution ismade. (4.) A glass stirrer for mixing the blood and solution
in the glass jar.t (5.) A brass stage-plate, carrying a glass slip, on which isa cell
Fic. 6.—Gowers’ Apparatus. A, pipette for measuring the diluting solution; B, capillary tube
for measuring the blood; C, cells with divisions on the floor, mounted on a slide; D,
vessel in which the dilution is made; E, glass stirrer ; F, guarded spear-pointed needle.
+ of a millimetre deep, The bottom of this is divided into 7, millimetre squares.
Upon the top of the cell rests the cover-glass, which is kept in its place by the
pressure of two springs proceeding from the ends of the stage-plate.”
The method of employing the instrument is as follows :—The diluting solution
used is a solution of sodic sulphate in distilled water, sp.gr. 1025, or the following :—
* For the above description and figure we are indebted to Landois and Stirling's
“Physiology,” vol. i. p. 5. Fourth edition.
{+ In practice error is apt to arise from variation in the depth of the cell, and it is
not easy to obtain one precisely} mm. Assuming that the same instrument is always
used by the observer, this is best corrected by ascertaining the true depth and allow-
ing for the error in mixing the solution. Suppose, for instance, the cell is found to
have a depth of 150 uw instead of 200 w, 5 parts of blood should be added to 945, of
the diluting fluid, instead of to955. The results so obtained will be absolutely accu-
rate (Z/art).]
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14 THE BLOOD.
Sodic sulphate, 104 grains ; acetic acid, 1 drachm; distilled water, 4 .0z. ‘995
‘cubic millimetres of the solution are placed in the mixing jar; 5 cubic millimetres
of blood are drawn into the capillary tube from the puncture in the finger and
then blown into the solution. The two fluids are well mixed by rotating the
stirrer between the thumb and finger, and a small drop of this dilution is placed
in the centre of the cell, the covering-glass gently put upon the cell, and secured
by the two springs, and the plate placed upon the stage of the microscope. The
lens is then focussed for the squares. In a few minutes the corpuscles have sunk
to the bottom of the cell, and are seen at rest on the squares. The number in ten
squares is then counted, and this, multiplied by 10,000, gives the number in a
cubic millimetre of blood.” #3]
To estimate the COLOURLESS corpuscles only, mix the blood with ten parts of 0.5
per cent. solution of acetic acid, which destroys all the red corpuscles [Thoma].
The instruments of Bizzozero, v. Fleischl, Hénocque, and Gowers * in-
volve the second principle to which allusion has been made, viz., the
estimation of the quantity of hemoglobin in the blood.
Hedin’s*° instrument for measuring corpuscles in bulk (see p. 40) is
applicable to the same purpose.
Finally, mention must be made of v. Limbeck’s ** researches on the subject of
the resistance of the red corpuscles and the isotonic property of blood serum,
since they may find a practical application by-and-by. The same potential
importance attaches to Laker’s*” observations on the resistance of the blood-
corpuscles.
(¢.) Bizzozero’s Chromo-Cytometer [According to Bizzozero 48 a know-
ledge of the number of coloured blood-corpuscles is of less practical
value than.to know the quantity of hemoglobin, and, as a matter of
fact, the amount of the latter is not necessarily in direct proportion to
the number of the former. For the purpose of estimating the amount
of hemoglobin Bizzozero has invented a small, practical, and handy
instrument, which he calls a chromo-cytometer * (fig. 7).
By means of this instrument we can estimate the amount of hemo-
globin in the blood, and it can be used either as a cytometer or as a
‘chromometer. In both cases it is essentially an expedient for varying
the thickness of a stratum of blood.
To use it as a cytometer, the blood is mixed with a definite volume
(z:50) of an indifferent solution, e.y., normal saline solution (0.75
gramme of sodic chloride in 100 cc. water), so that the corpuscles
remain intact in the fluid. The quantity of hemoglobin is estimated by
the thickness of a layer of fluid through which one in a dark room can
distinctly see the edges of a candle-flame placed at a distance of 14 metres
from the instrument.
In using the instrument as a chromometer, the blood is mixed with
a known volume of water, which dissolves out the hemoglobin from
the corpuscles. The amount of hemoglobin is then calculated from the
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BIZZOZERO'S CHROMO-CYTOMETER. 15
thickness of the layer of this mixture, which yields a colour exactly
equal in intensity to that of a red-coloured glass supplied with the
instrument.
The chief part of the instrument consists of two tubes (ab, cd), work-
ing one within the other, and closed at the same end by glass dises
(figs. 7 and 8), while the other ends are open. The one tube can be
completely screwed into the other, so that both glasses touch. Con-
nected with the outer tube is a small open reservoir (7), from which fluid
can pass into the variable space between the two glass plates at the
ends of the tubes. By rotating the inner tube, the space between the
two glass plates can be increased or diminished, on the principle of
Hermann’s hematoscope, and the screw is so graduated as to indicate
the distance between the two plates, z.¢., the thickness of the layer of fluid
between them. Each complete turn of the screw = 0.5 mm., and the subdi-
visions on it are so marked—z5 to one turn (index, fig. 7, cd)—that each
SeeaNel e oO. bi .
subdivision of the index=°2=0.02 mm. When the inner tube is
2
screwed home and touches the glass disc in the outer tube, the index
stands at o on the scale. If the instrument is to be used merely as a
cytometer, these parts suffice; but if it is to serve as a chromometer,
the coloured glass is needed also. ‘The instrument is also provided with
small glass thimbles with flat bottoms, containing 2 and 4 cc. respec-
tively ; a pipette graduated to hold 4 and 1 ce., and another pipette for
to and 20 cmm., the latter provided with an india-rubber tube, to enable
the fluid to be sucked up readily ; a bottle to hold the saline solution,
and a glass stirrer.
Method of Using the Instrument as a Cytometer.—1. By means of the
pipette place .5 cc. of normal saline solution in a glass thimble.
2. With a lancet or needle puncture the skin of the finger at the edge
of the nail.
3. With the pipette suck up exactly 10 cmm. of blood, observing the
precautions already indicated at p. 8. Mix this blood with the .5 cc. saline
solution, and suck part of the latter several times into the capillary tube,
so as to remove every trace of blood from the pipette. Mix the fluids
thoroughly. Carefully cleanse the pipette with water.
4. Pour the mixture into the reservoir (7) of the instrument. Gradually
rotate the inner tube, and as the two glass discs separate, the fluid
passes into the space between them.
5. Ina dark room light a stearin candle, place it at a distance of 14
metres, and, taking the instrument in the left hand, bring the open end
of the tubes to the right eye. With the right hand rotate the inner
tube to vary the thickness of the column of fluid, and so adjust it until
the outlines of the upper three-fourths of the flame can be distinctly seen
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16 THE BLOOD.
through the stratum of fluid. Vary the position of the inner screw so
as to determine accurately when this occurs. Read off on the scale the
thickness of the stratum of fluid.
Graduation of the Instrument as a Cytometer.—In this instrument
the graduation is obtained from the thickness of the layer of blood
itself, and the amount of hemoglobin is calculated directly from the
thickness of the layer of blood which is necessary to obtain a certain
optical effect, viz., through the layer of blood-corpuscles to see the out-
lines of a candle-flame placed at a certain distance.
From a number of investigations it appears that in healthy blood the
b (a
a O-+Y
m
Fic. 7.—General view of the instrument. ab and Fic. 8.—Showing how ed fits into ab. zand
ed. Two tubes, the one fits inside the other; 7. 2’, Plates of glass closing the ends of ab and
Reservoir communicating with the space be- ed; other letters as in fig. 7.
tween ¢ and J when cd is screwed into ab;
cr. Milled head, and index-scale to the left of
it; y for ast of fig. 9; m. Handle.
outlines of the flame of a candle are distinctly seen through a layer of
; IIO : ;
the mixture of blood ——— mm. in thickness.
100
Let the number 110 correspond to 1, or, better still, 100 parts of
hemoglobin ; then it is easy to calculate the relative value of the sub-
divisions of the scale on the tube of the instrument. Let g = the
degree of the scale for normal blood; g’, that for the blood being inves-
tigated ; e, amount of hemoglobin in the former; and ¢’, the amount
sought for in the latter.
Assuming that the product of the quantity of hemoglobin and the
thickness of the stratum of blood is constant, so that
eg=eg.
Then
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BIZZOZERO'S CHROMO-CYTOMETER. 17
Let us assume that the blood investigated gave the number 180;
then, using the above data :—
, _100.110 11,000
180 — 180
=61.1.
é
The blood, therefore, contains 61.1 hemoglobin. The following table
gives the proportion of hemoglobin, the normal amount of Taser loin
being taken as = 100 :—
Cytometer Scale. Hemoglobin. | Cytometer Scale. Heemoglobin.
110 : E . 100.0 170 5 2 OAS,
120 5 5 - 91.6 180 ‘ : ee Ore
130 : : . 84.6 190 : : - 57-9
140 5 5 7 O25) 200 5 0 - 55.0
150 - : - 73-3 210 : . « 52.4
160 ; ; - 68.7 220 , , + 50.0
If the instrument be used as a chromometer, the blood is mixed with a
known volume of water, whereby the hemoglobin is dissolved out of
the red corpuscles and the fluid becomes transparent. The quantity
GC
ANI
Fic. 9.—Coloured glass, 7, in a
blackened brass screen, 1 ; ast.
Stem for fixing itin y of fig. 7;
se. Brass tube in which f is se
fixed ; this is used when the
instrument is employed as a Ls
chromometer.
we
Oo
il
ast
Fic. ro.—Instrument seen from
above. Letters as in other
figs. (7, 8, 9).
of hemoglobin is calculated from the thickness of the stratum of fluid
required to correspond exactly to the colour-intensity of a tinted glass
which is attached to the instrument. The colour-intensity of the glass
is that of a definite solution of hemoglobin (fig. 9, /).
To use the Instrument as a Chromometer.—1. Place the coloured glass
with its brass frame in the instrument (ast of fig. 9 in y of fig. 7).
2. With the necessary precautions (p. 10) mix ro emm. blood with
.5 ce. distilled water, whereby in a few seconds a transparent solution
of hemoglobin is obtained.
3. Pour this solution into the reservoir (7), and rotate the inner tube
so that the fluid passes between the two glasses. Direct the mstrument
towards a white light or the sky, not towards the sun, and compare the
colour of the solution with the standard coloured glass, a proceeding
B
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18 THE BLOOD.
which is facilitated by placing a milky glass between the source of light
and the layer of blood so as to obtain diffuse white light. When the
two colours appear to have as nearly as possible the same intensity, read
off on the scale the thickness of the layer of blood, and from this by
means of the accompanying table ascertain the corresponding amount of
hemoglobin.
This is done in the same way as for the cytometer, but the graduation
is different, as in the one case we have to do with a candle-flame, and
in the other with a coloured glass.
In very pronounced cases of anemia, even with a layer of blood 6 mm.
in thickness—the limit for which the instrument is constructed—the
intensity of the mixture of blood may be less than that of the coloured
glass. In such a case, instead of 10 cmm. of blood, use 20 cmm.
Graduation of the Chromometer.—As the coloured glass has not abso-
lutely the same intensity of colour in all chromometers, one must first
of all estimate the colour-intensity of the glass itself. This is most
easily done by ascertaining in a given specimen of blood what degree
of the chromometer corresponds to the scale of the cytometer of the
same blood.
Suppose that a specimen of blood by means of the cytometer gave r110,,
and by the chromometer 140; the number 110 of the cytometer = 100.
hemoglobin, so that the chromometer number 140 must also be = 100.
With the aid of the formula (p. 16) a similar table can be constructed
for the chromometer. Suppose the blood investigated = 280; then by
the aid of the formula and the data from normal blood :—
ef — 100.140 _ 14,000 _
280 280
50.
This blood, therefore, contains 50 parts of hemoglobin.
Example.—Blood gives 130 with the cytometer and 190 with the
chromometer ; what is the initial number of the chromometer gradua-
tion corresponding to too parts of hemoglobin ?
If 130 (cytometer) corresponds to 190 (chromometer), then r1o cyto-
meter (?.e., graduation corresponding to roo parts of hemoglobin) corre-
sponds to « chromometer graduation :
190.
130:190=I110:2.°..¢= 9 TT = 20,000 = 160.7.
130 130
Blood containing 100 parts hemoglobin will correspond to 160 of the
chromometer scale, and beginning with this number as a basis, with the
aid of our formula it is easy to construct a table showing the relation.
Whilst the value of the cytometer scale remains the same for every
instrument, the chromometer scale varies with each instrument, as the
colour-intensity of the glass is not necessarily the same in all. But
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VON FLEISCHL’'S HEMOMETER. 19
it is easy to construct a scale for each instrument by investigating a
specimen of blood and comparing it with the cytometer graduation as
indicated in the foregoing paragraph.
Precautions to be Observed in Using the Instrument.—In using the
instrument certain precautions must be observed. The exact quantity
of the several fluids must be carefully measured ; evaporation must be
prevented by covering the blood-mixture. Further, do not look at the
fluid too long at a time, as the eye becomes rapidly fatigued.
In cases of leukemia, where there is a large number of white cor-
puscles rendering the mixed fluid opaque, the corpuscles may be made
to disappear by adding a drop of very dilute caustic potash. If the
opacity does not disappear by the addition of this substance, then the
opacity is due to the presence of fatty granules in the blood, so that by
this means we can distinguish lipemia from leukemia.
Further, the operation must be. carried out not too slowly, as the
saline solution only retards the coagulation of the blood, and does not
arrest it.
Bizozero claims that when the instrument is used as a cytometer
the mean error is not greater than 0.3 per cent. | *
Sadler,5° working in the author’s clinic, has found that Bizzozero’s
instrument gives very accurate results.
(¢.) Von Fleischl’s Hemometer.t—The application of this instru-
ment (fig. 11) depends upon the principle that the colour of the blood
diluted with water may be compared with that of a glass wedge tinted
with Cassius’s golden-purple, or some such pigment.
Its essential part is the red glass wedge, which is mounted movably
beneath a platform like that of a microscope, with a circular opening in
its centre. Upon this the light from a gas or oil lamp (daylight is
not admissible) is projected by a plate of plaster of Paris. Above the
wedge, and exactly over the circular opening in the platform, is fixed a
metallic tube 14 cm. long, closed at the bottom with a plate of glass
and divided by a vertical metallic partition, so that one half of the
metallic tube receives its light through the red glass wedge, the other
directly from the white reflector. When the apparatus is in use, the
former of these compartments is filled with pure water, the other with
water mixed with a known quantity of blood.
To secure this known quantity, von Fleischl has designed an auto-
matic blood pipette of such a capacity that, when healthy blood is used,
the resulting mixture corresponds in colour to that derived from the
part of the red glass wedge which is marked roo. From this point to
* The instrument may be obtained from F. Koristka, Via Circo, 14, Milan, and
costs thirty-five lires.
+ Von Fleischl’s instrument is made by Reichert of Vienna, and sold for 35 florins.
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2© THE BLOOD.
its sharp edge (where o stands), the wedge is graduated in ten divisions,
which represent its diminishing thickness, the Nos. 90, 80, &c., being
marked on the apparatus.
The instrument is employed thus:—The blood is obtained from a
puncture in the finger, and placed by means of the pipette in the proper
compartment of the tube. Both compartments are then filled with
water, and the red glass wedge is moved until the two fluids show an
equal intensity of red colour. The number indicated on the scale is then
read off. Suppose this should be 80,—then the blood examined con-
Fic. 1r.—Von Fleischl’s Hemometer.
tains but 80 per cent. of the normal proportion of hemoglobin, or the
quantity of hemoglobin is to that of healthy blood as 80: 100. Now,
assuming that in a healthy man 14 grms.* may be taken as the amount
of hemoglobin in too grms. of blood, we can calculate the latter abso-
lutely for the specimen examined by means of the formula:
wig
100
* J. G. Otto states the normal quantity at 13.77 per cent. 14 is taken here (as
by Hénocque elsewhere) as a simpler expression for the purposes of the calculation.
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HENOCQUES HAMATOSCOPE. 21
Where
X =the quantity of hemoglobin in 100 grms of blood ;
R=the figure obtained with von Fleischl’s apparatus to express the
relative proportion of hemoglobin in the blood ; and
14=the normal quantity of hemoglobin in the blood of a healthy
adult.*
Although it must be conceded that the results obtained with this
instrument are not absolutely correct, it still supplies a simple and
ready means of estimating the hemoglobin in the blood, and has the
further advantage that it needs but little of the latter to work upon.
It has proved a useful adjunct to the Thoma-Zeiss apparatus, or that
of Gowers, in the investigation of changes in the blood for clinical
purposes.°!
(e.) Hénocque’s Hematoscope.*?—This instrument has the advantage
over others employed for a similar purpose, that while comparatively
i
Fic. 13.—Heénocque’s Heematoscope filled with Blood.
little fluid is needed for its application, this consists of pure blood
undiluted with artificial serums.
It consists essentially of two glass plates superimposed in such a
manner as to enclose a prismatic capillary space. The inferior of these
plates is the broader. Upon the upper part of its surface is engraved
a millimetre scale, o to 60, reading from left to right, and at either
extremity it carries a cap of nickelled metal, in which is a groove for
the reception of one end of the smaller (upper) plate. These grooves
are so placed that whilst the plates are in immediate contact at one end,
that opposite o of the scale, they are separated at the other by an in-
terval of 0.3 mm. The smaller plate can be made to slide in the grooves
under gentle pressure, and can thus be removed for the purpose of clean-
* This number is chosen here so as to afford a basis of comparison between the results
obtained with v. Fleischl’s instrument and those with Hénocque’s, which will be
described presently.
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22 THE BLOOD.
ing the instrument. From the above description it will be seen that a
layer of blood introduced within the capillary chamber has a thickness
varying uniformly from o on the left to 0.3 mm. under the mark 60
on the graduated scale ; and it also follows that its depth increases by
0.005 mm. for every mm. distance towards the right. Thus its depth
at any point may be known by multiplying the corresponding figure on
the scale by five, when the result is expressed in thousands of a milli-
metre or micron.
The prismatic chamber is filled with blood obtained by pricking the
finger, and this is done best by bringing the lower lamina on a level
with the puncture and permitting the issuing drops to flow upon it ata
gentle decline. The blood will then arrange itself in an even layer, and
if its continuity be interrupted by empty spaces or air-bubbles, these can
be extruded by slightly tapping the glass wall with the fingernail. Six
drops generally suffice. The edges of the instrument, when filled, are
wiped clean, and the examination may be begun.
This is conducted in two different ways :—
(a.) The first (procédé diaphanométrique), the readier and simpler, has
for its object to estimate the relative opacity of the blood, and so to infer
the proportion of hemoglobin which it contains.
For this purpose there is supplied with the hematoscope a plate of
O/C OOOO Oe
van ta ai
Memalosiope a Ninocque
15. 14. 18. 12. 11. 10. 9.8.7.6.5.4.
Fic. 14.—Enamelled Plate belonging to the Heematoscope.
white enamelled metal, bearing on its upper part a millimetre scale pre-
cisely similar to that engraved upon the lower of the two glass plates,
and below a descending series of figures, of which the first underlies the
8 mm. mark above. Then follow at constantly diminishing intervals the
figures 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4. The markings upon this
plate are traced throughout in black. When in use, it is placed behind
the hematoscope filled with blood, and held there in such a position
that like markings upon the millimetre scales accurately correspond.
It is evident that the portion of the blood layer which is thinner, and
therefore less deeply coloured, will be transparent, and will suffer the
marks beneath to be visible, while these disappear towards the thicker
end. The examination consists in noting the point at which the figures
(15-4) in the lower series cease to be visible ; and it is clear that this
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HENOCQUES HAIMATOSCOPE. 2B
point will be attained the sooner according as the blood is richer in
hemoglobin. :
Further, Hénocque has arranged the series so that the second figure
(14) expresses in grms. the quantity of oxyhemoglobin in 100 grms. of
blood, and this figure terminates the series as seen through a layer of
blood of normal constitution. With blood taken from a case of anemia,
on the other hand, the figure 8 or 7 may be legible, and this implies
that such blood contains in 100 grms. only 8 or 7 grms. of oxyhemo-
globin. Finally, the thickness of the stratum of blood at the point of
requisite opacity may be ascertained from the mm. scale in the manner
already indicated.*
Hellstrom, Loos,®* and the author have satisfied themselves that the
results obtained in this way are not to be relied upon, and that the
figures generally indicate too high a proportion of oxyhemoglobin.
(f.) In the second and more accurate mode of using the hematoscope
the enamelled plate is dispensed with, and a Browning’s spectroscope is
required. The instrument, filled with blood as before, is placed opposite
the cleft of the spectroscope, and the point is observed at which the
characteristic spectrum of oxyhemoglobin is first distinctly formed,—
when the corresponding point on the millimetre scale of the glass plate
is read off. The less hemoglobin in the blood, the thicker must be the
layer from which a spectrum is obtained. In order to secure a correct
reading from the scale, it is well to place the apparatus holding a stratum
of blood upon a sheet of white paper against a window so as to examine
it by bright and diffused daylight, and then directing the spectroscope
over 1 or 2 cm. of its surface, the observer should several times judge
for himself concerning the point of earliest definition of the spectrum.
Of the numbers obtained in this way (which will usually differ by an
amount expressing only two or three millimetres) the mean is taken,
and employed for the purpose of the calculation. It must be allowed
that the conclusion in this respect is always somewhat arbitrary, and
leaves room fora difference of opinion as to when precisely the spectrum
is formed ; but once the eye has become accustomed to look for a certain
clearness in the outline of the bands, it seeks for and easily appreciates
it in every instance. f
From the reading on the scale at the point where the spectrum is
* [Hénocque’s hematoscope may be obtained from M. Lutz, 82 Boulevard Saint-
Germain, Paris. The price is 12 francs, and the enamelled plate costs 5 francs
additional.—(ED.)]
+ [This difficulty may be further obviated by the use of Hénocque’s double
spectroscope, by means of which two persons are enabled to make the observation
at once. For a description of this instrument the reader is referred to the original
communication, ‘ L’Hémato-spectroscope.” Compt. Rend., Soc. de Biologie, October
1886. ]
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24 THE BLOOD.
thus seen, the thickness of the blood stratum, and the quantity of
oxyhemoglobin in a known quantity of blood, can be readily deter-
mined. In the case of normal blood, which contains 14 grms. of oxy-
hemoglobin in 100 grms. of the fluid, the absorption-bands are plainly
visible in the situation of the figure 14 on the mm. scale ; and from what
has been already said it follows that the thickness of the blood stratum
at this point is 14 x 0.005 mm.=o0.07 mm. Let it be assumed now that
in a given case the bands just become distinctly evident at a point cor-
responding to the division 20 on the index; then the thickness of the
layer which yields them is 20x 0.005 =0.r mm. From these data the
quantity of oxyhemoglobin in 100 grms. of the blood may be calculated
by the following equation :—
@:14=0.07 : 0.005.y
14 x 0.07
B=
©.005,4
In this formula :
x =the quantity of oxyhemoglobin sought.
14 =the quantity of oxyhemoglobin in roo grms. of healthy blood.
0.07 = the thickness of the blood stratum, which will make the absorp-
tion-bands plainly evident where the blood, as in normal blood, holds
14 grms. oxyhemoglobin in roo grms, of the fluid.
0.005 =the thickness of blood stratum corresponding to 1 mm.
y =the number of mm. read off at the point where the absorption-bands
become distinctly visible. From this results the simple expression :
_14X0.07__ 196
~ 0.005.y ¥ °
In the example chosen :
196
Y=20-. 55= 9.8,
z.e., the blood investigated contained 9.8 grms. of hemoglobin in
100 grms.
To obviate the necessity for making the calculation afresh in each
case Hénocque has compiled a table from which the quantity of hemo-
globin may be deduced directly from the depth of the blood stratum.
Comparisons which the author has instituted between the results
arrived at in this way with others derived by means of v. Fleischl’s ap-
paratus, have shown that the two are sufficiently in accord. Henschen,54
however, is of opinion that the latter are more accurate, and accounts
for this by pointing out that they are obtained from oxyhemoglobin,
whereas with Hénocque’s hematoscope that body is still within the cells.
The preference will usually be given to v. Fleischl’s apparatus, because
of the greater quantity of blood needed for the application of Hénocque’s
hematoscope ; but the latter is especially suitable for the observation
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HEDINS HMATOCRITE. 25
of such changes in the blood as the formation of methemoglobin, Wc.,
which can be recognised by spectrum-analysis. To detect such changes,
Hénocque has applied it in a very ingenious manner. He observed the
development of oxyhemoglobin-bands in transparent parts, such as the
lobe of the ear and the ungual phalanges of the finger, capable of being
illuminated by diffuse sunlight.* Then, in the case of the ungual
phalanx, the part was ligatured, and he noted the length of time required
for the appearance of the broad absorption-band of reduced hemoglobin.
Proceeding in this way, he found that with a normal proportion of oxy-
hemoglobin, reduction took place in the course of 70 seconds, while
with anemic blood the interval was shortened to 30-40 seconds.
As a result of his researches, Hénocque has arrived at the following formula,
which is applicable to clinical purposes :
M
E= DS
where
E=the energy of reduction ;
M=the mean proportion of hemoglobin ascertained by his method ;
D=the time in seconds in which reduction is accomplished.”
The formula is derived from the following considerations :—In a specimen of
blood holding 14 grms. oxyhemoglobin in 100 grms., reduction takes place in 70
seconds, and in another holding 13 grms. in roo, it takes place in 65 seconds.
Inspection of the figures shows that in both cases a fifth part of the quantity
of oxyhzmoglobin (in 100 grms.) is reduced. Hence, to obtain the value of E
(energy of reduction), the quantity of oxyhzmoglobin found is multiplied by 5,
and the product divided by the number expressing the time (in seconds) in which
reduction takes place. Experiments are now in progress under the author’s
supervision which have for their object to ascertain how far this method of in-
vestigation may be of use in diagnosis. The apparatus may be employed also
for the examination of milk, in the spectrum-analysis of urine and morbid fluids,
and for the aniline dyes of so much consequence in staining processes. It seems
to merit a description here on account of its extended utility ; and in any case,
in connection with the spectroscopic examination of the blood, it must be classed
with the apparatus of Thoma-Zeiss, Gowers, and y. Fleischl as a valuable addi-
tion to our resources.
(f.) Hedin’s Hematocrite.°—This instrument is of great value.
It enables one readily to estimate the volume of the red blood-corpuscles.
Its parts are: (1.) A capillary tube for measuring and mixing the blood.
Hedin uses a special contrivance for this purpose, but the mixing-glass
noticed on p. 11 for counting leucocytes serves equally well. To prevent
coagulation Hedin sucks Miiller’s fluid into the tube and then blood in
equal quantities. These are then expelled into a small platinum dish
and well mixed. Daland,*" in the authoyr’s clinic, has found that a 2.5
per cent. solution of bichromate of potash answers best.
* [In researches of this character the double spectroscope is specially recommended
by Hénocque.]
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26 THE BLOOD.
(2.) Two glass tubes, 35 mm. long, with a lumen 1 mm. in diameter
and graduated into 50 parts.
(3.) A metallic frame, terminating at either side in an angle to sup-
port a small cylindrical recess, of the same diameter as the tubes (2.),
and covered with a caoutchoue disc. From the middle of this metallic
frame there projects downwards a hollow metal cylinder, by means of
which it can be made to rotate on a vertical axis (fig. 15). Connected
with the central cylinder are two metallic springs, placed opposite each
other, and carrying each at their upper ends, on a level with the recesses
ha
Fic. 15.—Hedin’s Heematocrite.
mentioned above, a caoutchoue cap. Between the recess and this
caoutchoue cap on either side is placed one of the glass tubes which has
previously been filled with the mixture of blood and Miiller’s fluid
(or bichromate solution). In this position the tubes are closed by the
caoutchouc cap, which is held against them by the pressure of the springs.
(4.) A vertical support which can be made to rotate.
The instrument is used thus: With Hedin’s capillary tube, or the
mixer for estimating leucocytes, a mixture is made of blood and a 2.5
per cent. solution of bichromate of potash, and with this the tubes are
filled by plunging one end in the fluid, which is then drawn into the
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HEDINS H#MATOCRITE. Ov,
tube by the mouth applied to a piece of india-rubber tubing attached to
the other end. The tubes being filled in this way are placed in position
in the frame—the extremity towards the recess of the frame being first
adjusted, and the caoutchouc caps of the springs being then made to
press on the other extremity. The frame is then attached by its
vertical cylinder to the body of the instrument and made to rotate
rapidly. The red corpuscles, in virtue of the centrifugal action, sepa-
rate from the leucocytes and serum. After 50-70 seconds (where the
bichromate solution is used) the volume of the layer of red corpuscles
remains constant. The contents of the tubes are then arranged in three
parts ; at the distal end are ‘collected the red corpuscles, forming a
dense dark-coloured mass; next in order a small turbid band, con-
sisting of leucocytes, and in health of a whitish colour ; finally, the clear
serum, which is coloured a bright yellow by Miiller’s fluid. To guard
against error, a sheet of white paper is placed behind the tubes, and the
volume of the red corpuscles is read off on the scale. The corresponding
number multiplied by four gives the volume of red corpuscles in one
hundred parts of blood, as will appear from the following considerations.
The volume of red corpuscles as read upon the scale is that contained in
a mixture of equal parts of blood and bichromate solution, forming a
column 35 mm. long and divided into 50 equal parts. The proportion
of corpuscles in pure blood would be twice as great, and in 100 parts
(instead of 50) again twice as great ; therefore the percentage bulk may
be expressed by the figure read off the scale multiplied by 4.
The description given here applies to an instrument furnished by Sendling
Sandstrém of Lund, in Sweden, and differs somewhat from that published by
//edin himself.
This method is very serviceable in discriminating between the various
diseases which affect the blood, and it may be used in part to replace the
more difficult processes for counting the corpuscles. It may be substi-
tuted for these in conditions where the relative bulk of the red corpuscles
depends only upon their number, and not also (as in many diseases, ¢.7.,
pernicious anemia) upon their size. As to how far the results obtained
in this way tally with those arrived at by counting, and under what
circumstances the one method may supersede the other, the reader
should consult Daland’s notice. In the same way it is possible to
estimate approximately the relative proportion of red corpuscles and
leucocytes, as, for instance, in certain cases of persistent leucocytosis.
Observations made within the last year, in three cases of leukemia,
have satisfied the author that the method suffices to determine the
defective state of the blood in that disease. Further, it can be applied
to the purpose of studying the leucocytes in the blood, and for the
detection of micro-organisms therein.*®
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28 THE BLOOD.
2. Leucocytosis.—By this term is meant a condition in which the
number of white corpuscles in the blood is temporarily much increased.
Such an increase occurs in health as part of the process of digestion.®®
One to two hours after the principal meal the white corpuscles are
found in the blood in the proportion of 1 : 150 or even 1 : roo of red
corpuscles, diminishing soon after to 1 : 350 or 600, or, according to
Griber,©© between 1: 521 and 821. and its association with the disease
has recently been confirmed by Jsrael©6 and Werchselbaum.15" The
bacilli are rod-like bodies, 2-3 « long and 0.3-0.4 u broad, often carry-
ing a spore at the extremity. They are found in the farcy buds and
ulceration of glanders, and also in the blood of persons suffering from
that disease. Fig. 26 represents the bacilli seen in a specimen of blood
taken from a case of glanders in the Vienna General Hospital. They
may be shown in the blood by means of the dried preparation, and they
are best stained by Loffler’s method for detecting these fungi. (See
Chapter VIIL.)
5. Bacillus of Typhoid Fever.—Bacilli have of late years repeatedly
been found inthe blood of typhoid patients, and they are doubtless the
exciting cause of the disease.8 Riitimeyer and Neuhauss 19 experi-
mented upon the blood taken from the roseolar spots of typhoid patients,
and succeeded in cultivating bacilli from it. Recent researches, as
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STREPTOCOCCI. 47
those of Janowshy,1°° show that the bacillus is very rarely present in
the blood during life, and that their detection should not be numbered
amongst the resources of diagnosis. Further information on this subject
will be found in the chapter on Feces.
6. Streptococci—V. Noorden 1! recently found streptococci in blood
taken from the body of a woman who had died of erysipelas. They
exhibited in their cultivation-properties the closest resemblance to the
well-known streptococci of Fehleisen and Rosenbach.
In like manner, Orthenberger,? by applying Weigert’s method to the
examination of the blood after death, has shown the presence in it of
pheumonicocci in six cases of uncomplicated lobar pneumonia.
In a series of cases in which the author examined the blood of pneumonia
patients, employing sterilised human blood-serum as the nutrient substance, he
failed altogether to obtain a cultivation of cocci.
Some years ago Klebs ascertained that micro-organisms existed in the
blood and endocardial vegetations of persons with endocarditis. In a
ees
ae ‘@
O
oOo -@
Fic. 26.—Bacilli of Glanders in Human Blood, from a preparation by Dr. Kolisko (eye-piece V.,
objective Zeiss j, homogeneous immersion ; Abbe’s mirror ; open condenser).
case of congenital heart-disease with endocarditis, Singer! has culti-
vated micro-organisms obtained from the blood during life. An instruc-
tive communication lately published by Weichselbawm 1** has also shown
that cultivations of cocci can be obtained from the blood during life in
cases of endocarditis. It is greatly to be desired that systematic investi-
gation of this subject should be made by means of Weigert’s method
and cultivation processes, with the object of establishing a secure stand-
point for clinical diagnosis. The researches of A. v. Hiselsberg, Levy,
and Brunner 1 encourage the hope that this may be accomplished. In
the clinic of Professor Chrobak at Vienna, the blood of patients in a
severe attack of puerperal fever has repeatedly been found to exhibit
micro-organisms of this class.1%
[Streptococcus Pyogenes.—A chain-forming micrococcus was described by Ogston
as occurring in abscesses. It was afterwards submitted to Koch’s cultivation
processes by Rosenbach, who gave it the name of Streptococcus pyogenes, and it
is now known to be associated with septic processes of all kinds, whether in men
or animals. It is apparently the same as Fehleisen’s 8. erysipelatis and Léfler’s
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48 THE BLOOD.
Diphtheriacoccus. It has been obtained from the pus of pyamic abscesses and
empyema, from the tissue-fluids in spreading gangrene, from the vesicles and
pustules of small-pox, and in contaminated calf’s lymph. It occurs in the blood-
vessels in certain cases of diphtheria, scarlet fever, puerperal septiczemia, measles,
and typhoid; but it must be regarded only as a secondary result of those affec-
tions. It may gain admission to the system in any disease attended with lesions
to the skin or mucous membrane, setting up destructive processes, when the
resistance of the tissues is greatly impaired by the working of a special virus
(Crookshank).187
Streptococcus of Scarlatina.—Dr. Klein has recently succeeded in separating a
micro-organism obtained from the blood of scarlatina patients, which he regards
as the contagium, virus, or actual cause of that disease. When cultivated by
inoculating the surface of nutrient gelatine with the post-mortem blood, the
micro-organisms bear a close resemblance to the Streptococcus pyogenes. Klein
is of opinion that the two are sufficiently distinguished, both morphologically
and by their pathogenic effects upon animals. The experiments upon which he
relies, however, are questioned by Crookshank,!® who maintains the identity of the
micro-organisms concerned. A Streptococcus which Klein believes to be the same
as that of scarlatina was found in the blood of cows in an outbreak of disease
amongst those animals at Hendon; and this, when inoculated upon calves, pro-
duced in them the post-mortem appearances of scarlatina. Moreover, the cow-
disease alluded to is thought to have caused an epidemic of scarlet fever amongst
men through the medium of the milk.1],
7. Micro-Organism of the Blood in Hydrophobia.—Bareggi!”° found constantly
present in the blood in hydrophobia a micro-organism which stained with
methylene blue. Placed on slices of potato at 25°-27° C., it developed in the
course of forty-eight hours in flattened hemispherical cultivations. of a colour
ranging between whitish-grey, yellow, and citron. In test-tube cultivations (see
the chapter on Bacteriological Methods) it behaved like the bacillus of Asiatic
cholera. Further research is needed to establish a connection between this micro-
organism and hydrophobia.
8. Bacillus of Tetanus.—Many authorities!" are of opinion that
tetanus is an infectious disease, produced by the agency of the ‘bristle-
bacillus” of Nikolaier. According to the observations of the latter
investigator, the bacilli in question are somewhat longer and thicker
than those of mouse-septicemia. They sometimes form in threads,
commonly in irregular heaps, and occasionally produce spores. The
bacilli themselves, or their spores, have been found in the blood (?)
(Hochsinger). They stain readily in dry cover-glass preparations, and
may be cultivated outside the system. The fact may be mentioned here
that from cultivations of the bacillus Brieger1” has isolated several
ptomaines—tetanin, tetanotoxin, and spasmotoxin—with which he has
induced tetanic poisoning symptoms in animals; and more recently the
same observer has obtained similar poisons from the blood of persons
who had died of tetanus.
Nissen 1"? also has experimentally demonstrated the presence of toxin
in the blood in cases of tetanus. [A. Bruschettini 1 has lately succeeded
in causing fatal tetanus in rats and rabbits by injecting the urine of
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PROTOZOA. AQ
patients suffering from that disease.] The researches of Aitasato!? in
Koch’s laboratory have definitely established the fact that the bacillus
is the specific cause of the disease. It is anzrobic, develops in pus
and forms spores there, but it is occasionally observed in the form of
rods free from spores, if the pus be examined in an early stage.176
B. Animal Parasites (Heematozoa).
1. Protozoa.—Under this heading are to be described the micro-
organisms of malaria,—parasites of very great interest, which occur in
the two principal varieties of Hamameba malarie and Laverania
malarie.
Historical.-—Alebs””" and Tommasi-Crudeli have described a bacillus which is
found in the soil of the Campagna, and they regard this as the specific cause of
malaria.
To Laveran,’8 who in 1880 observed flagellated organisms in the blood of
malaria patients, belongs the credit of the first step towards the ultimate patho-
logy of this disease ; but his discovery was too indefinite to lend itself to any
clinical purpose, and Marchiafava and Celli claim the honour of having first
distinguished and described the hamatozoon, which is the most abundant and,
clinically, the most important of this group of blood-parasites. These observers
detected amzboid bodies within the red corpuscles in the blood of persons
infected with malaria. The amzboid bodies (plasmodia) commonly contained
granules and particles of black pigment. They stain with methylene-blue. They
have not yet been cultivated outside the body,!*” but Marchiafuva and Celli, and
also Gerhardt,!8' by inoculation and intravenous injection with malarial blood
containing them, has succeeded in communicating the disease to other indi-
viduals, and the infected blood in its turn exhibited the plasmodia. The state-
ments of these authors are borne out by others.!**
[Fenton Evans has succeeded in obtaining pure cultivations of the hematozoen
outside the body by treating the nutrient media with living blood,—i.e., blood
taken before rigor mortis has set in. These cultivations, when inoculated upon
animals, produced a fatal disease, of which the symptoms were intermittent,
though not the same as those of classical intermittent fever. He believed also
that by altering the chemical composition of the media the hzmatozoon attained
a higher organisation. This statement is questioned by Dyer.!*3]
Metschnikof proposes to name the parasite Hematophyllum: malarie. TW.
Osler has examined the blood in seventy cases of malarial disease, and found
it present in all. It would appear from his researches, however, that the
organisms concerned assume a greater variety of forms than was previously
supposed.
Councilman,'* again, has recently supported the views of Laveran, Marchiafava,
and Celli. He describes several forms of the parasite, and opposes the doctrine
of Mosso,®> who sought to prove by his experiments that the plasmodium resolves
itself into degeneration types of the red blood-corpuscles ; and maintains that
similar appearances can be found in the blood apart from malaria. Finally,
L. Pfeiffer 1*° has also seen such in the blood after inoculation with vaccine and
in searlatina, Yommasi-Crudeli,'*’ on the other hand, regards the forms in ques-
tion rather as the result than as the cause of malarial disease, believing them to
be the product of the degeneration of the red blood-corpuscles, and further
maintains that the bacillus discovered by Klebs and himself is the true cause of
the disease.- This opinion is shared by Schiavuzzi,!8 who still more recently. has
D
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50 THE BLOOD.
succeeded in cultivating the micro-organism outside the system. ‘Ihe theory of
Danilewsky ® remains to be mentioned. That author supposes that the bodies
under discussion are identical with the hematozoa observed in the blood of many
birds. Ina recent communication he suggests for them the name of Polymitus
malariz, and from his researches, as well as those of Grassi, Felctti, Celli, and
Sanfelice,° it appears probable that birds are attacked by the same parasite
which is associated with malaria in man.
Observations which the author made in Rome in 1889 under the
direction of Marchiafava and Celli, and afterwards in his clinic at
Prague, have satisfied him that the blood in malaria contains specific
organisms, as Laveran first pointed out, and that these specific organisms
are the determining cause of the disease. The subject is thus invested
with great importance from the point of view of diagnosis ; but it must
be admitted that the micro-organisms in question display a great variety
of form, and many details of the life-history of this interesting parasite
remain yet to be discovered. For our purpose, it will suffice to mention
those particulars which at present admit of clinical application. The
following description is founded on the statements of Laveran, Marchia-
fava and Celli, Golgi, Celli and Guarnieri, Grassi and Calandraccio,
Canalis, R. Paltauf, Quincke, Dolega, Plehn, Chenzinshy, Rosenbach,
and Rosin, controlled by the author’s own observations.!®!_ Some of the
figures are borrowed from these writers.
The earlier researches of Laveran, which are so far confirmed by the
Italian observers, have established two facts—first, that the parasite of
malaria assumes a variety of forms in different cases, even within the
same locality ; and, secondly, that its form tends especially to vary with
the locality and with the clinical type of the disease. Hence the dis-
crepancies in the statements made by competent authorities, as by Laveran
on the one hand and Golg’ on the other, the former having had occa-
sion to see only or chiefly the spherical and crescentic bodies presently
to be noticed, while the amezboid parasite seldom came under his obser-
vation. 19?
We have it on the authority of Marchiafava, Celli, and Canalis,
and especially of Golgi and Canalis, that the hematozoon of malaria
occurs in three principal forms, each having a special relation to the
different clinical types of the disease—tertian and quartan ague, the
anomalous varieties, remitting and intermitting attacks, and cases of
fever with short periods of apyrexia (Febris perniciosa algida) (Marchia-
fava and Cellz), and that the development of the organism within the
system is intimately associated with the production of the various sets
of symptoms.
[Hehir 3 has very carefully investigated the blood of malaria patients
in India, and the results, which he has lately published, agree very closely
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PARASITES OF AGUE. 51
with the statements of Laveran and the Italian observers. He found
that there were constantly present in such blood eight different forms,
including the phagocytes, which may be observed to take an active
part in the morbid process. The micro-organisms are, in his opinion,
all varieties of a single polymorphous hematozoon, and in general they
correspond to Laveran’s description. The chief interest attaches to
a micro-organism with flagellated rapidly-vibrating processes, which was
very partial in its distribution through the body, was always most
abundant in the pyrexial period, and the vitality of which was controlled
by quinine. There was also found a spherical body with 3-6 well-
formed cilia-like processes. This is the Hematomonas malarie stellata. |
1. The Parasites of Tertian Ague.—A few hours after the
cessation of the febrile paroxysm the blood may be seen to contain
P
38 G yp aw
Fic. 27.—Parasite of Tertian Ague, as seen in the blood some hours after a paroxysm
(partly copied from other observers). 1%
very small movable bodies of a pale colour, and carrying from one to three
extremely delicate and pigmented thread-like processes (ektoglobular
parasite, fig. 27, on the left). Plehn and the author have observed
similar bodies during the fever-free period.
The parasite, as it is supposed, then invades, or has already invaded,
the red corpuscles (fig. 27, left), where it appears as an actively-moving
body, already, it may be, outlined, as it were, with a wall of melanin
granules. Within the corpuscle it grows in size, and as it does so, the
Fic. 28.—-Progressive Endoglobular Development of the Parasite during the Apyrexial
Interval (in part copied from Golgi).195
former becomes progressively despoiled of its hemoglobin. In this way
the parasite develops into a large freely-moving, deeply-pigmented mass
of protoplasm (Ameeba, see p. 53). The changes just described occur in
the fever-free period within twenty-four hours from the termination of
a paroxysm.
While the corpuscles which have been attacked rapidly lose their
colour (fig. 28), the newly-formed melanin accumulates towards their
centre, and the parasite comes to occupy the entire contents of the cor-
puscle. The parasite then undergoes segmentation, and from this result
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52 THE BLOOD.
the various forms described by Golgi, and represented in fig. 28. These
segmentation forms will be noticed at greater length presently.
The invaded corpuscle is disintegrated. Two more days are required
for this endoglobular development of the parasite. This terminates the
Fic. 29.—Parasite of Tertian Ague, at or just before the commencement of the attack (copied
from (Golgi).196 The figure shows the various segmentation forms of the parasite.
apyrexial period. A new generation of the parasite has matured, and
its presence in the blood determines a new paroxysm of fever.
The development of the parasite is often completed before the
paroxysm begins.
2. The Parasite of Quartan Ague.—The course of quartan ague
is marked by a development similar to that just described (Golgi).1%"
The endoglobular growth takes place in this case also during the fever-
free period. Its earlier phase is quite the same as that of tertian, only
paras O
a ae
Fic. 30.— Parasite of Quartan Ague. Various segmentation forms (from Golgi).1°8
the corpuscles are less rapidly decolorised, and the melanin granules
formed are of larger size.
The chief difference, however, is in the method of segmentation, the
resulting segments being much fewer in quartan than in tertian ague
(fig. 30). In the latter they may be as many as from 15-20 for each
plasmodium, whereas in the former they range from 6 to 12. Moreover,
the process of segmentation itself takes place in a more uniform manner
aes
Se O CO of
Fic. 31.—Parasites of Acyclical Intermittent Fever (from Celli and Marchiafava).
in quartan fever. The parasite requires three days for its development.
Golgi asserts that in quotidian fever the blood contains at once three
broods of the parasite of quartan, which mature successively at intervals
of one day.
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PARASITES OF AGUE. 53
3. The Parasites of Acyclical and Anomalous Forms of
Ague. — For a knowledge of these organisms we are indebted to
Celli and Marchiafava,'® and especially to Canalis. Marchiafava’s
observations were made with the blood of patients suffering from
the acyclic forms of intermittent fever which prevail at Rome in the
summer, autumn, and winter months. In Roman fever, just before the
paroxysm and at the end of the apyrexial period, the blood contains
small annular plasmodia, holding in their central part a mass of hemo-
globin or pigment granules ; also minute moving ameboid bodies with a
sinuous outline, and large round stationary forms which are almost
colourless, and which present at the centre or periphery a circular spot
of pigment. Unlike the parasites of tertian and quartan ague, the plas-
modia of the autumn and winter Roman fever are devoid of pigment
and retain their motility for a long time (Celli and Marchiafava).
In the varieties of Roman fever just noticed are often to be found
the crescentic and sickle-shaped bodies which were first described by
@) O
6 2
| f A 3 :
/ ie ) JR
fe a - a
| :
at oe
Fic. 32.—Crescentic and Falciform Bodies, and Free Organisms carrying Flagella
(Celli and Guarnieri 200),
Laveran. According to Celli and Guarniert the following forms may he
distinguished : Crescented or sickle-shaped bodies, others of a boat- or
spindle-shape, and again others with an oval or circular outline and pro-
vided with flagella (fig. 32).
‘Grassi and Feletti have urged that the name of Hemameeba malariz
should be appropriated to those forms of the plasmodium which have
been described as belonging to the recognised typical varieties of ague,
while the term Laverania malariz is reserved for the sickle-shaped micro-
organism. These writers are of opinion that the latter is associated with
recurring attacks and the malarial cachexia. Golgi holds the view that
the laverania occurs in cases of malarial fever, where the attacks are
separated by long and indeterminate intervals of immunity.
Canalis has directed his attention particularly to the study of the para-
sites which are to be found in cases where the successive febrile attacks
are separated by more or less considerable intervals, and which, for’ the
most part, result in the malarial cachexia. In this connection he has
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54 THE BLOOD.
described the life-history of two varieties of laverania ; and he also finds
that the period of maturation of one brood of the parasite coincides
with the development of fever.
Without entering into details, the author would observe that Canalis’ descrip-
tion applies to certain forms of the hematozoon which he himself has observed
in a case of reduplicated quartan ague with a very irregular course, and in certain
other particulars the observation is worthy of notice. Besides the usual amz-
boid forms, there were to be seen a remarkable number of pale, homogeneous,
red blood-corpuscles, and immediately after the febrile period—a double paroxysm
lasting for twelve hours—the blood contained free particles of protoplasm, en-
closing fine granular pigment and having attached long and well-formed flagella,
There were also present small round bodies segmented in the middle and pro-
vided with long, thick, freely-moving flagella, upon which black particles were
scattered. (See fig. 32.)
The most curious fact noticed was the presence, mostly towards the outer
eee OS r
Fic. 33-—lertian Ague; the Blood at the Commencement of the Attack. ‘he figure is com-
posed so as to represent the appearances observed in several cases. Zeiss’s compensation eye-
piece 4, apochromatic objective 2 mm., apert. 1.40, homogeneous immersion ; Abbe’s mirror,
and medium diaphragm.
boundary of the preparation, of spirally twisted bodies resembling the spirillum
of relapsing fever, but thicker and longer than the latter, and further distin-
guished by their outline being broken by very minute pigment particles. ‘These
bodies were actively mobile in the direction of their long axis. They never made
their appearance until some hours after the preparation had been mounted.2"2
Clinically, as has been said, the case was one of reduplicated quartan ague,
and pathologically it was found that distinct generations of the parasite matured
at separate intervals, their maturity corresponding with the access of fever.
Besides the parasites described here, the blood in malaria contains
pigmented leucocytes. These, however, are not characteristic of the
disease, occurring as they do in other febrile states, as, for instance, in
relapsing fever.
As the result of the foregoing description, it will be seen that the
parasite of malarial fever exhibits a singular variety of form.
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PARASITE OF MALARIA. 55
Notwithstanding, there are certain well-established facts available for
the diagnosis of the disease as it presents itself in European climates.
An examination of the blood at the outset, or during the period of fever,
will suffice to establish the nature of the disease in cases of tertian ague.
A number of the red corpuscles will be seen to be of a remarkably pale
colour, and within some of these pale corpuscles will be found freely-
moving colourless bodies, containing a fine granular pigment. Some of
the ved corpuscles are almost quite decolorised, and within these the
process of segmentation of the hemameba into 15-20 parts may be more
or less clearly distinguished. On the other hand, where this process can
be observed, and where the segments are fewer—6 to 8 in number—and
result in the characteristic marigold arrangement, the diagnosis of quartan
Jever may be made with equal certainty.
In view of the great importance of this subject, it is deemed advisable
to illustrate the foregoing remarks by a figure representing a specimen
of blood taken from a case of tertian fever at the commencement of the
paroxysm. The pale corpuscles contain the plasmodia (fig. 33).
This figure is drawn from appearances actually observed by the author
in three cases of tertian fever, and it will perhaps have an additional
value as affording a means of comparison with figs. 27-32, which were
partly borrowed from other sources, and in part merely diagrammatic.
In cases where the hemameeba is found in the blood, together with
the forms of laverania just described, the condition may be taken to be
one of atypical or anomalous intermittent fever.
It is unnecessary to dwell upon the great importance of these
researches. By their aid it has become for the first time possible to
distinguish malaria with absolute certainty by the result of an examina-
tion of the blood, and we have thus acquired an invaluable means of
discriminating other affections which closely resemble it, as obscure
sepsis, and certain cases of endocarditis and tuberculosis.?0?
4. Methods of Examining the Blood for the Parasites of
Malaria.—No more need be said to impress upon the reader the
expediency of being able to recognise the principal varieties of this
interesting parasite. For the purpose is needed an oil-immersion lens and
a moderately wide aperture of the diaphragm, or, still better, an apochro-
6 a RE His : et mao OMe: :
matic objective—as Zeiss’ apochromatic objective —— with compensating
1.40 - °
eye-piece IV. With such an instrument very little practice will secure
proficiency of observation ; indeed, the endoglobular pigmented parasite
can be discovered quite as readily as, for instance, the spirillum of re-
lapsing fever.
For the purposes of more precise investigation, and especially to avoid
the chance of being misled by the process of vacuolation in the red
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56 THE BLOOD.
corpuscles which has been noticed at p. 37, it is necessary to resort to
staining methods.
To distinguish the parasite of malaria from simple vacuolation it will suffice
to smear the under-surface of the slide upon which a preparation is mounted
with some blue fluid, as, for instance, a solution of aniline dye. The vacuoles
will then display the same colour as exists elsewhere in the field when not occu-
pied by corpuscles.?¢*
The parasite may be suitably stained in the following way :—
Methylene-blue is dissolved in normal (0.67%) salt solution until the
fluid is somewhat deeply coloured. The latter is then filtered, sterilised,
and set apart in small quantities in thoroughly sterilised test-tubes. The
point of the finger is then carefully cleansed, a drop of the staining fluid
applied to it, and through this the finger is pricked with a needle. The
flowing blood mixed with the staining fluid is brought in contact with a
Fic. 34.—The Blood in Tertian Ague at the Commencement of an Attack. Stained by Aldehoff’s
method; a. Plasmodia; b. Leucocytes; ¢. Eosinophil-leucocytes ; d. Blood-platelets (compen-
sation eye-piece VIII., apochromatic objective 2 mm., apert. 1.40, homogeneous immersion, Abbe's
mirror and open condenser).
cover-glass, and this is placed preparation-side downwards upon a slide
and examined. The preparation must be spread in a very thin layer,
and it is therefore necessary to guard against evaporation. This may be
done by sealing the edge of the cover-glass with paraftin-wax. It may
be examined first with a fairly wide aperture of the diaphragm, and
afterwards with an open condenser and a good oil-immersion lens.
The plasmodia, whether enclosed within the red corpuscles or lying
free in the blood, are stained a distinct blue of a light shade, and upon
this the pigment particles which they exhibit and the process of develop:
ment which they undergo may be easily discerned. It must be mentioned
that besides the plasmodia some red corpuscles which are free from them
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PARASITE OF MALARIA—VERMES. 57
may also take the stain, but with a little attention confusion will not
arise from this, since the corpuscles in question are stained uniformly
throughout. Instead of normal salt solution, diluted and _ sterilised
ascitic fluid may be employed for mixing the methylene-blue solution
(Guarnieri and Celli).
To mount a permanent preparation, the blood should be dried in a
very thin layer, the cover-glass heated for some time in the usual way,
and the preparation stained in eosin-methylene-blue solution (Chenzinshy,
Plehn).?o*
Plehn’s solution is as follows :—
A concentrated watery solution of methylene-blue . . 60 parts
3°/, solution of eosin in 75°/, alcohol . 2 : : . 20 parts
Distilled water . : : . 40 parts
To this is added 12 drops of a 20°/, solution of caustic potash.
The red corpuscles then appear a light red, leucocytes light blue, and
their nuclei a deep blue, the eosinophil granules of the leucocytes a
deep red; the parasites of malaria are stained blue. The method yields
good results.
The method of Aldehojf and Gabritschewsky for staining eosinophil
cells may also be applied for the detection of these parasites (fig. 34) in
the following manner :—
On cover-glasses prepared as laid down at p. 32, the blood is spread
out in a thin layer, and they are then immersed in a concentrated alco-
holic solution of eosin * for half-an-hour in the cold, or for 2-3 minutes
with heat, removed and washed with distilled water, then again stained
by dipping them once or twice into a concentrated watery solution of
methylene-blue, and finally well rinsed with distilled water. It is neces-
sary to obtain the blood rapidly, and to conduct the process without
undue delay. If this precaution be neglected, the blood-plates which
make their appearance (fig. 34 d) may be thought to have something to
do with the disease. R. Paltauf has directed attention to this as a
source of fallacy, and it may possibly explain the remarkable observa-
tions of Hochsinger.?°
It remains to be noticed that Loef and Pfeiffer °° have discovered in the blood
in SMALL-POX certain protozoa, to which they attribute a pathological signi-
ficance.
2. Vermes.—Under this heading we have to describe Distoma
hematobium and Filaria sanguinis hominis. Both are worms—the first
of the class Platodes and order Trematodes?® ; the second of the class
Annelides, order Nematodes, family Filariadew.
1. Distoma Hematobium (fig. 35).—Bilharz 28 has found this para-
* Kosin blaulich 22, Bayer, Elberfeld.
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58 THE BLOOD.
site in the main trunk and branches of the portal vein, in the splenic
and mesenteric veins, and in the venous plexuses of the bladder and
rectum. As the result of his investigations, he came to the conclusion
that more than half the adult Fellaheen and Coptic population of Egypt
suffered from it. Except in the blood, the eggs are more commonly
found than the parasite itself, and this in the liver, the lungs, the
bladder, the urethra, the large intestine, and the urine (see chapter on
Urine), giving rise to diarrhea, hematuria, and ulceration of the mucous
surfaces of these organs. Distoma hematobium has not yet, so far as
we know, been found in the peripheral blood-vessels, and on this account
it is seldom seen in the microscopic examination of the blood during life.
The parasite is of a white colour. The male and female are distinct
individuals. The former is from 12-14 mm. long, the latter 16-19 mm.
The male is thicker than the female. There are oral and abdominal
suckers anteriorly, and the genital opening in either sex lies close behind
Fic. 55.—Distoma Hematobium. Male and Female, with Eggs, from a preparation by
Dr. Schiess-Bey.
the latter. On the abdominal aspect of the male is a deep trench with
overlapping edges, which begins just behind the abdominal pore, and
serves for the reception of the female.
The eggs are slender bodies, about o.r2 mm. long and 0.04 mm.
broad, and furnished with a little spike, which projects from the
extremity or at the side.
Ringer *® discovered a new form of this worm at Tamsui in Formosa, and
Manson” found the eggs of the same species in the bloody sputa of a Chinese
who had lived for a long period in Formosa.
2. Filaria Sanguinis Hominis.—Waucherer 21 is said to have first
discovered this parasite in Bahia. Dr. Lewis”? of Calcutta, at all
events, was the first to describe it as occurring in the living body.
It is the larva of a filiform worm, which in the mature state measures
about 40 mm. in length. According to Bourne,?!3 the male is 1} in.
long, and carries two spicule. The larva, as it is found in the blood
of the living subject, is 0.0075 mm. in breadth and o-34 mm. long.
It has a short rounded head, with a tongue-like appendage, and a long
pointed tail. From the hinder extremity a ribbon-like proeess projects,
and when viewed with a high power of the microscope, this, like the
cephalic appendage, is seen to be the end of a closed sac in which the
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HEMOGLOBIN. 59
animal can coil or extend itself. This envelope is entirely structure-
less, but the contained parasite is seen under a very high power to be
transversely striated and very granular. In the blood the animal ex-
hibits for hours at a time the liveliest movements.2!4 At first it seems
to be homogeneous and transparent, but after some hours its motion
ceases, it assumes a darker tint, and the granular contents of its body
are easily discernible.
The parasite is rarely found elsewhere than in the blood and lymph
of persons who live, or have lived, in the tropics. It has recently, how-
ever, been met with in temperate climates.?)
It may infest the blood for months, or even years, without giving
Fig. 36.—Filaria Sanguinis Hominis (after Lewis and Leuckavt).
any sign of its presence ; but commonly, by blocking or perforation .of
capillaries and lymphatics, it leads to hematuria and chyluria, or to
hemorrhage and lymphatic exudation in different organs.
It would seem that the parasite is often conveyed by mosquito-bites.?16
Patrick Manson, Stephen Mackenzie, and others,? have shown that in
persons who suffer from the presence of Filaria sanguinis hominis, the
parasite is to be found in the blood only at certain periods, being absent
during the day, and abounding especially at night. Hence it is im-
portant that, when itis sought for, the blood should be taken from the
patient at night, and forthwith examined.
VI—CHEMICAL CHANGES IN THE BLOOD.
1. Colouring Matter.?!"—The most important constituent of the
blood is the Oxyhemoglobin—the combination of the colouring matter
with oxygen which is formed by the aération of the blood in the lungs.
The characteristic spectrum of dilute solutions of this body exhibits two
absorption-bands between D and E (of Fraunhofer’s lines). The band
nearest to D is darker, narrower, and more strongly marked ; that next
to E is less sharply defined and broader (fig. 37).
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60 THE BLOOD.
When submitted to the action of deoxidising substances, oxyhemo-
globin gives place to Reduced Hemoglobin. The spectrum of this body
is characterised by a single band, occupying a space about midway be-
tween the former two bands (fig. 38).
Red. Orange. Yellow. Green. Cyanblue.
—— —" 5 >
AGdBEC D Lb Ip
80 IO 100 116
pti
40 50
wlth tdi
Fic, 37. —Speetrum of Oxyhzemoglobin.
Under the action of acids of all kinds, of strong alkalies, and even of
CO,, hemoglobin is broken up into (1) a proteid resembling globulin,
and (2) the iron-containing body known as Hematin.
The spectrum of hematin in alkaline solution shows an absorption-
Red. Orange. Yellow. Green. Cyanblue.
AaB C D Eb F
0 50 80 90 100 110
ttt Gott the
Fic. 38.—Spectrum of Reduced Hemoglobin.
band lying between C and D of Fraunhofer’s lines (fig. 39). In an acid
solution its spectrum is identical with that of the methemoglobin acid
solution (fig. 42).
Hematin in alkaline solution, when treated with reducing agents,
Red. Oranye. Yellow. Green. Cyanbluc.
a a —— eee
AadBC D Eb FE
40 50 60 70 80 90 100 110
mob thot
fH
YY 4
Fic. 39.--Spectrum of Heematin in an Alkaline Solution.
yields Reduced Hematin. The spectrum of this body (fig. 40) exhibits
two absorption-bands between D and E. If the reduced solution be
shaken up with air or oxygen, these bands disappear again, and the
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TEICHMANN'S CRYSTALS. 61
spectrum shows once more the two absorption-bands of the alkaline
solution of hematin.
Hematin in combination with hydrochloric acid forms, even from
minute blood-traces, microscopic, highly characteristic, brown rhombic
crystals (fig. 41). These crystals were first discovered by Tetchmann.*!
They are of the utmost importance, inasmuch as their formation affords
an admirable test for blood-colouring matter under the most varied con-
ditions. We shall repeatedly have to revert to this later on.
To test for hemin crystals, the following plan may be adopted :—
The substance supposed to contain blood colouring-matter must be dried
Red. Orange. Yellow. Green. Cyanblue.
AaBeCe D Eb F
40 50 60 70 80 90 100 L10
ibid thy fbb drt
Fic. 40.—Spectrum of Reduced Hematin.
(if not already dry), powdered, and placed upon a slide. A crystal of
common salt is then added to it, and a cover-glass laid upon the pre-
paration. A few drops of glacial acetic acid are then allowed to flow
beneath the cover-glass. The whole is heated to a point below boiling,
and after a little while, if the substance contains blood colouring-matter,
hemin crystals (fig. 41) will be discernible by the microscope.
When an acid solution of hematin in alcohol is treated with reducing agents,
a series of colouring-matter derivatives are obtained. Of these, hwmatoporphyrin
Fic, 41.—Teichmann’s Hiemin Crystals (eye-piece III., objective 8a, Reichert).
(Hoppe-Seyler)° and heaahydro-hematoporphyrin (Nencki-Sieber)* have been
already isolated. If hzematoporphyrin be acted upon with tin and hydrochloric
acid in an alcoholic medium, it yields a body which cannot be distinguished
chemically or by its spectrum from urobilin (Hoppe-Seyler).?* According to C. le
Nobel,?"* however, this body is otherwise not identical with urobilin.
This substance can also be obtained from bilirubin by the action of sodium
amalgam (Maly).”4 There is another important derivative of hematin, which is
apparently identical with bilirubin. This is Hematoidin, a substance first dis-
covered by Virchow?” in extravasated blood. It was afterwards found in old
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62 THE BLOOD.
cerebral clots, in splenic infarctions, blood cysts, &c., and it has been met with
in human urine, in the sputum, and feces.*
From these facts, namely, that urobilin can be formed from hematin by the
action of reducing agents, and that this substance can also be formed from
bilirubin, Nencki and Sieber have established very simple relations between the
colouring matter of the blood and that of the bile. They have constructed a new
formula to express the constitution of hematin, and from this it would appear
that hematin is changed into bilirubin by the addition of two molecules of water
and the removal of one atom of iron, thus :—
Cy. Hz Ni O, Fe + 2H00 —- Fe = Cy Has Na Ob
———ae
Hematin. Bilirubin.
It follows from this, according to Nencki and Sicber, that bile pigment is JSormed
from the colouring matter of the blood, in that its molecules lose iron and take wp water.
Latschenberger 26 concludes, from experiments which he performed on animals,
that bile pigment, or rather its antecedents, to which he gives the name of Chole-
globin, results from the decomposition of blood colouring-matter, a dark-coloured
ferruginous pigment being formed at the same time. Choleglobin is elaborated
both in the tissues and in the interior of cells.
It seems to the writer not unimportant to consider these views here, in antici-
pation of much that will have to be said later on concerning the colouring-matters
of the blood and of the bile, in their relations to one another.
Red. Orange. Yellow. Green. Cyanblue.
Be ~—
AabBC D Eb F
40 50 na 70 80 90 100 ALO
titi tit
Fic. 42.--Spectrum of Methemoglobin in Acid and Neutral Solutions.
The colouring matter of the blood forms with oxygen another com-
pound, called Methemoglobin,??’ which is distinguished from oxyhemo-
globin by the more intimate union of the O with the Hb.
The spectrum of methemoglobin in acid and neutral solutions shows
four absorption-bands (fig. 42), one well marked (between C and D),
the other three in the yellow, green, and blue, being less easily seen.
This spectrum, as already said, is indistinguishable from that of acid
hematin in alcoholic solution. Any possibility of confounding these
two bodies is, however, excluded by the fact that when methemoglobin
is acted upon with sulphide of ammonium, its spectrum gives place, first,
to that of oxyhemoglobin (fig. 37), and after a while to that of reduced
hemoglobin (fig. 38); whilst, on the other hand, a solution of hematin
treated with ammonium sulphide yields a spectrum exhibiting two
absorption-bands between D and E (fig. 40). In alkaline solution, the
* See the chapters on these subjects.
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BLOOD-CHANGES IN DISEASE. 63
spectrum of methemoglobin shows three bands, viz., a narrow one
between C and D, but close to the latter, and two broader ones between
D and E (Jiderholm).2°8
1. Blood-changes in Dyspneea.—All conditions which interfere with
the giving off of CO, and the absorption of O in the lungs are attended
with certain characteristic changes in the blood.
The clinical symptoms of dyspnoea do not fall within our province.
They result directly from the condition of the blood, which shows itself
in the appearance of the patient. The arterial blood is laden with
carbonic acid, and in consequence has a darker colour, and this imparts
a bluish hue to the visible surfaces—cheeks, lips, nose, and finger-
tips. Microscopical examination of the blood shows no changes of a
special character. And further, in cases of the most severe dyspnoea
the blood is never so deficient in oxygen that its spectrum exhibits any
considerable change, such as, for instance, the disappearance of the oxy-
hemoglobin bands. v. Loos, by the application of Hénocque’s instru-
ment, has observed a notably diminished intensity in the oxyhemoglobin
bands in three cases of extreme cyanosis, while the proportion of con-
tained hemoglobin was approximately normal; and it is probable that,
with greater familiarity in the use of this method, we shall learn to
distinguish quantitative and qualitative spectroscopic changes as a result
of dyspnea.
2. Blood-changes in Carbonic Oxide Poisoning.—In carbonic oxide
poisoning the blood undergoes a change of colour which is appreciable
Red. Orange. Yellow. Green. Cyanblue.
—_— ——
AadBC D Eb F
40 50 60 70 80 90 100 140
pip bet ttt Ee
Fic. 43.—Spectrum of Carbonic Oxide Hemoglobin.
by the naked eye. It becomes of a bright cherry-red, alike in the
arteries and the veins. Spectrum-analysis shows the most important
change (fig. 43). The two absorption-bands of oxyhemoglobin are
replaced by two others between D and E, but placed slightly nearer to
the violet end of the spectrum. These bands indicate the union of the
hemoglobin with carbonic oxide,?*® and the most important quality of
this union is, that these bands cannot, as in the case of oxyhemoglobin,
be made to disappear by the action of deoxidising agents (ammonium
sulphide, Stokes’ fluid). Carbonic oxide hemoglobin in the blood of
the living subject may be recognised thus :—A few cubic centimetres of
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64 THE BLOOD.
blood are taken from the patient by means of a cupping-glass, and mixed
with water. Sulphide of ammonium is then added, and the solution is
placed in a glass vessel with parallel sides, or, still better, the blood
itself placed by means of Hénocque’s apparatus before the slit of the
spectroscope. If the specimen be one of blood poisoned with carbonic
oxide, the two absorption-bands will remain in spite of the admixture
with the reducing agent, sulphide of ammonium.
The presence of carbonic oxide in the blood can also be determined
by the following chemical test:—To a quantity of blood mixed with
water a 10 per cent. solution of caustic soda is added. When the mix-
ture is slowly warmed, a cinnabar-red colour appears. Under similar
circumstances a solution containing oxyhemoglobin will turn brownish-
green (Hoppe-Seyler, Otto).?°°
A modification of this test has been suggested by Salsozwsh?.251 The
blood to be examined is diluted with water to twenty times its bulk,
and a like quantity of a solution of caustic soda (sp. gr. 1.34) is added.
If the blood contains carbonic oxide, the fluid turns first white and
cloudy, and presently a bright red; when allowed to stand, red flakes
form and settle upon its surface. In the case of normal blood, when
treated in this way, a dirty brown colouration results. Kuniyost Kata-
yames method 78? is to add to the blood a little yellow sulphide of
ammonium and dilute acetic acid. The presence of carbonic oxide will
then be shown by the appearance of a beautiful red colour, whilst
normal blood so treated turns grey or greenish-grey.
Kunkel and Weizel 23° employ zinc chloride, or a very dilute solution of
platinum chloride. With these reagents carbonic oxide blood turns a
bright red, while normal blood becomes black. Other tests recom-
mended by Welzel are potassium ferrocyanide, acetic acid, and tannin.
Rubner *34 dilutes the blood with four to five times its bulk of acetate of
lead, which causes normal blood to take a chocolate-brown colour, while
if carbonic oxide be present it turns red.
3. Blood-changes in Poisoning with Sulphuretted Hydrogen (Hydvo-
thionemia).—The investigations of Hoppe-Seyler 23> tend to the conclu-
sion that hemoglobin will enter into combination with H,S, and form
a substance which that author has called Sulphide of Methemoglobin.
It is, however, noteworthy that in the severest cases of poisoning with
H,§, the two absorption-bands in the spectrum of oxyhemoglobin are
never known to disappear. In such cases, the blood becomes peculiarly
dark, and sometimes of a dull green tint. And it is further remarkable
that the distinction between venous and arterial blood entirely disap-
pears (Lewin).°°°
4. Blood-changes in Prussic Acid Poisoning.— Preyer 237 maintains
that hydrocyanic acid forms a crystalline compound with hemoglobin.
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BLOOD-POISONING—HAMOGLOBIN MIA. 65
However this may be, such a compound has not yet been found in the
blood of men or animals poisoned with the drug. According to Hoppe-
Seyler,”** the union of hydrocyanic acid with hemoglobin is of a very
unstable character, the resulting body readily decomposing when crys-
tallised or in presence of putrefaction.
5. Blood-changes in Poisoning with Chlorate of Potash. — Mai-
chand 8° discovered that when potassic chlorate was taken in great
quantities, the blood was profoundly altered, the most notable effect
being the formation of a sepia-like decomposition product, which was
afterwards shown to be identical with the methemoglobin of Hoppe-
Seyler mentioned above. Large doses of chlorate of potash cause the
production of methemoglobin itself in the blood, especially of children.
Stokvis and others 24° conclude from experiments upon rabbits that the
exhibition of the salt is not attended with the formation of methemo-
globin in the blood of the living subject ; while Marchand and Cahn*
have, in fact, obtained this result in certain animals, notably dogs.
The opinion of the latter observers finds support in a clinical notice
of Lenhartz, and also in a pathological observation recorded by JH.
Hammer?”
Chlorate of potash may be easily detected by spectrum-analysis
in fairly dilute solutions of hemoglobin, and the spectrum of methe-
moglobin, if present, will afford presumptive evidence of the poison.
Methemoglobin is produced also by the inhalation of nitrite of amyl
(Gamgee) and the injection of sodium nitrite into the blood-vessels 7#%
(Hoppe-Seyler), as well as by kairin, thallin, hydrochinon, pyrocatechin,
iodine, bromine, turpentine, ether, perosmic acid, permanganate of
potash (G. Hayem), and antifebrin (Fr. Miiller).** [The nitrites form
a compound with its oxygen, more firmly fixed than that of the oxygen
in oxyhemoglobin. They consequently tend to stop internal respira-
tion, but are more readily displaced by the products of asphyxia than
is carbonic oxide hemoglobin, and so again permit the aération of the
blood at the lungs. |
6. Poisoning with Nitrobenzol.—It has been asserted 74 that in dogs
poisoned with nitrobenzol the spectroscope has shown blood-changes
attributable to the presence of hematin. It would seem, then, that in
any case of suspected poisoning by this means in the human subject, the
blood should be examined in this direction by the spectroscope.
7, Hemoglobinemia.24°—By this term is meant the condition in
which hemoglobin is found dissolved in the blood. It is followed by
Humoglobinuria, whenever the spleen and the liver are unequal to the
task of eliminating the materials derived from the destruction of the red
blood-corpuscles within the vessels.
The presence of free colouring-matter in the blood may easily be
i
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66 THE BLOOD.
determined thus:—A little of the blood, drawn from the patient by
means of a cupping-glass, is placed immediately in a refrigerator, and
allowed to remain there for twenty-four hours. If the blood is normal,
perfectly clear yellowish-coloured serum will settle ; whereas, if heemo-
globinemia be established, there will be seen over the blood-clot a
beautiful transparent ruby-red stratum. The spectroscope shows in the
case of normal serum a feeble absorption-band in the blue part of the
spectrum (at /), said to be due to lutein (Thudicum) ;747 whilst with
serum containing colouring matter it shows the two absorption-bands of
oxyhemoglobin. The following method may also be employed :—Blood
serum is made to coagulate by heating it to 70°-80° C. If it contains
dissolved colouring matter it will appear of a more or less deep brown
colour, whereas healthy blood-serum when coagulated is light yellow and
of a milky turbidity. This method serves well for the detection of
heemoglobinemia.*48
8. Recognition of Changes in the Colouring Matter of the Blood.—
The changes in the character of the blood referred to above are chiefly
to be estimated by means of the spectroscope. Very perfect little
a b
é C
Fic. 44.—-Hering’s Spectroscope without Lenses,
instruments for clinical use have been invented by Desega of Heidel-
berg, Zeiss of Jena, and Hoffmann of Paris. Browning’s spectroscope
is also very suitable for the purpose.
To use one of these, artificial or day light is made to fall upon the
slit of the instrument. The telescopic tube attached to the apparatus
is focused until a spectrum is clearly defined, and if daylight be em-
ployed, the slit-like aperture is narrowed so as to bring Fraunhofer’s
lines clearly into view. The blood-solution to be tested is then fixed
between the aperture and the light. If the fluid be too concentrated,
it must be diluted beforehand. If the light be artificial, whether from
a lamp or some other source, it is well to place a little common salt or
some other salt of sodium in the flame, in order to define the situation
of the sodium line. Hénocque’s instrument is applicable to the same
purpose.
Very good results have been obtained in the investigation of blood
spectra with the aid of £. Hering’s 4° “ Lensless Spectroscope,” an instru-
ment which especially commends itself to the practitioner by reason
of its cheapness. It has been employed by the author together with
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PROTEIDS OF THE BLOOD. 67
Browning’s pocket-spectroscope, and shown itself to be quite as service-
able. The lensless spectroscope consists of two tubes, one sliding within
the other, and of about 24 cm. diameter. Of these, the outer one is
closed at its free end by a plate in which is a slit with a parallelogram
adjustment (fig. 44 c). The two parts of the plate which support this
parallel adjustment carry also a pair of clips destined to hold in posi-
tion a rectangular glass vessel or test-tube containing the fluid to be
examined.?6?
The tubes are lined with black, and the inner one (a) is provided at
(7) with a diaphragm to intercept reflected light. At that end of the
inner tube which is turned towards the observer, a prism (d) is fixed
in such a position that the spectrum is formed in a plane at right angles
to the proximal end of the tube, which is oblique, not vertical, in section.
In using the instrument, the eye must be directed at right angles to this
section, and not in the long axis of the tube. The tubes must also be
adjusted in such a manner that the spectrum is well defined and accu-
rately rectangular.
When this is done (by manipulation of the two tubes), a small but
very clear spectrum is obtained, in which the yellow is little developed,
but which very plainly exhibits absorption-bands such as those of oxy-
hemoglobin and urobilin. The instrument serves admirably for the
investigation of these bodies in blood and urine. Heénocque’s apparatus
is the most appropriate for the examination of undiluted blood.*
2. Proteids of the Blood.—The proteids of the blood are
diminished in all cases in which the total quantity of that fluid is
greatly lessened—temporarily, therefore, in hemorrhages of all kinds.
A permanent diminution of proteids occurs under such conditions as
disturb unfavourably the balance of waste and repair, whether of the
blood itself or of its contained albumin. Thus, in all diseases which
are attended with long-continued and excessive destruction of proteids
in the system, these bodies are found to be proportionally wanting in
the blood. It should be remarked, however, that such processes must
be long continued before this effect is reached, especially where the
digestive functions remain unimpaired. As a rule, a diminution of
proteids goes hand in hand with an unduly watery state of the blood
(hydreemia).
Hoppe-Seyler’s ?*! method is, perhaps, the best for determining the
proportion of proteids in the blood; but we shall not describe it
here, because it is very complicated, and its results are not altogether
accurate.
The occurrence of an absolute increase of proteids has not yet been
* This instrument can be had of Rothe, of Prague, for five florins.
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68 THE BLOOD.
established on satisfactory evidence. A relative increase is known to
happen in such diseases as are attended with the withdrawal of water
from the system more rapidly than it can be supplied, as in cholera and
acute diarvhcea.
In pneumonia and erysipelas there is an increase of fibrin. Hoppe-
Seyler 2 has devised a method for the estimation of the quantity of
fibrin in the blood, which is at once simple and adapted to clinical
purposes. It may be described as follows :—A beaker of about 80 ce.
capacity is provided with an india-rubber cap, perforated in the middle
by a close-fitting rod of whalebone. These are dried and weighed. Next,
30-40 cc. of blood, taken from the body of the patient with a cupping-
glass, are placed in the beaker, which is immediately covered by the
india-rubber cap and its whalebone rod. The blood is then defibrinated
by beating it up with the whalebone rod, allowed to cool, and weighed.
The cover is removed, and the beaker filled with water and beaten up
again. The fibrin is allowed to settle, washed with a solution of salt,
and placed upon a filter whose weight is known. Here it is again
washed with water until the fibrin is almost free from colouring matter.
It is next boiled with alcohol (to dissolve fat, lecithin, and cholesterin),
dried at r10°-120° C., then cooled, and weighed over sulphuric acid.
E. Ludwig? and the author have found peptones present in great
quantity in the blood in leukemia. Devoto, on the other hand, failed to
detect peptone in this condition, and Dr. Wagner (of Petersburg), by
examining fresh leukemic blood according to Devoto’s method, likewise
obtained a negative result. The same blood in a state of decomposition
showed abundance of peptone. In a second case in which the author
has applied Devoto’s method to the examination of leukemic blood no
peptone was found, and the same blood tested after death by this method
appeared also to be free from peptone, while Hoffmeister’s process showed
abundance of that body.
Further investigation is needed to explain the different results alluded to. It
is most likely that one or other of the two methods will serve for the detection
only of certain peptones. The observation of Devoto and Wagner, from which it
appears that Devoto’s method will not show the presence of peptone in leukzmic
blood which has been drawn during life, while in post-mortem blood it will, is of
much interest. In a third case—one of splenic leukamia—the author has lately
found much peptone by both methods in the blood during life.
To determine the presence of peptones in the blood, it is necessary
first to remove the other proteids by the action of metallic oxides, or by
coagulation with ammonium sulphate, and then to proceed in the manner
indicated in the chapter on Urine.
8. Urea.—Uvrea occurs only in traces in healthy blood (J. Picard)?
The following method will serve to detect its presence :—Blood is
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UREA. 69
diluted with 3-4 times its volume of alcohol, the mixture allowed to
stand for twenty-four hours, and filtered. The precipitate is washed
on the filter repeatedly with more alcohol, the filtrates are mixed, and
the alcohol distilled off. The residue is treated with nitric acid, and
the resulting crystalline pulp allowed to stand for some hours, when
the crystal masses which have formed are pressed between folds of
blotting-paper, dissolved in water, and treated with carbonate of baryta
until carbonic acid ceases to form, and dried on a water-bath ; the dry
residue is then extracted with boiling absolute alcohol. On evaporation,
the urea remains in long slender prismatic crystals belonging to the
rhombic system. If enough blood has been taken (at least 200-300 cc.),
or if the blood happens to contain urea in large quantities, the following
tests may be performed with the resulting crystals :—
t. Dissolve some crystals in a drop of water upon a slide, add a drop
or two of moderately strong pure nitric acid, and apply a cover-glass.
When looked at through the microscope, the characteristic hexagonal
plates of nitrate of urea will be seen.
2. To a somewhat saturated solution of the crystals add a little
metallic mercury and a drop of nitric acid, and heat; gas (CO, and N)
is rapidly evolved.
3. Heat the dried crystals in a test-tube, add a trace of caustic soda
and a drop of dilute solution of sulphate of copper. A violet colour
(biuret) indicates the presence of urea.
4. Over a erystal of urea pour a drop of fairly concentrated watery
solution of furfurol, and add immediately a drop of hydrochloric acid
of 1.10 sp. gr. A play of colours takes place from yellow through green
and blue to purple-red (Schiff).
This reaction does not occur with uric acid, but is yielded by allantoin, though
less promptly and clearly than by urea. It is given, moreover, by a number of
other bodies. 7°” :
When the above method* fails to exhibit the presence of urea—as,
indeed, usually happens in testing blood, on account of the very small
quantity of that body which it contains—resort must be had to the
more accurate process of Hoppe-Seyler,°> which can also be employed
whenever a quantitative analysis of urea is attempted.
[Haycraft?® recommends the following method :—20 ce. of blood are defibri-
nated and spread in a thin layer on a parchment-paper dialyser. This is then
floated on the surface of 50 cc. of absolute alcohol in a suitable vessel, where it
remains for twelve hours, the surface being kept moist by adding distilled water.
To the diffusate is added an equal bulk of concentrated oxalic acid solution, and
it is evaporated to dryness. To the residue is added naphtha-petroleum to remove
* The method has been described here because it serves well for the purpose of
examining the secretions and excretions generally for urea.
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70 THE BLOOD.
fats. The purified residue is then dissolved in a little water and barium car-
bonate added, next evaporated, the residue treated with boiling alcohol and
filtered. On concentrating the filtrate urea crystallises out, and may be sub-
mitted to the tests already described. ]
Dr. Miinzer has devised the following plan for the estimation of urea
in the blood :—The latter is treated with absolute alcohol and filtered,
&c., as above, the alcoholic extract evaporated, and the residue dissolved
in water. This is then submitted to Hufner’s process (see chapter on
Urine).
The method is not, perhaps, very exact, but by its means Miinzer has
determined the presence of great quantities of nitrogenous bodies in the
blood in cases of uremia.
Von Schroder’s method *° is, perhaps, the most delicate of all, but, on
account of its minute details, it is hardly applicable to clinical purposes.
Urea is found in increased quantity in the blood whenever its elimi-
nation is interfered with, either by disease of the kidneys or obstruction
of the urinary passages.
V. Schréder has shown that the formation of urea probably takes place in the
liver.
4. Urie Acid and Xanthin Substances.
1. Urie Acid.—Garrod found uric acid to the amount of 0.025-
0.175 in a thousand in the blood of persons suffering from gout. It
must be observed, however, that his method of testing for this substance
was far from exact.261
He took about 30-35 grms. of blood and allowed it to coagulate. Ten cc. of
the serum were then mixed with a dilute acetic acid solution in the proportion of
I: 10, and a delicate thread was placed in the fluid. When the blood contained
not less than 0.025 per 1000 uric acid, it was found that, after twenty-four to
forty-eight hours, the thread was covered with uric acid crystals.
In a few instances only did he precipitate from the blood with alcohol, and
apply the murexide test. 4 beles** has freed the blood from proteids by the
Schmidt-Mulheim process, and then tested for uric acid by Ludwig and Salkowski’s
method. Salomon? has observed an increase of uric acid in the blood during
the acute attack of gout.
For the detection of uric acid in the blood, the following procedure
may be adopted :?°4—roo—300 grms. of blood are removed by cupping,
and at once diluted with 3-4 times the bulk of water, heated on the
water-bath, and, when coagulation begins, treated with a few drops of
acetic acid (sp. gr. 1.0335 at 15° C.) until it has a feebly acid reaction.
It is left on the boiling water bath for 15-20 minutes, then removed
and filtered. The precipitate on the filter is repeatedly washed with
hot water and added to the filtrate. The fluid, which should now have
a slight yellow tinge, is again treated with a little acetic acid (sp. gr. as
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URIC ACID—-XANTHIN BASES. val
before), boiled over a flame, allowed to cool, and filtered. To the filtrate,
when cold, is added a little sodic phosphate, and it is then submitted to
the Ludwig-Salkowskt process. Should it happen that the pure blood
is deficient in salts, it may not coagulate on the water-bath so as to
yield a sufficiently clear filtrate. This may be remedied by the addition
of a little common salt.
The filtrate obtained by the Salkowski-Ludwig process, after the
addition of hydrochloric acid, is evaporated to the bulk of ro ec., and
allowed to stand for twenty-four hours; then, if visible crystals are
deposited, these ave obtained on an asbestos filter, washed first with
cold water and then with alcohol.?%©
1. Examine some of the crystals under the microscope. The character-
istic whetstone forms, and sometimes the rhombic tables, of urie acid
crystals are seen (figs. 110, IIT).
2. Some of the crystals may be submitted directly to the murexide
test (see below). If there should be no precipitate, or only a very slight
one, after the addition of nitric acid, the fluid containing hydrochloric
acid should be evaporated to dryness on a water-bath, pure nitric acid
added, and this again driven off by heat. To the residue is applied, by
means of pipettes, at one part a trace of ammonia, at another a little
caustic soda solution. If uric acid be present a red or purple coloration
develops at the spot touched by ammonia, and a blue round the soda
(murexide test). Nitric acid in the test may be replaced by bromine-
water, or chlorine-water, or nitrous acid (v. Jaksch).?°° The latter serves.
particularly well. The use of bromine-water or chlorine-water as re-
agents has for its object to distinguish between uric acid and the
xanthin bases.
The quantitative estimation of uric acid in the blood may be effected
in the same way. The blood is first freed from albumin, and Salkowshi
and Ludwig's process applied.?67
The blood in health does not contain uric acid in appreciable quantity.
Certain morbid states are marked by its appearance there. In croupous
pneumonia it may amount to 0.008 grm. in 100 grms. of blood. It is present
also in renal disease (acute and chronic nephritis and contracted kidney),
in severe anemia—finally, in all conditions which induce dyspnea,
notably in heart-disease and pleurisy. It is absent from the blood in
articular rheumatism and typhoid. It would appear that the febrile
state, as such, never leads to the production of uric acid in the blood.
From what has been said it follows that the presence of uric acid in
the blood is not characteristic of gout alone, and that it has not, there-
fore, the diagnostic significance imputed to it by Garrod.
2. Xanthin Bases.—Xanthin substances have been found in the
blood by various observers.?& They are closely allied to uric acid, and
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72 THE BLOOD.
the principal are xanthin and hypoxanthin. Very probably adenin,
paraxanthin, and guanin also occur. They may be detected in the
filtrate after the removal of uric acid in Salkowshkt and Ludwig’s process,
by the modified murexide test already described (p. 71), and by washing
the coloured residue after the application of the reagents mentioned
there (v. Jaksch).
5. Carbohydrates.
1. Grape-Sugar.—In health the blood contains a minute quantity
of sugar. To detect its presence there, the blood must first be freed
from proteids, and for this purpose the old method of Claude Bernard *°°
is the best. The blood is weighed, and its own weight of crystalline
sodic sulphate is added to it, and the mixture is boiled and filtered.
The filtrate may be tested for sugar as below. Another method for the
removal of proteids is to rub the blood in a mortar with solid ammonium
sulphate, and filter. In this case also the filtrate is free from proteids,
and the fact may be ascertained by testing it with alcoholic solution of
zine chloride (Abeles).
1. Moore’s test will serve where sugar exists in any quantity. (See
chapter on the Urine.)
2. Trommer’s test. (See chapter on the Urine.)
3. Lhe phenyl-hydrazin hydrochloride test is the best for detecting
slight traces of sugar in the blood. It is conducted as follows (v,
Jaksch) :?—
Add together two parts of phenyl-hydrazin hydrochloride and four ©
parts of acetate of soda ; add water and heat. Take 5 cc. of the proteid-
free filtrate (which is practically a saturated saline solution), obtained
by Claude Bernard’s process, and while still warm add it to 5 cc. of the
solution prepared as above. Place the mixture in a test-tube half filled
with water, heat it for half-an-hour on a water-bath, and allow it to
stand. Or a little of the phenyl-hydrazin salt and acetate of soda may
be added in a dry state to the warm proteid-free filtrate, and the process
conducted as described above. After it has cooled, when examined
under the microscope, it is seen to contain separately and in clusters the
characteristic yellow crystals of phenyl-glucosazon scattered amongst
colourless crystals of sulphate of soda. (See chapter on the Urine.)
To determine the percentage of sugar in the blood, Fehling’s fluid
may be employed (the blood having been previously freed from proteids)
in the manner afterwards to be recommended for testing for sugar in the
urine, and the polarimetric test* may be applied. It seldom happens,
however, that the filtrate contains sufficient sugar to be appreciable with
* See chapter on the Urine.
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GRAPE-SUGAR. 73
the polarimeters at present in use. Lippich’s instrument is the most
sensitive, and gives the best results in this connection.
[Pavey’s method, if somewhat tedious, serves well for the estimation of sugar
in moderately small quantity. The process may be divided into three parts :—1.
40 grms. of sodic sulphate are placed in a beaker, and 20 cc. of blood added,
The beaker and its contents are weighed ; the mixture is stirred, and about 30 cc.
of a hot concentrated solution of sodic sulphate added. The mixture is heated
till a coagulum forms, when the fluid is poured off, the coagulum washed, and
the washings added to the fluid in another vessel, which is then boiled and
filtered. 2, The filtrate is boiled, and an equal quantity of the copper test
solution added. The resulting suboxide of copper is collected on a glass-wool
filter and washed. It is then dissolved with a little peroxide of hydrogen and
nitric acid, boiled to drive off the excess of peroxide, and filtered through glass
wool, which latter must be carefully washed. ‘The filtrate contains the copper in
the form of nitrate. 3. The copper solution is placed in a vessel into which a
cylinder of platinum foil of known weight, connected with the negative pole of
a galvanic battery, is suspended. Within this a platinum spiral is made con-
tinuous with the positive pole of the battery. ‘he current is allowed to flow for
twenty-four hours, when the cylinder is removed, washed in distilled water and
alcohol, and weighed. The amount of copper deposited is the basis of a simple
calculation. One part of copper corresponds to .5678 parts of sugar; hence the
quantity of sugar in the blood used may be obtained by multiplying the weight
of copper deposited by this figure.
Claude Bernard’s "3 method :—Place 20 grms. of crystallised sodic sulphate in
each of six porcelain capsules, and to each add 20 grms. of the blood to be inves-
tigated. Mix the blood and salt together ; boil them till the froth above the clot
becomes white, and the clot itself is free from red specks; weigh again, and
make good the loss from evaporation by addition of water. The whole is then
placed in a small press, and the fluid part expressed, collected in a capsule, and
afterwards filtered. The filtrate is placed in a burette. Ina flask place 1 cc. of
Fehling’s solution, and to it add a few small pieces of caustic potash and 20 cc.
of distilled water. Boil this fluid, and from the burette allow the clear filtrate
of the blood to drop into the boiling dilute Febling’s solution until the latter
loses every trace of its blue colour. Asin all sugar estimations, the process must
be repeated several times to get accurate results. Hence the reason why several
capsules are prepared.
Read off the number of cc. used of the filtrate in the burette, ¢97., = n ce.
The formula
in grammes the weight of sugar per kilogramme of blood.
In Seegen’s method,” which may be taken as the type of the newer methods,
the proteids are precipitated by ferric acetate. The blood is diluted with 8-10
times its volume of water, acidulated with acetic acid, and heated. When the
precipitation of proteids commences, render the mixture strongly acid by the
addition of acetate of soda and perchloride of iron; then add sufficient sodic
carbonate until the mixture is faintly acid, and boil. Allow it to cool, and filter
it through a fine cloth filter, free from starch. The filtrate ought to be clear.
The residue on the filter is washed several times with water, and the remaining
fluid in it expressed by means of a small hand-press. The expressed fluid is then
mixed with the clear filtrate if the mixture has a slightly reddish tint from the
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74 THE BLOOD.
admixture of a small quantity of blood-pigment. Add a drop or two of per-
chloride of iron to precipitate the last traces of the proteids. Filteragain. The
sugar in the filtrate is estimated in the usual way by means of Fehling’s solution.]
In diabetes large quantities of grape-sugar are found in the blood.
Hoppe-Seyler 2” describes a case in which it reached as high as 0.9 per
cent. The researches of Freund 2° would make it appear that a deoxi-
dising substance—presumably sugar—exists in considerable quantity in
the blood in eases of carcinoma. This has been substantially confirmed
by Lrinkler.?7
2. Glycogen.—Salomon and Fr. v. Frerichs?"§ have studied the ques-
tion of glycogen in the white blood-corpuscles. Gabritschewshky?™ dis-
covered that this body occurs partly in the protoplasm of leucocytes, and
partly as free granules in the blood both of health and disease. For its
detection the blood is spread in a thin layer between two cover-glasses,
and dried in the air. A concentrated solution of gum arabic containing,
in roo grms., t grm. of iodine and 3 grms. of iodide of potassium, is
taken, and a drop is allowed to flow between the cover-glasses. The
presence of glycogen-containing leucocytes, which are the same as the
neutrophil cells described at p. 31, and also free granules of glycogen, is
made evident by a more or less deep brown coloration, whether of leu-
cocytes or granules. In health the blood examined after meals exhibits
little or no increase of glycogen. In diabetes and leukemia the glycogen
reaction is very pronounced (see Chaps. 1V., VIT., VIII.).
8. Cellulose.—According to Freund 8° the blood of tubercular
patients contains cellulose. For the detection of sugar, cellulose, and the
carbohydrates generally in the blood, the process of Baumann and
Udransky 8! may be employed with advantage. This is based upon
the fact that the carbohydrates are precipitated from their watery solu-
tions by the addition of benzoyl chloride and caustic potash, forming insol-
uble compounds. This combination of the carbohydrates with benzoyl
chloride when treated with sulphuric acid yields furfurol, a body which
may be recognised by its characteristic colour-reaction.
6. Organic Acids in the Blood (Lipacidemia). — Traces of
volatile fatty acids are sometimes present in the blood. The author has
frequently met with them. For their detection 20-30 erms. of blood
are taken from the patient by means of a cupping-glass, an equal
weight of sulphate of soda added, and the whole boiled and filtered.
The filtrate is evaporated to dryness, and the residue extracted with
absolute alcohol. The alcoholic extract in a large number of cases
contained no fatty acids, but, on the other hand, these occurred in
traces whenever looked for in fever and leukemia, and occasionally in
diabetes. *8?
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LIP MIA—CHOLAMIA. 75:
Lactic acid is also sometimes met with. Normal venous blood has
been said to contain 0.0079 per cent. of sarcolactic acid (Berlinerblau).
In regard to the latter and its tests, the reader may be referred to the
statements of Hoppe-Seyler and Berlinerblau.28* L. Hougouneng *** has.
found B-oxybutyric acid in the post-mortem blood of diabetes.
7. Lipgzemia.—The blood invariably contains small quantities of fat.
While digestion is in progress it abounds in this substance normally ;
but a permanent excess of fat is also a phenomenon of certain morbid
states. The blood in such cases is altered to the naked eye. It is.
turbid and usually paler than in health. Under the microscope a num-
ber of minute strongly-refracting globules are seen floating amongst
the proper cellular elements. The white corpuscles also often contain
fatty particles. [The lipemia of diabetes gives the blood a pink or
strawberry colour, and on standing a creamy layer collects on the
surface.] If any doubt remains in a given case as to the nature of these
particles, the addition of ether will settle the matter. If they are fatty,
a drop of ether poured upon the slide will dissolve them and cause them
to disappear.
Lipzmia has been met with in chronic alcoholism, chronic nephritis,
and severe cases of diabetes. It also occurs in wounds of the medullary
cavity of hones (embolic lipemia) when fluid fat passes into the blood.
8. Choleemia.—By this term is meant the condition in which the
constituents of the bile are found in the blood. In this connection the
biliary acids and colouring matters (bilirubin) are the points of chief
interest to the physician. And of these, again, the biliary acids must
probably be regarded as the real toxic agents, involving great possibili-
ties of mischief, leading to the disintegration of the red corpuscles, and,
as a consequence, to hemoglobinemia, disturbing the innervation of
the heart, and slowing the pulse. Even where such symptoms are
present, however, the quantity of biliary acids in the blood is always
very small—so small at times as to escape detection by the chemical
method presently to be detailed. This method, nevertheless, deserves
to be described, since it will serve where the biliary acids exist in com-
parative abundance in the blood, and in all cases where the secretions
are tested for bile. We shall, therefore, introduce it here :—
The blood 2° to be examined must first be freed from proteids by
precipitation with alcohol, or boiling it after dilution and filtering.
The proteid-free filtrate is treated with acetate of lead and ammonia.
The biliary acids combine with the lead and are precipitated as lead
salts. The precipitate is washed with water on a filter, boiled in
alcohol, and filtered. Carbonate of soda is added to decompose the lead
salt, The solution is again filtered, evaporated to dryness, and the
residue extracted by boiling with absolute alcohol. On evaporation, the
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70 THE BLOOD.
bile salts will crystallise out, or a dull amorphous substance may re-
main, from which the crystals can be derived by the addition of ether.
The amorphous substance itself may be tested for biliary acids by Petten-
kofer’s 86 method. This test depends upon the reaction of cholalic acid
in presence of cane-sugar and sulphuric acid. To apply it, dissolve
some of the crystalline or amorphous residue, obtained as above, in
water; add two-thirds its bulk of sulphuric acid slowly, so that the
temperature may not be raised above 60°. To the mixture now add a
few drops of a solution of cane sugar (1 to 5 of water), and a beautiful
violet colour indicates the presence of biliary acids. According to
Mylius,8" this test depends on the formation of furfurol from grape-
sugar, which then gives a play of colour with the bile acids. The
reaction may also, therefore, be well displayed with furfurol.?**
Mackay’s®*° physiological test may sometimes serve for the detection
of these substances in the blood. It depends upon the action of hile
acids, as observed in experiments, on the atropinised frog’s heart.
If a known quantity of blood be taken, the proportion of bile acids
in the blood may be determined in the manner described above. Efforts
have been made, unsuccessfully, to base an analytical test upon the
polarisation phenomena of biliary acids.
Bilirubin may be recognised by testing the serum obtained from
blood which has been allowed to coagulate on ice by any of the methods
described later on (wide chapter on the Urine). Huppert’s test is the
best for this purpose.
The same thing may be done more simply in a manner which the
author has recently adopted. Blood is taken from the patient with a
cupping-glass, sterilised in a fairly wide cylindrical glass, and allowed to
stand for an hour or two. The serum is then drawn off with a pipette
forced through an asbestos filter by means of an aspirator, and placed
in a test-tube. It is then shaken into froth. If bile pigment be present,
this froth is yellow. In all other cases (as, for instance, in hemoglobin-
emia, where the serum itself is tinted) the froth is quite colourless.2%°
Moreover, if more of the serum be now taken and left for three or four
hours in a warm chamber at 35° C., the development of an intense green
colour will mark the formation of biliverdin. A mere trace of bile pig-
ment will cause this green colour to appear, whereas normal serum
remains unchanged. A still simpler plan **! is to cause the blood-serum
to coagulate slowly at 70°-80° C. If normal, it will show a milky
yellowish tint; but if bile colouring matter be present, this is replaced
by a green colour of varying intensity, according to the proportion of
biliverdin formed from the bilirubin during the heating. In this way
the author has demonstrated bile pigment in the blood when none could
be found in the urine. He has also observed that in nearly every case
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URZMIA—AMMONIZMIA—ACETON AMIA. Taf
where urobilin exists in the urine, bilirubin may be found in the blood.
This is an unportant fact, as showing that bile pigment circulating in
the blood is transformed in the system—probably by the kidneys—into
urobilin.
The microscopical examination of jaundiced blood generally shows nothing un-
usual. According to Silbermann,2? this condition in newly-born infants is marked
by the following changes :—The red corpuscles are more or less disintegrated ;
they are often pale, or exhibit only round the pale centre of the corpuscle a ring
of hemoglobin of normal tint. Blood-plates, macro- and micro-cytes, and poik-
ilocytes are to be seen, together with nucleated red corpuscles and corpuscle-
holding cells. In a case which came under his own observation, however, the
author failed to find such appearances. ‘They are not to be regarded as constant
in jaundice.
9. Ureemia.**’—When urinary products accumulate in the blood,
the condition is termed Uremia. The retention of these products is
marked by certain well-defined phenomena, even though we are not at
present able to refer them to the action of any one substance in parti-
cular. The assumption that the poisonous material is urea, or carbonate
of ammonia resulting from its decomposition, has heen disproved. It is
now believed that the symptoms of uremia are due in general terms to
the excessive accumulation of fixed products in the blood. The interest-
ing researches of Bouchard *** go far to show that they may be referred
to the toxie effects of certain bodies resembling alkaloids (ptomaines)
normally existing in the urine. Stacdthagen, on the other hand, asserts
that no such substances can be found in the urine. Uremic blood
shows an increased quantity of urea and extractives. In a number of
cases reported by Horbaczewsk?,® no increase in salts was noted, even
in the salts of potash. The author himself, as also Pezper, has in
several instances observed that the alkalinity of the blood was greatly
less than normal,2%* and in some cases there was an excess of uric
acid.297 There are no other characteristic changes to be noticed as
occurring in the blood in uremia.
10. Ammonizemia.—Of this condition very little is yet known.
From observations hitherto made, it would appear that the poisonous
phenomena are due to the action of some hody—probably an alkaloid—
introduced into the system by absorption from the diseased bladder.
It would be essential in such cases to examine the blood for ptomaines
and toxalbumins.
11. Acetonzemia.—This term is applied to a condition in which
the blood is surcharged with acetone. Derehmiller and the author 2s
have succeeded, by extracting the blood with zther and subsequent dis-
tillation, in separating from it a substance which gives the reactions of
acetone. In many morbid states, and especially in fevers, it is found in
considerable quantity.
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78 THE BLOOD.
12. Changes in the Salts of the Blood.—The blood contains
about one-half per cent. of chloride of sodium,?® and this quantity
remains constant, whether much salt be taken with the food or not.
Moreover, Schen/:? has shown that in fevers, as, e.g., pneumonia,
where the chlorides disappear from the urine, the proportion of salt in
the blood is not notably altered.
In rickets and osteomalacia the salts are diminished.
The blood of tubercular patients, according to Freund,*° is relatively
deficient in sodium salts and phosphates, whilst at the same time the
salts of potash are increased.
The tests and methods for the qualitative and quantitative analysis
of the salts of the blood are to be found in the various text-books of
physiology and physiological chemistry.°°
[Note on the Specific Gravity of the Blood. —Hammerschlag’s method for determin-
ing the specific gravity of the blood is a modification of Roy’s, with the advantage
that it can be much more rapidly and conveniently applied. A mixture is made,
in a suitable vessel, of chloroform and benzol, two liquids of widely differing
specific gravity and which are freely miscible. In this mixture a drop of blood
is placed, and by the addition as required of more chloroform or benzol, the
density of the liquid is altered until the blood remains suspended in it. When
this point is reached, the specific gravity of the liquid is ascertained in the usual
way. ‘That of the blood is of course the same. Chloroform and benzol may be
supplied from two pipettes, and the whole proceeding may be accomplished in a
few seconds. This method has given the most satisfactory results ; and it dis-
penses with the troublesome necessity of preparing a series of solutions.?°?]
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CHAPTER II.
THH BUCCAL SHCRETION.
Tue saliva is a mixed secretion, derived in part from the mucous glands
within the mouth, and partly from the parotid, submaxillary, and sub-
lingual glands, which open by ducts within that cavity. Any dispro-
portionate activity, whether in health or disease, of one or other of these
glands will be attended with a corresponding modification of the physical
and chemical characters of the saliva.!
[To obtain the saliva fairly pure, the patient should be made to wash
his mouth with a warm solution of bicarbonate of soda, and afterwards
with cold water. The inside of the mouth should then be lightly
touched with a glass rod, moistened with dilute acid, and the secretion
collected. |
I. NAKED-EYE APPEARANCES OF THE SALIVA.—The saliva,
when freshly taken from the mouth, is a colourless or light blue fluid,
usually somewhat thick and stringy. When allowed to stand for some
time, it settles into two layers, of which the lower one is quite cloudy
and turbid, and contains in the greatest abundance the morphological
constituents presently to be described.
The reaction is distinctly alkaline. [The amount secreted daily is
variously stated at from 800 to 1500 grms.]
II. MICROSCOPICAL APPEARANCES.—The saliva, when examined
with the microscope, is seen to contain certain morphological elements
in varying proportions. These are :—
1. Salivary Corpuscles.—These bodies resemble white blood-cor-
puscles, but are larger, and their protoplasm is usually very granular.
2. Red Blood-Corpuscles.—These are seldom met with, and when
they occur are readily recognisable.
3. Epithelium.—Usually in the form of large irregular squamous
cells, derived from the mucous membrane of the mouth and tongue.
The quantity of epithelium to be found in the saliva varies greatly in
health ; and the cells exhibit much difference in shape, according as
79
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80 THE BUCCAL SECRETION.
they come from the superficial or the deeper layers of the mucous mem-
brane. They are, however, easily known by their polygonal shape and
relatively large size.
4. Fungi.—Mould- and yeast-fungi are very seldom seen in the saliva
in health ; when they occur, it is as an accidental constituent, probably
introduced with the food. In disease, however, their presence is frequent.
Fission-fungi, on the other hand, are met with in great number and
variety in healthy saliva. There are to be seen, thickly scattered through
the secretion, smaller or larger colonies of micrococci, of which some
possess the property of staining reddish in a solution of iodine and iodide
of potassium. W. D. Miller? describes four varieties, which he has
named Iodococcus magnus, parvus, vaginatus, &c. ; bacilli, too, of varying
size, which take a bluish red colour with the same reagent. There is
also an organism called the Spirochete buccalis, which occurs in ex-
Gb
wae
8 el
"No gone «*
Fic. 45.—Buccal Secretion, prepared by Friedliéinder’s and Giinther’s methods (eye-piece III.,
objective Reichert }, ; homogeneous immersion ; Abbe’s mirror; open condenser),
a, Epithelial cells. e. Spirochzete buccalis,
b. Salivary corpuscles. f. Comma bacilli of the oral cavity.
c. Fat drops. g. Leptothrix buccalis.
d. Leucocytes. h,i, k. Different forms of fungi.
tremely mobile spiral threads, very closely resembling the spirillum of
relapsing fever ; from this it is distinguished chiefly by its greater breadth
and by the smaller number of its coils. Forms resembling the comma
bacillus are frequently found in the saliva (Lewis, Miller).? They have
been obtained in considerable numbers from the secretion (Vignal).4
As many as twenty-one different micro-organisms have been separated
by the ordinary methods (see Chapter X.), and cultivated on plates and
by inoculation; and their behaviour in various food media observed.
Biondi® has recently been engaged in such research. According to
W. D. Miller,® the following list is a summary of the pathogenic fungi
which have hitherto been found in the buccal cavity, part of these
having also been isolated by cultivation methods :—Leptothrix buccalis,
Vibrio buccalis, Spirochete dentium, Micrococcus tetragenus, Micro-
coccus de la rage (Pasteui), Micrococcus of septicemic sputum, the
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FUNGI
CHEMISTRY OF SALIVA. SI
fungus designated § by Miller, the bacillus of decaying teeth, Bacillus
crassus sputigenus, Bacillus salivarius septicus, two pathogenic fission-
fungi not yet cultivated (Kreibohm), Staphylococcus pyogenes, albus and
aureus, and salivarius pyogenes, Coccus salivarius septicus, and Bacillus
septicus sputigenus.
Miller” has cultivated over fifty different fungi obtained from the
mouth. A special interest attaches to the presence in the mouth of
healthy persons of the bacillus of sputum-septicemia. Pure cultivations
of this bacillus have been made by Klein, Miller, and Friinkel,8 and
it would appear to be the same which the researches of Frdnkel and
Weichselbaum indicate as the specific cause of pneumonia (see pp. 120,
121). The observations of Léger and Velter® have shown that other
formidable parasites, as the bacillus of diphtheria, Staphylococcus, and
Streptococcus pyogenes are normally innocuous denizens of the mouth.
To show Spirochzte buccalis, a drop of pure saliva should be examined as it
is with a good oil-immersion lens, an Abbe’s condenser, and a narrow diaphragm.
It may be seen also in a preparation stained by Giinther’s process.
Under pathological conditions other pathogenic fungi are to be found
in affections of the mouth ; as, for instance, thrush-fungus, Actinomyces,
and the bacilli of tubercle. J rdnkel!® has obtained the bacillus of
typhoid from the lingual glands in a case of death from that disease,
and doubtless our acquaintance with such forms will extend with our
knowledge.
III. CHEMICAL CONSTITUTION OF THE BUCCAL SECRETION.
—This varies even in health with the activity of the different glands by
which the fluids are secreted. There are to be found traces of albumin
coagulable with heat, mucin, and occasionally sulphocyanide of potas-
sium (CNSK). The saliva contains, further, a ferment which changes
starch into sugar, and a trifling amount of salts. Oxygen, nitrogen, and
carbonic acid gases have been obtained from parotid saliva (Kuilz).U
It is seldom that opportunity offers for a chemical examination of the
saliva in disease. The quantity is then generally diminished rather
than increased ; and further, it is very difficult to obtain a pure secre-
tion from the patient.
Ptyalism (see below) is the only morbid state in which a large quan-
tity of pure saliva can be had. To examine the saliva, the patient
should be made to rinse the mouth with water carefully after each meal,
and the secretion collected for twenty-four hours in a clean vessel. The
reaction may be tested with litmus paper and the specific gravity taken.
It will be found to be alkaline, and of sp. gr. 1.002-1.006. A portion
of the fluid may next be tested for albumin in the manner to be described
in the chapter on Urine.
F
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82 THE BUCCAL SECRETION.
Another portion may be tested with solution of ferric chloride for
sulphocyanides. Should such be present, a bright red colour appears,
which does not disappear either with heat or on the addition of acid.
If the red colour is not thus obtained, roo ce. of the saliva should be
concentrated on a water-bath and tested as before. [Meconic acid yields
asimilar cherry-red colour with ferric chloride, and this may be obtained
from the saliva in cases of opium poisoning. The addition of mercuric
chloride causes the colour due to sulphocyanide to disappear, whilst that
from meconic acid is unaffected by it.] Colosanti advocates the fol-
lowing method :—The saliva is precipitated with alcohol and filtered.
The filtrate is evaporated on the water-bath, and the residue dissolved in
water. Cupric sulphate is then added. If sulphocyanide he present
an emerald-green colour develops.
Sugar may be tested for in the manner recommended for its detection
in blood, No. 3 (v. supra, p. 72).
The presence of diastatic ferment may be shown thus :—5 cc. of
saliva are mixed with 50 cc. of starch solution, and placed in a warm
chamber or in a water-bath heated to 40° C. When examined after one
hour, the fluid (which of course must have been tested beforehand to
ascertain the absence of sugar) will give all the reactions of grape-sugar
if amylolytic ferment be present.
Nitrites often occur in saliva. They may be detected by adding to
a little of the fluid a mixture of starch paste, iodide of potassium, and
dilute sulphuric acid, when, if nitrites be present, an intense blue colour
will be seen. A very useful test for nitrites has been suggested by
Greiss.14 Toa specimen of saliva diluted with five times its bulk of
water, a few drops of sulphuric acid are added, and then metadiamido-
benzol which melts at 63° C. The appearance of an intense yellow
colour shows the presence of nitrites.
IV. CONSTITUTION OF MORBID SALIVA IN GENERAL.—
The quantity of saliva is diminished during inflammation of the salivary
glands in febrile disorders and diabetes, and often also in nephritis.
[In high fever no saliva is secreted. That of moderate fever is thick
and scanty, and usually acid, and with the rise of temperature its dias-
tatic action is lessened. The secretion is arrested by certain drugs,
notably by belladonna.| It is increased in inflammations of the mouth,
by the action of certain poisons—as, e.g., pilocarpin and mercury /—
[in trigeminal neuralgia] and sometimes by the irritation of carious
teeth. The excessive secretion which attends poisoning by acids and
alkalies is rather due to irritation of the ducts than to any specific
action on the salivary glands. A long-continued flow of saliva will
sometimes occur without its being possible to ascribe it to any of the
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MORBID SALIVA. 83
causes mentioned. In such cases probably the disturbance is due to
some obscure changes in the innervation of the glands. Salivation has
occasionally been recorded as occurring in pregnancy (Schramm).1® [It
is frequently met with in hysterical women. ]
These are the cases (referred to above) which afford a favourable
opportunity for chemical analysis of the saliva.
In a case of ptyalism which the author observed, analysis of the saliva showed
that it contained 995.2 grms. of water and 4.8 grms. of solids. Its reaction was
alkaline. It held a small quantity of mucin, traces of serum-albumin, and some
sulphocyanides. The iodide of starch test showed the absence of nitrites ; and
no sugar was detected by phenyl hydrazin or other reagents (Salkowski).”
Certain diseases are attended with notable qualitative changes in the
saliva. [Its reaction may be acid in diabetes, acute rheumatism, and
mercurial poisoning.]18 In nephritis considerable quantities of urea
have been found in it by Wright, Picard, Rabuteau,!® and Fleischer.?°
For its detection Fleischer employs the following method :—An alcoholic
extract of the saliva is made and filtered, the filtrate evaporated, and
the residue dissolved in amylic-aleohol. Crystals of urea remain after
evaporation, and may be recognised by any of the tests described at
p. 70. Boucheron * found uric acid in the saliva of uremic patients by
employing the murexide test (p. 71). In such cases the author has
tested the saliva in the way described at p. 71, having previously pro-
moted its secretion by administering pilocarpin, and has never succeeded
in finding uric acid there.
Bile pigment and sugar have not yet been found in saliva. Even in that of
diabetic patients there seems to be no sugar. In three cases of diabetes the
author has carefully tested the secretion after the injection of pilocarpin, by
means of the phenyl-hydrazin test, but in each case without any result.
Certain drugs, and amongst them iodide and bromide of potassium, are readily
detected in the saliva soon after they have been taken into the system.”? (See
chapter on the Urine for the method of investigating this body.)
[The following method for the detection of mercury in the saliva is taken from
Ralfe.2 To the saliva secreted during twenty-four hours dilute HCl is added.
The mixture is heated for two hours in a water-bath, filtered, and the filtrate con-
centrated to half its bulk. The precipitate on the filter is placed in a beaker
three parts full of dilute HCl and heated, while small quantities of potassium
chlorate are added, and the mixture stirred to dissolve organic residue. It is then
filtered and the filtrate added to the previous one. The fluid is concentrated to
one-fourth its bulk. It containsall the mercury as bichloride. To test for this :—
1. Place a drop ona gold or copper coin and touch this with the blade of a knife ;
a bright silvery stain results. 2. Boil some of the fluid with pure copper foil ;
mercury is deposited on the foil, and may be volatilised in a test-tube.]
[V. THE SULPHOCYANIDE OF THE SALIVA.—The origin and
purpose of this salt in the economy have long been a subject of specula-
tion to physiologists. The researches of Dr. S. Fenwick ** have invested
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84 THE BUCCAL SECRETION.
the matter with a new interest, and their results go to prove that we
have in the variations of its quantity a valuable index to certain states
of the system. He has collected the records of a large number of cases
in which the saliva was examined, and the quantity of sulphocyanide
carefully compared. This was done by noting the colour produced by
adding to the secretion a certain quantity of a standard solution of per-
chloride of iron. For the purposes of comparison, the tint so obtained
with a mixture of the secretions from many healthy persons is taken
to indicate the normal amount of the salt, and a scale of colours. is pre-
pared by evaporating and diluting the fluid to certain proportions, and
copying the tints in each case.
As a result of his observations, Dr. Fenwick concludes that the sulpho-
cyanide of the saliva is a measure of the functional activity of the nutri-
tive organs, and that it is increased in general whenever an unusual
demand is made on them by the necessities of the system, provided those
organs are capable of responding to the call,—in the early stages of acute
inflammation, of cancer and phthisis, in acute congestion of the liver
from alcohol and over-feeding, in acute rheumatism, gout, and urticaria,
and in convalescence from typhoid and similar diseases. The quantity
is diminished in all conditions where the nutritive organs are unable to
supply the requirements of the system, in the later stages of phthisis
and malignant disease, in long-continued diarrhoea and dysentery, in
jaundice from obstruction, in lead-poisoning, and in ascites and similar
conditions impeding the portal circulation, and where the assimilation
of food is imperfectly performed. Where, in connection with articular
rheumatism, the sulphocyanide is greatly in excess, a tedious recovery is
to be expected, and frequent relapses may be feared.
Dr, Fenwick believes that the sulphocyanide is derived from the de-
composition of biliary compounds (? taurocholate of soda).
A more accurate method of ascertaining its amount is to collect the
saliva secreted during five minutes, add the tincture of perchloride of
iron in the proportion of one drop to a drachm, and filter. The colour
obtained in this way may then be compared with solutions of sulpho-
cyanide of iron carefully graduated. The bottles containing the tests,
and the solutions to be compared with them, should be of exactly equal
size. The flat-sided vessels or hematinometers used for the spectroscopic
examination of blood will serve well. |
VI. THE SALIVA IN SPECIAL DISEASES.
1. Catarrhal Stomatitis.—This affection is regularly attended with
a much-increased flow of saliva, which when examined microscopically
is found to contain an excess of epithelium and many leucocytes, but is
otherwise unaltered.” [Its reaction is acid. ]
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STOMATITIS—THRUSH. 85
2. Ulcerative Stomatitis (Mercurial, Scorbutic, §c.).—The saliva
is fetid, dark brown in colour, and strongly alkaline. It is loaded with
tissue débris, leucocytes, broken-down red blood-corpuscles, and various
forms of fungiin abundance. Friiiiwald ®6 believes that a specific bacillus
which he discovered has a special relation to ulcerative stomatitis. His
contention, however, remains to be proved.
8. Thrush.—The presence of this fungus in the mouth demands
a more detailed notice.** It occurs most frequently in children, but
is common also in adults, especially in association with tuberculosis.
Freundenberg *§ has detected it in healthy persons. It used to be taught
that the saliva of thrush is always acid ; but it is still a matter of doubt
whether the acidity is not due rather to the presence of other micro-
Fic. 46.—a. Thrush fungus; b. Conidia; c. Epithelial cells; d. Leucocytes ; ¢. Débris.
(From the mouth of a patient with a weak heart ; eye-piece III., objective 8a,
Reichert).
organisms than to the action of the thrush fungus. Kehrer has shown
that the latter parasite will thrive well in a medium where no free acid
exists, as in lactate of sodium or potassium. The outset of the disease
is marked by the formation of white patches on the mucous membrane,
and when examined microscopically, these patches are seen to enclose
sharp-bordered oval cells, each having one or two nuclei. The cells are
disposed in groups of two or three. After the lapse of some days the
patches run together, and form a membrane which may cover the entire
mucous surface of the mouth, and even line the fauces and cesophagus.
The membranes are at first firmly adherent, but later on loosen, and
may then be easily detached. When examined microscopically they are
seen to consist of epithelial cells, leucocytes, and débris, amongst which
the parasite appears as branching ribbon-like forms composed of long
segments. Each segment usually contains two strongly refractive nuclei
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86 THE BUCCAL SECRETION.
embedded in a clear substance, one at either end. The segments vary
_in length, and grow shorter towards the extremities of the parasite.
They are for the most part homogeneous, but occasionally finely granular.
There are also to be seen the oval bodies figured above, which are
thought to be the spores (conidia) of the fungus.
There is still much dispute as to the place of the thrush fungus in the vege-
table kingdom. Rees refers it to the yeast fungi; Grawitz*” supposes it to be
identical with the fungus studied by Cienkowsky; and Plaut* opposes this
view, regarding it (with both the above-named authors, and also Baginsky 3 and
Klemperer 33) as a yeast fungus.*4 According to the more recent investigations
of Plaut®* the thrush fungus is identical with the widely distributed Monilia
candida. :
The fungus can be easily examined by placing part of the loose mem-
brane with a little glycerine under the microscope.
Fic. 47.—Leptothrix buccalis.
The preparation was stained with iodo-potassic iodide solution (eye-piece III., objective 8a,
Reichert).
When pus containing Actinomyces has been discharged into the mouth,
the micro-organism can be found in the saliva. For its recognition,
see the chapter on Pus.
Fischer and Hauser*®® have repeatedly found sarcine in the buccal
mucus of wasting diseases.
VII. DEPOSIT ON THE TEETH.—TIf a little of the tartar be removed
from the teeth with a spatula and examined, it will be seen to abound
mainly in micro-organisms. These comprise :—
1. Spirochete buccalis (mentioned above), in small numbers.
2. Leptothrix buccalis.—Long bacilli, usually segmented and arranged
in large ribbon-like bundles. They stain bluish-red in iodine-potassic-
iodide solution (fig. 47). This micro-organism has been named Bacillus
maximus buccalis by Miller.27 He rejects the view that it has the
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DEPOSIT ON TEETH—COATING OF TONGUE. 87
power of penetrating dentine, but holds with other observers *> that
dental caries is brought about by various fungi, both cocei and bacilli,
which generate acids and destroy decalcified dentine. Mixed up with
‘the masses of Leptothrix are usually to be seen shorter bacilli, which do
not stain in the iodine solution.
3. Various forms of micrococci, occurring both separately and in
colonies.
4. A large number of leucocytes and epithelial cells, usually showing
advanced fatty degeneration (fig. 45).
VIII. COATING OF THE TONGUE.—1. In severe infectious dis-
eases the toneue is coated with a brownish fur, which consists partly of
the remains of food and partly of dried blood. Microscopical examina-
tion of the coating removed from the tongue exhibits, in such a case,
a profusion of epithelial cells and hosts of fungi of various forms. In
addition to these, there is a multitude of dark cellular bodies, derived
doubtless from the corneous and exfoliated epithelium of the part
(Bizzozero).
Schech,®*® again, has called attention to the occurrence of a black fur,
which is probably conditioned by the formation of pigmented papilla on
the tongue.*
2. The tongue of infants is normally coated with a white fur, and a
similar appearance is found in adults when the stomach is deranged.
Microscopical examination shows epithelium, a few salivary corpuscles,
and very many fungi.
[Dr. Dickinson ® has recently investigated the nature and significance of the
various morbid coatings of the tongue. He believes that a just conclusion can-
not be arrived at from the inspection of material scraped from the surface, and
his method was to obtain post-mortem sections through the substance of the
tongue, associating the microscopical with the naked-eye appearances during
life. Thus it is seen that the different varieties of coating distinguished as
‘« stippled,” ‘‘ coated,” “plastered,” ‘‘furred,” and “encrusted,” are all alike
derived from excess and alteration of the epithelial elements of the tongue;
the change, where most profound, extending first between the papille, and then
deeper, with hypernucleation of the deep cells of the corium and the diapedesis
of leucocytes. ‘The presence of non-pathogenic fungi is common to all, and may
be regarded as accidental ; even the thrush fungus occurs independently of the
grosser changes to which it commonly gives rise. The conditions of dryness
and moisture greatly modify both the character of the coat and its significance
as a symptom. ‘The colour of the encrusted brown variety is due to dryness
alone, while at the same time it must be mentioned that a profusion of micro-
organisms is especially associated with this form. Clinically the fact of most
importance is the thickness and exuberance of the coating, and a comparison
of instances has shown that such redundancy is especially connected with
pyrexia. ]
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88 THE BUCCAL SECRETION.
IX. COATING OF THE TONSILS.—The examination of morbid
deposits upon the tonsils is sometimes of the utmost importance in
diagnosis.
1. Croupous and Diphtheritic Tonsillitis. — The membrane
covering the tonsils both in croup and diphtheria is composed of glisten-
ing homogeneous fibrin, disposed in the form of a network, of which
the meshes vary in shape and size, and enclose epithelial cells, blood-
and pus-corpuscles, and micro-organisms of every description. The
differences between croupous and diphtheritic membrane cannot be dis-
tinguished by microscopic examination alone, as was formerly taught.
In both cases whitish layers are found on the tonsils. It should be
mentioned, however, that #. Wagner discriminates between croupous
and diphtheritic tonsillitis, in that the removal of the membrane in the
former affection leaves the underlying tissues simply hypereemic and
infiltrated with serum, while in the diphtheritie form a hemorrhagic or
even sero-purulent infiltration remains.
Hitherto even the newer bacteriological methods of investigation have
not thrown much light on the subject. The observations of Roux and
Versin, Zarnihko, Spronch, Wintgens, and van den Brink, Paltauf and
Kolisho, Escherich, Klein, and Bech, fully confirm the view that the
bacillus first discovered and described by Klebs and Liffler* is to be
regarded as the cause of diphtheria.
G. v. Hoffmann-Wellenhof “has shown that a micro-organism, morpho-
logically and in its life-history closely resembling the bacillus of A/ebs and
Léfler, occurs in the mucous membrane of diphtheria patients. This he
has named the pseudodiphtheria-bacillus. Kolisho and Paltauf, whose
observations have been confirmed by those of others, have again called
attention to a multiple infection in this disease—Strepto- and Botryo-
cocci being found in the interstices of the tissues, and diphtheria-bacilli
on the surface. These discoveries tend somewhat to discount the signifi-
cance of the diphtheria-bacillus as distinguished by Loffler’s indications.
More hopeful are the researches of 2oua and Versin, Brieger and
Frankel, Wassermann, Proskauer, which teach us that these fungi
elaborate proteid substances (toxalbumins) of a very poisonous nature.
When a method has been discovered by which it will be possible
to isolate these substances, either from pure cultivations of the fungi
or from the diseased tissues, we shall probably be in possession of
a more certain and simpler, and for that reason clinically more ser-
viceable, diagnostic resource than is afforded by the present cultivation
processes. Meanwhile, the method of d’Espine and A. de Marignac, as
adopted by Baginshy,*® serves the purpose. A portion of the diphther-
itic membrane is removed, washed in a 2 per cent. boracic acid solution,
and immersed in Loffler’s blood-serum. This consists of 3 parts blood,
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COATING OF THE TONSILS. 89
rt part bouillon, with 1 per cent. of peptone, common salt, and grape-
sugar. The resulting cultivations should then show the characters of
the diphtheria-bacillus ; and Baginsky is of opinion that this is twofold,
corresponding to two distinct clinical types of the disease. Of the latter
the more formidable is induced by the presence of Léffler’s bacillus,
while milder attacks are characterised by the presence within the tissues
of Streptococcus and Staphylococcus.
The author no longer has doubts as to the specific characters of the
diphtheria bacillus, and, with Kolisko and Paltauf, he would urge the
necessity of classing together, under the name of Synanche Contagiosa,
all those cases of ‘so-called croup and diphtheria in which the bacilli
mentioned above are to be found.
Peters*” discovered gregarina-like bodies (Coccidiwm oviforme ; see chapter on
the Feces) in diphtheritic membrane stained with alum-carmine and picric acid.
This fact is noteworthy, but further observation must show in what relation these
forms stand to the disease in man.
2. Pharyngomycosis leptothricia. — A special interest has
recently come to be attached to the nature of the plugs which block
the tonsillar crypts. They are found in almost every healthy person,
and consist of epithelial cells and of long seemented fungi, which stain
bluish-red with the iodo-potassic-iodide solution. In certain conditions
these micro-organisms extend outside the follicles, and cover the surface
of the tonsils with patches of varying size. They then give rise to
subjective symptoms, and their appearance may be mistaken for a com-
mencing attack of croupous or diphtheritic tonsillitis, They may be
readily recognised under the microscope by their reaction with the
iodine solution, as mentioned above, and the course of the disease will
afford a further indication of their nature (Zh. Hering).*8 O. Chiari?
is of opinion that this affection is not one sw generis, but should merely
be regarded as a modification of Angina follicularis, in which such
products are always found.
One or two minutes in the iodine solution suffice to develop the bluish-red
colour in a specimen containing leptothrix. This colour disappears in from
twenty-four to seventy-two hours.
Dr. O. Chiari has called the attention of the author to the fact that yellowish
plugs which do not contain leptothrix are often to be found in the crypts. Ina
very hard concretion from the tonsils, found on chemical examination to consist
of carbonates and silicates, the author met with splendid specimens of lepto-
thrix.
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CHAPTER III.
THE NASAL SECRETION.
I. NAKED-EYE AND MICROSCOPICAL CHARACTERS—
CHEMICAL CONSTITUTION.— Considering the great quantity of
glandular tissue with which the nasal passages is furnished, the secre-
tion in health is remarkably scanty.
Normal nasal mucus exhibits microscopically squamous and ciliated
epithelium in abundance, isolated leucocytes, and an enormous profusion
of fungi.
E. Weibel! has described a curved bacillus obtained from the nasal
secretion of healthy persons, which, when cultivated in nutrient gelatine
Fic. 48.—Nasal Mucus (eye-piece ILI., objective 8a, Reichert).
a, Ciliated epithelium ; b, Leucocytes; c. Encysted cocci; d. Bacilli; e. Micrococci.
and agar-agar, develops a spirillum-like body wound into several coils.
It is probable that further researches will show the presence of many
other forms. A great variety has been enumerated by Reimann.?
The normal nasal secretion is a thick fluid, faintly odorous, and of
an alkaline reaction. It abounds in mucin, but otherwise nothing
definite is known about its chemical constitution.
II. THE SECRETION IN AFFECTIONS OF THE NASAL CAVI-
TIES.—At the outset of an attack of acute nasal catarrh, the mucous
membrane is generally dry and much injected, and the secretion lessened
in quantity. Later on, however, there is a copious discharge of a thin
go
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SECRETION IN AFFECTIONS OF NASAL CAVITIES. gi
alkaline fluid, and this, when examined under the microscope, is seen to
consist of a great number of epithelial cells and fungi.
Where suppuration is in progress within the nose, the secretion par-
takes of the character of pus, and is seen microscopically to consist
almost entirely of pus cells. Occasionally, as in cases of wounds per-
forating the cranium and in brain tumours, cerebro-spinal fluid may be
discharged through the nose. Nothnagel® has reported a very inte-
resting case of this kind. Under such circumstances, chemical analysis
showing the absence of albumin and the presence of sugar, or, at least,
of a reducing substance, will determine the diagnosis. The import-
ance of the evidence so obtained in connection with cerebral tumours
is evident.
It is very necessary, in all cases of ulceration of the mucous membrane
of the nose, to look for certain of the pathogenic fungi already known
to us.
Thus, if it be a question whether a particular ulcer is tubercular or
not, a little of the discharge may be removed with the help of the nasal
speculum on a carefully sterilised platinum spatula, and examined for
tubercle bacillus in the manner indicated at p. 104.
Again, the discovery of the characteristic bacillus of glanders in such
a discharge will obviously determine the diagnosis of that disease.
This bacillus may be sought for in the same manner as in the examina-
tion of blood (p. 46). If this be not enough, fungi may be cultivated
on Koch’s plan (see Chapter X.) ; or, finally, in case of doubt, they may
be propagated in one of the lower animals, when a definite conclusion
will be arrived at.
LE. Frinkel* and Hajek ® observed various forms of fungi invariably
present in the discharge of the chronic ulcerative processes known as
ozena. Ldwenberg,® on the other hand, found that one large species of
diplococcus was almost the only form present in such discharge, and he
regards it as characteristic of ozena.
Tost" and Léwenberg® have shown that bodies resembling the pneu-
monia-coccus occur in the nasal secretion (fig. 48, c). H. v. Schrotter
and Winkler ® have isolated the Staphylococcus cereus flavus and another
similar micro-organism, which they designate albus, from the nasal dis-
charge in coryza. The discovery is obviously of no importance unless
it can be shown that these forms do not occur in health.
In a few cases, thrush-fungus and vegetations have been found in the
nose. Mould-fungi in this situation are another rare manifestation
(Schubert).0 Ascarides and other entozoa are very seldom seen there.
Proskauer ™ believes that he has found the embryo of Oxyuris. The
statement is very doubtful. Dipteral larvee are of most common occur-
rence (B. Frenkel).
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92 THE NASAL SECRETION.
The Charcot-Leyden crystals found in blood and sputum have also
been met with in the nasal secretion of an asthmatic patient. Leyden!
observed them associated with eosinophil cells in the nasal mucus in a
case of acute coryza, and Sticker 4 in blood discharged from the nose in
leukemia, after it had stood for some days. Lewy 5 has described them
in connection with nasal tumours (polypi).
Concretions (rhinoliths) occasionally form in the nasal cavities (0.
Chiari, Seifert).
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CHAPTER IV.
THE SPUTUM.
Unvber the term expectoration or sputum? are comprised all those sub-
stances which are removed from the air-passages by the mechanical effort
of coughing or hawking.
I. NAKED-EYE CHARACTERS OF THE SPUTUM.—The naked-
eye appearance of the sputum will often afford valuable information ; and
that this may be as accurate and exhaustive as possible, it is well to
collect the expectoration in glass vessels, after Mothnagel’s plan, and
then to examine it as to its quantity, specific gravity, reaction, colour,
smell, and tendency to stratification.
The quantity of expectoration discharged in twenty-four hours varies
within broad limits. Sometimes it does not exceed a few ce. ; in certain
conditions, on the other hand, as, e.g., where an empyema is discharging
into the lung, as much as 800 to 1000 ce. may be expectorated in twenty-
four hours.
H, Kossel? determines the specific gravity of the sputum in the
following manner :—The sputum is placed in a flask stoppered to pre-
vent evaporation, and gradually heated to 60° C. It is thus reduced to
a thinly-fluid state, and is placed in the pycnometer. The specific gravity
is seen to vary within very broad limits,—for mucous sputum, 1.0043-
1.0080; for purulent, 1.0155-1.0260; and for serous, 1.0375. The
question of density has in no case any clinical interest.
The reaction of the sputum is always alkaline.
In some diseases, as in abscess and gangrene of the lung, there is
marked stratification of its parts (see p. 121).
The colour of the sputum depends partly upon its microscopical and
partly upon its chemical character. When it consists entirely or chiefly
of mucin and a few cells, it is whitish. Green sputa are usually puru-
lent, but the presence of biliverdin or of pigment-forming bacteria may
also impart this colour.
The odour of the sputum is, for the most part, not characteristic ; but
in putrid bronchitis and gangrene of the lung it has a particularly
pungent and unpleasant smell.
93
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94 THE SPUTUM.
For many purposes it is convenient to collect the sputum in a cylin-
drical glass vessel containing water. In this way, for instance, the
nummular arrangement is made apparent. In other cases, again, cer-
tain constituents, as, e.g., spirals, fibrinous coagula, and shreds of tissue,
may be made more evident on a dark surface, such as that of a polished
black plate. A very suitable plate has been devised by Kroenzg.®
[The expedient of hardening the sputum and examining it in sections
was first adopted by Ad. Schmidt, and lately revived by Gabritschewshy.*
As fixing and hardening fluids the latter employs alcohol, Miiller’s fluid,
Flemming’s solution, picric acid, and sublimate in concentrated forms.
The hardened sputum is embedded in celloidin for cutting, and the
sections stained. This method is valuable for the detection of some of
the constituents of the sputum, which may be destroyed by pressure
under a cover-glass. |
Although much knowledge of a disease may be derived from a naked-
eye inspection of the sputa, it will never enable us to dispense with the
aid of the microscope, by means of which alone we can diagnose certain
affections—some forms of tuberculosis, for instance--with the utmost
certainty.
II. MICROSCOPICAL EXAMINATION OF THE SPUTUM.
1. White Blood-Corpuscles.—These bodies are always found in
large numbers in the sputum, commonly embedded in a viscid stringy
substance. Many of them are of large size and granular, and enclose
within them drops of fat and particles of pigment, such as carbon dust
and masses of hematoidin (see fig. 49, e). In cases where an abscess has
discharged into the lung, and in purulent bronchitis, such as is met
with in connection with emphysema, the sputum may consist entirely
of leucocytes.
2. Red Blood-Corpuscles.—These are also to be found in almost
all sputa, and their presence in small numbers is without significance.
In persons who smoke a great deal, or who spend much of their time in
an atmosphere of tobacco-fumes, the sputa are apt to be streaked with
blood in the morning. This blood, however, proceeds in most cases,
not from the lung-tissue proper, but from the bronchial mucous mem-
brane, and is due to catarrh.
When red blood-cells are present in very considerable quantity, the
sputa will be coloured by them. The individual cells are usually intact,
and in this they depart from the condition in which they are found in
urine and feces. In some cases, however, as in pneumonia, they are
altered and occur as pale discoidal bodies. Where blood has accumu-
lated for some time in the bronchial tubes, the red corpuscles may dis-
appear entirely and the pigment remain in the sputum either as irregular
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MICROSCOPICAL CHARACTERS. 95
particles or as red crystals of hematoidin (see fig. 49, e). The sputum of
pneumonia derives its colour from blood-pigment dissolved in it.
Finally, it is to be noted that in hemorrhage from the lungs the
sputum consists entirely of red corpuscles; in congestion the blood is
intimately mixed with mucus.
3. Epithelium.—The sputum abounds in epithelial cells. Squamous
cells (fig. 49, 2) come either from the mouth or from the surface of the
true vocal cords. Ciliated epithelium is less often scen, and occurs
chiefly in severe bronchial inflammation, when, too, it is probably derived
rather from admixture with nasal mucus® than from the surface of the
trachea, which, as is well known, is lined with ciliated epithelium. The
cells as found in the sputum are usually deprived of their cilia (fig. 49, ¢),
unless in quite recent expectoration, when cilia in active motion may
Fic. 49.—Epithelium, Leucocytes, and crystals of the Sputum (eye-piece III., objective 8a,
Reichert).
a, a, aw’, Alveolar epithelium. 6, Myelin forms. c. Ciliated epithelium. d. Crystals of
calcium carbonate. ¢, Hiematoidin crystalsand masses. jf, f’, ”. White blood-corpuscles.
g. Red blood-corpuscles. . Squamous epithelium.
still be seen on them. The mere presence of such cells in the sputum
is of little diagnostic import; but where they occur in great numbers
they may be taken as indicating the commencement of acute catarrh,
either in the back part of the nasal fosse or in the trachea and bronchi.
But there is another variety of epithelium whose appearance in the
sputum is a fact of great importance.’ It is known as “alveolar” epi-
thelium, a name which will serve provisionally, although its derivation
from the alveoli of the lungs has lately been called in question (Bizzozero).§
It consists of elliptical cells, each containing one nucleus, which usually
requires acetic acid to make it visible. The body of the cell is of finely-
granular protoplasm, and very often holds irregular pigment particles in
its substance. These particles consist usually of blood colouring-matter,
iron dust or carbon (fig. 49, a’). In the last case they are unaffected
by reagents generally. Iron dust may be known by its turning blackish-
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96 THE SPUTUM.
green with sulphide of ammonium, or blue with yellow prussiate of
potash and hydrochloric acid. These cells often contain one or more
fatty granules, readily recognisable by their high refractive power, and
at times they exhibit extreme fatty degeneration (fig. 49, a, a”), when
their protoplasm is replaced by oily drops of varying size. Sometimes
large bodies like drops of fat, presumably derived from the rupture of
these cells, are to be seen in the sputum (fig. 49, ¥). They were first
observed by Virchow,® who named them myelin droplets, from the
resemblance they bear to similar forms produced in the destruction of
nerve tissue. According to Panizza,!° however, this myelin (which is
only the outward form of a considerable number of different substances)
is probably mucin ; and in his opinion no diagnostic importance attaches
either to myelin or to myelin-holding cells.
Buhi™ thought that the appearance of alveolar epithelium in the
sputum was characteristic of the disease which he has named desqua-
mative pneumonia. It is certainly a fact that such cells are to be
found in great profusion only in quite fresh specimens of caseous infil-
tration of the lung, whether due to bacilli or not; but then they
occur also in pneumonia, in chronic bronchitis, and in chronic pul-
monary tuberculosis ;!2 sometimes, too, in very large numbers. It
follows from their manifestation in processes differing so entirely that
their diagnostic significance is on the whole slight.
[Troup 1® believes that the presence of alveolar epithelium in the
sputum belongs especially to obstinate catarrhs of the apex, when it
will be found associated with columnar and ciliated cells; he observes
that since such catarrhs tend forthe most part to run into phthisis, we
have in this an early and valuable sign of impending danger.] There
is a special form of alveolar epithelium, consisting of large flat cells con-
taining a golden yellow and brown pigment (failing-heart cells, Wagner),
whose presence in the sputum, according to F. A. Hoffmann, only
occurs in valvular heart-disease and adherent pericardium. They are
absent from the sputum in phthisis and pneumonia, and they may
therefore be taken, in doubtful cases, to point to brown induration
of the lung. Whilst agreeing in general with Hofimann’s view, the
author would insist that in the processes just mentioned the sputum
exhibits cells containing black pigment, which chemical examination
has shown to be a derivative of blood colouring-matter. Such cells
were noticed long ago by J. Sommerbrodt, who described them as
brown alveolar epithelium. He is in accord with Hoffmann as to
their meaning. Lenhartz° has observed them most frequently in con-
nection with mitral stenosis, and regards them as metamorphosed blood-
corpuscle-holding round cells (lymph corpuscles). Krénig}’ endorses
Hoffmann’s view.
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ELASTIC FIBRES. 97
To examine the sputum for epithelium, a small quantity should be
treated with acetic acid, to bring the nuclei and nucleoli into view; or
a specimen may be stained with a watery solution of methylene blue.
4. Elastic Fibres.—These fibres occur in the sputum singly or
in bundles, and they have commonly an alveolar arrangement (fig. 50).
They are of varying length and breadth, dark-coloured, slightly curved,
and generally exhibit a double contour.* Their diagnostic value is great,
as a sign of serious mischief, pointing to destruction of lung-tissue.
They occur, consequently, in tuberculosis, bronchiectasis, pulmonary
abseess, and occasionally in pneumonia, while the other signs of
abscess are wanting. The author has repeatedly found elastic fibres in
cases of pneumonia which otherwise ran a favourable course, and he
supposes that in such cases there was destruction of the pulmonary
parenchyma only over a very limited area. It is a notable fact that
Fic. 50.—Elastic fibres in the Sputum (eye-piece ILI., objective 8a, Reichert).
these fibres are rarely to be met with in the expectoration of pulmonary
gangrene, and the reason probably is that they are destroyed in site
by the ferments formed in that process. The fact was first noticed
by Traube.
Elastic tissue may be introduced with the food, and so find its way
into the sputum. =
+f aN
LOR eis )
oat ery es
; c \ 4
“ Jekino-
witsch,© Kuschew, and Paltauf,*" [and Lindt] have described such cases.
Paltauf has found the characteristic granular masses in the sputum in
cases of actinomycosis, and their peculiar ray-like arrangement is made
evident by the application of Gram’s method. Jehinowitsch and Kuschew
have shown that in the sputum the characteristic actinomyces occurs.
For a description of the ray fungus see the chapter on Pus.
Fic. 61.—Echinococcus Hooklets and Membrane of Hydatid Cyst (eye-piece III.,
objective 84, Reichert).
It should be mentioned here that organised bodies have often been
observed of late years in the sputum of whooping-cough, some of which
may have a causative connection with the disease. Thus Deichler*
has found in such sputa certain amceboid cells (protozoa), but his state-
ment needs confirmation. Burger and Letzerich established the presence
of bacilli, and Afanasstew* found in the sputum of affected children
bacilli to which he attributed an exciting influence; and since his
opinion is supported by Smtschenko °° (who performed careful cultivation
experiments to elucidate the subject), it is probable that the bacillus of
Afanassiew has really a close relation to whooping-cough.
2. Infusoria.—Infusoria were first found by Kannenberg®™ in sputa
derived from pulmonary gangrene. They were of the monad and cerco-
monad varieties. They occurred usually enclosed in small yellow droplets,
which also held margarine crystals, and exhibited sluggish movements.
Such organisms are described at length in the chapter on Fwces,
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IIo THE SPUTUM.
For their detection in the sputum Kannenberg has adopted the follow-
ine method:—A little of the fungoid substance mentioned above 1s
placed beneath a cover-class on a slide, and spread out by pressure in a
very thin layer. A few drops of a 1 per cent. solution of common salt are
then added. The cover-glass, with some of the preparation on its surface,
is next dried, and afterwards put to stain in a watery solution of methyl-
violet, washed in water, and, while still wet, placed in a concentrated
solution of acetate of potash. By this process the protoplasm of the
monads is stained a beautiful blue.
3. Vermes.—It very seldom happens that ascarides are found in the
sputum, and cysts of echinococcus in a perfect state have been but
rarely known to be expectorated. Hichhorst®* and also Hochsinger %*
have described cases in which this happened. Diagnosis in such cases
cannot be attended with difficulty. The cyst, however, is generally
discharged in fragments. These appear to the naked eye as whitish-
yellow shreds, and may be recognised microscopically by their uniformly
striped texture (fig. 61). The discovery of the hooklets of echinococcus
in the sputum is a fact of great importance in diagnosis. They may
be readily recognised by their characteristic form (fig. 61). Charcot-
Leyden crystals in great quantity commonly accompany them.
It would appear, too, that the expectoration may contain the eges of
Distoma hematobium. The author is indebted to Dr. Schiess-Bey of
Alexandria for a specimen which plainly shows that this parasite settles
in the lungs, and it follows that when the pulmonary structure breaks
down, it may be expelled with the sputum. Similar observations had
already been made by Manson.®4
10. Crystals.—Very many forms of crystals have been found in
the sputum, but for the most part their discovery is without great sig-
nificance in diagnosis.
1. Charcot-Leyden Crystals.—We shall consider these bodies first,
for the reason that they seem to possess some pathological interest.
Leyden® often found crystals in the sputum of asthmatic patients.
They abounded chiefly in the semi-solid greyish-yellow pellets dis-
charged during a paroxysm. ‘These crystals were colourless and of
the pointed octahedral form. They were insoluble in cold water, ether,
alcohol, and chloroform, but dissolved readily in acetic and mineral
acids, alkalies, warm water, and ammonia. They are identical with the
crystals to be seen in post-mortem blood, and described at p. 30, and
with those of the semen, and with others that are met with in the
feeces in cases of anchylostomiasis. According to Schreiner ® such
crystals are the phosphate of a new hase, which, according to the
researches of Ladenburg and Abel, is probably identical with ethyl-
eninim, or dizthylendiamin.®
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CRYSTALS—-H ZMATOIDIN—CHOLESTERIN. III
Leyden believed that the crystals were the exciting cause of the
asthmatic paroxysm. Friedreich and Zenker ® found them in expecto-
rated fibrin-coagula, and Bizzozero™ in the sputum of acute bronchitis
from patients who were not subject to asthma. The author can corro-
borate the statements of these observers. [Zroup™ asserts also that
neither spirals nor Charcot-Leyden crystals are pathognomonic of any
one disease, but points out that the former are invariably to be found
in asthmatic sputa, and by their presence cause the paroxysms. A
characteristic feature of the conditions in which both spirals and crys-
tals are found is marked desquamation of the mucous surface of the
bronchioles, and the same author refers the origin of Charcot-Leyden
crystals to the altered cells which are thus stripped off. |
2. Hematoidin Crystals.—Crystals of hematoidin, described by
Virchow, Friedreich, and Schultze, occur in the sputum as ruby-red
rhombic prisms, either solitary or in groups, or as needles or clusters of
Fic. 62.—Charcot-Leyden Crystals, from the Sputum of an Asthmatic patient (eye-piece III.,
objective VII., Hartnack).
needles. These crystals, or fragments of them, are often found enclosed
within the substance of white blood-corpuscles (fig. 49 e). Under such
circumstances hematoidin is also seen, either free or in the interior of
the white blood-corpuscles, as a mass of pigment in which no trace of
the crystalline formation can be discovered.
When hematoidin crystals appear in the expectoration, we may
conclude that blood has been effused and suffered to remain for some
time in the air-passages, or that an abscess has perforated the lune.
They occur most abundantly, therefore, in phthisis after hemoptysis,
when pulmonary clots are in process of absorption, very often in pul-
monary abscess, and when an abscess or suppurating hydatid cyst has
discharged into the lung. When the crystals are contained in cells, they
point to a previous hemorrhage ; but when free hematoidin is present in
considerable quantity, the inference is that an abscess has discharged
from some neighbouring organ into the lung.
3. Cholesterin Crystals.—Crystals of cholesterin were found in the
sputum of tuberculosis by Biermer,’ and in pulmonary abscess. by
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112 THE SPUTUM.
Leyden. In connection with the former disease they are often to be
seen there, but in very small quantity. The author has observed them
in great numbers in a girl who had a hydatid abscess in the lung, and
in a man suffering from chronic pulmonary inflammation. According
to Black,” cholesterin erystals are plentifully present in the remains of
old inflammatory exudation.
These crystals are distinguished by their powerful refractive action on
light. They are in the form of large, and often irregular, rhombic tables,
which have a tendency to cohere in groups. They are readily soluble
in ether; insoluble in water, acids, and alkalies (fig. 125). When the
erystals are treated with dilute sulphuric acid and a little tincture of
iodine, a violet colour is formed, which presently changes to blue, green,
and red. With sulphuric acid alone, they become first yellow and then
green, these colours spreading from the edges.
Pathologically, these bodies are of little consequence. They are per-
haps most apt to form when pus from some other organ has burrowed
into the lung, and lodged there for a time before being discharged
through the bronchi.
4. Fatty Crystals (Margarine Needles).—These are seen chiefly in
putrid bronchitis and pulmonary gangrene. They characterise the
discharge of unhealthy pus within the lungs, and belong to bronchi-
ectasis and occasionally to tubercle. They occur either singly or in
clusters as long sharp-pointed needles, and are occasionally vaulted or
saddle-shaped. They dissolve readily in ether and boiling alcohol, and
are insoluble in water and acids. This character facilitates their recog-
nition (fig. 142). Recently the author has found them in plugs, which
evidently originated in the crypts of the tonsils (see p. 89).
It follows from their occurring in so many different diseases that the
discovery of these crystals in the sputum lends but little aid to diagnosis.
As to their chemical constitution, they consist, most probably, of the
sodium, potassium, calcium, and magnesium salts of the higher fatty
acids, as palmitic, stearic, &e.
5. Tyrosin Crystals.—Leyden™ first found tyrosin crystals in the
sputum of a girl with putrid bronchitis, and again in the case of a man
who had an empyema discharging into the lung. They appear micro-
scopically as fine needles scattered separately or in clusters. As a rule,
they occur sparingly in fresh sputum, but form in greater quantity when
the specimen has been allowed to stand for some time.
Leyden and Kannenberg are of opinion that a profusion of tyrosin
crystals implies the existence of a perforating abscess of the lung,
It should be observed, however, that in many instances substances which
have been taken for tyrosin were, in reality, lime and magnesia salts of the higher
fatty acids.
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CHEMICAL EXAMINATION. 113
Tyrosin is usually associated with leucin in the sputum. The latter
occurs in faintly lustrous spherical particles (R. Fischer). It has the
same import as tyrosin.
For the detection of both these substances the method described in
connection with the Urine may be employed.
6. Oxalate of Lime.—fiirbringer "> has reported a case of diabetes in
which the sputum contained large quantities of oxalate of lime. It
occurs either in the form of octahedral (envelope-shaped) crystals (fig.
112), or as an amorphous conglomerate. Unga? found this body in
the expectoration of a knife-grinder, aged twenty-eight, who had suffered
for years from asthma.
The crystals of oxalate of lime are readily known from the fact that
they are soluble in mineral acids, and insoluble in water, alkalies, a
acids, alcohol, and ether.
7. Triple Phosphate.—The characteristic coffin-lid snyatalg have ocea-
sionally been met with (fig. 113). They are soluble in acids of all kinds,
and are, therefore, only to be found in the alkaline sputum. They are
for the most part a product of the decomposition of proteids, attended
with the liberation of ammonia. They are commonly to be seen in
purulent exudation, and consequently are very plentiful in the expectora-
tion from a discharging abscess.
Other crystals are also occasionally observed in the sputum. Fig. 49, ¢/,
represents some that were expectorated in a case of phthisis. They gave
the chemical reactions of carbonates (carbonate of lime), the evolution of
gas on the addition of acids, Xe.
III. CHEMICAL EXAMINATION.—The chemical examination of
the sputum throws little light upon disease.
1. Proteids and Allied Substances.—Of these, serum-albumin
and large quantities of mucin and nuclein (4. Kossel®) are normally
present. Peptone occurs in the expectoration of pneumonia and other
purulent conditions—in general, in all cases where the sputa contain
pus-cells in abundance.*!
The best method for the detection of proteids is that recommended
by Hoppe-Seyler *? as a test for albumin in serous fluids.
The “prune-juice” expectoration of pulmonary cedema is very rich
in serum-albumin. For the detection of this body, the sputum may be
extracted with very dilute acetic acid, and the filtrate tested with ferro-
cyanide of potassium, when its presence will be shown by turbidity or
a precipitate.
2. Volatile Fatty Acids.—Various volatile fatty acids may occur
in the sputum, and, notably in gangrene of the lung, acetic, butyric, and
sometimes caproi¢ acids are met with.** In testing for these bodies,
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114 THE SPUTUM.
the sputum is diluted with water and phosphoric acid added. The
volatile constituents are driven off by distillmg them in a vessel heated
by steam. The distillate is then tested in the manner laid down in the
chapter on Jeces. Some fat can be obtained from all sputa, and those
of tubercular patients contain a large quantity.*+
To separate the fats and non-volatile fatty acids, the sputum is acidu-
lated and extracted with ether, and by repeatedly shaking up the
ethereal extract with a watery solution of sodic carbonate, the acids
are converted into their corresponding salts, which remain dissolved in
the watery solution. The ether is pipetted or siphoned off, and the
fats obtained after evaporation of the ether. The sputum of pulmonary
gangrene contains several members of the aromatic group, as indol, phenol,
and scatol.®
8. Glycogen.—This body has been repeatedly detected in the
sputum by Salomon.®° Its presence may be demonstrated by Briicke’s
method.
4. Ferment.—Flehne, Stolnikow, and Stadelmann® found that the
sputa, especially in pulmonary gangrene and putrid bronchitis, contain a
ferment resembling in its action one of the pancreatic ferments. It is
soluble in glycerine, and may be extracted by that body from the sputum.
Escherich ® has been able to demonstrate its presence in the sputum in
all cases of extensive destruction of lung-tissue.
5. Inorganic Constituents.°°—-These are chiefly—
Chlorides: of sodium and magnesium.
Phosphates: of soda, lime, and magnesia.
Sulphates: of soda and lime.
Carbonates: of soda, lime, and magnesia.
Per-salts of iron (rarely)—phosphate of iron.
Silicates.
AREY DS o
The inorganic matter of the sputum has little bearing on clinical
diagnosis. For its analysis the organic constituents must first be
removed by incineration, when the usual tests may be applied to the
ash. (For further information consult Hoppe-Seyler’s Handbuch der
Physiologisch- und Pathologisch-chem. Analyse, 5th ed., p. 316.)
IV. THE CHARACTER AND CONSTITUTION OF THE SPU-
TUM IN THE PRINCIPAL DISEASES OF THE LUNGS AND
BRONCHI.
1. Diseases of the Bronchi.
1. Acute Bronchitis.—At the outset the expectoration is viscid,
white, and scanty, and occasionally streaked with blood. Microscopi-
cally it exhibits very few cells, and is devoid of specific fungi (tubercle
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THE SPUTUM IN DISEASE. I15
bacillus, §e.). At a later period it becomes more abundant, assumes a
pale-green tint, and under the microscope is seen to consist chiefly or
entirely of pus-cells. Elastic fibres are never present.
2. Chronic Bronchitis and Bronchiectasis.—The expectoration, which
is copious, green in colour, and without any characteristic odour, is
formed microscopically almost entirely of pus-cells, with which are
mixed a considerable number of fat-holding epithelial cells and myelin
particles, and a host of non-pathogenic micro-organisms. When ulcera-
tion of the bronchi takes place in the course of chronic bronchitis, lead-
ing to bronchiectasis, a very abundant expectoration is discharged in the
morning. The fluid, which is usually thin, tends to arrange itself in
three layers when allowed to settle. Of these, the topmost is frothy,
the next consists of watery fluid, and the third, which is of greater
consistence, 1s formed almost exclusively of cells.
In chronic bronchitis complicated with asthma, the sputum during
the paroxysms, and immediately afterwards, exhibits spirals (see p. 98),
and Charcot-Leyden (pp. 30, 99) and other crystals.
3. Putrid Bronchitis——The expectoration of this disease is thick,
greenish-brown, and has a very disagreeable sweetish odour. Micro-
scopically it contains a profusion of micro-organisms of various kinds,
and very often exhibits large tufts of fungi, which colour blue with
iodine and iodide of potassium solution, epithelium—usually in the pro-
cess of fatty degeneration—and fungoid plugs (p. 102), but no elastic
fibres, no shreds of alveolar tissue, and no specific fungi.
Lumniczer ° has separated by means of Koch’s plate cultivations (see
Chapter X.) a number of micro-organisms from the sputum, amongst
them Staphylococcus pyogenes citreus and albus, cereus flavus and
albus, and Diplococci; and also a fungus, the colonies of which, when
developed in nutrient agar-agar, emitted the odour belonging to the
expectoration of putrid bronchitis. It is a spore-forming bacillus,
1.5-2 » in length, thickest in the middle, and rounded off at the ends.
It was also seen ready formed in the sputum. When introduced within
the lungs and bronchi of rabbits it excited inflammation there.
Lebisch and Rohkitansky,®! by means of Baumann and Udranshky’s
benzol test, have detected cadaverin (pentamethylenediamin) and. an-
other diamin in these sputa.
4. Plastic Bronchitis.— The sputum contains fragments of the
croupous membrane and coagula of fibrin, with which are entangled a
profusion of epithelial cells and fungi (fig. 55). From these appear-
ances, and in the absence of pneumonic symptoms, the condition is
readily diagnosed. Occasionally it has to be distinguished from
chronic fibrinous bronchitis. The distinction will be made on clinical
grounds.
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116 THE SPUTUM.
2. Diseases of the Lung’ Tissue.
1. Pulmonary Tuberculosis.
(a.) Miliary Tuberculosis of the Lung.—The sputum in this condition
is merely that of acute catarrh, Tubercle bacilli are never to be found
ain it.
(b.) Acute Tubercular Infiltration of the Lung.—An early diagnosis
of the condition is of the utmost consequence, and happily it has been
rendered possible by Koch’s epoch-making discovery of the tubercle
bacillus. Two forms of the disease may be distinguished, according as
the symptoms partake of the typhoid or of the pneumonic character.
(a.) The Typhoid Type.—The symptoms are rigors at the outset, per-
sistent high temperature, enlarged spleen, extensive roseolar rash, which
at times suggests that of typhus exanthematicus, and commonly profuse
diarrhoea. The physical signs are those of severe catarrh in both apices.
There is no dyspnea. The pulse is frequent, respiration is but slightly
accelerated, and lividity is not marked, The sputum is viscid and
scanty. It contains but little tissue-débris, and only a few bacilli, which,
moreover, are always provided with spores.
After the lapse of a few days, dulness on percussion and bronchial
breathing may be obtained over the apices. The sputum becomes puru-
lent, and when again examined is found to contain swarms of tubercle
bacilli, There are also to be seen elastic fibres, showing an alveolar
arrangement, and a large quantity of epithelium. The physical signs
now give evidence of one or more large cavities, and the fever assumes
a remittent character. Death generally ensues in three or four weeks,
the mode of dying being that of chronic tuberculosis.
(8.) The Pneumonic Type begins with sustained high temperature,
marked lividity, and accelerated breathing. The physical signs point
to catarrh of both apices, and the sputum contains a few bacilli. Later,
the characteristic symptoms of infiltration of the lungs set in; the
expectoration becomes more profuse, and the contained bacilli more
numerous, The disease runs a very rapid course, often lasting only
for some days. Anatomically, the condition is one of acute tubercular
infiltration of both lungs.
(c.) Chronic Pulmonary Tuberculosis.—The diagnosis of this disease
has been greatly facilitated by Koch’s discovery of the bacillus of
tubercle. As a result of his experience of many hundred cases in the
clinic of Professor Nothnagel, the author has no hesitation in affirming
the principle so often laid down by other authorities, that the presence
of the tubercle bacillus in the sputum invariably implies the existence of
tuberculosis. Let this fact be granted, and no more is needed at once
to emphasise the importance of that recent contribution to our know-
ledge, and to impress upon the physician the necessity of rendering
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THE SPUTUM IN TUBERCULOSIS. 117
himself familiar with the very simple methods by which the bacillus
may he identified (p. 104). Experience has already accumulated cer-
tain data. In the first place, it must be mentioned that in most,
though not in all cases, the abundance of the bacilli is in proportion to
the severity of the disease; and again, the proliferation of bacilli is
apt to run parallel to the intensity of the febrile symptoms. The
supervention of hemoptysis is attended with an apparent (H. v
Frisch ®*) diminution in their number, but this may well be owing to
the fact that the sputa are in such a case diluted by the profuse admix-
ture of blood.
It is only when the tubercular process runs the very rapid course
described above that the bacilli, then usually carrying spores, are so
abundant as to fill the entire field.
It was held at one time that the appearance of elastic fibres in the
sputum was a sure token of incipient tuberculosis, but more recent
research has shown that they may be found equally in the course of
pulmonary ulceration of whatever kind; and so with other manifesta-
tions to which great importance was formerly attached. The signifi-
cance of all or any of them is very slight in comparison with that
belonging to the specific micro-organism, upon the detection of which
alone a positive diagnosis can be formed. [By the method of examining
the sputum in sections already referred to (p. 94), Gabritschewshy °° has
observed giant-cells in three out of four cases of pulmonary tuber-
culosis. |
It does not necessarily folow from the presence of the bacillus in
the sputum that a fatal termination is impending. The author has
met with such cases in which the patient eventually recovered, but they
are very rare. And doubtless an atmosphere crowded with the bacilli
of tubercle (as that of the consumptive ward of a hospital) must neces-
sarily give but little chance of cure. Possibly this is the reason why
the hospital physician has so seldom an opportunity of observing it.®+
Allusion may be made here to Koch’s process®® for the detection
during life of tubercular proliferation in inaccessible parts. The diag-
nostic value of the discovery is not yet finally settled. Numerous
clinical observations have shown that persons infected with tubercle
bacilli do in fact exhibit a reaction when injection has been made upon
them, while the healthy and those subject to other diseases generally
fail to do so. The process, however, zs neither entirely trustworthy nor
altogether free from danger. The initial dose should in all cases be less
than o.or ce.%
2. Chronic (Non-Tubercular) Inflammation of the Lung.—Under
this heading may be grouped all those conditions which would formerly
have been thought to present the typical character of tuberculosis—
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118 THE SPUTUM.
fever, night-sweats, &c.—but in which repeated search will fail to detect
the bacillus in the sputum. In one such case the autopsy showed caseat-
ing masses of considerable extent, but these, even to the naked eye,
were sufficiently discernible from tubercular deposit.
As regards the sputum, its essential characteristic is the absence of
tubercle bacilli. It further contains a large quantity of elastic tissue
and a profusion of epithelium cells, and especially of their myeloid
derivatives. If we may infer from the very slender data which have
as yet accumulated, the disease is attended throughout with slight
fever, and death by asthenia occurs sooner or later.°’ The author is
convinced that, with a little more care, we should learn to recognise
the non-bacillary form of phthisis in many instances where at present
it is not thought of.
3. Croupous Pneumonia.— and others, a distinction
is to be made between hyper-acidity and excessive secretion of the gas-
tric juice. By attending to this point it should be possible better to
discriminate between certain affections of the stomach, and especially
amongst those conditions which are still classed under the general
heading of gastric catarrh, dyspepsia, and the like (see p. 149).?°
A diminished acidity of the gastric juice occurs temporarily when a
large quantity of alkaline substances has been swallowed, and as a
persistent condition apparently in all febrile diseases.
The. acidity of the gastric juice may be measured in this way :—A
certain quantity—increased, if necessary, by the addition of water—is
filtered, and its reaction tested. If this be acid, a known quantity of
the filtrate is taken and coloured with a little neutral tincture of litmus.
Solution of soda of definite strength (the 1/10 normal or deci-normal
soda solution may be used with advantage) is now added slowly from
a graduated burette, until the point is reached finally at which the
onion-red colour of the fluid gives place to a violet hue. From the
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128 THE GASTRIC JUICE.
quantity of soda used, that of the acid present may be known, I ce.
of the normal soda solution employed in this way corresponding to
0.0365 grm. hydrochloric acid.°9 Instead of litmus an alcoholic solution
of phenolphthalein may be used. A few drops of this should be added
to the fluid before titration, and the alkali slowly supplied until a red
colour begins to develop.
The conclusions arrived at by this method are correct only when the
gastric juice contains hydrochloric acid alone, and not, as is generally
the case, several other acids as well (see below). On this account
Ewald* points out the fallacy of directly deducing the total acidity
from the amount of a deci-normal solution of soda required to neut-
ralise it. The expression 50 per cent. acidity implies that 50 cc. of the
deci-normal solution of soda will neutralise roo ce. of the gastric juice
experimented upon.
To determine whether the acidity is due to the presence of free acid
or to acid salts resort may be had to the methods of Ugelmann and Leo,
by which only free acid is detected. Leo*? uses calcium carbonate,
which in presence of acid is decomposed without heat, carbonic acid
being given off and the fluid acquiring a neutral reaction. If no free
acid, but only acid salts, be present, the fluid remains acid and reacts
to litmus paper as before. To carry out the test a quantity of the
gastric juice under examination is rubbed up with chemically pure
calcium carbonate, and the reaction obtained before and after the addi-
tion of the salt is compared. If in the second case this be neutral, the
original acidity was due to free acid; if, on the other hand, it be still
acid, but less so than formerly, the fluid contained both acid salts and
free acids. By an application of the same process it is possible to
estimate the quantity of free acid—hydrochloric and organic acids—in
a particular specimen. By Leo ** this is done as follows :—1o ce. of the
gastric juice is filtered, and 5 cc. of a concentrated solution of chloride
of calcium, and a few drops of an alcoholic solution of phenolphtha-
lein are added. The mixture is titrated with decimormal alkaline
solution. Next, to 15 cc. of the filtered juice is added 1 grm. of dry
powdered calcium carbonate, and the mixture is treated in the way
described above. It is then passed through an ash-free filter—asbestos
serves well—and the aspirator may be used to expedite filtration. Ten
ce. of the filtrate are measured out and placed in a small flask. The
stopper of this flask is perforated by two openings. Through one of these
a glass tube passes to the bottom of the flask; the other transmits one
end of a short right-angled glass tube, which reaches only just within
the flask, while the other end tapers a little and is connected by a
caoutchouc binder with a Bohm’s air-pump. By means of the latter the
carbonic acid which forms is drawn off. The fluid in the flask is then
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HYDROCHLORIC ACID. 129
treated with 5 cc. of calcium chloride solution and a few drops of
phenolphthalein, and titrated. The difference between the results of
this and of the former titration expresses the amount of acidity which
is due to the presence of free acid. Should it be ascertained, in the
way which will be described presently, that there were no organic
acids in the fluid, the difference depends upon the hydrochloric acid
alone, and its amount may be determined by the formula already given,
namely, that 1 ce. of the deci-normal solution of soda corresponds to
0.00365 grm. of hydrochloric acid. This method is sound in principle
and will be justified by its results. It must, however, be mentioned
that exception is taken to it by A. Hoffmann and A. Wagner ** on
theoretical grounds. According to MWossler,*> the process of filtration
may be omitted, and the conclusions both as to acidity and to the pro-
portion of free acid (see below) will be accurate.
(b.) HYDROCHLORIC ACID.—The gastric juice secreted during the
later stages of digestion appears normally to contain only free hydro-
chlorie acid. At an earlier period lactic acid is also present.
A. Detection of Free Hydrochloric Acid.The examination of the
gastric juice for free hydrochloric acid is attended with much difficulty,
since the chlorine salts yield nearly all the same reactions as the free
acid. To obviate this, many expedients °° have been suggested ; but
we shall notice here only those methods which will serve for clinical
purposes.
1. Mohr’s Tests.?’—(a.) ‘l'o the gastric juice to be tested is added first a solution
of iodide of potassium and starch-paste, and then a few drops of a very dilute
solution of ferric acetate. If free hydrochloric acid be present, a blue colora-
tion (starch iodide) appears. This very simple test is not altogether to be relied
upon, inasmuch as it will yield a negative result in presence of phosphoric acid
and its salts, even though free hydrochloric acid be present also.
(b.) The following test, also discovered by Mohr, answers its purpose admir-
ably :—It depends upon the fact that a very dilute solution of ferric acetate,
free from alkaline acetates, is unchanged by the addition of a few drops of
sulphocyanide of potassium solution, and retains its yellow hue, while, if a
mineral acid be present, it colours a deep red.
Ewald *8 has obtained good results by applying the test in the following
manner :—T wo cc. of a Io per cent. solution of sulphocyanide of potassium and
0.5 ce. of a neutral solution of ferric acetate are made up to 10 cc. (with water),
A few drops of the solution, which is of a ruby-red colour, are placed in a small
porcelain dish, and one or two drops of the fluid to be tested are allowed to
trickle slowly on to it. If hydrochloric acid be present, a light violet colour
forms at the point of contact of the two fluids, which gives place to a deep
mahogany-brown when they mix. This test, according to Hwald, has an advan-
tage over the aniline-dye tests in that its result is not materially affected by salts
or peptone ; but it is certainly less sensitive than the methyl-aniline-violet and
tropeolin tests.
2. The Aniline Dye-Tests.—(a.) Methyl-Aniline- Violet Reaction.—
This reagent was first used by Witz and Hilger *® for the detection of
I
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130 THE GASTRIC JUICE.
free mineral and organic acids. Maly has employed it for physiological,
Van der Velden for clinical purposes.4° To obtain the reaction, the
fluid to be tested is mixed with a violet-coloured watery solution of
methyl-aniline-violet. If very much free hydrochloric acid be present
(as is never the case in the gastric juice), the fluid will be bleached. If
a moderate quantity, it becomes green; and if very little, of a blue
colour. The direct examination of the gastric juice never shows more
than the transition from violet to blue. For the detection of a very
small proportion of acid, Maly recommends that the mixture should be
evaporated to the bulk of one or two drops on the water-bath. So
little as $ mgrm. of hydrochloric acid will then cause the change from
violet to blue.
Kost + recommends the addition of a 10 per cent. solution of tannin
before testing with methyl-violet, in order to precipitate peptones, which
would otherwise hinder the reaction.
(b.) Tropzolin (00) in alcoholic or watery solution yields a ruby-red
or dark-brown red colour in presence of free acids. Hwald # maintains
that this reaction constitutes the most sensitive test for free lactic as
well as hydrochloric acid. Boas,** who takes the same view, employs a
tropeolin test-paper for the purpose.
(c.) Fuchsin.—The test with fuchsin is far from sensitive, and on
that account of little utility.
(d.) Emerald-Green.*—The so-called “crystallised” emerald-green
affords a sensitive test for free hydrochloric acid. Concentrated solu-
tions of hydrochloric acid give reddish brown, and very dilute solutions
a grass- or a yellowish-green colour, with this reagent.
A brilliant-green, obtained from the same laboratory, has proved a
very efficient test. Five mgrms. of this reagent will serve to detect 0.48
mgrm. of hydrochloric acid dissolved in 6 cc. of water, giving to the
solution a bright green tint. It is to be noted, however, that a similar
effect is obtained where acetic, formic, or lactic acid is present in a higher
degree of concentration. Bourget # also uses a brilliant-green.
The other emerald-greens produced by Bayer, and distinguished as emerald-
green (extra crystallised) and emerald-green ii. and iii., proved useful, but less
sensitive. Of the other reagents tested, Kaiser blue (Guster, Berlin) was but little
sensitive. Its solutions turned a brown-green with concentrated hydrochloric
acid, and an azure-blue with dilute acid. A number of green pigments prepared
by Poirier of Paris were ineffective as tests for the acid.
Koster has recently employed malachite-green with good results as
a test for hydrochloric acid.
* This substance is made at B. Bayer’s laboratory, Elberfeld, and, with other
reagents, has been made the subject of experiment at the author’s request by Dr.
Voigt, on whose authority the statement in the text is made.
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CONGO-RED—BENZO-PURPURIN. 131
(e.) Congo-Red.—This is an aniline dye, which was first used as a test
for free acid by Herzberg. It may be employed most conveniently in
the form of filter-paper saturated with the reagent, as recommended by
Hosselin, Riegel, and his pupils,*° for the detection of free hydrochloric
acid.47 ‘This, when immersed in a fluid containing free hydrochloric
acid, turns blackish-blue or blue, according as much or little acid is
present. This effect is not obtained with organic acids or acid salts in
dilute solutions, and the intensity of the reaction is lessened in presence
of proteids and of salts in large proportion. The efficiency of the test
is undoubted, and notwithstanding that its use is subject to certain
fallacies,4#8 the Congo-red test-papers must be classed with benzo-
purpurin and the aniline-violet reagent as most suited to the purposes
of the practitioner.
(f.) Phloro-Glucin and Vanillin.—The reagent recommended by (iinz-
burg contains 2 grms. of phloro-glucin and 1 grm. of vanillin dissolved
in too parts of alcohol. When hydrochloric acid is added to this, it
deposits beautiful red crystals. For the detection of the acid in the
gastric juice it is employed thus :—To the fluid to be tested for acid an
equal quantity of the reagent is added, and the mixture evaporated on
the water-bath. The presence of hydrochloric acid is shown by a deli-
cate rose-red tinge on the surface of the porcelain dish. In this way so
little as 0.06 per cent. of the acid is discernible, and the reaction is not
impeded by organic acids, albumin, or peptone. By its means the
author ®° has often detected o.oo1 mgrm. of acid in ro cc. of gastric
juice. It is further commended by Haas.*! This observer has similarly
employed other colour substances, as eosin and methyl-orange, but
experience does not justify their use.°? Boas and Puriz®* have recom-
mended resorcin for the purpose, but it is less sensitive than Giinzburg’s
reagent.
(g.) Benzo-Purpurin.—A still more sensitive colour-test is that fur-
nished by benzo-purpurin 6 B. Five mgrms. will serve to show 0.39
merm. of acid dissolved in 6 cc. of water (Hellstrim), causing the dark-
red colour of the solution to give place to a light violet. A similar
change is effected with acetic, formic, and lactic acids ; but the colour
obtained with organic acids is rather a brownish-violet, and requires a
ereater quantity of the latter for its production ; in the case of acetic
acid, not less than 0.84 mgrm. Test-papers may be prepared by soaking
strips of filter-paper in a saturated watery solution of benzo-purpurin
6 B, and subsequently allowing them to dry. If one of these be placed
in the gastric juice, it will immediately stain a dark blue, provided
hydrochloric acid be present in a proportion not less than o.4 germ. to
100 cc. A brownish-black tint may be due to the presence of organic
(lactic or butyric) acids, or to admixture of these with the hydro-
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132 THE GASTRIC JUICE.
chloric acid. The ambiguity in this case may he dispelled by placing
the paper so stained in a test-tube and shaking it up with sulphuric
ther, when so much of the colour as is due to the presence of organic
acids will speedily disappear, leaving a lighter stain, or restoring the
paper to its original tint. If hydrochloric acid alone be present, no
change will be effected in this way, and even after the lapse of twenty-
four hours the blue stain will be only slightly displaced. It is important,
of course, that the ether used should itself be free from acid. To ascer-
tain this its reaction may be tested with blue litmus paper.
The action of the benzo-purpurin test is not seriously interfered with
by peptone and serum-albumin, even when these bodies are present in
large quantity, and acid salts have no effect upon it.
The following experiments are of interest, as showing the various effects
obtained from benzo-purpurin with hydrochloric and organic acids :—
Two solutions were made, one of 4 grms. hydrochloric acid in 100 cc. of water,
and another of 0.1 grm. benzo-purpurin 6 B in 600 cc. of water. On mixing to-
gether 3 cc. of each, a beautiful blue colour inclining to violet developed, and a
coloured flocculent precipitate formed on standing. The addition of hydrochloric
acid caused this precipitate to dissolve, and it reformed on the further addition
of the dye.
The same effect was produced whether the solution contained 0.4 or 0.04 grm.
hydrochloric acid in 100 cc., 3 cc. being taken in each case, Three cc. of a solu-
tion holding 0.004 grm. hydrochloric acid, when added to 3 cc. of a solution of
0.1 grm. benzo-purpurin in 600 cc, of water, gave an evident violet coloration
with slight turbidity.
With formic or butyric acid, to obtain the reaction rather less than 0.04 grm.
in 100 cc. of water was required; with acetic acid, something more than 0.04
grm.; with lactic acid, over 0.004 grm. in 100 cc. In all cases alike 3 cc. were
taken of each solution.
A comparison of the Congo-red and benzo-purpurin 6 B test-papers
shows that the latter are the more sensitive, and they deserve the pre-
ference for practical purposes. Hyper-acidity and the preponderance
of organic acids in the gastric juice can be shown by this simple pro-
cedure in the space of a few minutes.
None of these coloration processes give entirely satisfactory conclusions.
In cases where the reaction is positively obtained, free hydrochloric acid
is undoubtedly present ; but we may fail to obtain the result when the
gastric juice contains albumin, peptone, or salts in considerable quantity,
even when free hydrochloric acid is present also.64 The reactions with
methyl-aniline-violet, Congo-red, and benzo-purpurin are the most to be
depended upon. They will not serve for scientific purposes, but in view
of their simplicity they are of the utmost value in bedside observation.55
3. Uffelmann’s Tests.—U/felmann *® has employed the colouring-matter of claret
in testing for free acids in the gastric contents, and quite recently, as a still
more sensitive reagent, the amylic alcohol extract of bilberries, which he applies
by means of blotting-paper soaked in it.” The reaction depends upon the fact
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ULTRAMARINE AND ZINC SULPHIDE. ae
that the colour of such a test-paper changes in presence of hydrochloric acid
even when peptone, albuminates, and salts are present, from greyish-blue to a
rose tint, which persists after the paper has been washed with ether.
Lactic, acetic, and butyric acids give similar reactions, but only when in such
a degree of concentration as is never found in the gastric juice ; and, moreover,
the reaction obtained with them is destroyed by the addition of zether.
[Dreschfeld ® employs Uffelmann’s test in a modified form. The test solution
consists of 0.5 cc. of claret (unadulterated), 3 cc. of 90 per cent. alcohol, and 3 cc.
of zther; the solution is almost colourless, and is rendered a rose colour by
the presence of a minute quantity of hydrochloric acid. This test is said by
Dreschfeld not to be interfered with by the presence of peptone or albumin.
Lactic acid gives a similar reaction only when occurring in a more concentrated
form. The mixture does not keep long, and has to be freshly prepared.]
4. Ultramarine and Zinc Sulphide.—These substances were suggested by Maly,
and employed by Kahler® as a test for free hydrochloric acid in the contents
of the stomach. Ultramarine, according to Kraus," is a test for free acids
in general. It is decomposed by them even in dilute solutions, sulphuretted
hydrogen being given off, while silicic acid and sulphur are precipitated, Zinc
sulphide, again, is dissolved in dilute acids with the evolution of sulphuretted
hydrogen. It is, however, insoluble in acetic acid.
In testing for hydrochloric acid the process is as follows:—About 20 cc. of
the fluid under examination is placed in a crystallising crucible, and so much
ultramarine is added as will suffice to give it immediately a blue tinge. The
crucible is then covered with a watch-glass, from which depends a strip of filter-
paper soaked in solution of sugar of lead, and the mixture is gently heated in the
water-bath. After the lapse of a quarter of an hour, if hydrochloric acid be
present, the blue colour of the fluid will have given place to a brown tint, while
the-lead-paper will be stained brown or black. Sulphide of zinc (as much as
will fit on the point of a knife) is then added to another specimen, and the same
process repeated, when the brown or black stain upon the lead-paper will again
show the presence of hydrochloric acid. The reactions are rendered more feeble
by the presence of salts and of phosphates in particular. They can be obtained
also with organic acids (lactic and acetic) in more concentrated solutions.
These circumstances, and the comparative complexity of the process,
render its application at the bedside a matter of difficulty. Whereas, on
the other hand, we possess in the methyl-aniline-violet, benzo-purpurin,
and brilliant-green reactions a series of tests which are at once ready
and accurate.
B. Quantitative Estimation of Free Hydrochloric Acid.—This can be accurately
effected by the very complicated process of Bidder and Schmidt.*! All the acids
and bases in the gastric juice are quantitatively estimated, the proportion of
each in 100 cc. of fluid ascertained, and their equivalents computed. The
remaining hydrochloric acid is that which is free in the secretion.
Another method for the determination of this body depends upon the fact
that the acid is insoluble in ether, whilst organic acids are soluble in that
medium. To utilise this property for the purpose in hand, Richet® shakes up
the gastric juice with zther, and determines by titration the quantity of acid
which is taken up by the latter together with what is retained in the watery
solution.
Recently, v. Meriny and Cahn ® have adopted the expedient of collecting the
volatile acids by distillation, lactic acid by extraction with zther, and combining
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134 THE GASTRIC JUICE.
the hydrochloric acid separated from the organic acids with cinchonine, shaking
up the newly-formed hydrochlorate of cinchonine with chloroform, changing
the acid into its silver salt, and finally weighing the chloride of silver obtained.
Koster (see p. 130) has endeavoured to determine the quantity of hydrochloric
acid in the gastric juice by a process of titration with alkalies after the addition
of methyl-aniline-violet.
Giinaburg’s reagent, according to Zwald,*4 will also furnish a means of approxi-
mately estimating the quantity of hydrochloric acid present.
1. Leo’s Method.—This has been already described (p. 128). If fatty
acids and lactic acid be present, their proportion must be determined
(see p. 139), and deducted from the total acidity. The difference. will
express the quantity of HCl. According to Kossler,® the method
is accurate. Both it and that which follows serve well enough for the
estimation of physiologically active hydrochloric acid.
2. Sjéqvist’s Method.—Sjoqvist % has recently introduced a process
for the estimation of free hydrochloric acid in the gastric juice founded
upon the following facts :—The acids of the secretion may be changed
into their barium salts by the action of barium carbonate, and when
these are incinerated, the baryta salts of the organic acids leave barium
carbonate, whilst the chloride of barium resulting from the combina-
tion with hydrochloric acid remains unchanged. The latter may then
be separated from the insoluble carbonate by extracting the ash with
warm water, and its quantity estimated by titration with chromate
solution. The details of Sjoqvist’s method are these :—Ten cc. of the
gastric juice are filtered and placed in a platinum or silver crucible,
and barium carbonate free from chlorides added in excess. The fluid
is then evaporated to dryness at a gentle heat, and the residue charred
and strongly heated for some minutes. After cooling, the residue
is treated with 10 cc. of water, the mixture rubbed up, extracted
repeatedly with boiling water, and filtered until the filtrate has a bulk
of 50 cc. The quantity of chloride of barium in solution is best esti-
mated by titration with bichromate of potash. This body gives with
salts of barium a precipitate of barium chromate, which is insoluble
in water and acetic acid, and soluble in hydrochloric acid. A solution
of bichromate of potash of known strength is added from a_ burette,
until all the barium present is precipitated in the form of chromate.
A subsequent excess of bichromate of potash would give to the fluid
a deep red colour, which would tend to mask the result. This may be
prevented by the use of tetra-paper (tetramethylparaphenyl-diamine),
which has the property of staining blue with oxidising substances.
In the process of titration, therefore, the filtrate is mixed with one-
fourth or one-third its volume of alcohol and 3-4 ce. of a solution
holding ro per cent. acetic acid and ro per cent. acetate of soda, and
titrated with a solution of bichromate of potash (8.5 grms. to the litre)
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ESTIMATION OF HYDROCHLORIC ACID. 135
until a faint trace of blue appears upon the test-paper. The addition of
acetic acid and acetate of soda has for its object to promote the precipita-
tion of chromate of barium, and at the same time to prevent the forma-
tion of chromate of lime from the small quantity of lime salts and free
hydrochloric acid that may be present. From the quantity of bichro-
mate of potash used, that of the barium salt formed, and also of
sulphuric acid present, results directly.97
This process is attended with difficulty, and it is open to the objection
that it depends too much on the judgment of the observer. The follow-
ing modification of it is more accurate.
3. V. Jaksch’ Modification of Sjéqvist’s Method.—It is the author’s
practice to convert the chloride into barium sulphate, and by weighing
the sulphate to calculate the amount of hydrochloric acid in 10 ce. of
gastric juice. To that end the unfiltered gastric juice (10 ce.) is treated
with chlorine-free carbonate of barium in excess, and placed on a furnace
in a thin porcelain crucible, where it is evaporated to dryness, then
gently fused in a muffle; the residue cooled, extracted with boiling
water, and filtered ; the filtrate evaporated on the water-bath to a volume
of roo cc., and dilute sulphuric acid added. The precipitate (sulphate
of barium) is placed on a thick ash-free filter, washed with water, fused
in a platinum capsule, thence removed with the usual precautions.®
The result is calculated thus :—233 parts by weight of barium sulphate
(BaSO,) correspond to 73 parts of hydrochloric acid (HCl). And the
quantity of the latter contained in 1o cc. of the gastric juice may be
calculated from the formula
eee LS. M=0.3132 x M
233
where M = thequantity of barium sulphate obtained from ro cc. gastric juice
x =the quantity of hydrochloric acid sought in ro ce.
This method enables the examination to be effected within a compara-
tively short time. Its accuracy is attested by Leo, Lenbuscher, Pfungen.®
The objections made to it on the ground of its being too complicated are
ill-founded.” It serves for the estimation of HCl equally when free,
and when combined with organic digestive products (proteids). It is
doubtless true that there are proteids which enter into combination with
HCl in such a way that the acid is no longer perceptible by this process,”
but the author’s investigations have satisfied him that such combinations
do not in fact oceur in digestion. Quite lately Leo"? has contended
against the principle of Sjéqvist’s method, adducing considerations which
gravely affect the pretensions to accuracy both of that method and of the
modification of it just described ; the result of Kossler’s'? researches, how-
ever, has greatly diminished the force of Zev’s objections. It would
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136 THE GASTRIC JUICE.
appear, indeed, that the method is inapplicable where phosphates are
present, and its utility is much curtailed by this fact. In any case it
is only the absolute values as determined by the method which are
affected. The conclusions based upon them remain good. Finally, the
observations of Rosenheim™ show that the fallacies which Leo has
pointed out do not apply to a bedside examination. The modifications
of Salkowshkt and Fawitzky™® and of Boas" offer no special advantages.
Of Bourget’s process’? the author has no experience. That of Winter
and Wagner, according to Kossler,’$ yields an estimate of HCl, free and
combined with proteids, which is somewhat too high.
4. A. Braun’s Method.”—A certain quantity—5 cc.—of the filtered
gastric juice is taken and its acidity determined by titration with 35
normal soda solution in the manner described at p. 127. To another
5 ce. of gastric juice is added soda solution a little in excess of
what was needed to neutralise it. The fluid is now incinerated (see
p. 134), and to the ash is added as many ce. of 7'5 normal sulphuric
acid solution as were needed of 4, normal soda solution to neutralise the
specimen taken, z.e., 5 cc. of the filtered juice. The ash is thus dis-
solved ; the fluid is warmed, and carbonic acid driven off, after which
a solution of phenolphthalein is added to it, and it is titrated with
iy normal alkali solution. The number of cc. of 7'5 normal soda solution
employed, multiplied by 0.00365 (see p. 129), gives the quantity of HCl
in 5 ce. of gastric juice. This method is founded on the same principle
as Sjéqvist’s, but, according to Kossler,®° it is not accurate, since the
acidity which is due to acid phosphates is not allowed for.
5. A. Hoffmann’s Method.*! —In testing the proportion of HCl in the
gastric juice, Hoffmann has availed himself of the property which HCl pos-
sesses of inverting cane-sugar, ze. of breaking it up into dextrose and lvu-
lose, so that the polarisation-phenomena of its solutions are altered. ‘The
following preparations are required :—z. A fluid containing known quan-
tities of cane-sugar and HC]. 2. Equal quantities of cane-sugar and gastric
juice. 3. Gastric juice alone. 4. Gastric juice with cane-sugar and sodium
acetate in equal quantities. The rotatory power of each of the four fluids is
ascertained by means of the polarimeter, and they are then allowed to stand
in a warm place for some hours, and their rotatory power again investigated.
The calculation is then made by the formula, log A—log (A-«x)=C, where
A=the quantity of sugar originally present, «=the quantity which has been
converted at the termination of the process. This method is undoubtedly
ingenious, but it is subject to the drawback that it requires a very accurate
polarimeter, eight polarimetric examinations, and a highly-complicated calcula-
tion. Recently it has been much simplified by substituting titration with
methyl acetate for inspection with the polarimeter.® The researches of Kossler ®%
have shown, however, that it serves only for the estimation of free HCl, to the
exclusion of that which is combined with proteids.
In addition to those described here, many other methods have been brought
forward for the estimation of HCl, but they possess no superior advantages, such
of them as are easier of application being proportionately wanting in accuracy.
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HYDROCHLORIC AND ORGANIC ACIDS. 137
Amongst them are those of C. Th. Morner, Mintz, Jolles, Kronfeld, and Czyr-
nianski.5* Of the method recently suggested by Liittke® the author has no
personal experience. The principle upon which it depends—namely, estimation
of the total quantity of chlorine and chlorides—is not new.
(c.) THE QUANTITY OF HYDROCHLORIC ACID PHYSIOLOGI-
CALLY ACTIVE IN THE GASTRIC JUICE, AND ITS DIAGNOS-
TIC IMPORT.—Concerning the quantity of hydrochloric acid which is
secreted normally during digestion the recorded observations are very
few. Moritz, Wohlmann, and v. Jaksch 6 have investigated this subject.
According to the latter, the quantity formed during digestion in healthy
children varies greatly with the nature of the food, and generally attains
its maximum within one to three hours aftera meal. With milk, which
combines very readily with acids, the increase is slow; it is more rapid
with nitrogenous, slowest, but with greatest initial rapidity, with fari-
naceous food. The greatest quantity of effective HCl was obtained
with a diet of milk alone, a smaller quantity with a meat diet, and the
least with carbohydrates. The quantities were respectively :—o.1615
gim. (mean of fourteen observations), 0.1563 grm. (mean of eleven
observations), and 0.1102 grm. (mean of ten observations), in 100 cc.
of the gastric contents. The facts are the same in healthy adults.
Thus with the method described at p. 135, the author has found that
when 200 grms. of ham have been taken, there are in roo ce. of the
gastric contents 0.0643 grm. of HCl in thirty minutes, 0.1529 grm. in
forty-five minutes, and 0.0992 grm. in an hour. From this it follows
that, as a preliminary to basing any inference upon the quantity
of HCl secreted, it is necessary to consider what food the subject
of the inquiry has taken, and at what time he has taken it. The
absence of free HCl, or its presence only in very small quantity, fifteen
to thirty minutes after a meal, has no pathological significance. But
should there be little or no free HCl present one to three hours after
taking milk or nitrogenous food, the fact is evidence of a grave defect of
function. A large quantity of HCl, even so much as 0.33 per cent. three
hours after food, does not necessarily imply functional disorder (hyper-
secretion). Such considerations must always be weighed in forming an
inference for diagnostic purposes. Again, for practical purposes, those
tests alone are satisfactory which yield information concerning the
physiologically-effective acid. From this point of view the colour-tests
are insufficient, but they have the advantage of being easily applied, and
where approximate results are desired they serve well enough. For
scientific purposes the requirements are :—1. The application of such
methods as dispense with the necessity of filtering the gastric juice,
since this process is attended with much waste of the acid (v. Jaksch).®
2. That the method chosen should be one which takes account of that
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138 THE GASTRIC JUICE.
part of the acid which is physiologically effective. These requirements,
as Kossler has shown, are fulfilled only by Leo’s method, when applied
to artificial digestion. Whether this is true of the natural gastric juice
also remains to be proved. Approximately accurate results, however,
may be obtained by the author’s modification of Sjdqvist’s process. One
of these methods may be used with advantage to control the other.
We shall return to this point presently in treating of the contents of
the stomach in different gastric disorders.
It may be suggested here that for the terms “free” and “ combined ”
hydrochloric acid, “ physiologically active” and ‘physiologically in-
active” should be substituted. By the first would then be meant
either that portion of the acid which has already discharged its function
and has entered into combination with proteids, or that which is still
available, and therefore in the literal sense free.’8
The investigation of the functions of the stomach in disease of all
kinds, and especially with reference to the secretion of hydrochloric acid,
has of late years been pursued with the utmost energy. The contri-
butions to the subject which possess the chief diagnostic interest may be
briefly mentioned. Jmmermann and Schetty*®® found that in tubercu-
losis there was no change in the secretion of HCl. Their conclusions
are supported by Chelmonshi, Klemperer, O. Brieger, Hildebrand, and
Schwalbe.© Grusdew,® on the other hand, observed a diminished pro-
duction of the acid. vile? states that in heart-disease the acid is
deficient, but this is not in accordance with the observations of Hinhorn,
Adler, and Stern.%
Biernackt®* and the author have noticed a considerable deficiency of
the acid in renal disease in many cases.°° Lenhartz®° has collected much
information upon this subject. In acute and chronic dyspepsia there
was a remarkable deficiency of free acid ; in chlorosis a similar deficiency
was observed in 45.6 per cent. of the cases investigated, whereas in
gastric ulcer the condition was inconstant.
From these facts it results that the presence or absence of free hydro-
chlorie acid is a symptom of doubtful import, and that it must be
weighed in conjunction with the other circumstances of the case. It is
much to be desired that measures should be taken for the acquirement
of accurate data concerning the production of hydrochloric acid in
diseases of the stomach and other parts, and this may be done by the
use of the more scientific methods indicated here, and especially by
observance of the precautions mentioned on p. 137. It is sufficient here
to point out that a failure of the secretion on the one hand, and its pro-
duction in excess on the other, are alike evidence of Gisease.97 Their
precise significance will be dealt with later (pp. 146, 148).
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ESTIMATION OF ORGANIC ACIDS. 139
(d.) ORGANIC ACIDS OF THE GASTRIC JUICH.—In this con-
nection we have to deal with lactic, acetic, and butyric acids.
1. Lactic Acid.—A. Qualitative Tests.—In the detection of this
hody in the gastric juice the carbolo-chloride of iron test is to be recom-
mended (Ujelmann, see ref., p. 132), (Kredel).8 To a mixture of to ce.
of a 4 per cent. solution of carbolic acid with 20 cc. of water, a few drops
of perchloride of iron solution are added, and the resulting amethyst-
blue colour changes to yellow in presence of a few drops of lactic acid.
Alcohol, sugar, and phosphates, however, yield a similar reaction (Ewald).
A further test for this body is derived from a very dilute solution of
perchloride of iron—two to five drops of a watery solution of perchloride
in 50 cc. of water. The faint yellow colour of the fluid, whilst not
affected by the addition of hydrochloric, butyric, or acetic acid, is inten-
sified in presence of dilute lactic acid. To separate lactic acid from the
gastric juice, the distillation residue (see below) of the gastric juice, in
which the acid is dissolved, may be extracted with ether, and submitted
to the tests described elsewhere (see chapter on Urine).
B. Quantitative Estimation.—This may be effected by Cahn and
v. Mering’s method (see p. 133), or by that of Leo.°! 10 ce, of gastric
juice are taken, and when the fatty acids have been removed (see below),
extracted six times with reo cc. of ether in a separator-funnel, the
resulting ethereal extracts collected, the ether driven off by exposure to
the air by heat from a water-bath—(a flame must not be used)—and the
residue dissolved in water. The acidity of the solution is then deter-
mined by a 35 normal soda solution. Since 1 ce. of the soda solution
corresponds to 0.090 grm. of lactic acid, the quantity of the latter con-
tained in 1o cc. of gastric juice may be obtained by multiplying the
number of ce. of alkali used by 0.090.
2. Butyric and Acetic Acids.—(a.) Qualitative Tests.—If the gastric
contents be extracted with ether, butyric and acetic acids may b2 recog-
nised by their smell (Ufelmann). To separate these acids, the gastric
juice is distilled and the distillate tested in the manner laid down for
the examination of the urine.
Hammarsten'? prefers not to distil the gastric juice directly, but to
neutralise it first with caustic soda, and then to extract with alcohol,
proceeding afterwards in the manner to be described for the detection
of fatty acids in the urine. The object is to avoid the error of including
fatty acids derived from proteids.
Uffelmann (ref., p. 132) directs attention to the importance of a syste-
matic analysis of the gastric juice for the detection of free acids. To
do this the contents of the stomach are filtered and their reaction tested.
Should this be acid, they are submitted to the following process :—The
total acidity is determined by titration with a decinormal solution of
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140 THE GASTRIC JUICE.
caustic soda, and a portion is tested with dilute solution of perchloride
of iron for the presence of lactic acid. Another portion is then tested
for free hydrochloric acid with bilberry-dye test-papers. A rose colour
obtained when the degree of acidity is slight, and persisting after the
addition of ether, indicates the presence of hydrochloric acid. If, on the
other hand, the colour is entirely destroyed by treatment with ether, it is
evidence of considerable quantities of lactic, butyric, and acetic acids.
Riegel! and Koster (ante, p. 134) have employed similar methods
with success; and attention may also be directed to the process de--
scribed at p. 135.
(b.) Quantitative Estimation.—Leo’s 1* method is the following : 10 ce.
of the gastric juice are taken, and the total acidity determined in the
manner described at p. 128. Another ro ec. are filtered and boiled until
the fumes no longer present an acid reaction. The residue is allowed to
cool, and is then titrated with deci-normal solution of soda. The differ-
ence between the acidity of this and the former specimen is that due to
the fatty acids. The method is not absolutely accurate, since HCl may
be driven off by boiling.
4. Proteids.—Proteids occur in the gastric contents during digestion,
being partly formed in that process, and in part derived from the food.
Their recognition affords valuable evidence as to the functional condition
of the stomach ; and to make its import clearer, it will not be out of
place to refer to certain facts in physiology. The period of digestion
may be divided into two stages. (1.) The first of these, which lasts
but a short time (15-20 min.), is occupied chiefly with the digestion of
starchy matter, and is characterised by the presence of the resulting
products, and especially lactic acid. (2.) The second stage commences
with the secretion of pepsin and an active gastric juice, by means of
which the albumin of the food is changed. The two stages pass gradu-
ally into one another, and authorities are not agreed as to whether lactic
acid occurs only during the first (Hwald, Boas, and others) or in the
second stage of healthy digestion also, when it is said by some (Cahn
and v. Mering, Ritter and Hirsch) to be present together with the more
abundant hydrochloric acid.
For the purpose of an examination, whether in a healthy individual
or otherwise, a test-meal should be administered on an empty stomach.
This, according to Hwald, should consist of a dry, well-baked roll and
water or weak tea; whilst Leube and Riegel recommend a meal of
water-broth,* semolina and flour-gruel,t and meat. Ewald’s regimen
* Wassersuppe, translated here as water-broth, is made of boiling water with
small squares of dry rolls, some salt and fresh butter.
+ Griessuppe, semolina soup, consists of semolina boiled in water and seasoned
with salt and butter or extract of meat.
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PROTEIDS—-UREA—-AMMONIA. 141
has the advantage that digestion is at its height within an hour after
the food has been taken, whereas in the other case it is necessary to
wait for four to six hours before the examination can be begun The
contents of the stomach are obtained in the manner described at p. 125.
A test-meal of this kind is very useful for many purposes. Klemperer
and the author! administer milk in the same way. It is probably
advisable that the test-meal should be of the simplest possible character,
a single proteid, as, for example, ego-albumin, or a carbohydrate being
given, and the choice will be made in accordance with the subject under
investigation. The proteids in question are albumin, hemialbumose,
peptone, and syntonin.
Albumin and hemialbumose may be detected by the process detailed in
the chapter on Urine. Should these bodies and syntonin be absent, the
biuret reaction (red coloration) will serve directly to show the presence
of peptone. If, on the other hand, following the method referred to,
other proteids (and especially those which are coagulable by heat) are
found to be present, these must first be removed in the usual manner
(see chapter on Urine), provided a sufficiency of material remains to
work upon. The filtrate may then be submitted at once to the biuret
test, the previous precipitation with phosphotungstic acid not being
necessary.
Syntonin may be known by its being precipitated by neutralisation
from its acid solutions.
About 30-40 cc. of gastric juice will suffice for an examination of
this kind when a little skill has been attained in conducting it. The
pathological specimens which come to hand rarely exhibit other nitro-
genous bodies than peptone, as is the case also when the contents of
the stomach are examined several hours after the test-meal has been
taken.
5. Urea.—For the detection of urea, one of the methods adopted for
the same purpose in connection with the blood (p. 69) may be employed.
Considerable quantities of this body are found in the stomach in cases
of ureemia.
6. Ammonia.—Salts of ammonia are abundantly present in the
stomach in rare instances. Where a considerable bulk of the gastric
contents can be obtained (as by vomiting), the quantity of ammonia
present may be estimated, after the removal of the proteids, by Sai-
kowski’s method. For this purpose, 50 cc. of the vomited matter are
taken, 20 grms. of pure powdered chloride of sodium first added, and then
too cc. of a mixture holding seven parts by volume of a saturated solu-
tion of chloride of sodium and one part of acetic acid (1.040 sp. gr.).
The whole is then mixed together, allowed to stand for fifteen to twenty
minutes, when it is measured and filtered. .Of the proteid-free filtrate
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142 THE GASTRIC JUICE.
50 to 100 ce. are measured off, treated with milk of lime, and placed
under a bell-glass containing a known quantity of 1/100 normal solu-
tion of an acid. After the lapse of from three to five days, the latter
is removed and titrated with 1/100 normal alkali solution coloured
with rosolic acid. In this way the quantity of ammonia absorbed may
be determined.1°7
The same process is applicable to the determination of ammonia salts in the
blood and other fluids.
7. Carbohydrates.—Grape-sugar may sometimes be found in the
stomach, having either been introduced with the food, or formed
there by the action upon starch of saliva which has been swallowed.
This latter mode of origin belongs especially to conditions of hyper-
secretion of HCl (Riegel, see p. 127, Hwald).°S The mode of testing for
sugar is the same here as in the blood (p. 72), the proteids being first
removed.
The phenomena of the digestion of starch, and the formation of its
intermediate products, involve some points of interest. An hour after
food has been taken, under ordinary circumstances, neither starch
(blue colour with iodine and iodide of potassium solution) nor erythro-
dextrin (red with the same reagent) can be discovered in the filtered
gastric juice. Should it happen otherwise, some cause tending to delay
the amylolytic process may be inferred, and this may be sought either
in the fact that the saliva is deficient in diastase, or that there is an
excessive secretion of free acid by the stomach at the outset of digestion
(Ewald, Boas, Rosenheim"). In health, also, when amylaceous food
has been taken in quantity, starchy particles may be found, and their
nature determined chemically (see p. 145).
5. Estimation of the Rate of Absorption of the Gastric
Contents.—The rapidity with which the gastric contents are absorbed,
and consequently the functional activity of the stomach in this respect,
may be determined thus, after Penzoldt and Faber..! A capsule con-
taining o.1 grm. of iodide of potassium is given to the patient to
swallow. The saliva is then tested for iodine every two or three
minutes, by placing a little of it upon filter-paper saturated with
starch-paste, and adding a drop of fuming nitric acid. The presence
of iodine is shown by a blue colour, which usually appears in 8-15
minutes. According to Zierfel,!!? this period is prolonged—-thus indi-
cating a deferred absorption—in various affections of the stomach, as
dilatation, cancer, and gastric ulcer.
6. To Determine the Contractile Activity of the Stomach.—
For this purpose various expedients have been adopted. Amongst them
may be mentioned those of Lewbe, Klemperer, Stevers, and Ewald.
Leube assumes that the motor function of the gastric walls is impaired
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THE INTESTINAL JUICE. 143
when the use of the sound shows the presence of food seven hours after
it has been taken. Klemperer’s method is objectionable on the score of
discomfort. Ewald introduces within the stomach a gelatine-capsule
containing 1 grm. of salol. This decomposes into phenol and salicylic
acid as soon as it reaches the small intestine, and rapidly appears in the
urine, where it may be detected by solution of ferric chloride (see chapter
on Urine). The interval which elapses before the drug appears in the
urine may be taken to indicate the length of time required for the
stomach to discharge its contents. In health this is from 4o to 60
minutes, but a much longer time in gastric atony and dilatation. The
results obtained in this way have no utility in diagnosis.!4
7. A Summary of the Chemical Examination of the Gastric
Contents.—It is seldom that sufficient material can be obtained for
the systematic examination suggested here, and it will be necessary to
make the investigation by successive evacuations of the stomach, the
administration of test-meals, &c., before the different processes can be
applied.
1. The reaction is to be tested.
2. A known quantity of the fluid, say 10 cc., is taken for the deter-
mination of acidity.
3. Another quantity of 10 ec. is examined to show the presence of
pepsin and milk-curdling ferment.
4. The benzo-purpurin, Congo-red, and brilliant-green tests for free
hydrochloric acid are applied, and the latter estimated quantitatively by
Sjoqvist’s method.
5. A rough estimate is made of lactic, butyric, and acetic acid in the
manner described at p. 139.
6. Examination for proteids, this being confined to serum-albumin
and peptone where sufficient material cannot be had.
7. Test for starch and its digestive products.
8. The remainder of the fluid is distilled, and the residue shaken up
with ether, to determine accurately the quantity of lactic acid which it
contains (p. 139). The distillate is tested for fatty acids in the manner
described in the chapter on Urine.
II. THE INTESTINAL JUICE.—In the present state of our know-
ledge the investigation of the intestinal juice lends but little aid to
clinical study. Notwithstanding this, the subject is worthy of attention,
and it is probable that before long it will be brought within the scope
of a practical inquiry.
1. Naked-Eye Characters.—The intestinal juice is 2 mixed secre-
tion derived from several glands, and its character varies with the part
of the tract from which it is taken. In the small intestine it is the
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144 THE GASTRIC JUICE.
product of Brunner’s and Lieberkiihn’s glands, the liver, and the pancreas.
It is only this fluid, which is a compound of bile, pancreatic fluid, and
the secretion of the intestinal glands, that will be noticed here. It
is a clear yellow thin fluid of a strongly alkaline reaction, and sp. gy.
1.009—1.011. On standing exposed to the air it turns to a grass-green
colour.1%
2. Formed Elements.—Concerning these nothing is accurately
known.
8. To Obtain the Intestinal Juice.—According to Boas," it is
first ascertained whether the stomach is empty. Should it be so, the
patient is made to lie down, and the abdomen over the region of the
gall-bladder is massaged ; then the patient is made to stand upright, and
the sound is again introduced, when he once more assumes the horizontal
position, and the fluid is pressed out.
4. Chemical Constitution of the Intestinal Juice.—The
intestinal juice contains bile-acids and hile-pigments, syntonin, peptone,
a small quantity of leucin and tyrosin (comp. Chapter VII.), and a
number of ferments, of which the chief are the tryptic, fat-splitting, and
emulsifying * (pancreatic), diastatic, and inverting ferments.
Concerning the changes which the secretion undergoes in disease
nothing is yet known. Boas was the first to introduce the subject of
digestion in the small intestine. Physiological research has yet to pave
the way before our knowledge in the matter can be applied to the pur-
poses of diagnosis. Nevertheless, the few facts which have been brought
to light by Boas and Noorden™" afford ample prospect of a rich harvest
both of physiological and clinical results from further study in this
direction. "8
III. EXAMINATION OF THE VOMIT.—The vomit includes the
secretions of the mouth and nasal passages which have been swallowed,
and are, for the most part, already undergoing digestion, the gastric juice
and ingested substances, in part altered by the action of the stomach,
and partly unchanged. Further, it sometimes contains bile.
The naked-eye and microscopical appearances vary with its constitu-
tion, and chiefly with the abundance and character of the food. Apart
from such constituents as are derived from the mucous membrane of the
mouth and nasal passages, and which have been already described, the
vomit almost invariably presents—(1) Columnar and squamous epithe-
lium, both usually much altered in form; (2) isolated white blood-cor-
puscles, generally so transformed by the action of the gastric juice that
little more than the nuclei remains ; (3) isolated red blood-corpuscles,
* [It is, however, doubtful if there is an emulsifying ferment.]
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CONSTITUENTS OF THE VOMIT. 145
usually seen as colourless rings, and very seldom in a quite perfect state ;
(4) the following derived from the food :—
1. Muscle fibres, readily recognisable by their transverse striation.
2. Fatty globules and fat-needles, which are sufficiently characterised
by their refracting property and their solubility in ether.
3. Elastic fibres and connective tissue.
4. Starch granules, to be recognised by their concentric arrangement
and by their property of staining blue with iodo-potassic-iodide solution.
These bodies are frequently disintegrated and more or less dissolved hy
the process of digestion.
5. Vegetable cells of various forms.
Fic. 64.—Collective View of Vomited Matter (eye-piece III., objective 8a, Reichert).
a. Muscle fibres. e. Fat globules. i. Various micro-organisms, such
b. White blood-corpuscles. jf. Sarcina ventriculi. as bacilli and micrococci.
c, c’. Squamous epithelium. g. Yeast-fungi. k, Fat-needles; between them
ce’. Columnar epithelium. h. Forms resembling the com- connective tissue derived
d. Starch grains, mostly al- ma-bacillus, found by the from the food.
ready changed by the author once in the vomit|/. Vegetable cells.
action of the digestive of intestinal obstruction.
juices.
In addition, the vomit in disease displays a great variety of fungoid
growths (W. de Bary"), depending upon the nature of the underlying
process. Amongst these :—
1. Mould-Fungi and scattered conidia have occasionally been found.
These are, so far as we know, devoid of pathological significance.
2. Yeasts.—(a.) Saccharomyces cerevisiz. These are about the size
of leucocytes, and refract light powerfully. They cohere in groups of
three or more, and stain deeply a brownish-yellow with iodine and iodide
of potassium. Very often there are also to he seen elliptical bodies
resembling Saccharomyces ellipsoideus (Zees).1°°
K
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146 THE GASTRIC JUICE.
(b.) Very small yeast-like fungi in thick clusters (fig. 64, 9).
(c.) More seldom highly-refracting rod-like bodies, of considerable
length and thickness, which generally exhibit a single nucleus. They
are rounded off at the ends, and are sometimes separate, sometimes
strung together in strands. It would seem that these are the agents
in lactic acid fermentation of sugar.
3. Fission-Fungi—The forms belonging to this class are many and
various.!21 They include rod-like bodies, which stain blue with iodo-
potassic-iodide solution, bacilli and micrococci of every description, and
in particular a bacillus which possesses the property of changing glyce-
rine into alcohol by fermentation (fig. 64, 7).
Sarcinz ventriculi 122 may easily be known by their shape, resembling
that of wool-packs, their dark silver-grey tint, and their property of
staining a deep mahogany-brown to reddish-brown with the iodo-potassic-
iodide solution (fig. 64, /).
After this general view of its microscopical appearances, we shall
advert to the physical, chemical, and microscopical characters of the
vomit in certain diseases.
4. Acute Gastritis.—In this condition the vomit consists partly of
mucus which has been swallowed, and partly of half-digested food
residues. Microscopically it displays the appearances already detailed,
which, however, are here subject to much variety, and notably a few
red blood-corpuscles are generally to be seen.
Its chemical character varies greatly (wald).!°3 At the outset of the
affection, hydrochloric, and commonly lactic, acid in the free state are
wanting. The addition of the former will establish a slow digestive
process. Ewald 14 has been unable to determine the presence of fatty
acids in notable quantity, and the proportion of pepsin would appear
to be considerably diminished.
The vomit usually is coloured green from the admixture of bile pig-
ment (biliverdin). It often also contains biliary acids. The first may
be recognised by Gmelin’s test (see chapter on Urine), and the latter by
Pettenkofer’s (see p. 76), or by means of the furfurol and sulphuric
acid reaction (see Urine). Much remains to be learnt as to the chemical
peculiarity of the gastric contents in this condition.
2. Chronic Gastritis.—The vomit is a thin mucous fluid (vomitus
matutinus), of alkaline, or it may be weakly acid, reaction. Van der
Velden has shown that it always contains pepsin and hydrochloric acid,
also organic acids, especially acetic and butyric acids. It is commonly
rich in proteids, and notably peptones, which may be easily distinguished
by the tests which will be subsequently described in connection with
the examination of the urine. Bile pigment is also generally present.
Recent observations seem to show that it is possible to distinguish
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CHRONIC ULCER OF THE STOMACH. 147
the different forms of gastric catarrh by the results of the chemical
methods described above. Following the conclusions of Hwald, we may
discriminate (1) Simple gastritis, (2) acid gastritis, (3) mucous catarrh,
(4) atrophy.
1. In the first form, simple gastritis, the test-breakfast is never
followed by increased acidity ; the proportion of hydrochloric acid is
diminished; the secretion contains little pepsin and milk-curdling
ferment, and generally, though not always, includes lactic and fatty
acids. On the addition of acid the secretion shows digestive activity.
2. In acid gastritis acidity is increased, especially that due to hydro-
chloric acid. In other respects the condition is that of simple gastritis.
3. In the third form, mucous catarrh, acidity is always slight and
hydrochloric acid absent ; there is abundance of propeptone, but no pep-
tone. Milk-curdling ferment is absent, or it may develop only after a
prolonged interval. Artificial digestion requires the addition of hydro-
chlorie acid.
4. In atrophic gastritis the fasting stomach is usually empty, and its
contents, after the administration of the test-meal, is free from mucus,
and altogether wanting in pepsin, hydrochloric acid, and the milk-
curdling ferment. !?°
The observation of Mathieu °° that mucus is indigestible has an im-
portant bearing on the study of these conditions. The fact noticed by
John 12" that excessive acidity of the gastric juice impedes salivary
digestion, and that acids, organic and inorganic, promote the secretion of
saliva, is equally instructive. In the case of a gastro-duodenal catarrh
complicating gastritis, the gastric juice exhibits the same variety in
respect of the presence or absence of appreciable quantities of physio-
logically effective hydrochloric acid. The author has investigated three
cases of this kind. In one the acid was altogether wanting, while in
the other two it occurred in diminished proportion.
8. Chronic Ulcer of the Stomach.—The microscopical appear-
ances of the vomit in this disease are those detailed under (2) in the
last section. Otherwise it exhibits nothing distinctive. There can be
no doubt that we have in the hyper-acidity which Riegel’s 128 observa-
tions have connected with this condition in a large number of instances,
a fact of the highest clinical significance. It may be estimated accu-
rately by the method detailed at p. 135, or by titration. The proportion
of hydrochloric acid in the stomach in a case of chronic gastric ulcer is,
according to Riegel, o.4—0.6 per cent., as against O.1-0.2 per cent. in
health.129 It must be mentioned, however, that the researches of Ewald,
Ritter and Hirsch, and Jaworski'®° go. to show that the increased
acidity in connection with round ulcer of the stomach may undergo
diminution with the further progress of the disease.
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148 THE GASTRIC JUICE.
According to Lenhartz! acid may be deficient in gastric ulcer. The
digestion of carbohydrates is accomplished slowly. There is still need
to verify these assertions by the application of trustworthy methods,
such as those described at pp. 133, 136, and especially with reference to
the precautions enjoined in a previous paragraph (p. 137). The conflict-
ing statements quoted here must be in part referred to the want of
such accurate observation.
The presence of blood, and its character, are facts of great significance.
1. When the hemorrhage is considerable, clots of blood are found,
which are not at all, or but slightly changed.
2. More commonly the effused blood remains for a longer time in
contact with the gastric juice, and is thereby altered in such a way that
the oxyhemoglobin is converted into hematin, and the vomit has the
appearance of coffee-grounds.
When examined under the microscope in such a case, no blood-cor-
puscles whatever are to be seen in it, but in their place larger or smaller
pigment masses. The blood may best be identified as such by Tezch-
manns hemin test and by the spectroscopic appearances of hematin.
To obtain the latter, a portion of the vomit should be treated with
caustic potash, filtered, and then examined with the spectroscope for the
spectrum of hematin in alkaline solution (fig. 39).
It should be borne in mind that the exhibition of preparations of iron
will impart to the vomit the same appearance as that due to blood; so
also will the abundant partaking of red wine ; and finally, the presence
of bile-pigment may cause it to assume a brownish-black colour.
Large quantities of blood (blood-pigments) may be found in the vomit
in cases of duodenal ulcer with hemorrhage into the intestine.
4. Carcinoma of the Stomach.—The physical and microscopical
character of the vomit in cases of cancer of the stomach are, in general,
those of gastric ulcer. Sarcine in large quantities are a remarkably
frequent manifestation. The blood is very seldom discharged unaltered,
and it is usually represented only by colouring-matter.
The chemical constitution of the gastric juice in cases of cancer has
been made the subject of research by many observers, van der Velden
(p. 130), Uffelmann (p. 132), Hwald,? and Kredel ;!3 also by v. Mering
and Cahn (p. 133); and more especially by Riegel (p. 131), Korczynsk,
and Jaworski.84 Absence or diminution in quantity of hydrochloric
acid is a point of special interest, and has been recently studied by
many investigators. 18°
The author has analysed the contents of the stomach in a great
number of cases of cancer, and he has found that in many no trace of
free hydrochloric acid could be shown by the colour-tests employed for
the purpose. He has had seventeen cases of cancer under observation
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DILATATION OF THE STOMACH. 149
during the last two years. Either the vomit or the gastric juice with-
drawn after the administration of a test meal—usually of milk or ham—
was repeatedly examined. In fourteen out of the seventeen cases the
reaction with Congo-paper, benzo-purpurin, and Gunzburg’s test, was
either absent or very feebly evinced. The total acidity was also very
low, ranging from 48-4, and the higher figure was obtained in only one
instance. In one case, where the gastric juice was examined an hour
after the administration of half a litre of milk, no result was obtained
by the method described on p. 135, while the same method applied to
the gastric juice of a healthy person under like conditions showed
0.0301 grm. HCl in roo ce. In three cases of cancer the acidity was
remarkably high, viz., 90, 100, 126, and all the tests for free HCl gave
decided results. The experiences of O. Iosenbach and Waetzhold 1%
have been similar to these. The absence of hydrochloric acid, however,
is by no means so constant as to warrant an absolute diagnosis on this
ground alone. Moreover, in other conditions, such as amyloid degenera-
tion of the gastric mucous membrane,!*” in stagnation of the contents of
the stomach, in diabetes,!*8 and in the febrile state, even without demon-
strable disease of the stomach,!? the hydrochloric acid reactions may
also fail.
Aceording to Wolfram, the gastric juice is devoid of HCl in the
course of the infectious fevers, whereas in chronic febrile disorders it is
of quite normal character. Taken, however, in conjunction with the
other clinical symptoms of cancer, we have in this circumstance impor-
tant evidence of the disease. Riegel points out the important fact that the
gastric juice in this affection has entirely lost the digestive property.
Concerning the secretion of pepsin in carcinoma, it would appear that
this, as well as the milk-curdling ferment, are secreted to the end. The
tests for pepsin are described at p. 126, and its quantitative estimation
may be effected by #. Schiitz’s method.
5. Dilatation of the Stomach.—The character of the gastric
contents in this condition is subject to variety, according to the cause
of the dilatation. Nevertheless, there are certain general features which
belong to all cases, and these will be considered first. The remnants of
undigested food are visible many hours after a meal. Microscopically
there is a profusion of micro-organisms of all kinds, and yeast-forms are
rarely absent. Chemical analysis usually discloses an excessive proportion
of volatile fatty acids.
In dilatation from chronic gastritis the contents partake of the
character of the latter disease.
When the primary condition is pyloric stenosis, with gastric ulcer
physiologically active HCl is present in great excess. In one case the
author found that the unfiltered gastric juice withdrawn in the morning
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150 THE GASTRIC JUICE.
before food had been taken contained 0.4629 grm. HCl to roo ce. ; and
when the stomach had been thoroughly washed out, and milk admini-
stered, the gastric juice examined half-an-hour afterwards contained
0.1374 grm.
In dilatation from cancer of the pylorus free HCl is either absent or
diminished in quantity. This is true also of dilatation with atrophy of
the stomach, but the rule is not without exceptions.
6. Parasitic Affections of the Stomach.—(a.) In but one
instance as yet—a case of favus—have the characteristic appearances
of this condition been detected in the stomach (Kundrat).
(b.) Extensive patches of thrush are sometimes formed in the stomach,
and in such cases the vomit contains masses of the thrush fungus
(p. 85).
7. Croup and Diphtheria.—It very rarely happens that a croup-
ous or diphtheritic condition of the mucous membrane extends from the
upper part of the alimentary canal as far as the stomach. When it is
so, the vomit exhibits the appearances described at p. 88.
8. Fecal Substances in the Vomit.—Formed masses of faces
are never discharged by the mouth, but in cases of occlusion or partial
paralysis of the intestine, its contents may become mingled with those
of the stomach, and brought up with the vomit, which then has an
intensely feeculent odour, a yellowish-green colour, and a feebly acid or
alkaline reaction. When derived chiefly from the small intestines the
vomited matter will contain bile acids and pigment, and abundance of
fat. These may be detected by chemical examination. Microscopically
it shows nothing distinctive ; but on one occasion the author found in
such a discharge a quantity of large fungi which closely resembled the
comma-bacillus (fig. 70).
9. Pus.—In rare cases pus occurs in the vomit. It indicates sup-
puration in the walls of the stomach, or the rupture into it of an abscess
from some neighbouring viscus.
10. Animal Parasites.—Amongst the Entozoa, Ascaris lumbri-
coides, Oxyuris vermicularis, and Anchylostoma duodenale have been
obtained from the stomach. Other worms, such as Trichina, are excep-
tional manifestations, and the hooklets of Echinococcus and hydatid
cysts are occasionally present. Gerhardt has found dipteral larve
in the secretion, where they give rise to the symptoms of gastritis.
Similar observations have been made by Senator,? Hildebrandt,'** and
Iinlayson.
11. Constitution of the Vomit in Poisoning.**
1.. Poisoning with Acids.—In all cases of poisoning with strong
mineral or organic acids, the vomit acquires a powerfully acid reaction.
It displays a blackened mass of altered blood and charred tissues in
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CONSTITUTION OF THE VOMIT IN POISONING. 15.
cases where the quantity of the poison has been sufficient to cause these
effects. The appearance presented in all cases of poisoning with strong
acids is the same. To distinguish one from the other in the contents of
the stomach, the sense of smell will serve in some instances, as, @.g.,
for acetic acid, while in others resort must be had to the methods of
analytical chemistry. It is important in certain cases to remember that
the vomit may contain an abnormal proportion of organic and inorganic
(hydrochloric and lactic) acids, altogether independently of poisoning.
(a.) Detection of Sulphuric Acid.—The presence of sulphuric acid may
be ascertained thus :—The vomit is mixed with a large bulk of distilled
water, and put aside for several hours, during which it is frequently
stirred. It is then filtered, and the precipitate repeatedly washed with
water on the filter. The filtrate is then collected, and evaporated on the
water-bath until the fluid begins to blacken. It is then allowed to cool,
mixed with twice its bulk of alcohol, and, after standing for some hours,
again filtered. The filtrate, diluted with water, is once more evaporated
on the water-bath until the alcohol is entirely driven off. The fluid
remaining may then be tested for sulphuric acid. The addition of
chloride of barium solution or of lead nitrate should give a white pre-
cipitate, showing the presence of sulphuric acid or its salts.
(b.) Detection of Nitric Acid.—The vomit, which is generally stained
somewhat of a yellow hue from the formation of xanthoproteic acid,
is mixed with water, boiled, and filtered. The reaction of the filtrate is
tested, and if found to be acid, it is neutralised with caustic potash, and
evaporated to a small bulk. When allowed to cool, it should deposit
erystals of nitrate of potash, which will give the following reactions :—
1. To asolution of the crystals concentrated sulphuric acid is added,
and when the mixture is quite cool, a little sulphate of iron solution is
poured upon its surface. At the point of contact of the two fluids, a
deep brown zone shows the presence of nitric acid. The test is appli-
cable only where the brown coloration is not obtained with sulphuric
acid alone.
2. A solution of brucin in sulphuric acid is placed in a test-tube,
and a little of the fluid supposed to contain nitric acid is poured on its
surface. At the point of contact of the two, a red coloration takes
place if nitric acid is present.
The modes of testing for hydrochloric acid have already been given
(p. 129).
(c.) Oxalic Acid.—The contents of the stomach are partially evapo-
rated and extracted with alcohol, the alcohol evaporated, and the residue,
dissolved in water, is treated with acetic acid and solution of chloride of
calcium. A precipitate of oxalate of calcium forms, and the character-
istic crystals may be distinguished by the microscope.
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152 THE GASTRIC JUICE.
2. Poisoning with Alkalies.—The vomit in such cases is a viscid,
glistening, and strongly alkaline fluid. Where a concentrated solution
of a caustic alkali has been taken, the ejected tissues are charred and
brown, as in the case of acids. The determination chemically of the
character of the poison is often attended with great difficulty, and in
other instances, again, it is very easy.
Where ammonia has been taken, the vomit, if examined immediately
after the poisoning, will emit the characteristic odour of that body, and
further evidence of its presence may be obtained by holding over the
fluid a glass rod moistened with hydrochloric acid, when fumes of sal-
ammoniac will be given off. The detection of caustic potash and of
caustic soda, on the other hand, involves much difficulty on account of
the readiness with which they are converted into their carbonates.
The process for the detection of chlorate of potash in the vomit de-
mands a special notice. £. Ludwig’s!4* method is as follows :—The
vomit, if not already acid, is rendered slightly so by the addition of
acetic acid, heated and maintained for one minute at the boiling-point,
filtered, the filtrate evaporated to a small bulk on the water-bath, and
allowed to settle undisturbed. The salt then separates in the form of
crystals, which are dried between folds of blotting-paper and tested in
the following manner :—
1. They are treated with dilute hydrochloric acid and warmed ; the
fluid assumes a greenish-yellow colour, and chlorine gas is evolved. The
reaction may be obtained at ordinary temperatures by the addition of
strong hydrochloric acid.
2. The crystals are dissolved in water, or, where none have been
deposited, the liquid is evaporated and a solution of indigo and dilute
sulphuric acid is added. If chlorate of potash be present, on the further
addition of a watery solution of sulphurous acid or hyposulphite of soda,
the fluid changes from blue to yellow, or altogether loses its colour.
8. Poisoning with Metals and Metalloids.—(a.) Poisoning with
Salts of Lead.—After the lapse of a few hours, a quantity of grey or
blackish-grey substance is vomited. For the detection in this of com-
pounds of lead, it should be partially evaporated on the water-bath, and
organic matter decomposed by treatment with reagents.
For this purpose 4. Ludwig !45 recommends the process of Fresenius
and Babo :—The vomit is placed in a large porcelain dish, mixed with
about its own weight of a 20 per cent. solution of hydrochloric acid, and
3 to 5 grms. of chlorate of potash added, when the vessel is covered
and allowed to stand for about twelve hours. The mixture is then
heated to 60° in the water-bath. When the evolution of gas has ceased,
more chlorate of potash is added to the brown mass, and this process
is continued until the fluid ceases to form a brown colour. Should
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POISONING WITH METALS AND METALLOIDS. 153
the fluid become unduly concentrated, it should be further diluted with
water. If in this way the organic material is not entirely decomposed,
hydrochloric acid must be again added, and the requisite quantity of
chlorate of potash supplied as before. The mixture is then evaporated
on the water-bath until the odour of chlorine is no longer perceived,
when it is diluted with twice its bulk of water, passed through a filter
which has been moistened with water, washed with a large quantity of
water, and the washings finally collected and added to the filtrate. To
the fluid so obtained sulphuretted hydrogen is added to saturation. The
resulting dark precipitate is then filtered off, washed with sulphuretted
hydrogen water, dried, and dissolved in nitric acid in the following
manner :—It is placed in a porcelain dish, and pure (chlorine free)
nitric acid is added in drops until the whole has the consistence of a
thin fluid, when it is evaporated to dryness on the water-bath, and the
residue dissolved in boiling water and filtered. A white insoluble
residue of sulphate of lead may remain. This may be reduced to
metallic lead by the addition of soda and combustion on charcoal in
the reducing zone of a blow-pipe flame.
The addition of sulphuric acid will cause the formation of a azhzte
precipitate of sulphate of lead, and chromate of potash will give a
yellow precipitate if lead be present.
The quantitative estimation may be effected in the same way.
Salts of lead in the vomit may be detected by another very simple
process :—A strip of magnesium, free from lead, is placed in the fluid,
when metallic lead will be deposited upon it, and can then be dissolved
in nitric acid, and subsequently proceeded with as above.
(b.) Poisoning with Salts of Mercury.—Poisoning with compounds
of mercury is very often attended with vomiting. The vomit in such
cases differs greatly according to the strength of the poison. When
large quantities of corrosive sublimate have been taken, pain is expe-
rienced in the region of the stomach, and shreds of tissue stained brown
with hematin are apt to be discharged in the vomit.
The salts of mereury may be detected in the vomit in the same manner
as the compounds of lead. Sulphide of mercury is formed in the pro-
cess, and from this the metal is obtained thus:—To the precipitate
carbonate of soda and cyanide of potassium are added, the mixture dried,
placed in a test-tube and heated, when the metal is sublimed in the
upper part of the tube.
The presence of mercury in the vomit may be shown directly as
follows :—Granulated zine (£. Ludwig) 4° or brass wire (Mirbringer) 16°
is placed in the substances to be examined, which have been previously
acidulated with hydrochloric acid; the mixture heated for an hour in
the water-bath, and exhausted first with water and then with alcohol,
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154 THE GASTRIC JUICE.
and finally washed with ether and allowed to dry in the air. The brass
wire is then placed in a test-tube and heated, when the metal is de-
posited on the sides of the tube. If now, while the test-tube and it’
contents are still hot, a small piece of iodine be introduced, the vapour
of iodine given off will change metallic mercury into mercuric iodide
with the development of a beautiful red colour (Schneider)! In a
similar manner, mercury obtained by other methods may be converted
into mercuric iodide. If, at the same time, the vomited matter contains
an abundance of organic substances, it will be necessary to remove the
latter by Fresenius and Babo’s method before introducing the granulated
zinc or brass-foil.
It should be mentioned that in the distillation of the suspected vomit,
metallic mercury may pass over with the watery vapour (Lecco 1°), and
it may also form from the reduction of corrosive sublimate in the process
of distillation.
(c.) Poisoning with Salts of Copper.— When sulphate of copper has
been taken, it imparts a greenish-blue tint to the vomit. In poisoning
with the copper salts of acetic acid (verdieris, the commonest form), the
green colour may be present, or there may be nothing distinctive in
the appearance of the gastric contents. The recognition of the poison
may be effected by the process described under (a.) Poisoning with Lead
Salts. The sulphide of copper so obtained is dissolved in nitric acid,
when the presence of the metal will be shown by the blue colour of the
solution, which becomes deeper on the addition of ammonia. If the
latter reagent causes a precipitate to fall, the fluid is filtered and the
filtrate acidulated with hydrochloric acid. A portion of the filtrate is
treated with yellow prussiate of potash, when a reddish-brown precipi-
tate forms. In another portion a piece of iron-foil is placed, and after
a little while the metallic copper present is deposited on its surface as a
red coating.
It must not be forgotten that traces of copper occur in every organ.
(d.) Arsenic Poisoning.—The administration of large doses of arseni-
ous acid, Fowler’s solution, or of certain mineral waters abounding in
arsenic (such as those of Roncegno and Levico), is followed after a
short interval by the vomiting of a copious fluid deeply stained with
bile. Where arsenious acid (white arsenic) is the poison in question,
a careful naked-eye and microscopical examination of the vomit will
often afford accurate information as to its nature. In such a case, larger
or smaller particles of this substance are usually to be seen. When
these white. particles are removed with forceps, freed from other impu-
rities by repeated cleansing, washed with cold water, and dissolved in
a test-tube containing a small quantity of boiling water and then
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ARSENIC AND PHOSPHORUS POISONING. 155
allowed to cool, crystals of arsenious acid separate and may be recog-
nised microscopically as small octahedral forms. When the crystals
are heated with soda on a piece of carbon in the reducing zone of the
blow-pipe flame, the characteristic odour of garlic is evolved, and if a
specimen be heated with carbon in a test-tube, a metallic deposit forms
in the upper cool part of the tube.
A more accurate method is to remove organic substances with chlo-
rate of potash and hydrochloric acid, then to heat the remaining fluid
for a long time at 60° with sulphuretted hydrogen. A yellow preci-
pitate of sulphide of arsenic forms. This is dissolved in sulphide of
ammonium, filtered, the filtrate evaporated to dryness, allowed to cool,
some drops of concentrated nitric acid added, heated with more nitric
acid until the evolution of gas has ceased and reddish-brown fumes are
no longer given off. The fluid is then concentrated to a small bulk in
the water-bath, diluted with a little water, and treated with sodium car-
bonate until its reaction is distinctly alkaline. It is then evaporated to
dryness on the water-bath ; the dried residue is fused with a quantity of
carbonate and nitrate of sodium, allowed to cool, several times exhausted
with water, and filtered. The filtrate is repeatedly treated with small
quantities of dilute sulphuric acid until effervescence has ceased, when
more sulphuric acid is added, and the fluid evaporated first on the
water-bath and afterwards over a flame until white fumes are given off.
The residue is then allowed to cool and is dissolved in cold water. Zinc
and sulphuric acid, both free from arsenic, are placed in an apparatus
for generating hydrogen.¥? The hydrogen set free is purified and dried
by being passed through a tube which is fitted to the apparatus, and
contains solid caustic potash and granular chloride of calcium. To the
first tube is adapted, by an air-tight connection, another tube con-
stricted in two or three places and terminating in a point. When all
the air has been driven out, the hydrogen escaping from the point of
the terminal tube is ignited, and then the fluid to be tested is poured
into the apparatus. The tube is next heated in front of the place
where its calibre begins to diminish, and if arseniuretted hydrogen is
mixed with the hydrogen gas evolved, metallic arsenic is deposited in
the constricted portion.
A further test is as follows:—The flame is extinguished and the gas
conducted into a solution of nitrate of silver. A blackish-grey precipi-
tate of metallic silver separates, and the filtrate, on the careful addition
of ammonia, will give a further yellow deposit of arsenite of silver.
(e.) Phosphorus Poisoning.—Poisoning with phosphorus is always
attended with persistent and severe vomiting, which may last for
whole days. The discharged substances are free from blood, shreds
of tissue, and the other signs of a formidable organic lesion. When
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156 THE GASTRIC JUICE.
solid phosphorus in large quantity has been taken, the gastric contents
emit the characteristic odour of phosphorus and are luminous in the
dark, It should be noted, however, that these properties are lost in
presence of alcohol, oil of turpentine, and chloroform.
For the detection of phosphorus, the vomit is distilled with sulphuric
acid in the dark, and the retort connected with a glass condenser
(Mitscherlich). The presence of the poison is shown by the appearance
of luminous rings where the phosphorus fumes come in contact with the
cold water.
Scherer has also devised an admirable method for this purpose. The
vomit is enclosed in a flask provided with an air-tight stopper, and two
test-papers—one saturated with nitrate of silver and the other with
acetate of lead—are placed in it. Jf phosphorus be present, the first of
these will be blackened, whilst the other remains unchanged.!4
4. Poisoning with Alkaloids.*—(a.) Morphia Poisoning.—The
earlier stages of poisoning with morphia are generally attended with
vomiting, and in all cases where it has been taken by the mouth, the
alkaloid can be detected in the ejected contents of the stomach. Alt 1°
has shown that, even when it has been injected subcutaneously, the
drug will be found in the stomach about an hour afterwards. In such
a case, therefore, the stomach should be washed out, and the washings
tested for morphia. The Stas-Otto method °° for its separation may be
employed. In this, the vomit is placed in a flask, and digested with
alcohol and tartaric acid on the water-bath, allowed to cool, and filtered ;
the alcoholic extract is heated on the water-bath at a moderate temperature
(60°) until the spirit is entirely driven off, when the remaining watery
solution is filtered. The new filtrate is evaporated to a syrupy consis-
tence on the water-bath, and the residue extracted with alcohol. In
doing this, the latter should be cautiously added, little by little, until
a flocculent precipitate forms, and then in greater quantities until no
further turbidity occurs. The alcoholic solution is then filtered, and the
filtrate evaporated on the water-bath and dissolved in a little water.
The still acid watery solution is next shaken up with ether, in order
to eliminate other alkaloids and resinous substances, after which it is
rendered alkaline with caustic potash, and again shaken up with ether.
Any nicotin and atropin present (see below) are dissolved in this way.
The residue is treated with sal-ammoniac and repeatedly extracted with
warm amylic alcohol, which takes up morphia. The amylic alcohol
extract is next collected, filtered, and evaporated to dryness on the water-
* In this connection we shall consider only such alkaloids as are most frequently
the subject of investigation by the physician. For more detailed information on the
entire subject, the text-books of F. C. Schneider, J. Otto, Kobert, and E. Ludwig may
be consulted.
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POISONING WITH ALKALOIDS. 157
bath. The residue is dissolved in acidulated water, which is repeatedly
added for the purpose. It is then filtered, extracted with amylic alcohol,
neutralised with ammonia, and again extracted with warm amylic alcohol,
which is driven off by evaporation. Finally, the residue may be tested
thus :—
1. To one portion a freshly prepared solution of molybdate of soda
and concentrated sulphuric acid (1 cc. sulphurie acid and 5-10 grms. of
molybdate of soda—Fdhde’s reagent) is added. If morphia be present,
the fluid turns first violet, and, changing through blue and green, becomes
finally a pale red.
2. Another portion is dissolved in water acidulated with hydrochloric
acid, evaporated on the water-bath to dryness, and treated with a few
drops of a very dilute solution of perchloride of iron, which should be
Sree from hydrochloric acid. A blue colour shows the presence of
morphia.
An acid-free solution of perchloride of iron may be best pre,ared by dissolving
the sublimated silt in water (Ludwig).
(b.) Poisoning with Nicotin.—Vomitine frequently occurs in this
condition, and the poison may be separated from the gastric contents by
the Stas-Otto method. The alkaloid is extracted with ether from the
alkaline solution of the evaporation residue (vide supra), and when the
ether is driven off at a low temperature (30° C.) on the water-bath,
nicotin remains as a brown or yellow mass. If this be dissolved in
zther and an ethereal solution of iodine added, an oily substance forms,
from which ruby-red needles (2ouwssin’s crystals) slowly separate.
(c.) Poisoning with Atropin.—In atropin-poisoning with the pure
alkaloid, whether taken by the mouth or administered subcutaneously,
vomiting rarely occurs; but it is a frequent event in poisoning with the
berries of the deadly nightshade. Under sucli circumstances, the con-
dition is usually rendered evident by the discovery of the berries in the
ejected substances, together with the clinical symptoms (mydriasis, &c.).
If there should be any doubt as to the character of the toxic agent,
recourse may be had to the Stas-Otto method, when the alkaloid will be
taken up by ether from an alkaline solution of the residue, and may be
recognised by the following tests. The ether being driven off :—
1. A portion of the residue dissolved in water, to which a trace of
acid has been added, is dropped upon the conjunctiva of an animal (cat
or rabbit). After the lapse of from 6-20 minutes paralysis of the
sphincter fibres of the iris ensues, and the pupils are widely dilated :
0.01 merm. of atropin suffices to produce this effect.
2. A specimen of the residue is dissolved in a few drops of fuming
nitric acid, and the solution evaporated on the water-bath : a colourless
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158 THE GASTRIC JUICE.
substance remains, and this, when allowed to cool, and subsequently
treated with alcoholic solution of caustic potash, turns first violet, and
afterwards a cherry-red colour.
(d.) Poisoning with Ptomaines and Toxalbumins.'°*—The ingestion
of putrid flesh is occasionally attended with severe symptoms of poison-
ing, and there can be no doubt that in many cases of so-called acute
gastritis, where the use of certain articles of diet—such as liver, kid-
neys, and oysters—has been followed by nausea, vomiting, and profuse
diarrhoea and a retarded pulse, the true cause is to be found in the toxic
effects of ptomaines and toxalbumins. To the same category may be
referred the conditions known as ammoniemia (retention-toxicosis,
v. Jaksch,° see Urine), and the cerebral symptoms (coma carcinoma-
tosum, v. Jaksch °°), which sometimes develop in the course of cancer.!®1
The poisonous substances are probably diamines and toxalbumins, which
are known to be formed in these processes. Further research is needed
for the elucidation of this subject, and in questionable cases the vomit
should be tested for ptomaines. In doing this, the observer should be
euarded in his conclusions, since peptone (which is normally a con-
stituent of the gastric contents) is known to yield toxic substances of an
alkaloid nature.
In view of the great importance which the study of these bodies has
acquired of late years, and also because it enters into the pathology of
other secretions besides that now under consideration, the subject is
dealt with here at some length. The references, which are omitted, will
be found in Brieger and the other authorities quoted.
The Stas-Otto method may be employed for the separation of
ptomaines from the vomit. Such of these bodies, however, as have
yet been distinguished exhibit a very remarkable variety in respect of
their chemical character. Some may be derived by extraction with
ether from an acid, others from an alkaline medium, whilst a third class
is distinguished by the fact that its members are soluble only in amylic
alcohol, chloroform, or benzol. Others again are insoluble in amylic
alcohol. It will be seen from this that the application of the Stas-Otto
process must be supplemented by extracting the derived substances with
various media, and even then it will sometimes happen that the effort
is attended with failure.
For such cases Brieger’s method? may be employed. This is briefly
as follows :—If the material to be examined contains solid substances,
these are first reduced to small particles; sufficient hydrochloric acid is
then added to render the whole feebly acid, and the mixture boiled for
a few minutes and filtered. The filtrate is evaporated, at first over a
flame, and subsequently on the water-hath, until it has attained a syrupy
consistence. It may be noted, however, that in view of the instability
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ANIMAL ALKALOIDS. 159
- of the bodies sought, it is advisable to evaporate in vacuum, and at the
lowest possible temperature (v. Jaksch)—a precaution which, as Brieger 1°
suggests, should also be taken where foul-smelling substances are the
subject of manipulation. The thick fluid is mixed with 96 per cent. of
alcohol (filtered), and the filtrate treated with warm alcoholic solution
of acetate of lead. The lead precipitate which forms is now filtered off,
and the filtrate concentrated—here again preferably in vacuum—to the
same consistence as before, when it is again taken up in 96 per cent. of
alcohol. The alcohol is driven off by evaporation, and the residue, dis-
solved in water, is freed from lead by the addition of sulphuretted
hydrogen and filtering. The filtrate is acidulated with a little dilute
hydrochloric acid, and concentrated (in vacuum) to the consistence of
syrup. It is then diluted with alcohol, and alcoholic solution of mer-
curic chloride added. The resulting precipitate is boiled in water, and
certain ptomaines may separate at this stage in consequence of the
different solubilities of the double salts of mercury. The better to
secure this, the precipitate may be treated successively with water at
various temperatures. Should it be thought that the lead precipitate
may have retained some of the ptomaines, it may be suspended in water,
the lead converted into its sulphide, and the fluid treated in the manner
just described.
The solution obtained as above is filtered, and the filtrate, already
freed from alcohol and mercury, is evaporated, the hydrochloric acid
all but completely neutralised with sodium carbonate, and the residue
again extracted with alcohol, after which it is dissolved in water,
neutralised with soda, again acidulated with nitric acid, and precipitated
with phosphomolybdic acid. The double phosphomolyhdate is filtered
off and decomposed by neutral acetate of lead—an object attained more
readily by the application of heat on the water-bath. The lead is then
removed by means of sulphuretted hydrogen, and the fluid concentrated
and treated with alcohol. Several ptomaines are thus separated as
hydrochlorates, and may be obtained in the form of double salts of gold
or platinic chloride and of picric acid. From these the hydrochlorates
are again derived by precipitation with sulphuretted hydrogen; and in
the case of the picric acid compounds, extracting with water, acidulating
with hydrochloric acid, and finally removing the picrie acid by shaking
it up with ether.
The next step is to ascertain if any ptomaines remain in the phos-
phomolybdic acid filtrate after the precipitation of phosphomolybdic
acid.
The above is a mere sketch of the process, which, moreover, needs to
be modified in many instances.
For the detection of the basic compounds which occur in the secre- -
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160 THE GASTRIC JUICE.
tions as diamines, the best method is that of Bawmann and v. Udransky,
in which these bodies are converted into their benzoic compounds by the
action of benzoyl chloride and caustic potash. By this means these
observers discovered cadaverin (pentamethylendiamine) in the urine,
and established the identity of Brieger’s putrescin with tetramethyl-
endiamine 164 (see chapter on the Urine).
Ptomaines (animal alkaloids) yield the characteristic reactions of
alkaloids ; but otherwise they are not known to possess any distinctive
chemical or physiological properties. :
The characteristic reactions which are common to all the alkaloids are the
following (Otto, £. Ludwig).6 With—
1. Iodine and iodide of potassium solution, a brown flocculent precipitate ; most
readily obtained from the solution of the alkaloid which has been acidulated with
sulphuric acid.
2. Mercuric and potassium iodide, a white or yellow precipitate, insoluble in
water and dilute acid.
3. The iodide of bismuth and potash, an orange precipitate in a solution acidu-
lated with dilute sulphuric acid.
4. Phosphomolybdic acid, a bright or brownish yellow precipitate, insoluble in
water and dilute mineral acids.
5. Metatungstic and phosphotungstic acids, a white flocculent precipitate, with
difficulty soluble in water and diluteacid. (This, according to LZ. Ludwig, affords
a particularly sensitive test.)
6. Tannin, in neutral or feebly acid solutions, a yellow or white precipitate.
7. Platinic chloride, a whitish-yellow or citron precipitate, which is sometimes
readily soluble in water, and but slightly so in alcohol.
8. Chloride of gold, a yellow or whitish-yellow precipitate, which may be amor-
phous or crystalline.
The animal alkaloids already distinguished as occurring in the human
system are sufficiently numerous. They have been detected in the
feeces, the urine, and the milk, and they will find appropriate notice
under the separate headings in this work. They are known by their
effects both in health and disease, and, in many instances, have been
separated as definite bodies from the secretions. Such products result
from the decomposition of articles of food. Thus Vaughan 1 obtained
one of these bodies (tyrotoxin) from rotten cheese and bad milk, and he
supposes that the substance in question is diazobenzol. Ehrenberg 168
found a similar body in putrid sausages. Special mention should be
made also of ptomato-atropin, a basic compound, which has been dis-
covered in the latter food. In all cases where the clinical symptoms are
those of poisoning, and include severe vomiting, the methods described
above may serve to elucidate the matter ; but it should not be forgotten,
meanwhile, that the presence of peptone may be a source of ambiguity,
since it may yield similar poisons. If the vomit or secretion is to be
tested for toxalbumins, Brieger and Frankel’s process 1 may be used.
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ETHYLIC ALCOHOL—CHLOROFORM. 161
5. Poisoning with Ethylic Alcohol.—In acute poisoning with
alcohol (ethylic aleohol), the vomit emits the characteristic odour of that
substance. For its more accurate recognition, the gastric contents are
first diluted with water, and, if very acid, carefully neutralised with
caustic potash, and then distilled by steam.
The distillate may then be submitted to the following tests :—
1. Toa portion a few drops of benzoyl chloride and a little caustic
potash are added. When the mixture is heated and again allowed to
cool, the presence of alcohol is shown by the characteristic odour of
benzoylethylic ether (Berthelot)!
2. With a small portion an equal volume of concentrated sulphuric
acid is cautiously mixed, a little powdered sodium acetate added, and
the mixture heated. The characteristic odour of acetic ether shows the
presence of alcohol (Otto, Z. Ludwig).™
6. Poisoning with Chloroform.—Chloroform may he detected
either directly in the vomit or in the fluid obtained from its distillation.
In either case, the following reactions will disclose its presence :—
1. A little thymol dissolved in caustic potash is added to the fluid to
be tested, and the latter is then heated. If chloroform be present, the
preparation assumes a dark violet tint (Vital/ 1"), and if B-mnaphthol be
used instead of thymol, a blue colour results (Lustyarten).1°
2. A few drops of alcoholic solution of caustic potash and a little
aniline are heated with the distillate of the gastric contents. If chloro-
form be present, isocyanphenyl] is formed, and may readily be recognised
by its unpleasant odour (Hofmann).
In a case of poisoning with chloroform, where the drug was taken by
the mouth, the author was unable to find any trace of it in the sub-
stances vomited three hours afterwards, although the toxie symptoms
were well marked.
7, Poisoning with Carbolic Acid.—When a poisonous dose of
carbolic acid has been administered by the mouth, the vomit usually
emits the characteristic odour of that substance. The presence of
carbolic acid in the ejected substances may be ascertained directly by
the following tests :—
1. Bromine water yields with a fluid containing carbolic acid a yellow
crystalline precipitate of tribromophenol.
2. A solution of perchloride of iron colours dark violet in presence
of carbolic acid.
In testing for these reactions, it is well previously to filter the vomit,
if necessary washing it upon the filter with water. If the reactions
are not obtained in this way, the filtrate is distilled with a little sul-
phuric acid, and both tests are again applied to the distillate.1”*
It is to be borne in mind that carbolic acid may form in considerable
L
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162 THE GASTRIC JUICE.
quantity in the intestine in certain morbid states, and may then, as in
intestinal obstruction, find its way into the vomit. (See chapter on the
Urine.)
8. Poisoning with Nitro-Benzol and Aniline. —(a.) Nitro-
Benzol.—The presence of nitro-benzol in the vomit may be detected
frequently by the characteristic odour, which resembles that of the oil
of bitter almonds. To separate this substance from the gastric contents,
the latter is distilled with a little sulphuric acid. The distillate will
contain oily drops, which are soluble in ether. Aniline may be derived
from nitro-benzol by the addition of granular zine and dilute hydro-
chloric acid. When reduction is effected in this way, the fluid is ren-
dered alkaline with caustic potash, and the aniline formed is extracted
with ether. The oily residue after the expulsion of the ether will yield
the following reactions :—
1. If the aniline solution be treated with hydrochloric acid, and a
shaving of pine-wood be placed in it, the latter assumes a deep yellow
colour.
2. A drop of the oil is suspended in water, and a few drops of dilute
solution of chloride of lime or of a very dilute solution of sulphide of
ammonium added: the fluid assumes a rosy-red colour (Jacquemin).1
3. A very sensitive test is that of H. Ludwig :17°—A watery solution
of aniline colours a dark blue on the addition of a watery solution of
carbolic acid and hypochlorite of soda; and this colour changes to red
on the further addition of hydrochloric acid.
4. The isocyanphenyl test serves well for the detection of aniline
formed in the decomposition of nitro-benzol. It was introduced by
A, Flickiger *” as a test for acetanilide (antifebrin). To the fluid under
examination a few drops of caustic potash and chloroform are added.
It is then shaken up and heated, and when again allowed to cool, should
emit the disagreeable odour of isocyanphenyl.
(0.) Aniline.—Poisoning with aniline also is often attended with
vomiting. The vomit is diluted with water, and distilled with a little
sulphuric acid. The distillate is extracted with ether, and when the
latter has been driven off by evaporation an oily substance remains,
to which the above tests (1 to 4) for nitro-benzol may be applied.
9. Poisoning with Prussie Acid.—This condition may usually be
recognised by the characteristic odour of oil of bitter almonds. For the
detection of the poison the vomit is treated with a small quantity of
tartaric acid, and distilled. Hydrocyanic acid passes over with the
distillate. From its presence, however, poisoning with the drug is to
be inferred only when it can be ascertained that the vomit is free from
innocuous double salts of cyanogen, as, for instance, the yellow or red
prussiate of potash.
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PRUSSIC ACID. 163
The best test is to add solution of ferric chloride and sulphate of iron
to a little of the filtered fluid. With this last reagent yellow ferro
cyanide of potassium gives a white precipitate, which soon changes to
a bright blue, while with the perchloride of iron it forms a Prussian-
blue precipitate. Red ferricyanide of potassium gives a dark blue preci-
pitate with sulphate of iron, and a deep brown coloration with the
perchloride. Should both the above-mentioned substances be present,
the following process may be applied :!’’—The fluid is acidulated with
sulphuric acid, and treated with an excess of carbonate of lime. The
corresponding lime-salts take the place of ferro- or ferri-cyanide of
potassium, and only so much hydrocyanie acid as is not combined in
the double salts of cyanogen passes over with the distillate. The latter
is then tested for hydrocyanic acid in the following manner :—
1. To a few cc. rendered alkaline with caustic potash, a few drops of
a freshly-prepared solution of cupric sulphate are added ; the mixture is
heated, maintained for the space of one minute at boiling-point (Ludwig),
and allowed to cool. It is then rendered strongly acid with hydrochloric
acid. A blue coloration of the fluid results, and when allowed to stand
for some time, a flocculent Prussian-blue precipitate settles in it.
2. To a few drops of the distillate a yellow (holding poly-sulphide of
ammonium) solution of sulphide of ammonium is added, and the mix-
ture boiled until the yellow colour entirely disappears. It is then
allowed to cool and perchloride of iron and hydrochloric acid added.
If hydrocyanic acid be present, the preparation assumes a red colour
(sulphocyanide of iron). #. Ludwig' applies this test in a different
manner :—The fluid is treated with yellow solution of sulphide of ammo-
nium in excess, a few drops of caustic potash added, and the mixture
evaporated to dryness. The residue is exhausted with water, treated
with hydrochloric acid, and filtered. The filtrate is then tested with
solution of perchloride of iron, when a blood-red colour should develop.
3. Another very admirable test has lately been suggested by Vort-
mann.189 To the fluid to be tested a few drops of nitrite of potash are
added, and then two to four drops of the solution of perchloride of iron,
and finally dilute sulphuric acid, until the yellowish-brown colour of
the basic ferric salt formed in the beginning of the reaction has changed
into a light yellow. The solution is then heated to boiling, allowed to
cool, treated with ammonia and filtered, and to the filtrate a small
quantity of a colourless solution of sulphide of ammonium is added.
The presence of a minute quantity of hydrocyanic acid will be shown
by a bluish-green, of large quantities by a beautiful violet-red colour.
Vortmann has named this the ‘“nitro-prusside test.”
The vomit induced by a number of other poisons, as carbonic oxide gas, sul-
phuretted hydrogen, &c., exhibits no distinctive properties.
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CaLIVAGE Waliriaeey ale
THE FACES.
Unper the term feces! are comprised all those substances which,
being formed from the food in the process of digestion, and mixed
with the residues of the secretions of the alimentary canal, are finally
expelled from the body by the rectum.
I. NAKED-EYE CHARACTERS OF THE FACES.—The char-
acter of the faeces varies considerably in health, depending chiefly as it
does on the nature of the food ingested. The labours of Nothnagel,
however, have obtained for us a knowledge of some points which are
more or less characteristic of healthy stools. Such a stool is moulded,
and of a certain consistency. Its reaction is sometimes alkaline,
sometimes acid. It is alkaline in certain morbid states, as, eg.,
typhoid ; but in others, as the acute enteritis of children (and, in the
author’s experience, of adults as well), the reaction is acid. The
so-called “clayey” stools of dyspepsia in children, however, are nearly
always strongly alkaline,—a fact which is due to the presence in them
of carbonate of ammonia. Nothnagel concludes that there is little to
be learned from the reaction of the feces.
The colour, too, is very inconstant. It depends upon the food taken,
and is greatly modified by drugs supplied to the system. When, eg.,
bilberries are eaten freely, the faeces are coloured black. So, too,
they are rendered black by preparations of iron, manganese, or bismuth,
the colour in these cases being due to the formation of the sulphides
of those metals. After a meal of cocoa-nibs or chocolate, the stools are
apt to be coloured grey (Widerhofer).2 The exhibition of calomel will
turn them green, an appearance which was formerly attributed to the
formation of sulphide of mercury, but which is now thought to be
caused by the presence of biliverdin (Betz, A. Vogel, Monti, Zawadshi).8
Researches which the author has made with the green stools passed
after the administration of calomel have shown that these contain
abundance of urobilin, but no biliverdin. Hence it would appear that
the colour is not due to the latter substance. Lesage distinguishes
164
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CHARACTERS OF THE FACES. 165
two varieties of the green stool of children. The colour in the first is
due to biliverdin, but in the second it is caused by a definite bacillus
which produces a green colour-substance. This bacillus can be culti-
vated outside the body, and inoculated upon animals. Its presence in
great abundance in the feces is associated with a
severe form of cholerainfantum. Santonin, rhubarb,
and senna will stain the feces yellow.
The presence of unaltered bile pigment in the
feces is always pathological (Pettenkofer).5 Healthy
excrement contains a pigment which has been
named stercobilin (Vanlair, Masius®), and which
Maly asserts to be hydrobilirubin (urobilin). This
latter body can be prepared artificially from bile
pigment, and it is probable, @ priori, that a simi-
lar change is effected in the process of intestinal
digestion, when we would expect to find urobilin
in the feces. For a further description of this
body and the tests by which it may be recognised,
see the chapter on Urine.
The quantity of feces passed by a healthy man
in twenty-four hours averages 120-200 grms. The
remains of undigested food are often to be found
in the excrement, as berries, fragments of potatoes
and apples, and shreds of fibrous tissue. Virchow"
relates a case in which orange-skins voided with
the feeces were taken for a parasite, and Hichhorst §
one in which great coils of hard, woody asparagus
were passed unaltered by digestion.
Amongst the occasional constituents of the faces
visible to the naked eye, must be mentioned the
cylindrical shreds of mucous membrane, of larger
or smaller size, which are passed in the affection
known as tubular intestinal catarrh (Colica mucosa, 46y
Enteritis membranacea or tubulosa), (Mothnagel).®
; P F FIu. 65.—Mucous Cylin-
The cases in which such mucous formations are Heuinemiiheikecest
found are not very rare. Their discharge is attended
with violent tenesmus, and unaccompanied by the passage of feces. They
are ribbon-like or reticular in form, and consist chemically of mucin and
fibrin (Litten).1° They are often of great length. In one instance they
had the appearance of coiled brownish-yellow strings, 0.5 cm. thick, with
here and there shreds of transparent membrane. The material under
description was readily compressible beneath the cover-glass, and when
looked at through the microscope, exhibited a profusion of transformed
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166 THE FACES.
intestinal epithelium involved amongst long, spirally-wound, and twisted
threads. These bore some resemblance to the Curschmann-Leyden
spirals (p. 98), but had no central thread, nor did they exhibit crystals.
The specimen represented in fig. 65 was derived from a child of two years,"
It consisted of mucin and fibrin concentrically arranged, and enclosed bubbles
of gas.
In all probability the presence of these bodies implies chronic catarrh
of the large intestine, usually associated with obstipation and copious
secretion of mucus.?2
A patient, suffering apparently from chololithiasis, whilst under the
author’s observation, passed with the feces a shred of tissue 5 cm. long
and 3 cm. broad, which proved to be intestinal mucous membrane. No
cause could be assigned for its detachment.
Virchow and Nothnagel '* describe the occurrence of bodies resembling
frog-spawn or cooked sago-grains in the stools, and some observers
have supposed that they were derived from ulcerating intestinal fol-
licles. Verchow thinks they come from an excess of farinaceous food.
Nothnagel has also met with particles about the size of a poppy-seed,
which chemically had the constitution of mucus. It must, however,
be mentioned that this author has never found mucin in any quantity
as a constituent of healthy excrement. Avtagawa' found that these
bodies in many cases consist of vegetable débris, but that others, which
‘are distinguished by being more viscous and of softer consistency than
the rest, are formed of mucus.
Foreign bodies of all kinds are occasionally to be seen in the feces of
lunatics and children.
Finally, tumours or parts of tumours originating in the alimentary
canal, and stones or concretions formed in the gall-bladder or intestine,
may be passed with the stools.
The presence of gall-stones is a fact of great clinical interest. They
may in all cases be detected by a careful examination with the naked eye.
The feces of a woman suffering from various symptoms of dyspepsia
were found to contain a number of soft, white and yellowish particles
about the size of a pin’s-head. These proved to contain cholesterin and
carbonate of lime, and it is probable that they were multiple small
biliary concretions.
II. MICROSCOPICAL CHARACTERS OF THE FHCES.—To study
the microscopical appearances of the faces, a small particle should be
pressed between a cover-glass and slide. If the stools are fluid, a drop
may be placed upon a slide, and so examined. Much, of course, depends
upon the character of the food, and the following description applies to
the feeces of an adult living chiefly upon animal diet.
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CHARACTERS OF THE FZCES. : 167
1. Constituents Derived from the Food.
(a.) Vegetable Cells.—These are of very variable form, and occur
separately or in organic connection with one another. They sometimes
exhibit starch granules or remnants of chlorophyll (fig. 66, e-7, 1).
(d.) Muscle Fibres are almost invariably found in the feces. Their
quantity depends upon the supply of flesh-meat. They are relatively
fewer after a mixed diet (Wothnagel).1® They are usually much altered,
stained yellow by the bile, and swollen; but with a high power of the
microscope, their transverse striation can usually be made out.
(c.) Elastic Fibres are readily to be distinguished by their double
contour and curved form. They are always derived from the food, and
occur both in health and disease.
Fic. 66.—Collective View of the Feeces (eye-piece III., objective 8a, Reichert).
a. Muscle-fibres; 6. Connective tissue; c. Epithelium; d. White blood-corpuscles ; ¢. Spiral
cells ; f.-i. Various vegetable cells; &. Triple phosphate crystals in a mass of various micro-
organisms; J. Diatoms.
(d.) Connective Tissue is found occasionally in the excrement of
persons who eat much animal food, and is then of no pathological con-
sequence. But if areolar fibres occur plentifully where flesh is sparingly
eaten, they afford an indication of digestive disturbance.
(e.) Fat.—Fatty globules are occasionally seen, but fat occurs more
commonly in needles, arranged separately or in clusters (Nothnagel).
Such needles are found in greater quantity when much fat has been
taken with the food. The stools in alcoholic poisoning are always rich
in fat, so also with the fatty diarrhcea of children (see p. 203).
(f) Starch Granules.—These particles may be easily detected by
their reaction with a solution of iodine and iodide of potassium. They
are commonly to be found, but sparingly and of small size, in healthy
stools. They are also found in the interior of vegetable cells. Moth-
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168 THE FACES.
nagel asserts that an excess of such substances in the excrement points
to a derangement of the intestine.
(g.) Coagulated Proteids.—Undigested milk occurs in the stools,
especially in children and in persons suffering from diarrhea. Noth-
nagel has described a substance resembling coagulated albumin which
is occasionally to be seen in cases of intestinal trouble. It occurs in
round yellow particles, varying from the size of a bean to that of a
millet-seed. Their substance is readily soluble in a 5 per cent. solution
of HCl, is precipitated from alcoholic solution by acetic acid, and redis-
solves in excess of the acid, from which it may be again precipitated
by ferrocyanide of potassium. They resemble the mucous particles of
Nothnagel, to which reference has already been made. That author
thinks that the substance in question is casein.1°
The discharges of infants at the breast are of a very different character
from those of adults. Here muscle-fibres, areolar, and elastic tissue are
Fic. 67.—Degenerated Intestinal Epithelium (eye-piece IL., objective 8a, Reichert).
absent, coagulated proteids taking their place. Microscopically they
abound in fat and crystals of the fatty acid salts.
2. Formed Elements Derived from the Intestinal Tract.
1. Red Blood-Cells.—Red blood-corpuscles are rarely to be found in
the feces. Mothnayel has examined the freshly-voided excrement of
typhoid, when it was deeply stained with blood, but could find none of
these cells. In such hemorrhagic stools, however, are seen larger or
smaller masses of reddish-brown pigment (hematoidin), and the rhombic
crystals of hematoidin are also occasionally present. In cases where
the blood is derived from the upper part of the alimentary canal or has
remained for a long time in the intestine, the feces are no longer red
like blood, but are stained a dark brown or black. We have already
seen that a similar effect may be produced by certain drugs (see p. 164),
and consequently it is not possible to infer a hemorrhage from this
appearance alone; neither will red blood-cells be visible under the
microscope. In such cases the presence of blood may be determined
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BLOOD-CORPUSCLES AND~ EPITHELIUM. 169
with absolute certainty by the application of Teichmann’s test to a dried
particle of the faeces (see p. 61).
2. Leucocytes.—In healthy stools leucocytes are rarely to be met
with. They are always loaded with fatty particles. As a pathological
condition, the appearance of leucocytes in great quantity in the excre-
ment is far from common. Nothnagel found absolutely no increase
in the number of these bodies in simple intestinal catarrh. When a
considerable increase does occur, it affords a presumption of ulceration
of the gut.
Pure pus is found when an abscess has discharged into the intestine
and in dysentery. (See p. 208.)
3. Epithelium.—Epithelium is always found in the feces in health.
Squamous epithelium comes from the region of the anus. Columnar
epithelium is more rarely met with (fig. 66, c). The latter is usually
uncoloured, but occasionally stained yellow. The cells occur either
separately or in masses. Their boundaries, as a rule, are not easily to
be recognised, but well-formed goblet-cells are sometimes seen (Woth-
nagel). Sometimes, too, they contain fat, and are then very large.
Altered epithelial cells are often found in the feces. In their typical
manifestation they constitute what Nothnagel has termed “fusiform
degeneration.” They are, for the most part, small, non-nucleated,
homogeneous, and somewhat glossy bodies, tending towards the spindle
shape (fig. 66), but exhibiting every variety of form between this and
the ordinary epithelial structure. Mothnagel’s opinion is that these
bodies are epithelial cells altered by abstraction of fluid, and he remarks
that he has found them most typically shown in the mucous coating of
scybalous masses. The mere presence of epithelium in the stools is a
fact of no clinical consequence. When in disproportionate quantity, it
points to intestinal catarrh.
4. Detritus.—There are certain indeterminate substances always to
be found in the feces, which are usually either derived from the food
or belong to the waste products of digestion. They occur separately or
in masses, and are little affected by reagents, although sometimes they
are soluble in alcohol. Their constitution is very various.
3. Parasites.—There is no part of the body so apt to be infested
by parasites as the intestine. Such parasites belong both to the animal
and the vegetable kingdom, and it is not unreasonable to conclude, from
the vast numbers in which some of them are always to be found, that
they exercise an important function in the final processes of digestion.
This may be said especially of certain vegetable forms, and among them
the fission-fungi, presently to be mentioned, hold a prominent place.’
[Researches by MacFadyean** point to a physiological distinction be-
tween the bacteria inhabiting the small and those of the large intestine.
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170 THE FACES.
The former are stated to act only, or almost only, on carbo-hydrates,
producing ethylic alcohol, which is constantly present in the small intes-
tine ; while the bacteria of the large intestine aid in the disintegration
of proteids. |
A. Vegetable Parasites.—It will be useful to divide these para-
sites, as before, into two classes,—the pathogenic and the non-patho-
genic ; but in doing this, it must be premised that some of the organisms
classed as non-pathogenic may also at times be closely associated with
morbid states. As an instance may be mentioned, the Bacterium coli
commune, which under certain circumstances acquires noxious properties
(Wyss), The non-pathogenic parasites will first engage our attention,
and we shall adopt the usual classification into moulds, yeasts, and
fission-fungi.
1. Non-Pathogenic.
1. Moulds.—The only specimen of this class which has yet been found
in the intestine is the thrush-fungus. It occurs in children suffering
from thrush, and its presence in the stools is clinically of no significance.
2. Yeasts.—Yeast-cells (Saccharomycetes) are the commonest form
of parasite in the intestinal discharges, whether of health or disease
(Nothnagel), (fig. 66, between } and c). Uffelmann *° asserts that yellow
yeast-fungi are often also to be seen in the fresh stools of infants at the
breast. Micro-organisms of this kind are most abundant in the acid
stools of children. They are round or oval ; lie together in groups of three
or four; and commonly exhibit their characteristic sprouting arrange-
ment. Well-formed yeast-fungi, however, such as are seen in fermenting
saccharine solutions, are very rarely to be met with. Nothnagel saw
such once in a case of typhoid in a child. In the bile-stained and acid
discharges of acute catarrh of the small intestine in adults the author
has not infrequently found fungi which closely resembled the form
described by Rees! as the Saccharomyces ellipsoideus, except that they
were somewhat smaller (p. 145).
The yeast-fungi of feces stain a mahogany-brown with the iodo-
potassic-iodide solution. This property depends upon the fact that they
hold glycogen in their substance.
There are other forms to be met with morphologically resembling
yeast-cells, but distinguished from them by giving a blue colour with
the iodo-potassic-iodide solution mentioned above (see p. 171).
3. Fission-Fungi.—These organisms exist in swarms in the intestine,
and they are to be found in greater profusion in the feces than in any
other of the excretions (Vothnagel, Brieger, Uffelmann, Escherich, Bien-
stock, Stahl, Kuisl, Miller, Suchksdorf?*); indeed, it is not incorrect to
say that they always constitute the bulk of these discharges. Bacilli
and micrococci of the most varied kinds are the commonest forms.
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FUNGI FROM THE INTESTINAL TRACT. 171
They occur separately or in colonies, and often exhibit lively movements.
It may be said, as a rule, that micrococci predominate in the solid, and
bacilli in the fluid motions. The former are sometimes found in shapes
resembling torule and sarcine. The organism which occurs most com-
monly and in greatest abundance is the Bacterium termo (Bacterium coli
commune), and there can be little doubt that this body is intimately
associated with putrefactive processes in the intestine ; although it must
be stated at the same time that we are ignorant of its functions in
health, where also it exists abundantly, and that the host of other
micro-organisms which make their appearance when putrefaction is
going on throws a great deal of doubt over this question.
Bacillus subtilis is found in the discharges both of health and disease.
It was first discovered by Nothnagel, and may be seen as long threads
with spores attached, or as separate spore-bearing rods, and elsewhere
the spores alone occur in clusters. Its relatively thick edges and the
remarkably glossy appearance of the spores facilitate its detection. Its
presence has no clinical significance.
The various micro-organisms above alluded to stain brown or brownish-
yellow in solution of iodine and iodide of potassium or of ammonium
iodo-iodide ; and this property belongs especially to the groups of micro-
cocci, which are coloured very deeply a brownish-yellow by contact with
this reagent.
In addition to such forms, the feces exhibit other micro-organisms,
which stain blue or violet in the iodo-potassic-iodide solution. Mothnagel
has described many of these, and one especially which he holds to be
identical with the Clostridium butyricum of Prazmowski.8
The author has investigated this subject with great care, and he is in
a position to confirm Vothnagel’s statements in every particular, and
would venture to add something to his description of the fungi which
stain blue with the iodo-potassic-iodide solution.
To begin with the minutest forms. There is a micrococcus which
occurs in swarms of uniformly and finely granular zoogleaform bodies,
which colour a reddish-violet with the solution.
Next in order is a micro-organism in the form of short delicate and
somewhat pointed rods, which recall the baczllus of septicemia in the
mouse, and which stain in a similar manner with the reagent mentioned.
These rods occasionally contain one or two spherical granules, which do
not stain in the solution.
There are other rods, of varying length, which resemble the Leptothrix
bucealis in the manner of their reaction with the iodine fluid; and a
further variety, which differs from the Bacillus subtilis only in that the
fungus threads stain blue, while the bodies referred to above as the
spores remain uncoloured (fig. 68).
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172 THE FACES.
The author has often had an opportunity of observing the Clostridium
butyricum of Nothnagel. It takes the form of large round cells, usually
visible in uncoloured preparations by reason of their somewhat lustrous
appearance, and in other respects resembling yeast-fungi. In some
cases they adhered to one another like a string of beads, and in others
were simply disposed in groups (fig. 69). These bodies, as Lictheim
and others have observed, stain with the Ziehl-Neelsen fluid in the same
@ > f
Keay Yoo
SS et
~ eS Ee La
iS Z a erliaee
Fic. 68.—Bacilli from the Feeces, staining Blue with the Iodo-Potassic-Iodide Solution
(eye-piece III., objective 84, Reichert).
manner as tubercle bacilli, but they are not likely to be mistaken for
these, since they are sufficiently distinguished by their size, shape, and
peculiarity, of arrangement.
A micro-organism of oblong and somewhat pointed form also occurs
in the feces, and cultivations of this have been made by H. Fischer.
It must be mentioned that although these bodies all stain some shade
ex (a eo
_ 6%, “a”
9 “w 99 ®le
ee “Re eo ~
Fic. 69.—Nothnagel’s Clostridia and Stunted Bacilli from the Feces, staining Blue with the
Iodo-Potassic-Iodide Solution (eye-piece III., objective 8a, Reichert).
of blue with the solution of iodine and iodide of potassium, the tints
which they derive from that reagent exhibit notable differences; for
whilst, on the one hand, the micrococci are but slightly coloured, and
of a purple tint which tends towards red, the rod-like micro-organisms
stain very deeply, and of a dark-blue colour. The stain is in all cases
transitory, fading in from twenty-four to forty-eight hours, and disap-
pearing altogether within a few days.
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PATHOGENIC FUNGI. 173
Those fungi whose characteristic it is to stain blue in iodo-potassic-
iodide solution occur probably in all stools, but in relatively small
numbers in those of health. They are in profusion only in certain
morbid states, and especially in intestinal catarrh. They do not seem
to bear any relation to the reaction of the discharges, having been found
alike when this was alkaline and when it was acid. To conclude, they
are constantly present in health and in disease, and in the discharges
of infants at the breast, as well as of older children nourished on a
meat-diet.
Hence it follows that no definite clinical significance attaches to any
of the parasitic forms hitherto described. It is a matter of observation
that in certain pathological conditions of intestinal derangement one
form or the other is apt to preponderate, but we have no evidence that
they are in any case the cause of disease, or that the multiplication of
a particular micro-organism is not rather the consequence of the dis-
turbance which it is found to accompany.
The intestine is apt to be infested with microbes of a pathogenic
character, which in form closely resemble those innocuous parasites
which have just been described. Much light has been thrown upon
their nature by the researches of recent years, and for their detection
we have to make use of a number of special methods. But these alone
will not suffice. Without an accurate knowledge of the commoner, at
least, of the non-pathogenic organisms which normally inhabit the
intestine, the discrimination of the others is impossible. It is for this
reason that we have dwelt at some length—though still in a far from
exhaustive manner—on the description of the innocuous micro-organisms
which are most frequently to be found in the feces.
2. Pathogenic Fungi.—We pass now to a consideration of the
pathogenic parasites, the bacilli of cholera, typhoid, and tubercle.
1. Cholera-Bacillus (Comma-Bacillus).—To Robert Koch,?* the
pioneer of the modern science of bacteriology, belongs the honour of
having first discovered the micro-organism which causes that most
terrible of the epidemic diseases of our time—cholera.
We shall not attempt to give an account of all that has been written
upon this subject, but shall content ourselves with making here and
there a reference to the leading authorities for the information of the
reader ; and we shall avoid the discussion of controverted points of
which we have no personal knowledge. Nevertheless, there can be no
doubt whatever of the fact that a definite and morphologically distinctive
parasite occurs in the discharges of cholera patients ; and it is a task at
once difficult and of the utmost importance to define the form of this
organism, and to devise methods for its recognition.
Koch described the cholera-bacillus as a short rod-like form, curved
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174 THE FACES.
or semicircular, and somewhat thicker than the bacillus of tubercle.
Such bodies often lie two together, with the concavity of their curves
turned in opposite directions and their extremities in contact, so as to
from an S-shaped figure. Neuhauss?° describes flagella upon them.
Lofler 26 has demonstrated their existence by the method described in
Chap. X. They produce by division peculiar screw-like spirals, which
remind one of the spirillum of relapsing fever, only that these are
thicker (fig. 24). Koch did not find any separate spores belonging to
these organisms, but it would seem that Hweppe?’ has succeeded in
doing so. Such bacilli were discovered by Koch in the intestine and
discharges, rarely in the vomit, of Asiatic cholera, and never in the
blood, saliva, tears, urine, or breath of patients suffering from this
disease. The discharges, according to this authority, sometimes contain
almost unmixed colonies of bacilli. Koch’s statements have been borne
FiG. 70.—Koch’s Comma-Bacillus (pure cultivation ; eye-piece III., objective Zeiss y,,
homogeneous immersion ; Abbe's mirror and open condenser).
out by the subsequent investigations of Babes, Vandyke-Carter, Nicati,
Rietsch, van Ermengen, and others.?8
It follows from what has been said of the enormous profusion in
which micro-organisms of various kinds infest the intestine, that the
cholera-bacillus, when not very plentiful, may easily escape detection ;
and therefore it will not suffice to submit discharges which are supposed
to contain it to a simple microscopical examination. To meet the exi-
gencies of the case, Koch has studied the mode of growth of the bacillus,
and he has devised for its cultivation certain special processes, on the
application of which the diagnosis of Asiatic cholera may very safely
rest. The first requisite is to separate some of the bacilli or their germs
from the mass which contains them, and this may readily be done in
the manner to be described in another part of this volume (vide chapter
on Methods of Bacteriological Research).
A complete and exhaustive search for the cholera-bacillus may be
performed as follows :—
1. A particle of the discharge is placed upon a slide, and examined
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BACILLUS OF CHOLERA. 175
microscopically for the bacillus. In doing this, the expedient of
Schottelius®® may be adopted with advantage. He puts a little of
the stool in an open glass, together with an equal quantity of alka-
line meat-broth, and allows the mixture to stand at a temperature of
30-40° C. for twelve hours. At the expiration of that period, the
bacilli will be found in swarms on the surface of the glass, and a
specimen may be obtained which will consist almost entirely of them.
2. A particle of the discharges or a drop of the infected broth
(Schottelius) is next spread out in a very thin layer between two cover-
glasses, dried, passed three times through the flame of a Bunsen burner,
stained with one of the basic aniline dyes (fuchsin, methylene blue) and
examined under the microscope.
3. Plate-cultivations are made from the suspected stools with nutrient
gelatine and agar-agar, as described in Chapter X.
4. If comma-bacilli develop in these, cultivations are to be made by
inoculation in the depth of nutrient substances.
5. The bacillus is to be cultivated in hanging drops (vide Chapter
X.)—(it is well to apply this test at once, in the event of comma-bacilli
being found in Schottelius’ preparation)—and the micro-organisms
developed in the medium are to be compared with those derived by
plate-cultivation.
When the discharges examined belong really to Asiatic cholera, the
processes 1 and 2 will generally show the comma-bacillus of Koch. The
inference to be drawn from the third process depends upon the fact
that the cholera-bacillus, cultivated on a nutrient gelatine plate at
22° C., forms after twenty-four hours white colonies, with irregular,
jagged, or sinuous outlines. These exhibit a light-yellow or rosy tint,
and present an appearance like that of a layer of powdered glass over-
lying the gelatine plate. The colonies grow gradually darker towards
their centre, and presently begin to liquefy.
Plate-cultivations in nutrient agar-agar form a greyish-yellow, fur-
rowed, slimy surface, and do not cause the underlying nutrient medium
to liquefy.
When cultivated by inoculation in the depth of the nutrient sub-
stance contained in a test-tube (v. supra), after the lapse of twenty-
four hours the nature of the bacillus is shown by a white coloration,
which extends along the track of the needle, and the formation of a
funnel-shaped cavity, which increases gradually from the circumference,
and acquires the appearance of an air-bubble. It is only at its super-
ficial part that this liquefaction occurs, the lower layer of the inoculated
substance remaining unaltered for days.
In hanging-drop cultivations, the comma-bacillus exhibits the follow-
ing peculiarities (v. swpra):—When examined on the day following
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176 THE FACES.
the inoculation, or, it may be, after the lapse of a few hours, and with
an oil-immersion lens and a constricted diaphragm, mobile swarms are
seen in the centre of the mass, while at its circumference appear the
spirocheete-like bodies, which sometimes exhibit as many as twenty
spiral twists. Suppose that a specimen, which Schottelius’ method had
previously shown to contain micro-organisms when cultivated in this
manner, displayed some forms which resembled the comma-bacillus, it
will then be necessary to transfer some of these drop-cultivations in the
manner described in Chapter X. for cultivation by the plate and deep-
inoculation methods.
Bujwid has recently recommended his chemical process (see below), in
combination with that of Schottelius for the purpose of disclosing the
cholera microbes, even without the aid of the microscope.
It should be mentioned that the cholera-bacillus will thrive at a tem-
perature of 37°, and even on boiled potatoes. Its cultivations resemble
those of the bacillus of glanders to the naked eye, but their growth is
slower and needs artificial heat. The bacilli are very sensitive to drying
and to exposure to a 5 per cent. solution of carbolic acid.
Bitter and Rietsch®° have shown that the cholera microbes elaborate a peptonis-
ing ferment.
Poehl and Bujwid* found that the addition of a 5 to 10 per cent.
solution of hydrochloric acid will, in a few minutes, impart to cholera
cultivations, and to no others, a violet-rose colour; and Brieger®? has
been able to separate from them a colour-substance, to which he gives
the name of “ cholera-red,” but which Salkowski *° identifies with indol.
Bujwid’s cholera reaction does not seem to merit the commendations
bestowed on it. Other fungi, pathogenic and innocuous, behave in a
similar manner with mineral acids.
The foregoing observations were confirmed by Kitasato.34
Cantani*° notices, as a result of his experiments upon animals, that
cholera-bacilli elaborate a poison ; and Brieger *° has actually separated
from its cultivations specific toxic substances, which occur together with
cadaverin and putrescin, and result from the agency of cholera microbes.
The method he employed is that detailed at page 158. It remains for
the clinical observer to detect these substances ready-formed in the
discharges of cholera patients ; and some progress has already been made
in this direction (Pouwchet).*” Recent research has made it doubtful
whether it is these toxines which play so important a part in the morbid
process, and not rather the toxalbumins from which they are known to
originate.
There are two other micro-organisms which bear a considerable resemblance
to the comma-bacillus. One of these, the bacillus of cholera nostras, is a
pathogenic micro-organism ; the other is Deneke’s spirillum of cheese.
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DETECTION OF CHOLERA BACILLUS. 7:
2. The Bacillus of Cholera nostras.—Finkler and Prior *8 have observed a
micro-organism resembling the comma bacillus in the discharges of cholera
nostras. It is distinguished from the bacillus of Asiatic cholera chiefly by its
size (fig. 71), being both longer and broader than the latter. In addition to
this, the two exhibit notable differences in life-history, When a colony of the
Finkler-Prior bacillus is cultivated on a plate in nutrient gelatine, it is seen to
be of a uniformly round figure with well-defined edges ; and when examined with
a low or medium power, it has a granular appearance, and is usually of a brown
colour. Moreover, the gelatine rapidly liquefies, and emits a very foul and
penetrating odour.
The comma-bacillus of Koch, on the other hand, develops less rapidly. The
colonies are never coloured brown, but of a tint ranging from light-yellow to
rose-colour ; and the figure which they form, as already mentioned, is bounded
with a ragged contour (see p. 175).
Again, when cultivated by inoculation in the depth of nutrient substances,
this bacillus develops in a very characteristic way ; for whilst the comma bacillus
swarms in the funnel-shaped manner already described, the cultivation in this
case assumes a saccular shape, somewhat comparable to that of a stocking. V.
Hovorka and Winkler * employ plover’s egg-albumin as the food medium. This is
Fic. 71.—Finkler-Prior Bacillus of Cholera nostras (pure cultivation ; eye-piece III., objective
Zeiss Yo, homogeneous immersion ; Abbe's mirror ; open condenser).
rapidly liquefied by the Finkler-Prior bacillus, while the comma bacillus is pro-
pagated only along the track of the needle and does not decompose it.
The pathological import of the Finkler-Prior bacillus is still a matter of dispute,
but it is plainly of the utmost consequence to be able to distinguish this com-
paratively harmless organism from the very fatal microbe of Asiatic cholera.
Spirillum of Cheese.—Deneke ” found a micro-organism in ripe cheese which
bears a close resemblance to the comma-bacillus of Aoch. But this, like the
Finkler-Prior bacillus, can be distinguished by certain peculiarities in its life-
history. The nutrient gelatine medium is rendered fluid sooner than by Koch’s
bacillus, but more slowly than by that of Finkler and Prior. This micro-
organism, moreover, will not develop in potato, while the other two will thrive
upon this food. The crucial test, however, is the result of inoculation upon
animals. Deneke’s bacillus has no morbid influence on the intestine.
3. Bacillus of Typhoid Fever.—A characteristic parasite was dis-
covered in 1880 by Kberth*! in the implicated viscera in typhoid.
Similar observations were afterwards made by Klebs and Eppinger,*?
and these have been confirmed by the researches of R. Koch, Meyer,
and Friedidnder, and more recently by Gaffiy and very many others.4
M
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178 THE FASCES.
Gafky describes the funeus as consisting of rods, in length equal to
one-third the diameter of a red blood-corpuscle, and occasionally forming
threads of greater length by the aggregation of several segments. They
are about three times as long as they are broad, and rounded off at the
extremities. Spores are sometimes to be seen within the rods. They
stain best in a concentrated watery solution of methylene blue, and
Lofler’s process (p. 43) is the most appropriate to the purpose. They
are not stained by Gram’s method. Friinkel and Pfeifer,4* using
Léjfler’s process for staining flagella, have observed these processes on
the bacilli of typhoid and of malignant cedema.
Gaffky* has ascertained certain facts connected with the life-history
of the typhoid-bacillus. It develops readily in a medium of nutrient
gelatine. In a preparation of this kind the cultivations make their
appearance after the lapse of twenty-four hours. When examined with
a medium power of the microscope, they seem to be yellowish, and they
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do not render the gelatine fluid. Rods and threads appear, and they
are endowed with an evident and peculiar motion. The parasite
develops on prepared potato. The colonies can be distinguished with
difficulty by the naked eye. When cultivated in a medium of prepared
potato at a temperature of 37° C., spores begin to form after three or
four days. According to Birch-Hirschfeld,*® solitary and segmented
spores are to be seen, the first in hanging-drop cultivations, and the
latter when cultivated in an incubator. This observer recommends that
the nutrient medium be stained with phloxin-red or benzo-purpurin, by
means of which the spores are deeply coloured. There is much doubt
as to the true character of these so-called spores (Buchner, Pfuhl).¥
The fungi are easily cultivated in hanging drops in sterilised broth.
The bacillus occurs also in the stools of typhoid patients; but on
account of the vast number of micro-organisms constantly to be found
in the dejections, it is impossible to recognise it with the aid of the
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BACILLUS OF TYPHOID. 179
microscope alone. Neither does it possess, like the bacillus of tubercle,
any characteristic staining properties. For its complete recognition,
therefore, we must resort to Koch’s methods for obtaining pure cultiva-
tions, and separate it from the fecal substances. Pferfer 48 was the first
to do this, and he made use of the nutrient agar-agar plate. A useful
adjunct is the employment of a 0.25 per cent. solution of carbol-gelatine,
after the manner of Chantemesse and Widal.49 According to Holtz,°°
however, this is impracticable, since he found that the development of
the bacilli was suspended in presence of 0.1 per cent. of carbolie acid.
The best medium is neutral potato-gelatine containing 0.05 per cent. of
carbolic acid. For the recognition of this micro-organism, Holtz, follow-
ing Grancher and Deschamps,®*! recommends weakly-acid bouillon or
similarly-prepared milk stained by Noeggerath’s*? process. Kitasato >
relies upon the absence of the indol-reaction from such a cultivation as
evidence of the typhoid-bacillus.°4 The researches of Babes and Cas-
sedebat®® have shown that the investigation is attended with much
difficulty, since there are a great many distinct fungi which, when culti-
vated, present appearances quite similar to those of the typhoid-bacillus.
It is difficult to effect the separate cultivation of typhoid-bacillus derived from
the faces in nutrient gelatine, because the discharges contain other micro-
organisms (hay bacillus), which liquefy that medium before the colonies of
typhoid-bacilli appear in it.
When the micro-organism under discussion has been experimentally
communicated to animals, it causes them to manifest the symptoms of
typhoid ; and the researches of L. Frankel, M. Simmonds, and C. Seitz,°°
seem to leave no doubt as to its pathogenic character. Bewmer and
Peiper,®" on the other hand, have come to a different conclusion. Bear-
ing in mind Brieger’s discovery of animal alkaloids (ptomaznes) as a
product of bacillary life, it seems probable that such play an important
part in connection with typhoid, and this may well explain the contro-
verted results obtained in the experiments upon animals reported by
Friinkel, Simmonds, and others.
Finally, it may be noticed that many recent investigations tend to prove the
possibility of typhoid-bacilli being disseminated by means of drinking-water and
by milk.*8
4. Bacillus of Tubercle.—Lichtheim®® and other observers have
found tubercle-bacillus in the stools in cases of tubercular ulceration
of the intestine. For its recognition there, the methods are employed
which have already been described in connection with the sputum
(vide p. 104).
The detection of this bacillus in the feces invariably implies the
existence of tubercle, but not necessarily tubercle of the intestines, since
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180 THE FACES.
it may be derived from sputa which have been swallowed. Still, in
cases where it has been repeatedly found in the stools, and where it
occurs in great profusion, so as to resemble pure cultivations (vide fig. 108),
and especially where the other symptoms of tubercular ulceration of the
intestine (purulent discharges, &c.) are present, the diagnosis is estab-
lished on the firmest basis.
B. ANIMAL PARASITES.
1. Protozoa.—Adopting the classification of Leuchart, these in-
clude Rhizopoda, Sporozoa, and Infusoria.
1. Rhizopoda.
(a.) Monadines.—NVothnagel | found these organisms repeatedly in
the stools of consumptive and typhoid patients, and of persons suffering
6. Cercomonas intestinalis (Davaine). e. Monadines, living.
c. Ameeba coli. J. Monadines, dead.
a, Trichomonas intestinalis. | d, Paramecium coli.
from heart-disease. They were always dead unless the stools were
examined directly upon being passed, and then appeared as more or
less circular bodies of various sizes (fig. 73, /).
The still living monadines are pear-shaped, and usually possess a
long pointed process, which moves about rapidly (fig. 73, e). According
to Wothnagel, they have no pathological significance. Grassi 6? found
similar bodies in the stools of a patient suffering from entero-colitis.
Bodies altogether resembling these, but not as yet identified with them,
occur in the discharges of infants and children (see v. Jaksch).®
(b.) Ameeba coli. Ldsch % has described certain cellular bodies of
large size which he found in the feces in a case of intestinal ulcer of a
quasi-tubercular character. These bodies were contractile, and some of
them, of circular form, had a diameter of 20-35 ~. They consisted of
hyaline and coarsely granular protoplasm, with a round nucleus and
hyaline vesicle, but no distinct cell-wall (fig. 73, ¢).
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ANIMAL PARASITES—PROTOZOA. 181
Similar organisms have been found in the intestine by Lambl,® and
Kartulis, Massuitin, Osler, and Dock have seen amceba-like organisms
in the stools of patients suffering from dysentery and chronic enteritis.
2. Sporozoa.—Again reverting to Leuckart’s classification, the sporozoa
which chiefly concern us here are the oval psorospermia, the group to
which belong the coccidia which infest the intestinal tract of man
(Dressler, Gubler, Kjellberg, Eimer) ®™ and the liver (Podwyssoki).®
They appear in the feces as elliptical forms, 0.022 mm. long, furnished
with a thin membrane, and enclosing within their substance a number
of granular nuclei, arranged for the most part in groups. They are to
be found in great numbers. Their favourite seat is the intestinal mucous
membrane, where they burrow, doing much damage to its structure.
For this reason Leuchart appropriately names the parasite Coccidium
perforans.
3. Infusoria.—1. Cercomonas intestinalis.—This protozoon was first
Fic. 74.—Cercomonads from the Stools.
a. Megastoma entericum (Grassi).
b, b'. Encysted forms of Cercomonas intestinalis.
c. Cercomonas intestinalis after loss of its tentacles (Lamb/).
found by Lambi° in the jelly-hke mucous discharges of children, and
it was afterwards observed by Davaine, Marchand, and Zunker. It is
of piriform shape, clearly nucleated, and furnished with eight tentacles
of varying length (see fig. 74, @). Davaine discovered it in cholera,
Marchand in typhoid, and Zunker in nine cases of diarrhoea. It would
appear from these facts that the Cercomonas intestinalis is apt to thrive
in a gut which is already diseased, and when present tends to cause
severe diarrhcea. The observations of Zunker especially strengthen this
conclusion. According to Grassi and Schewiakof'™ the parasite causes
anemia and diarrhoea in human beings, and by the changes which it
effects in the mucous membrane interferes with absorption from the
intestine. The Cercomonas was observed by Miller 7 in the jejunum
of a healthy man.
The Megastoma entericum, lately described by G'vassz, is almost cer-
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182 THE FACES.
tainly identical with Lambl’s Cercomonas.” Per roncito ™ has observed
the encysted forms of the parasite in the intestine (fig. 74, 6)—observa-
tions confirmed by the author in the case of children.”
Other Cercomonads have been seen in the same situation (Davaine),
(see fig. 73, 0).
2. Trichomonas intestinalis.—This is a pear-shaped organism, some-
what larger than Cercomonas intestinalis, and distinguished from it by
bearing a ciliated dise at one extremity (fig. 73, a). It has been obtained
from the intestine by Marchand and Zunker.
3. Paramecium coli (Balantidium col/).—An entozoon first found
by Malmsten™ in the discharges of diarrhcea, and afterwards observed
by Stieda, Graziadet, Perroncito, and K. Ortmann."8 It is oval, o.1
mm. long, and covered with cilia, which are planted more thickly around
the buccal (2) orifice. The anterior extremity is smaller than the posterior,
and the opening (anal) in this situation is but sparingly provided with
cilia. The abdominal surface is less arched than the dorsal. Internally
it is furnished with a nucleus and two contractile vesicles, and frequently
contains amylum particles and fatty granules. Its presence appears to
be associated with diarrhcea, but it has no other clinical significance.
In addition to the varieties mentioned here, other infusoria are occa-
sionally present in the intestine (V. Jalsch).7
2. Vermes.—The investigation of the feces for intestinal worms
has become of late years a matter of special interest to physicians,
because experience daily teaches us that, even in temperate climates,
the alimentary canal is apt to be beset with certain parasites of this
class, which must be reckoned amongst the most formidable pests of
mankind ; and it often happens that an accurate diagnosis of their
nature can alone enable the physician to adopt intelligent methods for
their removal, and so, it may be, to save his patient’s life.
Class I.—Platodes.
(a.) Cestodes.—The following tapeworms concern us here :—
1. Tenia saginata (mediocanellata).
Tenia solium.
N
Tenia nana.
Tenia flavopunctata.
Tenia cucumerina (elliptica).
Bothriocephalus latus.
Tenia saginata (mediocanellata).°—This parasite is longer than
the Tznia solium, attaining to four or five metres, and its segments
are also longer. The head is surrounded with four large and usually
black-pigmented suckers, but is not provided with a rostellum, and is
without a circle of hooklets. The segments increase in length more
ec
gradually than in Tenia solium, and are commonly pigmented.
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TAPEWORMS. 183
The uterus is very much branched, and the genital pore is situated
at the side of the proglottis. The eggs resemble those of Tzenia solium,
but are more oblong, and exhibit the primordial yolk membrane.
Hooklets are not discernible in the embryo (fig. 75).
Fic, 75.—Tenia saginata: Head ; Proglottis; Egg. (Reichert’s eyepiece III., objective IV.)
2. Tenia solium.*'—The Tenia solium may measure upwards of
two or three metres. Its head is quadrilateral, about as large as a
pin’s-head (;; to =; of an inch), and dark in colour. This is succeeded
by a delicate, thread-like neck, about an inch in length, and unjointed.
The segments, or proglottides, which form the rest of the body, are
Fic. 76.—Tznia solium, Head (magnified), Proglottis (actual size), and Egg (maguitied).
short and relatively broad near the neck; but as they increase in size
this relation ceases, and still growing in both dimensions, their quadri-
lateral form becomes evident about three feet from the head. Their
average length is from 9 to ro mm., and their breadth 6 or 7 mm.
Under the microscope the head is seen to present four. prominent
suctorial discs, usually pigmented, and between them a rounded elevation
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184 THE FACES.
or rostellum, which is surrounded with about twenty-six hooklets of
different sizes.
The sexual apparatus first becomes visible about a foot from the head
(Bristowe). The uterus is but little branched, and the genital pores are
situated somewhat behind the middle of each segment.
The eggs are oval in shape, about 0.03 mm. in diameter and 0.036
mm. long, and surrounded with a thick shell, which is radially striated.
When the eggs are mature, they may be seen to contain embryos fur-
nished with hooklets (fig. 76).
3. Tenia nana.S2—This parasite averages from ro to 15 mm. in
length, and its greatest breadth is about o.5 mm. It has a globular
head 0.3 mm. in diameter, furnished with four circular suckers, and a
rostellum o.06 mm. long, carrying twenty-two to twenty-four hooklets
at its anterior extremity, which is rounded off. The rostellum can be
protruded to a considerable distance from the head or entirely withdrawn
Fic. 77.—Teenia nana: Head (with Rostellum drawn in ; Proglottis Egg.
within it. Jn the latter position it has the form of an hour-glass. The
body is attenuated in its anterior third, but proceeding backwards grows
quickly in bulk. The segments are short, and towards the end of the
body are scarcely one-fourth so long as they are broad. The uterus is
oblong and loaded with eggs of 0.03 to 0.04 mm. in diameter. The
shell does not exhibit the rod-like structure, but consists of a double
membrane, within which are a spiral thread and amorphous matter, in
which granules are embedded. Jn the interior of the ege may be seen
the embryo, already provided with five or six hooklets (fig. 77). The
parasite may be present in great numbers in the intestine, and is apt to
produce severe nervous symptoms, such as epileptic seizures, insensi-
bility and mental derangement, and melancholia (Grass¢, Comint).8*
Recent observations go to prove that the Tenia nana is very widely
distributed. It especially attacks children and young persons. It was
first discovered by Bilharz in Egypt, and since then has been recognised
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THENIA FLAVOPUNCTATA—CUCUMERINA. 185
as of common occurrence in Italy and Sicily.8! It is probable that it
exists elsewhere more frequently than is supposed. tanson has pub-
lished an account which goes to prove that it-was observed in England
so long ago as 1856.8 According to Grassi, Tenia nana is in Sicily the
commonest parasite. The number present in a single individual may
reach 4000-5000.
; 4. Tenia flavopunctata.—This bears a close resemblance to Tenia nana, but it
is of greater length (12 to 20 mm.), has no rostellum, and only two suckers. The
eggs are like those of Tenia solium (Parona), and larger than those of Tzenia
nana. The occurrence of the parasite in man rests upon the testimony of Leidy
and Parona,® but is disputed by others; and Grassi‘? identifies it with Tzenia
leptocephala, which has hitherto been found only in certain species of mice and
rats (Mus decwmanus and Mus rattus).
5. Tenia cucumerina (elliptica).—This is a worm which averages
18-25 cm. in length. The head is situated at the thinner end, and has
Fic. 78.—Tenia cucnmerina: Head ; Proglottis (magnified).
some sixty hooklets irregularly disposed around the rostellum, which is
a coarse club-like process when projected. The first forty proglottides
are of small size, but increasing as they proceed backwards both in length
and breadth, and especially in the former dimension, measure at the
extremity 6 to 8 mm. by 2 mm. in breadth. The mature segments are
of a reddish colour, and readily separate from those nearer to the head.
The eggs, when shed, have a diameter of 0.05 mm., and contain an
embyro furnished with hooklets.
The parasite is not at all rare amongst human beings;** it especially
infests children, and is acquired by them from dogs.
It is sufficient merely to mention here the rarer forms of tape-worm known to
be present in the human intestine. These are Tzenia, madagascariensis (Grenet) *
and Tenia leptocephala (Grassi), which possibly is the same as Tenia nana.°°
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186 THE FACES.
6. Bothriocephalus latus.°1—This worm attains a length of 5-8
metres. The head is ovoid, and 2 mm. long by 1 mm. broad. It is
cleft, and provided with two lateral suckers, placed on either side of the
middle line. It has no hooklets. The proglottides are at first short
and small. They increase in breadth as they proceed, and towards the
end of the parasite approach the square form. ;
The uterus of mature proglottides containing eggs exhibits a reti-
form arrangement, and appears superficially as a small rosette. This
uterine rosette is characteristic of Bothriocephalus latus.
The eggs are oval, and measure 0.07 mm. by 0.045 mm. They are
covered with a brown shell, and open by a small lid at one end. They
contain centrally-transparent masses of protoplasm of uniform size.
Bothriocephalus latus has recently acquired an increased clinical signi-
ficance, inasmuch as it has been found frequently by different observers
in conjunction with the symptoms of pernicious anemia.?2
Other varieties of this parasite have been observed, as the B. cordatus in
Greenland,® and the B. liguloides in Japan and China. The latter infests the
sub-peritoneal tissue, and especially that of the lumbar region in man.
The presence of one of the tape-worms here described is made evident
—apart from clinical symptoms, which do not concern us here—by the
discovery of proglottides in the stools.
lic. 79.—Head of Bothriocephalus latus (eye-piece IL1., objective 1V., Reichert).
a. Seen on edge; b. Seen on the flat; ¢. Proglottides; d. Eggs.
A careful microscopical examination with a medium power (Hart-
nack objective IV., Zeiss objective C., Reichert objective IV.) may
show the eggs in the feces. When it is supposed that a patient is
suffering from tape-worm, whilst yet no evidence of the parasite can
be derived from a careful inspection of the stools, it is well to mix
these with water, which is constantly poured off and renewed until the
greater part of the fecal mass has been dissolved. An examination of
the sediment will then inevitably reveal the eggs, if the suspicion be
well founded. To determine to what form of tape-worm a particular
proglottis belongs, the best proceeding is to examine the specimen,
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. DISTOMA. ; 187
mounted in glycerine, with a low magnifying power; and the same
thing may be done if a head be obtained.%
Cysts of echinococcus and hooklets may be found in the feces when a hydatid
cyst has burst into the intestine. Heller °° was able by the discovery of such a
cyst to diagnose a doubtful liver complaint as one of hydatids.
(0.) Trematodes.*’—The varieties of distomata, D. hepaticum and D.
lanceolatum, have been found in rare instances in the intestine or
biliary passages of man.
_ 1. Distoma hepaticum.—This is a leaf-shaped worm, measuring
28 mm. by 12 mm. The head is short, and furnished with a sucker.
There is another sucker on the ventral aspect, and between the two the
Fic. 80.—Distoma hepaticum.
genital pore is situated. The latter leads to a uterus, which is convo-
luted like a ball of wool.
The eggs are oval, 0.13 mm. long and 0.08 mm. broad, brown in
colour, and covered with a shell consisting of two layers; one end is
broader than the other, and opens by a small lid. Bvermer, Bostroem,
and Baelz,°® have described these parasites as occurring in human beings.
2. Distoma lanceolatum.—This entozoon is from 8 to 9 mm. long
and 2-3.5 mm. broad. It is lance-shaped, as its name implies, and
pointed at either extremity, but more so in front than behind. In
other respects its form resembles that of Distoma hepaticum.
The eggs are 0.04 mm. long and 0.03 mm. broad, and they contain
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188 THE FACES.
the mature embryo. Bizzozero® maintains that when the worm is
present in the intestine, its eggs are to be found in the stools. The
observations of Baelz,!° corroborate this view. Perroncito 1! found the
eggs of this fluke in the case of persons infested by anchylostoma.
The last two forms of parasites but rarely occur in man, and con-
sequently neither they nor their ova are often to be seen in the feces.
Moreover, they very seldom cause serious symptoms.
3. Distoma rathonisi.'°°—This distoma was described by Rathonis, who observed
the first specimen in a Chinese woman, thirty-seven years of age. The host
suffered from severe pains, referred to the liver. The parasite resembles D. hepa-
ticum, but is larger (25 mm.); the ramifications of the alimentary canal are less
complex, especially towards the hinder end.
Fic. 81.—Distoma lanceolatum (eight times actual size) and Egg:.
CLASS II.—ANNELIDES.
1. Order Nematodes (Round Worms).
a. Family Ascarides.10
1. Ascaris lumbricoides (common round worm).—This is a cylindrical
worm, of some size, with a body that tapers from before backwards.
The male is 250 mm. and the female 4oo mm. long. The head, which
is distinct from the body, consists of three conical prominences (lips)
furnished with tactile papille and minute teeth. The caudal process of
the male is folded hook-like on the abdominal surface, and is provided
with papille. In the female, the vulva lies deeply behind the anterior
third of the body. The eggs are nearly round, and brownish yellow in
colour. Their diameter is 0.06-o.07 mm. In the fresh state they are
covered externally with an albuminous layer, and beneath this is a tough
shell, which in turn encloses the very granular contents.
The Ascaris lumbricoides infests the small intestine in man, and it
appears to be common to all climates. It occurs also in cattle and in
sheep. It has no special medical interest ; but it is thought by Lutz 1
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ASCARIDES. 189
to cause spasm and tympanitis, and to impede nutrition in children.
Kartulis!© records a case of death in a man following directly upon an
invasion of the liver by ascarides. Severe nervous symptoms also, as
Fic. 82.—Ascaris lumbricoides. a. The Worm; b. Head; c. Egg.
a, half natural size; 6, slightly magnified ; c (eye-piece I., objective 84, Reichert).
amaurosis, strabismus, and evidence of meningitis,}°° have been found
to accompany their presence in great abundance. They have caused
death by invading the liver.’
Fic. 83.—Ascaris mystax.
a. Male; b. Female; c. Head; d. Egg.
2. Ascaris mystax (round worm of the cat).—This worm closely
resembles the preceding, but is smaller, and is readily distinguished
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190 THE FACES.
from it by the shape of its head, which is pointed, and bears two lateral
wing-shaped processes. The male is 45-60 mm. long, and the female
110-120 mm. The eggs are globular, larger than those of A. lum-
bricoides, and covered with a dimpled shell (fig. 83).
3. Oxyuris vermicularis (common thread-worm or teat-worm).—The
female is ro mm. in length, and exhibits two fully-developed uteri,
which extend symmetrically backwards from the vaginal orifice. The
male is rather less than half the length of the female, and its tail is
provided with six pairs of papilla. The head of both sexes is similar.
It displays a remarkable cuticular enlargement and small prominent
lips.
The eggs are irregularly oval, and measure 745 (0.05 mm.) by 7755
(0.02-0.03 mm.) inch. The shell is membranous, and consists of two
Fic. 84.—Oxyuris vermicularis.
a. Head; b. Male; c. Female; d. Eggs.
or three lamin. Its contents are coarsely granular. The eges often
contain an embryo with an indistinct alimentary canal and a tail equal
to half the entire length. The presence of the parasite is attended with
uncomfortable sensations, among which itching in the situation of the
anus is prominent. 105
B. Family Strongylides (Leuckart).!°°—To this family belongs one of
the most important and formidable of the parasites which infest the
human intestine. This is—
Anchylostoma duodenale (Dochmius duodenalis, Strongylus duo-
denalis).—It was formerly believed that this worm occurred only in
the tropics and in certain districts of Italy.4° Of late years, numerous
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ANCHYLOSTOMA DUODENALE. I9QI
observations in Italy (Perroncito and others"), Germany, Switzerland
(Menche and others 112), and Belgium 13 have made it clear, together with
the older researches, that the inhabitants of temperate regions are not
free from its attacks.115
The Anchylostoma is cylindrical in form. The male measures 8 to
12 mm. in length, the female 10 to 18 mm. The anterior extremity
is pointed, and reflected towards the dorsal surface. The oral orifice
is armed with four claw-like teeth. The caudal extremity of the male
expands into a pouch with three flaps; that of the female is pointed
and conical ; the vulva is situated behind the middle third of the body.
The eggs are smooth and oval, measure 0.05 to 0.06 mm., and usually
contain two or three large daughter-cells. The embryos develop rapidly
Fia. 85.—Anchylostoma duodenale.
d. Female (magnified).
e. Head (eyepiece II., objective C, Zeiss).
i. Eggs.
a. Male (natural size).
6, Female (natural size).
c. Male (magnified).
outside the human body. In stools which contain eggs, the embryo:
may be seen and observed after the lapse of twenty-four to forty-eight
hours.
Except when anthelmintics have been administered, the eggs are the
only signs of the parasite to be found in the discharges, and it is con-
sequently of the utmost importance to be familiar with their appearance.
The accompanying figure shows this at various stages of their develop-
ment (fig. 85, /).*
The presence of Anchylostoma is to be suspected in all cases where
a severe form of anemia occurs in labourers (and especially in brick-
burners, miners, and tunnel-borers), without any obvious and sufficient
* [An instructive case of this disease is reported in the Lancet, February 1, 1890.],
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192 THE FACES.
cause. It is, however, necessary to bear in mind that Bothriocephalus
latus produces similar symptoms (p. 186). Examination of the stools
will then afford the means of diagnosis. If the intestines contain
Anchylostoma, the characteristic eggs with their large blastomeres will
be seen. If any uncertainty as to their nature should persist, the fecal
substances containing them should be allowed to remain for some days
in a warm place, and again examined microscopically. The process of
segmentation of the egg will then be seen to have advanced, and fully
developed embryos will be visible here and there. The administration
of anthelmintics, and especially of the ethereal extract of male-fern,
will cause the expulsion of the mature worm, and an inspection of the
resulting discharges cannot fail to establish the diagnosis.
The character of the stools in this affection varies greatly. Diarrhcea
Fig. 86.—Trichocephalus dispar.
a. Male; b. Female; c. Eggs; a, 6. Slightly magnified ; c. (eye-piece 11., objective 8a,
Reichert).
is usually present, and blood is frequently passed. But it may happen
that the discharges are altogether normal. They have been known to con-
tain great quantities of Charcot-Leyden crystals (Levchtenstern, see ante).
[In the report of the Ceylon Commission, 1887,"6 anchylostomiasis
was stated to be a cause of beri-beri. The-association is probably
accidental (Sonsino). | 11"
y. Family Trichotrachelides (Leuchart)..8
1. Trichocephalus dispar (whip-worm).—This worm has a whip-like
form, consisting of a short, stout hinder-part, and a long, spiral, filiform
process anteriorly. The male is 40 mm., and the female 50 mm. long.
The short hinder part measures 1 mm. in thickness (fig. 86, a, b).
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TRICHOCEPHALUS DISPAR—TRICHINA. 193
The eggs, which are occasionally to be found in the feces, are brown
in colour, 0.05-0.06 mm. long and 0.02 mm. broad. The shell consists
of two layers and is flattened at either end, where it is furnished with
a small lid, formed of a glossy substance. The yolk is very granular
(fig. 86, ¢). According to Erni" and others, this parasite, together
with Anchylostoma and an insect-larva, produces the beri-heri disease
which is endemic in Sumatra. This view is, however, opposed by other
writers (Scheube, Scheffer).
2. Trichina spiralis.!2°—Trichina occurs in two different forms in
the human body, according as its habitat is the muscular tissue or the
Fic. 87.—Trichine.
a. Male, and ), Female Intestinal Trichine, slightly magnified; ce. Trichina of muscle
(eye-piece III., objective IV., Reichert).
intestine. It is with the trichina of the intestine that we have to do
here, since this form alone is found, though rarely, in the feces. The
male is 1.5 mm. in length, and the female 3 mm. The former has four
prominent papille situated between the conical protuberances at the
extremity. The sexual organs of the female consist of a tubular ovary,
which is placed at the hinder part of the body, and a tubular uterus,
with which the ovary communicates in front (fig. $7). Impregnation
takes place in the intestine. The eggs develop into embryos while still
within the uterus, and the newly-born parasite almost immediately per-
forates the gut, and becomes imbedded in the muscles of its host.
N
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194 THE FACES.
Of their own accord these worms rarely pass with the stools. But
in any case where there is reason to believe that trichinous meat has
been eaten and trichinosis is apprehended, an anthelmintic may be given,
and the detection of intestinal trichina in the feces will establish the
diagnosis in a very early stage of the affection.
8. Rhabdonema Strongyloides (Leuckart).—Certain nematode worms
have been discovered in the stools in cases of Cochin-China diarrhcea
(Normann, Bavay, Seifert). They occur commonly in conjunction
with Anchylostoma (Grassi, Parrona, Perroncito).!22 It was formerly
thought that there were two distinct parasites of this kind, viz., Anguil-
lula intestinalis and Anguillula stercoralis; but more recent observa-
tions by Leuekart and Grassi "3 have shown that the latter is only an
Fic. 88.—Anguillula stercoralis.
a. Female; b. Male; c. Head (eye-piece II., objective 8a, Reichert).
intermediate form in the development of A. intestinalis. A complete
knowledge of the subject, however, implies an acquaintance with this
form, as it may be confounded with other Helminthide. The life-
history, according to Grassi, is as follows :—
The Anguillula which infests the human intestine deposits eggs, from
which the young are produced as embryos or larve. These are dis-
charged with the stools. As found there, they already exhibit sexual
maturity (Anguillula stercoralis) and produce embryos, which undergo
no further change in the human system. The body of this worm is
round, and shows faint traces of transverse striation. The head is in
the form of a blunted cone (fig. 88) and sessile upon the body. It is
furnished with two lateral jaws, each bearing a pair of teeth. The
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ANGUILLULA STERCORALIS—INSECTS. 195
male is 0.88 and the female 1.22 mm. long. Anguillula intestinalis
measures 2.25 mm. in leneth and 0.04 mm. in thickness at its middle.
It has a triangular mouth closed by three small lips. The vulva lies
at the junction of the middle with the posterior third. Its habitat is
the small intestine. The egos resemble those of Anchylostoma duode-
nale, but are longer, more elliptical, and pointed at the poles. In recent
stools the larve alone are to be seen. It is doubtful whether the para-
site 1s directly mischievous ; but its constant association with Anchylos-
toma, and the readiness with which the two may be confounded, render
its recognition a matter of consequence.
3. Insects.—It requires to be noticed that insect larve infest the
stools. Joseph !*4 has reported a number of species, which are for the
most part taken into the intestine with food (cheese, meat), and give
rise to a variety of morbid symptoms, as colicky pains, vomiting, Xe.
(see p. 158). Special mention may be made of the immature cheese-
maggot (Piophila casei) and Drosophila melanogastra, which are derived
from curdled milk, and may attain the chrysalis form in the intestine
before they are discharged per rectum. Of other species are the larvee
of three varieties of Homalomyia, of Hydrothza meteorica, Cyrtoneura
stabulans, Calliphora erythrocephala, Pollenia rudis, Lucilia caesar and
regina, Sarcophaga hemorrhoidalis and hematodes, and Eristalis arbus-
torum, all of which are apt to occur. Rembold, Lampa, and Kohn 1°
have also observed in the stools certain lancet-shaped bodies, 8 mm,
long, which are covered with hair and indented on the surface, and
these have been identified by V. Graff as the larve of Anthomyie.
[ Finlayson °° records a case in which swarms of larve were passed alive
from the bowel of a man. He identified the insect as Anthomyia
canicularis or scalaris. |
4. CRYSTALS.—Crystalline bodies are a common constituent of the
feeces, and in some cases are to be found in great quantities. They may
be organic or inorganic.
1. Charcot-Leyden Crystals.—These bodies, of which an adequate
description has already been given in connection with the Blood (p. 30)
and the Sputum (p. 110 and fig. 62), are comparatively rarely to be seen
in the feces. Nothnagel has met with them in typhoid fever, and
Leichtenstern 2" in phthisis and anchylostomiasis. Their presence, how-
ever, has no pathological significance.
2. Hematoidin Crystals.—It is surprising that so little attention has
been paid to this subject. Ufelmann,!* indeed, remarks that crystals
of hematoidin are sometimes present in the discharges of infants at
the breast ; but apart from this notice the matter has been passed by in
silence. The author has found these crystals often enough in the feces,
especially in chronic intestinal catarrh from over-eating, and in many
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196 THE FAECES.
instances in which blood had been discharged into the intestine some
time (several days) before the stools were passed. They usually exhibit
an ill-marked crystalline structure. Particularly good specimens were
seen in the stools of a patient suffering from nephritis. The crystals
are sometimes free, and sometimes enclosed in masses of a shining
Fic. 89.—Hematoidin Crystals from Acl olic Stools (eye-piece III., objective 8a, Reichert).
substance which resembles mucin (fig. 89). Similar crystals were found
in the liquid motions of a man who suffered from pernicious anemia
(v. Jaksch).
8. Cholesterin.—This substance enters normally into the constitution
of the feces, and can always be obtained from them.
It seldom appears in its crystalline form (fig. 125), according to Noth-
nagel, and the statement is undoubtedly correct. (For the microscopical
and chemical character of cholesterin, vide infra and chapters on Sputum
and Urine.)
4. Fat Crystals.—Nothnagel, in his well-known monograph,! states
that fatty substances occur in the feces in the form of needles.
Fic. 90.—Acholic Stools (eye-piece 11I., objective j;, oil immersion, Reichert >
Abbe’s mirror, narrow diaphragm),
Gerhardt 1° found quite an enormous quantity of organic crystals in the
stools of jaundice (fig. 90). He was himself of opinion that such bodies ©
consisted of tyrosin; but one of his pupils, named Oéesterlein,31 who
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CRYSTALS—INORGANIC SALTS. 197
ed the investigation farther under Gerhardt’s auspices, came to the
clusion that chemically they were lime and magnesia salts of the
her fatty acids, and that, therefore, soaps of lime and magnesia hases
form a part of such discharges. According to Stadelmann,!? they are
sodium soaps. The author, however, can add his own testimony to
Gerhardt’s statement, for he has repeatedly seen great quantities of
crystals arranged in clusters in acholic stools; and is disposed, on the
grounds of separate investigation, and especially of the ascertained
character of similar bodies occurring in other excretions (see chapter on
Urine), to believe that such crystals do not consist of tyrosin, but rather
of a combination of the alkaline earths with the higher fatty acids.
Uffelmann, 8° who had already observed these crystals in the discharges
of infants, arrived independently at the conclusion that they could not
consist of tyrosin. According to #r. Jfiller,!** their presence indicates
an impediment to the absorption of fat from the intestines,
In cases of jaundice, so frequent among children, such crystals are
profusely present in the stools, and they are normally found in those
of infants during lactation (v. Jahsch).
5. Oxalate and other Organic Salts of Lime.—Ovxalate of lime is a
sufficiently common constituent of the feeces, and appears on micro-
scopical examination (see fig. 112). According to Nothnagel, it is always
derived from the food. It is most abundant after a vegetable diet, and
when manifested in considerable quantity the discharges also contain
abundant débris of plant-tissues.
Uffelmann'® asserts that crystals of lactate of lime occur in the
discharges of children as sheaves of radiating needles. Other organic
salts of lime, as the acetic and butyric acid salts, have been observed in
the discharges of persons suffering from acute gastric and intestinal
catarrh (v. Jahsch) 1%
6. Carbonate of Lime occurs rarely in the stools as amorphous par-
ticles and dumb-bell figures (fig. 124).
7. Sulphate of Calcium.—This salt is very seldom present in the
stools. It can be obtained, however, by the action of sulphuric acid
on the feces, which shows that other lime salts are present. Its form
presents the same variety here as in the urine (fig. 116).
8. Phosphate of Lime.—This substance crystallises in stout or elon-
cated wedges, grouped together so as to form larger or smaller gland-
like masses (fig.115). The presence of such crystals in the feeces is without
pathological significance.
Other salts of lime are occasionally met with. They are impregnated
with bile-colouring matters, and deeply stained a yellow colour.
9. Triple Phosphate-—The phosphate of ammonia and magnesia
occurs sometimes as well-formed coffin-lid crystals (fig. 66, 7), some-
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198 THE FECES.
times in ill-defined crystalline masses, and very rarely in the elder-leaf
arrangement (fig. 121).
Perfect crystals are most commonly to be found in fluid motions,
and in the mucus which adheres sometimes to the feces, whether liquid
or solid. Fragments of coffin-lid crystals alone may be visible, and
these often exhibit fissures and flaws, or there may only be mere
splinters (Nothnagel). It is notable that these crystals seldom take
up bile pigment. By their chemical constitution they may he readily
recognised ; and they dissolve easily, as has been already mentioned, in
acetic acid (p. 113).
10. Sulphide of Bismuth Crystals —When preparations of bismuth
have been taken internally, the stools may be found to contain crystals
which bear a remarkable resemblance to those of chloride of hematin
Fic. 91.—Sulphide of Bismuth Crystals from the Stools (eye-piece III., objective 84, Reichert).
(hemin). They consist of sulphide of bismuth, as may readily be shown
by a comparison with the bodies formed when nitrate of bismuth is
added to ammonium sulphide.
IiIl. CHEMICAL EXAMINATION OF THE FACES.—In striking
contrast with the valuable information to be derived from the naked-eye
and microscopic investigation of the feeces is the very slight assistance
which the chemical examination of those discharges lends to the purposes
of diagnosis.
A. Organic Substances.
1. Mucin.—Mucin, as Hoppe-Seyler 1°" has said, may be looked upon
as the basis of the fecal substances, a statement which can be confirmed
by the author. #7. Miller, on the other hand, asserts that mucin is
not so abundantly present in the stools. For the detection of mucin
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ORGANIC SUBSTANCES. 199
in the stools the following process may be recommended :—The feces
are stirred up with water, their own bulk of lime-water added, and the
mixture allowed to stand for some hours. It is then filtered, and the
filtrate tested with acetic acid for mucin (see chapter on Urine).
2. Albumin.—The presence of albumin may be shown as follows :—-
The feces are mixed with a large quantity of water, to which a trace
of acetic acid has been added, and a watery extract is thus made. This
is repeatedly filtered, and the filtrate may be submitted to the tests for
albumin mentioned in the chapter on Urine (q. v.). Under ordinary
circumstances no proteid reactions can be obtained, but albumin occurs
in considerable quantity in the stools of typhoid and diarrhcea. In one
instance, much serum-albumin was found in the discharges of a chlorotic
woman, who passed pale stools almost devoid of bile; and once again in
the case of a patient whose stools were deficient in bile, but who was
not jaundiced (v. Jaksch).
3. Peptone.—For the detection of peptone, the feces should be
mixed with water so as to form a thin pulpy fluid, then boiled, and
filtered while still hot. The filtrate will be clear or slightly tinged with
red. When it has cooled, it may he tested for albumin with acetic
acid and ferrocyanide of potassium. It usually happens that the liquid
becomes a little turbid when the acetic acid is added (mucin), but the
turbidity does not extend on the addition of ferrocyanide of potassium.
When this is so, the mucin may be precipitated with acetate of lead,
the filtrate tested in the manner afterwards to be described (chapter on
Urine) with phosphotungstic acid, and the fluid which finally remains
may be submitted to the biuret test. Should it happen that the fluid
after boiling contains albumin as shown by the acetic acid and ferro-
cyanide of potassium test, this substance must be removed by combina-
tion with ferric acetate (see chapter on Urine), and the remainder of the
process conducted as above.
The author has never found peptone in healthy feces, but has met
with it repeatedly in disease. He has collected the records of some fifty
or sixty cases bearing upon this matter, and the results which were
obtained depend upon seventy or eighty separate analyses.
Out of seven cases of typhoid, peptone occurred in the liquid stools
in large quantities in five. Its presence remained doubtful in one, and
it was absent from the discharges of the seventh.
It was present in all cases where the stools contained pus, as in dys-
entery (two cases), tubercular ulceration of the intestine (three cases),
and suppurative peritonitis discharging pus into the intestine (one case).
In hepatic affections, the character of the feces in this respect was
very inconstant. In a series of cases of catarrhal jaundice with more
or less acholic stools, no peptone was to be found; whilst, on the other
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200 THE FACES.
hand, the thin non-purulent discharges from a patient with syphilitic
inflammation of the liver exhibited it in considerable quantity. It
occurred plentifully in certain cases of atrophic cirrhosis and of car-
cinoma of the liver.
Acholie stools without jaundice were generally rich in peptone, but
the results of analysis in these cases show much variety (v. supra).
4. Urea.—The presence of urea may be best ascertained by the
method previously described (p. 69). For the estimation of metabolism,
it is necessary to ascertain the total quantity of nitrogenous substances
contained in the feces. To do this, the stools should be treated with
dilute acid (to prevent the evaporation of ammonia) and dried. The
usual method for the analysis of organic compounds will then serve to
determine the proportion of nitrogenous bodies present (see chapter on
Crine).
5. Carbohydrates.— Various carbohydrates occur in the feces. Of
these starch is the most prominent. It may be recognised at any time
by the aid of the microscope. Hoppe-Seyler 8 asserts that grape-sugar
and certain gummy carbohydrates may be contained in the stools.
To ascertain the presence of these substances, the feeces must be
boiled with water, filtered, and the filtrate partially evaporated on a
water-bath. One part of the fluid may then be tested with Trommer’s
or the phenyl-hydrazin test for sugar. To another part a little of the
iodo-potassic iodide solution may be added, to show the presence of
starch. The remainder of the fluid may now be distilled, and the
residue extracted with alcohol and ether (see chapter on Urine); the
extract boiled with water and filtered ; the filtrate partially evaporated ;
treated with dilute sulphuric acid, and boiled; saturated with caustic
soda; treated again with cupric sulphate, and boiled. The reduction
phenomenon will show the presence of dextrin and gums (Hoppe-
Seyler).
The property of benzoyl chloride to form insoluble compounds with
carbohydrates in alkaline solutions may also be utilised as a test.
6. Acids.
(«.) Bile Acids.—For the detection of bile acids, the distillation
residue of the feces may be tested in the manner already described in
connection with the blood (p. 75). If biliary acids be present in great
quantity, the application of Pettenkofer’s test directly to a watery
extract of the feces (p. 76) will suffice for their recognition. They
may also be detected by the addition of a watery solution of furfurol
and sulphuric acid (p. 76, and chapter on Urine).
(8.) The Volatile Fatty Acids.—To obtain these bodies from the
feeces, the following plan may be adopted :—Dilute the fecal mass with
water, add phosphoric acid, and distil. The distillate contains these
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ORGANIC ACIDS. 201
acids together with indol, phenol, and scatol. If this distillate be
neutralised with carbonate of soda and again distilled, the indol, phenol,
and scatol will pass over, and the sodium salts of the fatty acids remain
behind. Let these now be evaporated to dryness on the water-hath,
the residue extracted with alcohol, and after the evaporation of the
latter dissolved in water. The solution may then he tested for fatty acids.
The separation of the different fatty acids may be accomplished by
fractional distillation when they are present in abundance. Moreover,
they may be partially isolated by precipitation of the sodium salts with
ether in alcoholic solutions of varying degrees of concentration (v.
Jaksch).4° When there is sufficient material at hand, it is a good
plan to convert the acids into their silver or barium salts, and to effect
their separation on the principle of their different degrees of solubility
in water,
The estimation of the silver, barium, or sodium constituent in the
corresponding salts may be effected in the reactions given below, and
the proportion of the respective acids determined accordingly. Of the
volatile fatty acids, butyrie and acetic acids are those most readily to
be found in the feces.!4! Formic and propionic acids do not appear to
have been recognised with absolute certainty, but we shall take account
of them here, since it is certain, at any rate, that they occur in another
secretion (urine).1#
(a.) Formic Acid.—This is a colourless liquid, of a pungent pene-
trating odour, which freezes at o° C., boils at 100° C., and is miscible
with alcohol and water.
1. Free formic acid is not precipitated by nitrate of silver, but. this
reagent will precipitate the alkaline salts of the acid from concentrated
solutions. The silver compound blackens quickly in the cold,, and
when heated reduction takes place.
2. If a solution of perchloride of iron be added to a solution of a
neutral salt of formic acid, a blood-red colour appears. This hue disap-
pears on boiling, and a rust-coloured sediment remains.
3. If formic acid or an alkaline salt of the acid be heated with
mercuric chloride to 60° or 70° C., a precipitate of subchloride of
mercury forms. This reaction is impeded by the presence of free
hydrochloric acid or of excess of an alkaline chloride.
(b.) Acetic Acid is a fluid with an acrid, pungent odour. Its boiling-
point is 119°, and it crystallises at o° C. Heated with ferric chloride,
its salts behave like those of formic acid. Nitrate of silver yields a
precipitate in neutral solutions of a salt of acetic acid, and this preci-
pitate dissolves in boiling water without being reduced.
When a salt of this acid is heated with sulphuric acid and alcohol,
the characteristic odour of acetic ether is obtained.
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202 THE FACES.
(c.) Propionic Acid.—This is an oily fluid. It boils at 117°C. Pro-
pionic salts exhibit the same reactions with nitrate of silver as those of
formic acid. With ferric chloride they do not yield a red colour.
(d.) Butyric Acid.—In the pure state butyric acid is an oily fluid,
with a goat-like odour, which boils at 137° C. It is miscible in all
proportions with alcohol and ether. Its salts, when treated with
mineral acids, develop the characteristic goaty smell. Ferric chloride
solution does not give a red colour in solutions of such salts, while
nitrate of silver forms a crystalline sediment which is insoluble in cold
water.
To isolate butyric acid from the isobutyric acid in the feces, the portion which
distils at 158° C. should be treated with carbonate of guanidin (Brieger 4%), and
the guanidin salt obtained converted by heating into the corresponding guanamin.
The base examined under the microscope will then exhibit the characteristic
pointed rhomboids of the guanamin of isobutyric acid.
Valerianic, caproic, and others of the higher fatty acids are also present in the
feces. Wegscheider 4 asserts that oleic, palmitic, stearic, capric, and caproic
acids occur in the discharges of infants.
7. Phenol.—This substance is always a constituent of feces. When
the fatty acids have been converted'‘into their sodium salts in the
process described above for the separation of the volatile fatty acids,
phenol passes over in the distillate. To isolate it from indol and
scatol, the distillate must be rendered alkaline with caustic potash and
again distilled. The phenol remains behind, and may be purified by
distillation with sulphuric acid.
(1.) If a portion of the distillate now be treated with a solution of
ferric chloride, a violet colour will show the presence of phenol.
(2.) The addition of bromine-water to another portion will cause the
deposition of a crystalline sediment of tribromophenol.
(3.) Millon’s reagent gives a red colour.
8. Indol and Scatol.—Both these bodies occur in the feces, the
latter having been detected there by Brieger.14° To separate them
from the phenol present, the distillate in the above process (see ante,
Volatile fatty acids) should be treated with an alkali and again distilled,
when indol and scatol will pass over. Indol forms in small colourless
scales like those of benzoic acid. It dissolves in boiling water and
very readily in alcohol, and is decomposed by strong alkalies.
Scatol, which also crystallises in colourless scales, is much less readily
soluble in water, and possesses a disagreeable pungent smell. It is not
decomposed by fairly strong alkalies.
To obtain either of these bodies separately, we avail ourselves of the
lesser solubility of scatol in water, or of its property of resisting the
action of alkalies.
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CHOLESTERIN—FATS. 203
(1.) If nitric acid which contains nitrous acid be added to a solution
of indol, a distinct red colour is produced, or a red precipitate if the
solution be concentrated.146
(2.) Pine-shavings steeped in hydrochloric acid are tumed red in an
alcoholic solution of indol. The first test, when applied to scatol, does
not produce a red coloration, but at most a slight turbidity. The second
entirely fails. Jointly they will serve sufficiently for the discrimination
of these two substances. 17
9. Cholesterin, Fats, and Non-Volatile Organie Acids.—
Cholesterin, as we have seen, seldom occurs as crystals in the feces,
but, according to Hoppe-Seyler, is in one form or the other an invari-
able constituent of those discharges. For its detection chemically, the
residue which remains when the volatile fatty acids and phenol group
have passed over in the process of distillation is to be treated with
excess of sulphuric acid, and extracted first with alcohol and then with
ether. (1.) The ethereal extract is filtered, the wether removed by
distillation, and the residue first digested with carbonate of soda on the
water-bath, so as to remove any traces of the volatile fatty acids that
may have failed to pass over with the ether, evaporated to dryness,
and again extracted with ether. (2.) The alcoholic extract is also
filtered, treated with carbonate of soda, the alcohol distilled off, the
residue dissolved in water, and finally, as before, extracted with ether.
In the alkaline watery residue are contained the biliary acids (v. supra),
oleic, palmitic, and stearic acids, which, according to Hoppe, may be
separated by converting them into their barium salts.
Cholesterin and fat are taken up by the ether. The latter is evapo-
rated, the residue treated with alcoholic solution of caustic potash, the
alcohol removed by evaporation on the water-bath,48 and the remain-
ing fluid diluted with water and extracted with ether. The fats remain
as soaps in the watery solution, while the cholesterin is dissolved by
the ether.
Cholesterin may be recognised by the following tests :—
(1.) A little concentrated sulphuric acid applied to the crystals on
a slide will cause them gradually to colour a reddish-yellow round their
borders, and finally to grow smaller and disappear.
(2.) When the crystals are dissolved in chloroform and sulphuric acid
is added, a blood-red colour forms, presently changing to purple-red.
The sulphuric acid at the same time shows a strong green fluorescence.
(3.) A particle of cholesterin to which a little nitric acid has been
added is placed in a small dish and evaporated to dryness in the water-
bath. . It leaves a yellow stain, which turns a yellowish-red on the addi-
tion of ammonia (Schulze).
The soap-solution obtained in the above process is to be rendered
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204 THE FASCES.
acid with dilute sulphuric acid, and the resulting fatty acids removed
by filtration. If the filtrate be neutralised with ammonia, evaporated,
and extracted with alcohol, it will be found to contain glycerine. The
fatty acids may be again dissolved in ether, repeatedly saponified,!°?
collected and dried, and then identified, first by ascertaining their
melting-points, and again by converting them into their barium salts,
and determining in each case the value of the barium constituent
( Hoppe-Seyler).11
Fats, and especially neutral fats (tri-glyceride), soaps, non-volatile
fatty acids, and cholesterin, are present in all feces. Acholic stools
present them in relatively large quantities. According to Miiller,'>?
clinical inferences can be based on a. knowledge of the melting and
solidifying points of the fatty acids.“? Both points are higher in pro-
portion to the efficiency of intestinal absorption. When the fatty acids
of the feces contain a proportion with a melting-point so low as 50° C.,
this function is probably impaired.
For the quantitative estimation of fats in the stools the methods of
Hoppe-Seyler and Benedikt + may be employed. That of Atiller! is
more expeditious and serves well for clinical purposes. To determine
the amount of fats formed with a given diet, as milk or flesh, powdered
animal charcoal is administered with the first meal, which should be
taken on an empty stomach. The earliest resulting feces are thus
stained black. A portion is dried at 100° C., and by extraction with ether
in Soxhlet’s apparatus the neutral fats and free fatty acids are obtained.
These are dissolved in warm alcohol and a little ether, and submitted to
titration with phenol-phthalein solution and alcoholic solution of caustic
potash. The result of titration shows the proportion of fatty acids
present. Another portion of the dried feces is extracted first with acid
alcohol and afterwards with ether to determine the amount of soaps
contained in it. In intestinal disease, especially such as involves the
lymphatics, and where the flow of bile is suspended (M/ziller) °° the feces
contain great quantities of fat, showing that absorption is impeded.
10. Colouring Matters.
1. Urobilin—This is the normal colouring matter of the feces
(p. 164). It can readily be obtained from the stools by treating them
with acid alcohol.
Mehws*’ method for the isolation of urobilin in feces yields
excellent results. A watery extract of the feeces is made, and to this
is added sulphuric acid in the proportion of 2 grms. to the litre, and
solid ammonium sulphate. The fluid is then filtered, and the pre-
cipitate washed with a warm. saturated solution of ammonium. sul-
phate, dried on a water-bath, and extracted with a boiling alcoholic
solution of ammonia. Urobilin may be shown in the extract so formed
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COLOURING MATTER—GASES. 205
by its characteristic spectrum in acid solutions. This exhibits a well-
defined absorption-band between the lines ) and F' (Fraunhofer) of the
solar spectrum (fig. 130).
It should be noted that urobilin may be present even in acholie stools.
2. Blood Colouring-Matter.—Pure blood occurs in the stools only
after very profuse and rapid hemorrhage into the intestine. In all
other cases where its constituents are found they are greatly altered.
Hematoidin crystals are rarely seen. Hematin is the form in which
blood pigment occurs most commonly. This substance may best be
recognised by Teichmann’s test, or with the spectroscope (pp. 61, 66).
3. Bile Pigment.—The feces never contain bile pigment in health,
but it is found abundantly in the discharges in cases of catarrh of the
small intestine. It may be best detected by the application of G'melin’s
test (nitric acid). On the addition of a little impure nitric acid to a
specimen of feces in which bile pigment is present, the mass changes
colour quickly, and the separate drops of the acid are surrounded with
rings of green, red, and violet. The appearance of a green ring is very
characteristic of bile pigment, and is due to the formation of biliverdin.
We have already spoken of the other pigments which may occur in the
stools (see p. 165).
11. Intestinal Gases.—These consist of hydrogen, carbonic acid,
nitrogen and volatile carburetted hydrogen (methan).* It is not yet
definitely determined whether sulphuretted hydrogen is formed in the
intestine or not. Senator and Ottavio Stefano,? however, maintain that
in certain morbid states this gas is generated in such quantity as to
cause symptoms of poisoning. The fact that sulphide of bismuth is
formed in the alimentary canal when nitrate of bismuth has been taken
(v. Jaksch), lends probability to the assumption that sulphuretted hydro-
gen is also produced there. According to Hammarsten,! the latter
occurs in small quantity in normal feces.
12. Ptomaines. — Putrescin and cadaverin are present in the
stools, and may be recognised by the methods already laid down.
Moreover, the ptomaines known to be produced by pure cultivations of
certain pathogenic fungi have recently been obtained directly from the
feeces, as by Powchet1®! in cases of cholera. Bawmann and Udranshy,
Stadthagen and Brieger1® have separated diamines from the stools of
patients with cystinuria (see chapter on Urine). They believe that these
substances are absent from normal feces. See the methods described at
p- 158.
13. Ferments.
Diastase and Invertin are generally present in the stools of healthy
children (v. Jaksch).1°* For the detection of diastase see p. 82.
B. Inorganic Substances.—The consideration of such inorganic
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2060 THE FACES.
substances as assume a crystalline form has already engaged our atten-
tion (p. 195). Chloride of sodium may be detected in the feeces thus :—
An extract is made with water, acidulated with nitric acid, filtered, and
the filtrate tested with nitrate of silver. A white precipitate (chloride of
silver), soluble in ammonia, will show the presence of the sodium salt.
In Hoppe-Seylei’s 1+ method for the quantitative analysis of inorganic
matter in the stools, the substances which are soluble in alcohol are
separated from those which are soluble in dilute acetic and hydro-
chloric acids before the process of incineration is commenced. If this
is not done, there is danger that the nuclein, which is nearly always
present in feces, will be decomposed, setting free its phosphoric acid,
which may then either remain uncombined or displace other acids from
their compounds. The analysis, both quantitative and qualitative, of
the incinerated ash is conducted according to methods which are suffi-
ciently familiar.!%°
IV. EXAMINATION OF THE MECONIUM.—The term ‘meco-
nium” is applied to the substance discharged from the rectum of the
child immediately after birth. It is a thick, sticky, viscous fluid, of a
greenish-brown colour. When examined by the microscope, meconium
exhibits some intestinal epithelium cells, fatty particles, both fluid and
solid,!®* numercus cholesterin crystals, a quantity of more or less well-
formed crystals of bilirubin, and some downy hairs. There are imme-
diately after birth no fungi, and (according to Escherich 1%") no spores.
After the lapse of twenty-four hours, however, the discharges exhibit a
very different character. They now contain abundance of micro-organisms,
and Escherich obtained from them by Koch’s plate-cultivation methods
three distinct microbes.
After the child has taken the breast, the bacteria of the stools,
according to the same authority, are represented by two species of micro-
organisms. The first consists of thick, curved, rod-like bodies, measuring
1-5 “in length by o.3-0.4 w in thickness. The other is a micro-organism
which closely resembles the lactic acid bacillus of Hvippe.168
In addition to the above, the meconium contains numerous squamous
epithelium cells, derived from the pharynx and esophagus, or from the
anal orifice (Bizzozero).1
Zweifel and Hoppe-Seyler, who have investigated the chemical con-
stitution of the meconium, found it to contain bilirubin, biliverdin, and
bihary acids, but no hydro-bilirubin (urobilin), Wegscheider 17! found
traces of peptone, fats, and soaps, bilirubin, and traces of hydro-bilirubin
in infantile stools. In a specimen which the author examined, there
was no serum-albumin, peptone, or sugar. There was abundance of
mucin, Pilirubin was the only pigment present.
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ACUTE AND CHRONIC INTESTINAL CATARRH. ZOY
V. CHARACTER OF THE FACES IN CERTAIN INTESTINAL
AFFECTIONS.
1. Acute Intestinal Catarrh.—In this condition the quantity of
the stools is subject to great variety. They are usually fluid, thin, and
slimy, yellowish-brown in colour, and emit a most unpleasant smell.
Their reaction is alkaline, except in the case of acute enteritis of chil-
dren, when it may be acid. Such stools usually contain great quantities
of mucus, and there are often visible to the naked eye food remnants in
great quantity.
Microscopical examination reveals an abundance of fungi of vari-
ous descriptions, large quantities of intestinal epithelium, and isolated
leucocytes.
2. Chronic Intestinal Catarrh.—In this disease the stools
exhibit no very distinctive characters, whether to the naked eye or
microscopically.
Vothnagel 1"? lays down the following rules for the localisation of
chronic idiopathic intestinal catarrh, according to the character of the
feeces :—-
1. When the large intestine is alone involved, a single discharge
takes place within twenty-four hours. Diarrhcea, however, is apt to
recur at certain regular intervals.
2. When the small intestine alone is engaged, the motions are also
likely to be sluggish.
3. When both the large and small intestines are the seat of catarrh,
continuous diarrhea is apt to ensue.
4. Solid or semi-solid stools containing hyaline particles of mucus,
which can be recognised only with the microscope (see p. 166), and
devoid of mucus visible to the naked eye, point to implication of the
upper part of the large intestine.
5. The presence of bile pigment in the stools, as shown by Gmelin’s
test, invariably indicates a catarrh of the ileum and jejunum. In such
cases also the feces are usually found to contain epithelial cells and
mucus, deeply stained yellow by the bile colouring matter.
In certain forms of chronic catarrh, where the large intestine is
especially involved, it sometimes happens that the bodies described at
p. 165 are to be found in the stools. Such an affection is then called
enteritis tubulosa or membranacea; but it is probable that these mani-
festations accompany other sufficiently dissimilar morbid states. Our
present knowledge of the subject is defective.
3. Ulcerative Enteritis. —The diagnosis of this condition is
always attended with difficulty. It is usually (though not always)
accompanied with diarrhea. In a questionable case, the appearance
of blood in the stools makes ulceration probable ; but we cannot derive
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208 THE FACES.
any conclusive evidence from either the physical or the chemical char-
acter of the feces to establish the diagnosis. A diligent examination
of the discharges, however, may in certain specific forms of ulceration
disclose the presence of the pathogenic organisms to whose influence
the process is known to be due. The detection of the tubercle-bacillus
especially is in this way a fact of the utmost clinical significance
(see p. 103).
4. Typhoid Fever. — This disease is usually characterised by
abundant foul-smelling discharges of the colour of pea-soup. They
contain large quantities of bile pigment, a fact which points to a catarrh
of the small intestine, and to which also Nothnagel attributes the
peculiarly offensive character of the smell emitted,
The reaction of typhoid stools is in all cases alkaline.
Microscopical examination shows numbers of bile-stained epithelial
cells, some leucocytes, abundance of triple phosphate crystals, and a
profusion of fungi. Nothnagel’s clostridia are especially prominent
amongst these. The typhoid-bacillus, of course, infests the discharges
of this disease ; but it cannot be distinguished from the other micro-
organisms by a simple microscopical examination. This can be done
only by the bacteriological methods indicated at p. 178.
The stools of typhoid in its later stages may be those of intestinal
ulceration. Thus, when hemorrhage results from the extension of
typhoid ulcers, the feeces will be blackened, and yield the chemical
reactions which denote the presence of a derivative of blood pigment
(hematin).
5. Dysentery.—The discharges of dysentery are subject to a great
variety of character ; but there is one respect in which they are constant,
for they always contain abundance of mucin, and in the author’s experi-
ence also some serum-albumin and much peptone.
Under the microscope there are to be seen great quantities of
leucocytes, intestinal epithelium, and fungi. Tolerably perfect red
blood-corpuscles are occasionally visible. The number of these latter
varies within broad limits, but the other microscopical appearances are
remarkably uniform.
The grosser properties of dysenteric stools, on the other hand,
display notable differences. Founded upon these, Heubner 1”? distin-
guishes :—
1. Mucous and muco-sanguineous discharge.—A pale yellow, viscous,
transparent substance tinged with blood, cohering in masses, with or
without admixture of feces.
2. Sanguineo-purulent discharge.—A reddish or yellow fluid, contain-
ing floceulent or solid particles as large as a pea or a bean. Such stools
may be compared to raw minced meat.
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DYSENTERY—CHOLERA. 209
3. Discharge of pure blood.—This oceurs when a vessel has been
opened by the extension of a dysenteric ulcer.
4. Discharge of pure pus.—This consists almost exclusively of leuco-
cytes, and belongs to the later stages of dysentery.
5. Gangrenous stools.—Such stools are brownish-red or brown-black
in colour, from the presence of altered pigment. They emit a putrid
odour. They indicate extensive gangrene of the intestinal mucous
membrane.
It was in dysentery that the stools were first noticed to contain those
mucous particles which have been compared to frog-spawn (see p. 166),
and which Nothnagel afterwards observed in other intestinal diseases.
They have no special clinical significance in this disease.
On the whole, it may be said that the naked-eye characters of dysen-
teric stools are so remarkable that they will ordinarily suffice to establish
a diagnosis without the aid of the microscope.
Amebe, which have lately been found in such stools, have been
credited with a causal relation to the disease (Hlava and Kartulis)."*
A similar importance is attached by others to a pathogenic fission-fungus
(Klebs, Chantemesse and Widal),° but with less reason.
6. Cholera.—During an epidemic of cholera, there is usually pre-
valent a form of diarrhcea which is distinct from that disease, and it is
of the utmost importance to possess the means of discriminating between
the two. The discharges of the less formidable complaint are not charac-
terised by any special changes ; but, in a doubtful case, the investigation
in the stools for cholera bacillus (as indicated at p. 173) may be needed
to establish the diagnosis.
In a pronounced case of Asiatic cholera, on the other hand, no kind
of ambiguity can exist. The discharges are thin, and devoid of smell
and colour. They have been aptly termed ‘“rice-water” stools. Micro-
scopically they abound in leucocytes and epithelium, and their specific
micro-organism, the comma-bacillus, may be readily detected. It must,
” stools are not by themselves
pathognomonic of cholera. They are seen repeatedly in heat-apoplexy
and arsenical poisoning ; and in such connection, as well as in cholera,
they hold a profusion of intestinal epithelium. It follows that the
diagnosis of Asiatic cholera will rest on an absolutely secure basis only
when the comma-bacillus has been found, separated from the stools,
and cultivated by the methods with which we are already familiar
(p. 174). Chemically, the discharges of cholera contain serum-albumin 17°
however, be borne in mind that “‘vice-water’
and much mucin.
7. Hemorrhagic Stools.—Blood is discharged with the stools in
cases of great venous congestion of the intestine, in typhoid, in tubercular
and dysenteric ulceration of the stomach or intestine, and in round
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210 THE FACES.
ulcer of the stomach or duodenum, ‘These cases are always attended
with symptoms of severe intestinal trouble. The blood is usually '
profoundly altered (p, 205); but when the hemorrhage has taken place
in the lower part of the alimentary canal, as the sigmoid flexure or
rectum, pure bright blood may be passed.
8. Acholic Stools.—The stools may he deficient in bile in cases of
jaundice from obstruction of the biliary ducts, or they may be so in the
absence of this condition.
’ They are characterised by (1) their whitish-grey colour, (2) the abun-
dance. of fat which they contain, and (3) a profusion of fat crystals,
probably soaps of soda, lime, and magnesia (fig. go).
Such stools in. connection with jaundice imply an obstruction to the
flow of bile by blocking of the ducts. When they occur independently
of obstruction, the underlying cause is not yet sufficiently understood.
Many theories have been framed to account for the phenomenon :—(1.)
It may be either that the bile pigment has undergone some change in
the intestine which prevents the formation of its metabolic product
(urobilin) ; or (2.) the secretion of bile may be so scanty that there is
not enough pigment for the elaboration of urobilin ; or (3.) it is possible
in such cases that the latter is replaced by certain colourless metabolites
of bilirubin (v. Nencki’s leucohypobilin). The latter view is supported
by the fact that considerable quantities of urobilin may be obtained
from acholic stools by extraction with acid alcohol (v. Jaksch, Pel,
Le Nobel)."" The stools may be devoid of bile in cases of the most
varied origin—as in tuberculosis of the intestine, chronic nephritis, and
chlorosis—where no trace of jaundice is present. They are commonly
so in the fatty discharges which accompany indigestion in children
(Biedert)."8 Berggriin and Katz" have observed acholic stools in
the chronic tubercular peritonitis of children. In these cases, as usual,
the feeces contained excess of fat. It follows, therefore, that we cannot
infer the character of the stools from the presence or absence of this
symptom. But in all cases where colourless stools concur with jaundice,
the cause is to be found, as has already been said, in obstruction of the
biliary passages.
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CHAPTER VII.
EXAMINATION OF THE URINE.
THE urine is the secretion of the kidneys.!* employs the albuminimeter to determine the proportion
of albumin in a urine. From another portion of the same urine he
precipitates globulins with magnesium sulphate, as Hammarsten does,
and again tests the “ globulin-free” urine with Esbach’s albuminimeter.
From the difference in the two results he infers the quantity of
globulins present. This plan is commended by its author, but the
process obviously partakes of the uncertainty which is inseparable from
the use of the albuminimeter.
It may be noticed that Huppert and Zdhor® have endeavoured to found a
quantitative method of estimating albumin upon the comparative specific gravity
of the urine. Its efficiency has not yet been sufficiently tested, but it may prove
to be of service clinically.
2. Peptonuria.—This condition has been invested with very great
interest since the discovery by Hofmeister! of a comparatively simple
chemical test for the detection of peptone.
So far as our present knowledge extends, the causes of peptonuria
are quite different from those to which the other forms of albuminuria
are due. Neither nephritis, circulatory disturbances, nor anemia, will
bring about the appearance of peptone in the urine. Its presence there
associated with such pro-
is most commonly—though not invariably
cesses as are characterised by the collection and subsequent destruction of
leucocytes under such circumstances that the products of disintegration,
including the peptone constituent, of these bodies can obtain admission
into the blood-stream, to be subsequently eliminated by the kidneys.
_ To the condition arising in this way the name Pyogenie peptonuria
has been given (Hofmeister, Maixner, v. Jaksch).7 Tt occurs chiefly
in the resolution stage of pneumonia, in purulent pleuritic exudation,
and, in general, in suppuration wherever situated, provided that the
conditions are favourable to the absorption of the constituents (peptone)
of the pus.
Peptone has further been found abundantly in the urine in purulent
meningitis, acute articular rheumatism, the suppuration of phthisis—-
briefly, in nearly all those states which are attended with the formation
and breaking down of pus.
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PEPTONURIA. 265
It follows, therefore, that the detection of peptone in the urine goes
far to warrant the inference that suppurative changes are in progress
in some part of the system, but such an inference must, in all cases, be
strengthened by the exclusion of the other known causes of peptonuria.
Amongst these are severe cases of scurvy, tending towards a fatal
termination (heematogenic peptonuria) (v. Jahisch).
Maixzner ®° has also shown that in ulceration of the intestine, peptone
derived from the food may pass directly into the blood through the
ulcerated parts, and so give rise to this condition (enterogenie peptonuria),
an observation confirmed indirectly by those of Pacanowshi.\8! A
number of cases have also been reported in which peptone found in the
urine was attributed to phosphorus poisoning ; and Jischel 18? has shown
that it is normally a constituent of the urine in the puerperal state
(puerperal peptonuria).
These facts are mentioned chiefly to show that peptonuria does not
always imply suppuration; but these other conditions being excluded,
it is a valuable diagnostic sign of that process. It is, moreover, avail-
able as a means of prognosis and of testing the progress of certain
diseases attended with the resolution of pus. Thus, when peptone is
found in the urine in the course of pneumonia, it indicates that the
stage of softening has begun. Again, in connection with abdominal
tumours or pleuritic \effusion, it shows their purulent character; and
in purulent meningitis its manifestation varies with the severity of the
disease—peptonuria occurring together with a relapse, and so on.
As a means of discriminating between tubercular and epidemic cere-
bro-spinal meningitis, the presence of peptone in the urine is occasion-
ally a fact of crucial significance. It is characteristic of the latter disease,
and its absence in presence of the clinical symptoms of meningitis in all
cases implies a tubercular character. Obviously, however, peptonuria
may arise accidentally in the course of tubercular meningitis ; and in
basing a diagnosis upon this condition, care must be taken to ascertain
that it is not due to ulcerative processes in other organs, and especially
to exclude implication of the lungs.
Again, in the condition which has been called “sepsis occulta,” and
which is commonly so difficult to recognise, peptonuria is an important
symptom. By its aid especially it will be possible to distinguish the
symptoms of septicemia from those of latent disseminated sarcoma,
which present quite a similar clinical character (high fever, rigors).
In acase which came under Prof. Nothnagel’s care, there had been rigors and
a high temperature maintained for a long period, and no other symptoms what-
ever. These were ascribed to the formation of a deep-seated abscess. ‘he urine
was repeatedly examined for peptone without result. The post-mortem showed
disseminated sarcomatous nodules.
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266 THE URINE.
The author has been engaged for many years in investigating the
subject of peptonuria, and he feels warranted in asserting that its
clinical value as a symptom is very great. It may be that further ex-
perience will extend and distribute its import; but there can be little
doubt that the significance attaching at present to the form with which
we are best acquainted—that of pyogenic peptonuria—will not diminish
with the progress of knowledge. Recent investigations tend in the
fullest manner to confirm this view.!%* Peptonuria is frequently met
with in connection with syphilis (PvenZ).15* Modern science furnishes
an adequate explanation in many instances where the condition is found ;
for, granting that micro-organisms have the property of changing albumin
into peptone, it is probable that they can also cause the latter to appear
in the urine (Mya, Belfanti).1*
Detection of Peptone.—The methods of Hofmeister and Devoto 186 will
be described here.
1. Hofmeister’s Method.—The urine should first be tested for albumin
by the three processes described above (pp. 255, 257). If tests 1 and 2
give no result, and no precipitate forms on the addition of acetic acid
alone, the presence of peptone may be shown by the biuret test (see p.
257), but. only when this body is in great abundance. If it is not so,
the result in this case will be also negative. A further preliminary test
may be applied by adding first concentrated acetic acid, and then a
muxture of acetic and phospho-tungstic acids. If clouding takes place
either directly or after the lapse of a short interval, it may be concluded
that peptone is present. The inference is rendered still more certain if,
before the application of the test, a little neutral acetate of lead be added
(to precipitate mucin), until a flocculent precipitate appears. If the
test again gives positive results, peptone is present ; if it remains nega-
tive, the urine is peptone-free. This, however, only holds good where
the urine contains a considerable amount of peptone.
Hofmeister’s test is more accurate. Assuming that the previous
methods have failed to disclose albumin, the urine is treated with
neutral acetate of lead and filtered. The clear filtrate, which should
amount to not less than 500 to 600 cc. in volume, is acidulated with
hydrochloric acid, and phospho-tungstic acid is added until a precipitate
ceases to form with it. The fluid is then filtered without delay.
Phospho-tungstic acid may be prepared thus :—Commercial tungstate of soda
is dissolved in boiling water and phosphoric acid added until the mixture exhibits
an acid reaction. _ It is then allowed to cool, rendered strongly acid with hydro-
chloric acid, and filtered after standing for twenty-four hours (Huppert).187
The precipitate consists of peptone combined with phospho-tungstic
acid, and various other substances (ptomaines, &c.). It is now washed
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DETECTION OF PEPTONE. 267
on the filter with five parts concentrated sulphuric acid in 100 of water,
until the fluid which passes through is colourless. In this way the salts
are got rid of. The precipitate, while still wet, is washed from the
filter with as little water as possible, and is received in a watch-glass.
Barium carbonate is added until the mixture is alkaline, and the latter
is then placed on a water-bath at boiling-point, and heated for ten to
fifteen minutes, and the biuret test (p. 257) applied. Peptone is shown
by the formation of a colour ranging from bluish-red to violet, and
varying in intensity according to the quantity present. If this be only
a trace, the resulting colour is of a dirty red or dull violet. The accom-
panying precipitate of baryta need not confuse the experiment; but
should any doubt exist as to its result, the entire preparation may be
placed in a test-tube and allowed to stand for a few minutes. The
precipitate then falls to the bottom, and the fluid displays the charac-
teristic tints—from dull red to violet—if it contains peptone. If that
body be absent, it has a greenish colour.
If either of the first two tests (p. 255) should show the presence of
albumin, whilst the addition of acetic acid and ferrocyanide of potas-
sium after filtration causes only very slight turbidity, the albumin must
be removed by combination with a metallic oxide—and best with
oxide of iron—in the following manner :—A solution, first of acetate of
soda and then of perchloride of iron, is added to the urine. This is
exactly neutralised with caustic potash, boiled, filtered, and allowed to
cool. Tests 1 and 2 are next applied. If neither discloses albumin, and
if also with test 2 no blue colour forms, thus showing that the fluid
is free from iron, the further process is that described above—hydro-
chloric acid is added, and a precipitate obtained by the use of phospho-
tungstic acid, and so on, as before.
If, however, after the precipitation of albumin in the manner indi-
cated, one of the tests alluded to should show that the fluid is not yet
free from that body, the previous tests must be repeated until the
filtrate exhibits no trace either of albumin or of iron. Should the former
substance be present in the urine in great quantity, it may be removed
in large proportion by heat, and what remains may be subsequently got
rid of in the manner described above.
The application of this method in the case of highly coloured albu-
min-free urine has the contingent advantage that it involves the
removal of colouring matters whose presence might be a source of
fallacy. J. A. Schulter 188 recommends that the urine be first saturated
with ammonium sulphate, and the filtrate proceeded with as before.
The quantitative estimation of peptone may be effected by the colori-
metric process of Hofmeister and Maixner.1®°
2. Devoto’s Method.—The difficulties attending the application of
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268 THE URINE.
Hofmeister’s method are a serious impediment to its use. That of
Devoto, which will now be described, is at once simple, expeditious,
and efficient.
The two tests have given identical results when the author has employed
them for the investigation of urine. When, however, they were applied to the
examination of the blood and the viscera, there was less conformity between
them, Hofmeister’s usually indicating peptone where Devoto’s failed to do so.’?!
To 2c0-300 cc. of urine is added pure crystalline ammonium sulphate
in the proportion of 80 grms. to 100 ce., and the fluid is placed in a
beaker in a boiling water-bath for half-an-hour, at the end of which the
greater part of the salt should have dissolved. It is then steamed for
half-an-hour in a Budenberg’s steam-steriliser, the vapour being kept at
100° ©. In this way all the proteids (serum-albumin, globulin, hemo-
globin, deutero-albumose, peptone, nucleo-albumin) are precipitated, but
only serum-albumin, globulin, and nucleo-albumin (mucin) are thoroughly
(and hemoglobin partly) coagulated. The fluid having been heated to
100° C. is at once filtered. The filtrate should be straw-coloured, and
free from albumin, as indicated by tests 1 and 2, p. 255. A slight
cloudiness appearing quickly with test 2 does not necessarily imply the
presence of albumin. A decided turbidity or a precipitate would be due
to a proto-albumose, or more probably hetero-albumose. Should the hot
filtrate be cloudy, or give the proteid reactions (pp. 255, 257), the investi-
gation has miscarried, and must be repeated from the beginning. The
residue on the filter is washed first with hot and then with cold water.
The resulting filtrates have a more or less decided brownish tint. These
are collected, and to one portion of the fluid acetic acid and ferrocyanide
of potassium are added to test for albumin. Should no result be
obtained, the biuret test is performed with a portion to which caustic
soda has been added in excess. Any albumin shown to be present is
certainly peptone. The filtrate from the hot washings may exhibit it,
but it often happens that peptone first becomes recognisable with the
biuret test in the filtrate derived from the cold washings. Several
specimens both of the hot and cold washings may be tested until a
positive result is obtained.
[<. Martin! has found that in many cases of supposed peptonuria—especially
of peptonuria in connection with purulent disease—the morbid constituent of
the urine was deutero-albumose and not peptone. The two are distinguished
by their behaviour in solutions with ammonium sulphate; deutero-albumose is
precipitated by saturation with this salt, while peptone is not.
Macwilliam + recommends salicyl-sulphonic acid as a test for albumoses and
peptone. Primary albwmoses are precipitated by a saturated watery solution of
the acid; the precipitate disappears with heat, and reappears when the liquid
cools. Deutero-albumose is precipitated by the reagent when the fluid examined
is mixed with two to three times its bulk of a saturated solution of ammonium
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ALBUMOSURIA. 269
sulphate. Peptone is readily precipitated by salicyl-sulphonic acid in saturated
ammonium-sulphate solutions, and the precipitate clears up on heating, and
reappears when the liquid cools. The peptone precipitate is dissolved by the
addition of water, glycerine, or excess of the reagent. ]
3. Albumosuria.—The distinctive character of this condition was
formerly thought to be the presence in the urine of a single body, to
which the name of propeptone or hemialbumose had been given. The
researches of modern times, however (Kiihne, Chittenden, Herth1*),
have placed the matter in a new light, and the first two observers have
sought to show that propeptone is really a mixture of four different
proteids. However this may be, these interesting observations cannot
as yet be brought to bear upon our clinical knowledge.
Albumose has been found in the urine in connection with various
diseases—as osteomalacia, dermatitis, intestinal ulcer, &c. (Senator, Ter
Gregoriantz, v. Jaksch).! In severe cases of osteomalacia, which were
recently under treatment by Professor Nothnagel, v. Helly, and Schauta,
the author failed to discover albumosuria ; neither has he detected it in
advanced rickets.
Loeb’ believes that he has discovered propeptone in the urine in
measles and scarlatina (in this he is confirmed by Heller 1%"), and from
the observations of Kahler and Huppert® albumosuria would seem
to be a frequent occurrence in inflammation of the medulla of bones.
Koppner™® has observed albumosuria in mental derangement. The
clinical significance of this state is modified by the fact that Posner
has detected propeptone in the seminal fluid (see Chapter IX.). The
presence of albumose, when it occurs alone, may be determined by the
consideration of results derived from the tests given for the detection
of albumin generally. If, on the application of tests, a precipitate first
forms on cooling the specimen, or when it has been allowed to stand for
a long time (vide supra), and if this precipitate, when separated on the
filter, is shown by the biuret test to consist of albumin, a fresh specimen
of the urine may be submitted to test 2. In doing this, it may be
necessary to add water, since albumose is readily soluble in concentrated
salt solutions, and therefore in concentrated urine. Whether with or
without this precaution, a further precipitate with test 2 suggests the
presence of albumose. Another specimen should now be saturated with
common salt, and further treated with acetic acid. If albumose be
present, a precipitate forms, which, after the addition of a large amount
of acetic acid, dissolves when heated and reappears on cooling. A
nitrogenous body resembling albumose was found by Thormdhlen*° in
the urine in a case of hydatids of the liver, with jaundice and
nephritis.
When the urine holds albumose in conjunction with serum-albumin,
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270 THE URINE.
the latter must be removed by boiling with acetic acid and chloride of
sodium before the tests are applied.?0?
4. Globulinuria.—Globulin probably never, or almost never, occurs
alone in the urine, but generally in conjunction with serum-albumin.
Consequently its import in disease is the same as that of the latter body.
{Serum-albumin is usually present in greater quantity, but in severe
organic renal disease and in diabetes Maguire 2” finds that the proportion
of globulin to albumin is often 2.5: 1. Senator? asserts that more
globulin is present in lardaceous kidney than in other forms of Bright’s
disease. ]
To Kauder?% belongs the credit of discovering a simple method for
the detection of this body in presence of serum-albumin. The urine is
rendered alkaline with ammonia, allowed to stand for an hour, then
filtered, and to the filtrate is added its own volume of a saturated solu-
tion of sulphate of ammonium. If globulin be present in any quantity,
a flocculent precipitate falls.
By an extension of this method the quantitative estimation of globulin
may be effected. With this object the precipitate formed is treated in
the manner described before when speaking of the estimation of albumin
by weight (p. 259), (Pohd).?°
[Halliburton ?°" adopts the following method :—The urine is neutral-
ised and then saturated with magnesium-sulphate. If globulin be pre-
sent, a precipitate forms. This precipitate may be collected on a filter
and dissolved by the addition of water. The solution coagulates at
75°C. When the urine holds a large quantity of globulin, Si William
Roberts’ test will serve for its recognition :—A deep glass vessel is filled
with water and the urine is added, a drop at a time. Each drop leaves
a milky track behind it, and when much urine has been added, the fluid
becomes opalescent, and clears again on the addition of acetic acid. ]
5. Fibrinuria.—Fibrin is found in the urine in cases of hematuria
and chyluria (v. infra). It then usually forms coagula. It is found,
moreover, as a consequence of inflammatory exudation in the urinary
passages. The coagula occur most commonly in croup and diphtheria,
and occasionally in tuberculosis.
To detect fibrin the clots should be separated by filtration, washed
with water, dissolved by boiling in solution (1 per cent.) of soda or
(5 per cent.) hydrochloric acid (Huppert °S), and the fluid tested when
cold by the process described on p. 256.
6. Hematuria.—The blood which occurs in the urine may be derived
from several sources, from the kidney, renal pelvis, ureters, bladder, or
urethra (see p. 218).
In well-marked cases, the presence of blood is directly suggested by
the colour of the urine, which varies from that of an extract of raw
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HAMATURIA—H AMOGLOBINURIA. 271
meat to a ruby-red ; but inasmuch as a similar appearance may be due
to hemoglobin in solution (hemoglobinuria), it is never safe to base
the diagnosis of this condition upon inspection alone. It may be
accurately determined by—
1. Spectroscopic Examination.—The freshly-passed urine, which, if
deeply coloured, should be diluted with water, will exhibit the two
absorption-bands of oxyhemoglobin (p. 60, fig. 37), and these, on the
addition of sulphide of ammonium, give place to the absorption-band
of reduced hemoglobin. Lastly, when blood containing urine has stood
for some time, occasionally even in fresh urine, the spectrum of methe-
moglobin may be looked for (p. 62, fig. 42).
2. Heller's Test.2°°—The urine is treated with caustic potash and
boiled. The (basic) earthy phosphates are then precipitated, and to-
gether with them the hematin derived from the oxyhemoglobin present.
The phosphatic sediment is consequently coloured a bright red. Should
it happen that the urine contains abundance of colouring matter (bile-
pigment, &c.), which renders it difficult to appreciate the colour of the
sediment, the latter should be separated on a filter and dissolved in
acetic acid. The solution then becomes red if blood be present, and its
colour vanishes gradually on exposure to the air.?!°
Rosenthal” applies the test for hemin directly to the dried preci-
pitate (see p. 61). Struve’s 2!" method serves well for the detection of
blood-pigment. The urine is treated with ammonia or caustic potash,
and the fluid then rendered acid with tannic and acetic acids. The
presence of blood is shown by a dark-coloured precipitate, which, when
dried and treated with a little chloride of ammonium and glacial acetic
acid, should yield Teichmann’s crystals. This test is very sensitive, but
less practicable than Heller’s, which, with the spectroscopic examination,
best meets the requirements of the physician.
3. Almén’s Blood Test.?\°—A mixture in equal parts of tincture of
guaiacum and mature oil of turpentine is poured on the surface of about
ro cc. of the urine. The presence of blood is shown by the appearance
at the junction of the fluids of a ring at first white and afterwards
turning blue.
If, in addition, the microscope reveals the presence of red blood-
corpuscles (p. 218), the existence of hematuria may be inferred, and
it only remains to judge of its origin on the principles already laid.
down. For its clinical significance the reader may refer to p. 219.
7. Hemoglobinuria.—Sometimes the colouring-matter of the blood
is also found dissolved in the urine (see p. 65). This condition is
apt to arise in the course of acute infectious diseases, in burns, and in
various forms of poisoning. In the latter class of cases it is always
a serious, and even ominous symptom. It has been observed in poison-
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272 THE URINE.
ing by naphthol? and carbolic acid,?!® and in erysipelas.?4° Hemo-
globinuria is known as an idiopathic affection?!" (paroxysmal hemo-
globinuria), and as such often occurs in connection with severe syphilis,
[and also in malaria and rheumatism, when the attacks appear to be
determined by exposure to cold (Zaylor)].?8
The occurrence of hemoglobinuria may be inferred when it is made
evident by spectroscopic analysis and the application of Heller’s and
Almén’s tests that the urine contains blood colouring-matter, whilst at
the same time the microscope discloses smaller or larger masses of brown
pigment, and either no red corpuscles, or so few as are inadequate to
account for the results obtained. The spectroscopic appearances are
usually those of methemoglobin (p. 62, fig. 42); and Hoppe-Seyler 1
maintains that in this condition the blood-pigment is always in the form
of methemoglobin.”° [In seven cases of paroxysmal hemoglobinuria
investigated by Halliburton,??! methemoglobin was the only pigment
present in three. In the remaining four there was found only methemo-
globin at first, but in a few hours the amount of pigment increased, and
oxyhemoglobin appeared as well. In such a specimen the spectra of
methemoglobin and of oxyhemoglobin occur together. In three of
Halliburton’s cases serum-albumin was present in the beginning of the
attack, and in one its appearance preceded that of the blood-pigment.
Albuminuria has been observed to alternate with hemoglobinuria, and
Fragge has described a paroxysmal albuminuria which he believed to be
a mild form of the latter (see p. 252)].
8. Mucinuria (Nucleo-Albuminuria).—The presence of small quan-
tities of nucleo-albumin (mucin) 7? in the urine is not a pathological
symptom ; when found in greatly increased proportion in women, it is
often derived from the vagina. Such an increase, originating in the
urinary passages, invariably points to catarrh of those parts. The urine
in question is usually turbid when passed, and after a little while it
deposits a bulky cloud. The latter is seen by the microscope to contain
leucocytes and epithelium (p. 218). When a great quantity of mucin
is passed, it forms a viscid gelatinous sediment at the bottom of the
urine-elass, and no further evidence of its character is needed.
For the detection of mucin chemically, the urine is treated with an
excess of acetic acid, when it is rendered turbid if much mucin is
present. It may be necessary to dilute it previously, since concentrated
urine, being rich in salts, will retain mucin in solution even in presence
of acetic acid. In testing for the presence of mucin in albuminous
urine, the great bulk of the albumin should be removed by boiling and
filtering previously, and the filtrate allowed to cool.
The best method for precipitating mucin from urine is by the addition
of acetate of lead (vide supra).
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CARBOHYDRATES—GLYCOSURIA. 273
Fr, Miiller ??5 found mucin very abundantly present in the urine of
leukemia. Obermayer 224 maintains that it is invariably to be met with
in jaundice.
II. Carbohydrates.
1. Glycosuria.—Although various forms of sugar are occasional con-
stituents of the urine, as, ¢.g., sugar of milk after parturition, and inosite
and levulose rarely, the consideration of these will nevertheless hardly
detain us, since their manifestation, from the point of view of frequency
and importance, possesses but little practical interest in comparison with
that of the hexose 2” orape-sugar (glucose, glycose, dextrose). Our re-
marks here will be confined to the occurrence and tests for the latter
body.
(a.) Physiological Glycosuria.—It must be mentioned at the outset
that normal urine contains a trace of sugar. The fact of a physio-
logical glycosuria was long ago laid down by v. Briicke,?”" and has
quite recently derived remarkable confirmation.22° Wedenskv has made
use of Baumann’s discovery that benzoyl chloride forms insoluble
compounds with the carbohydrates ; and applying this to healthy urine,
he succeeded in separating from the precipitate a body which gave all
the reactions of grape-sugar. The proportion to be found in health,
however, is so small, that it may be neglected as a disturbing factor,
even in the most sensitive of the tests to be described. [According to
Dr. G. Johnson 7 normal urine is quite free from sugar; and Mr. G. 8.
Johnson ?8 has shown that when all the uric acid and kreatinin have
been removed from such urine by precipitation with mercuric chloride,
all reducing action disappears and no trace of sugar can be found. ]
(b.) Pathological Glycosuria.
(a.) Transitory Glycosuria.—Grape-sugar may appear temporarily in
the urine in the course of many diseases, as cholera, intermittent fever,?29
[typhus and typhoid], cerebro-spinal meningitis, and scarlatina,™° [after
attacks of whooping-cough, asthma, and epilepsy (Taylor) 2°], in affec-
tions of the brain involving the fourth ventricle, in diseases of the heart,
liver, and lungs, in gout, and in tertiary syphilis (Ord).?°! It has also
been occasionally observed in small quantities in cirrhosis of the liver.
Glycosuria in connection with these diseases is, however, very rare. It
is commoner as an effect of certain poisons, notably morphia and carbon
monoxide [after the inhalation of chloroform, ether, and amy] nitrite, and
in poisoning with prussic acid, mercury, and curare. In some of these
cases, however (morphia, curare, chloroform, &c.), it has been shown
that the substance which reduces Fehling’s solution in the urine is not
sugar, but glycuronic acid (Halliburton) ?**], The author has found
grape-sugar in the urine in two cases of advanced asphyxia from breath-
ing irrespirable gases (a mixture of carbonic acid and nitrogen).?°*
Ss
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BPA THE URINE.
In certain diseases the function of sugar-assimilation is depressed
(Hofmeister), and when that substance is taken as food, it appears tem-
porarily in the urine. This happens especially in hepatic cirrhosis
(Moritz, Kraus, Ludwig 4), and in brain disease (v. Jaksch).
(8.) Persistent Glycosuria.—The continued excretion of grape-sugar in
appreciable quantities belongs exclusively to diabetes mellitus, and it is
the most certain symptom of that disease. Its great clinical importance
lies in the fact that it ordinarily becomes apparent at a time when all
other symptoms of diabetes are wanting. In such cases, however, one
can be certain that diabetes exists only when, by repeated investigation,
grape-sugar is found, and especially when its quantity is observed to
increase with the administration of other carbohydrates, as cane-sugar,?”
and still better, starch.
Determination of Grape-Sugar.
(«.) Qualitative Tests.—It is very easy to determine the presence
of a considerable proportion of sugar in the urine ; but sometimes, when
that body occurs only in traces or in very small quantity, the tests
hitherto most commonly employed, namely, those of Moore and Trommer,
are hardly sufficient for its detection. We have only recently become
acquainted with a method which is in all cases adequate to the purpose.
1. Moore-Heller Test.?°>—The urine is treated with liquor potasse
and boiled. If sugar be present, it is decomposed. Lactic acid and a
number of volatile compounds are formed,27 and with them certain
coloured substances, which impart an intense deep-brown tint to the
fluid. This test is by no means accurate, and conclusions drawn from
it are open to fallacy, since healthy urine turns brown with caustic
potash from the action of that body upon mucin (nucleo-albumin).
Moreover, the change of colour is proportional to the quantity of mucin
present, independently of sugar.
2. Trommer’s Test.°8—The urine is rendered alkaline with caustic
potash, and a fairly strong solution of cupric sulphate is added, drop
by drop, until the cupric oxide formed ceases to be dissolved. The
mixture is then heated in a test-tube. If sugar be present in greater
quantity than a mere trace, a yellowish or red precipitate of the sub-
oxide of copper falls before the boiling-point is reached, and at the
same time the fluid loses colour somewhat.?8® This test is very sensitive.
Trommer was able with it to detect sugar to the amount of 0.001, or
even o.ooor per cent. Unfortunately it is also ambiguous. The pyro-
perty of reducing cupric oxide in alkaline solutions belongs to a number
of bodies which occur in healthy and morbid urine. Amiongst these are
uric acid, kreatin and kreatinin, allantoin, mucin, milk-sugar, pyroca-
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GLYCOSURIA—TESTS FOR SUGAR. 275
techin, hydrochinon, and bile-pigments. In addition to these, the
ingestion of benzoic and salicylic acids, glycerine, and chloral leads to
the formation in the system of substances which possess a similar
reducing power. Hence it happens that the urine is sometimes thought
to contain sugar on the evidence of Trommer’s test when none can be
found with other methods. The error is especially apt to arise when
the boiling is continued for a long time. The test can be depended on,
therefore, only when reduction takes place at a temperature belov boiling,
which, however, occurs only when the urine contains a relatively large
proportion of sugar.
Lehling’s fluid (p. 281) may be substituted for the copper sulphate
and caustic potash in the process. [ Pavy’s 4° fluid, which is much used
in England, is a modification of Fehling’s. It has the following consti-
tution :—(i.) neutral potassic tartrate 640 grs., potassa fusa 1280 grs.,
water ro 0z.; (ii) cupric sulphate 320 grs., water 10 oz. The two
solutions are kept apart and mixed for use. Of the mixture 40 to 60
minims are boiled in a test-tube, and a drop or two of the suspected
urine is added. If heat be continued, the yellow precipitate shows
itself in the upper part of the test-tube, and by adding more urine the
fluid will be made to lose its blue colour entirely. |
A useful modification of Trommer’s test has been suggested by Worm-
Miller. A mixture is made of 1.5 cc. of a 2.5 per cent. solution of
cupric sulphate, and 2.5 ec. of an alkaline solution of tartrated soda
and potash (prepared by dissolving 100 grms. of Rochelle salts in a
normal solution of caustic soda), and heated to boiling-point ; and in a
separate test-tube 5 cc. of the urine to be tested are boiled. The boil-
ing fluids are added together without shaking them, and if sugar be
present in any quantity, the suboxide is precipitated directly. Should
no such precipitate form, the process is repeated with 2, 3, or 4 ce. of
the cupric sulphate solution. This test is said to be very sensitive.
It should be mentioned that the power of a urine to dissolve cupric
oxide does not necessarily imply the presence of sugar in the urine, since
the property belongs to ammoniacal and albuminous urine, whether it
contains sugar or not.
3. Fermentation Test.—This depends upon the fact that grape-sugar
decomposes in presence of yeast into alcohol, carbonic acid, and a number
of other products (succinic acid, glycerine). It is conducted in the
following manner :—A test-tube is filled for two-thirds of its depth
with mercury, and in the remaining third with the urine, to which a
little tartaric acid has been added. In this is placed some yeast which
has been carefully washed. The mouth of the test-tube is then closed
with the thumb, and it is inverted over a vessel containing mercury.
If sugar be present, fermentation takes place directly, and the carbonic
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276 _ THE URINE.
acid formed collects over the mercury. When yeast is placed in normal
urine a limited fermentation takes place and some gas is disengaged.
It is, therefore, well to compare the result of fermentation in saccharine
urine with a healthy specimen (Moritz?#). There are special fermenta-
tion tubes made for such purposes, and the experiment is greatly facili-
tated by their use.22 This test is sufficiently sensitive. It will serve
to indicate o.1 per cent. of sugar in the urine.”4+ [According to Halli-
burton,2% the fermentation-test is the best for distinguishing sugar from
other substances that reduce Fehling’s solution in the urine. These
substances are uric acid, hippuric acid, kreatinin, pyrocatechin, and
glycuronic acid. ]
4. Phenyl-Hydrazin Test.—In this we have a method for the detec-
tion of sugar which is greatly to be preferred to those already mentioned.
Fic. 127.—Phenyl-Glucosazon Crystals, from Diabetic,Urine (eye-piece II., objective 8a, Reichert).
Several years’ experience has convinced the author that it is entirely
accurate, simple in its application, and in every way suited to the needs
of the physician. It depends upon the property of phenyl-hydrazin to
form with grape-sugar a highly-characteristic crystalline compound,™®
called phenyl-glucosazon. This body has the form of yellow needles,
and is but little soluble in water. The test is conducted in the follow-
ing manner (v. Jaksch **"):—Two parts of hydrochlorate of phenyl-
hydrazin * and three of acetate of soda are placed together in a test-
tube containing 6-8 cc. of urine. If the salts do not dissolve when the
fluid is warmed, a little water is added, and the test-tube containing the
mixture is placed for 20-30 minutes in boiling water. After this it is
taken out and put into a vessel containing cold water. If sugar -be
* Twice as much of the phenyi-hydrazin salt as will lie on the point of the blade
of a knife.
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PHENYL-HYDRAZIN—BOTTGER'S TEST. 277
present, even in very moderate quantity, there forms directly a yellow
crystalline deposit, which may appear amorphous to the naked eye, but
which when examined under the microscope is seen to contain yellow
needles detached or arranged in clusters (fig. 127). If the urine holds
but a very small proportion of sugar, the preparation should be placed
in a conical glass, and the sediment examined carefully. In a case
where only a mere trace of sugar exists, detached crystals of phenyl-
glucosazon cannot fail to be seen. The discovery of smaller and larger
yellow scales, or of powerfully refracting brown granules, must not, how-
ever, be mistaken for evidence of sugar. This test gives very good
results with every variety of morbid urine,”4§ and it is equally applicable
whether albumin be present or not. In the former case, however, it is
well to get rid of the excess of albumin previously by boiling. Phenyl-
glucosazon crystals melt at 205°, and their character may be ascertained
beyond doubt by submitting them to that temperature. The efficiency
and utility of this test is amply proved.249 The objections to its use
made by Geyer, Moritz, and Luther*™® seem to be without weight.
Doubtless the test requires much practice, but in expert hands highly
satisfactory results are obtained.”°!
In addition to the foregoing methods, which especially merit atten-
tion, other tests for sugar have been suggested, and some of these call
for description.
5. Bottger’s Test.%’—A quantity of the urine is mixed with its own
bulk of a concentrated solution of carbonate of soda, and a little basic
nitrate of bismuth is added. The preparation is then boiled. If sugar
be present, it turns black from the reduction of oxide of bismuth.
This process has no advantage which does not belong to Trommer’s
test, and it is less sensitive. If the urine contains the principles of
rhubarb taken as food, a black precipitate will fall independently
of sugar.*? In albuminous urine, too, sulphide of bismuth will
form a similar black deposit.%+ These conditions must therefore be
excluded.
The modification of Bdttger’s test by Nylander ?? is more accurate.
The reagent employed (called Almén’s fluid) is prepared by dissolving
4 grms. of Rochelle salts (tartrated soda and potash) in roo grms.
and of an 8 per cent. solution of caustic soda, warming the fluid,
adding as much basic pernitrate of bismuth as will remain in solu-
tion. The mixture so formed is added to the urine to be tested in
the proportion of 1 in 11, and the whole is then heated. The fluid
should blacken in the course of a few minutes. In this way it is
asserted “6 that sugar in the proportion of o.1 per cent. can be
detected. It has, moreover, the advantage of simplicity, but is also
open to certain fallacies. It is inapplicable, as we have seen, to the
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278 THE URINE.
case of albuminous urine, and the reaction occurs in presence of
melanin or melanogen, or where the fluid contains a large proportion
of reducing substances but no sugar.
6. Rubner’s Test.25'—The urine is treated with an excess of acetate of
lead (sugar of lead), filtered, and to the filtrate ammonia is added until
a permanent precipitate forms. The fluid is then heated, but not boiled.
If sugar be present, the precipitate formed on the addition of ammonia
gradually assumes a rose-red colour, which vanishes slowly on standing,
more quickly on the application of heat (60°-70° C.), giving place to a
yellowish-coffee colour.
Rubner believes that the precipitate consists of sugar of lead. Milk-
sugar does not give this reaction when the process is conducted as above,
but when a solution of that body is boiled for 3-4 minutes with acetate
of lead, and ammonia then added, a similar precipitate forms. In the
author’s experience, the best plan in performing the test is to heat the
precipitate gradually at a temperature not exceeding 80° C. By its use
Penzoldt has discovered sugar to the amount of o.o1—o.02 grm. in Io cc.
of urine. That writer employs a very simple and practical modification
of Rubner’s test.2°> He adds to the urine a few drops of basic acetate
of lead (subacetate) and a few of ammonia, and then warms the mixture.
The presence of sugar causes a red precipitate as before. This method
is not less sensitive than the other.
7. Mulder’s Test.—'the urine is treated with carbonate of soda in solution, and
solution of indigo-carmine is added until the whole is freely coloured. If sugar
be present, the colour changes to yellow on heating, and becomes again blue
when the fluid is shaken up with air.
This test may be conveniently applied thus :7°—Two pieces of filter-paper are
taken. One is placed in a concentrated solution of carbonate of soda, and the
other in a solution of indigo-carmine. Both are then dried. When wanted for
use, a small piece of the indigo-carmine paper is placed in about 10 cc. of water,
the urine under examination is added, and finally a large slip of the paper satu-
rated with carbonate of soda is placed in the fluid. ‘The result should be as
above. ‘The convenience of its application in this manner is the only merit of
Mulder’s test. It is neither sensitive nor accurate. [Dr. G. Oliver? recom-
mends the use of indigo-carmine papers alone. The test solution is made from
these with heat, and is again boiled with the urine. The colour obtained ranges
from violet to straw-yellow, according to the quantity of sugar present. This is
not a satisfactory test.]
8. Johnson’s Test (Picric Acid).—Both Johnson and Thiéry*®! have employed
picric acid as a test for sugar. A few drops of a solution of picric acid are added
to the urine, which is then treated with caustic potash. If sugar be present,
the fluid assumes a ceep-red colour ; but a red colour may also be obtained from
caustic potash and picric acid alone, or in presence of kreatinin; and conse-
quently, as a test for sugar, the process is not trustworthy.°* [Dr. G. Johnson
claims for picric acid the advantage that solutions do not change with keeping.
When a drachm of normal urine is boiled with the same quantity of picric acid
and half a drachm of caustic potash, a claret-red colour is produced, which in
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TESTS FOR SUGAR. 279
a test-tube of half-inch diameter will transmit light. This colour is due to
kreatinin. he presence of the smallest quantity of glucose in addition will
render the fluid so intensely dark that no light passes through.]
9. Penzoldt’s Test.?3_In this the reagent is diazobenzol-sulphonic acid dis-
solved in water, 1 : 60, without the aid of heat, but a drop of caustic potash may
be added to facilitate solution. A few cubic centimetres of the urine under
examination is placed in a test-glass, and rendered strongly alkaline with caustic
potash. A like quantity of the reagent, which should be feebly alkaline, is now
added. The process is repeated with healthy urine of the same tint and concen-
tration, and the two specimens compared. Both are at first of a reddish-yellow
colour, but whilst the healthy specimen remains unchanged, or nearly so, that
containing sugar becomes a bright claret-colour after some time. If sugar be
present in abundance, the fluid eventually becomes dark-red and opaque.
Penzoldt asserts that 0.1 per cent. sugar is appreciable in this way; but for
practical purposes the test is not to be recommended, since acetone and diacetic
acid have a similar reaction.**4 Moreover, the substance used is highly explo-
sive,265
10, Molisch’s Reactions.—Molisch -®§ has recently devised two methods, by the
aid of which he believes that sugar can be detected in the urine, whether of
health or disease.
(a.) The first depends upon the reaction of sugar with a-naphthol and sulphuric
acid. To obtain this, he takes 4 to 1 cc. of the fluid containing sugar—urine
should be highly diluted for the purpose—places it in a test-tube, and adds to it
two drops of a 15-20 per cent. alcoholic solution of a-naphthol. The fluid
becomes turbid from the precipitation of some of the a-naphthol. Concentrated
sulphuric acid is now added in excess, and the whole is well mixed. ‘he pre-
sence of sugar is shown by the transitory appearance of a blue colour, and the
formation of a violet-blue precipitate on the subsequent addition of water.
(b.) This reaction is obtained with thymol and sulphuric acid. The urine
which is thought to contain sugar is highly diluted, and to 4-1 ce. in a test-tube
is added first two drops of a 15-20 per cent. alcoholic solution of thymol, and
then sulphuric acid in excess. When the mixture is shaken, the momentary
development of a “cinnabar-ruby-carmine red” discloses the presence of sugar,
this colour giving place to carmine when the fluid is diluted with water.
By this method Molisch maintains that so small a proportion as 0.00001 per
cent. of sugar can be detected. Similar reactions, however, may be obtained
with cane-sugar, fruit-sugar, and maltose. Secgen**’ has further investigated
the subject, and found that chemically-pure solutions of proteids, and especially
of serum-albumin, behave in like manner. The author has repeatedly performed
the test with albuminous urine, with the result that the a-naphthol reaction was
obtained when the fluid was diluted in a much higher degree than that (1 : 100)
recommended by Molisch in the case of sugar. In presence of albumin, the dark-
violet coloration of the fluid was followed by the deposition of a greenish-black
precipitate. The thymol and sulphuric acid reaction with this body was almost
identical with that displayed by sugar.
For these reasons, Molisch’s reactions, which no doubt find a valuable applica-
tion in vegetable physiology, are not to be recommended as a test of glycosuria.
The researches of Mylius and v. Udransky*° have made it clear that Molisch’s
reaction is identical with the furfurol reaction, which takes place not only with
sugar, but with any carbohydrate.
It remains to mention that experiments have been instituted by
several investigators (v. Briicke, Seegen, Abeles, Salkowski®) with the
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280 THE URINE.
object of separating the sugar when it exists in very small quantities in
the urine, and submitting it in the concentrated form to the action of
Trommer’s and other tests.
The separation and detection of grape-sugar, as of the carbohydrates
generally, may he effected by the action of benzoyl chloride, which with
the carbohydrates forms insoluble benzoic acid ethers. For this pur-
pose the urine is treated with benzoyl chloride and caustic potash. If
to a litre of urine there be added 200 ce. of a 10 per cent. soda solution
and ro cc. of benzoyl chloride, the nauseous smell of the latter disappears
on shaking the mixture, and a precipitate results. The addition of
concentrated sulphuric acid and a few drops of an alcoholic solution of
«-naphthol causes an intense red colour if a trace of a benzoyl combi-
nation with the carbohydrate be present, and the coloured fluid will
exhibit a well-defined absorption-band in the green part of the
spectrum. 7?
It is indispensable that both the sulphuric acid and the naphthol
solution should be absolutely pure. To ascertain that they are so, a
ro per cent. solution of «-naphthol in chloroform is prepared, and to a
drop of this in a test-glass is added first 0.5 cc. of water, and then 1 ce.
of pure sulphuric acid. If the reagents are serviceable, the mixture
assumes a yellow tinge. A little is next added to the fluid to be investi-
gated,—.e., to a benzoic acid ether precipitate suspended in water. A
reddish-violet ring is evidence of sugar or a carbohydrate (Luther,
Roos).2 This proceeding, though simple, is open to fallacy, since many
other substances, as albumin, fats, &c., form acid ethers with benzoyl
chloride. In other words, it is a form of the furfurol reaction, and
partakes of its ambiguous character. The necessity of securing abso-
lutely pure reagents is a further disadvantage which detracts from its
value as a clinical test.
(8.) Quantitative Estimation of Grape-Sugar.
1. Titration Method (Fehling).?"°-—The principle upon which this
method is founded depends upon the property which grape-sugar pos-
sesses of reducing cupric oxide to its suboxide in alkaline solutions. It
has been applied in various ways, and most of these are to be found
described in the text-books of urinary chemistry. Fehling’s process has
hitherto been chiefly in vogue, but, in common with most of the others,
it is tedious and difficult, and consequently but little suited to the
requirements of the physician. At once the simplest and most satis-
factory mode of procedure is that adopted by Leube and Salkowski.2°
An opinion is first formed from the density of the urine as to the
quantity of sugar which it probably contains. It is then diluted to
such an extent that this shall not exceed 0.5 per cent. of the entire
fluid—6-1o times its volume of water may be needed for the purpose.2”4
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ESTIMATION OF GRAPE-SUGAR. 281
The diluted urine is placed in a burette. Ten ce. of Fehling’s solution
are measured into a white porcelain capsule, 40 cc. of water added,
and the bluish mixture heated until it begins to boil. The diluted
urine is now slowly added, and a precipitate of suboxide (red) or
its hydrate (yellow) falls, whilst the fluid loses its blue colour. It
is important to ascertain the precise point at which this colour has
disappeared entirely, showing that the fluid no longer contains free
sugar. When this is reached, 1 cc. of the fluid is taken and filtered
through thick filter-paper. The filtrate, which should be quite clear,
is acidified with acetie acid, and a little ferrocyanide of potassium
is added. The presence of copper will be shown by a brown colour,
and 0.5-1 cc. of the diluted urine must then be added until the brown
colouration no longer takes place. On the other hand, should it happen
that the fluid when tested is seen to be free from copper, the whole
process must be repeated with a smaller quantity of urine. Finally,
when, as sometimes happens, suboxide of copper is not precipitated,
and passes through with the filtrate, the experiment is entirely frus-
trated. When these points have been attended to, the process is
repeated, that quantity of urine being taken at the outset which was
found to be requisite. A calculation is then made by multiplying the
number which expresses the dilution (in volumes) of the urine by 5
(10 cc. of Fehling’s fluid correspond to 0.05 grm. sugar), and dividing
the product by the number of cc. of diluted urine employed. The
result is the percentage of sugar in the original urine. Salkowshki 2
has suggested that the cuprous oxide formed should also be weighed.
And Munk.?"6 recommends that a few drops of a 15.8 per cent. solution
of chloride of calcium be added to the mixture of urine and Fehling’s
solution, to promote the precipitation of the copper salt.
Fehling’s fluid is prepared as follows :—(1.) 34.639 grms. of pure crystalline
cuprous sulphate are weighed out and dissolved in water with the aid of a little
heat, water is then added to 500 cc., and the whole placed in a tightly-stoppered
flask. (2.) 175 grms. of Rochelle salts (potassium and sodium tartrate) and 100
cc. of caustic soda of 1.34 sp. gr. are dissolved in 500 cc. of water, and well
mixed, and also placed in a well-stoppered bottle.
When required for use, equal parts of these solutions are measured with a
pipette, and the mixture constitutes Fehling’s fluid.
[Mr. Martindale recommends the following formula :—(1.) Sulphate of copper,
181 grains; distilled water to 6 ounces. Dissolve. (2.) Tartrate of potassium,
neutral, 728 grains; caustic soda, 360 grains; distilled water to 6 ounces,
Dissolve.
Of a mixture of these two solutions (Fehling’s fluid) in equal volumes, 10 cc.
will be decolorised and reduced by 0.05 grm. of glucose or diabetic sugar in
solution.
Titration with Pavys Ammoniated Cupric Solution.—This is a
fluid composed as follows:—Cupric sulphate, 4.158 grms.; potassic
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282 THE URINE.
sodic tartrate, 20.4 grms. ; caustic potash, 20.4 grms. ; strong ammonia
(sp. gr. 0.880), 300 ce. ; water, 1 litre. The object of the ammonia is
to prevent the precipitation of the suboxide, and so to render the de-
coloration of the copper solution more evident. In preparing the fluid,
the caustic potash and the tartrate are dissolved together, the cupric
sulphate by itself; the two solutions are mixed, and when cold the
ammonia is added, and water supplied to the specified bulk. Ten ce. of
this solution are decolorised by 0.005 grm. of sugar. Dr. Pavy recom-
mends for clinical convenience the use of hermetically-sealed tubes of
glass, each containing 10 cc. of the solution.2"7]
2. By Fermentation.—This method of analysis was first suggested by
Roberts,?"> and Worm-Miller 2°. applied it to determine the proportion
of sugar in the urine from the density of that fiuid before and after
fermentation. According to Worm-Miiller, this method, with the aid
of a thermometer and a pycnometer fitted with a graduated index-scale,
gives good results where so little as o.5—1 per cent. of sugar is present.
Roberts concluded from experiments that a difference of 0.001 sp. gr
corresponded to 0.23 per cent. of sugar, and arrived at the following
formula :
ae Dx 0.230
0.001
Where
x= the percentage of sugar.
D=the difference in the density of the urine before and after fer-
mentation.
It is possible to obtain good approximate results from the application
of this method clinically. The following apparatus is required : Two
hydrometers accurately graduated to four places of decimals, and each
provided with a thermometer carrying a fractional index, and capable
of registering ;4,° C. These instruments should measure densities
ranging between 1.000-1.025 and 1.025-1.050 respectively up to four
places of decimals.
The first step is to take the sp. gr. of the urine at the iemperatute for
which the hydrometer in use was constructed. This may be done by
placing the test-glass containing it in a vessel of water, which may be
cooled or heated as required. 100-200 cc. of the urine are then placed
in a flask, together with some fresh yeast which has been carefully
washed on an ash-free filter to secure removal of inorganic impurities.
The flask is next closed with the arrangement represented in fig. 128,
by which evaporation is prevented. Fermentation is allowed to go on
for 24-48 hours. After this, the fluid, which should be clear, or nearly
so, is passed rapidly through a filter, and its density again taken at the
appropriate temperature, the latter being secured and ascertained as
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FERMENTATION PROCESS—POLARISATION. 283
before. From the observations made, the percentage of sugar is calcu-
lated by the formula given above.
In twelve cases of diabetes this method proved most valuable. Its
simplicity renders it very suitable for clinical use.
The figures in the following table afford the means of comparing the results
obtained by fermentation and by means of Lippich’s polarimeter in a series
of cases :— P
Percent. Percent. Percent, Percent, Percent. Percent, Per cent, Per ceut.
I, Fermentation: 2.22; 3.55; 4.49; 5.38; 6.06; 6.23; 60; 6.1
2. Polarimetry : 2.253; 3-655 4.67; 5.60; 6.01r3 6.00; 6.1; 5,7 280
3. By Polarisation.—Grape-sugar possesses a dextro-rotatory power
for polarised light, and upon this fact a quantitative test for that body
is based. Such a test must necessarily be open to fallacy, inasmuch as
the urine in diabetes is apt to contain other substances, such as B-oxy-
butyric acid and levulose, which rotate light in the opposite direction..
It is well, therefore, in applying it, to do so both before and after fer-
mentation (Hoppe-Seyler, Kulz, Worm-Miiller, and K. A. H. Morner),
when the difference in the results will be a measure of the quantity of
grape-sugar in solution. The advantage of the method is that it dis-
penses with delay. In recent times it has been invested with great
accuracy by the use of a polarimeter constructed on the principle devised
I'ic. 128.—Flask for the Approximate Estimation of Sugar by Fermentation (}).
by Lippich. This instrument is represented in fig. 129.°8! It is em-
ployed thus :—
The graduated disc is turned towards the observer, and the tube
towards the lamp, and the cap which covers the telescope and the
posterior end of the apparatus is removed. The lamp is placed at a
distance (45 cm.) equal to the length of the instrument itself. Car-
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284 THE URINE.
bonate of soda is placed in the cage attached to the lamp, and fused
until the receptacle is full. The latter is then fixed in the lamp in such
a way as to be in contact with the flame at the side only, and a screen
is so placed that the light passes only through the aperture in it.
The following description will sufficiently explain the construction of
the instrument :—At the hinder end of the polarimeter is a rod sup-
porting the arc of a circle, and behind this, in the direction of the lamp,
another rod, with a notch marked upon it. The second rod is fitted
with a screw, by means of which it moves upon the first, and can be
fixed in contact with the latter. When the line upon the upper surface
of the adjustable rod corresponds to the central point (0) of the metallic
are, and this with the o of the vernier, the entire field is dark, and by
rotating the are (which is done with the ivory lever in front) both
halves will be obscured or illuminated equally. In experimenting with
the instrument, the adjustable rod is deflected slightly to the right or
to the left. It is practically a lever attached to the box containing a
Nicol prism (d in the section, which is represented as seen from above),
and rotates the prism on its axis.
In conducting an observation, the tube containing the urine or other
fluid to be examined is placed in the capsule, and the second rod is
moved right or left, say as far as the mark 4. The observer then looks
through the telescope, and adjusts the instrument in such a manner
that the field is illuminated to the utmost in one half at least; after
which he moves the telescopic tube until the vertical line dividing the
field into two equal parts is rendered as narrow and well defined as pos-
sible, and the position of the flame is again looked to. The ivory lever
is now moved forward, and the inner notched vim of the disc is rotated
to the right or the left, until both halves of the field are equally obscure.
The lever is next reversed, and the observer works the micrometer screw
at the lower part of the disc, whilst he looks for a difference in the
degree of illumination of the two halves of the field. If this does not
occur, the latter was.either too bright or too obscure. It may be
rendered brighter by increasing and inverting the angle between the
two rods (c, d) to which the polarisers are connected ; and the less this
angle, the less will be the variation with equal differences of adjustment.
When the proper degree of illumination is obtained, a number of read-
ings are taken with different adjustments.
The number of degrees to the nearest 4°, from the zero-point of the
dise to that of the vernier, are read off; and then, proceeding in the
same direction, the first line on the vernier which exactly corresponds
with a division on the disc is noted. This is easily found by inspecting
the divisions to the right and left of that one which is assumed to be
correct. Both are on the inner side of the corresponding marks on the
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286 THE URINE.
circle. The longer lines on the vernier correspond to 0.01’, the short
ones to 0.005". In practice, the adjustments should not differ by more
than 0.005”.
The way in which the readings are taken may best be shown by an
example :—Supposing the zero-point of the disc stood to the right of
the zero-point of the vernier, and that, between the two, 2° in addition
to twenty long vernier marks and one short one had been counted,
then + 2°, 205 is written down. With further readings, the vernier
marks only are noted, added together, and the average taken. Should
the result again be 205, then
2° =0.75°, 0.75° +0.205 = +0.955.
One long mark =0.01", 20 long marks= 0.200".
One short mark = 0.005”, 1 short mark = 0.005".
Finally, the zero-point is fixed by taking the tube out of the capsule
without otherwise altering the arrangement of the instrument.
The field of vision is unequally illuminated, and the mark no longer
distinct. The telescope is focussed to show the mark, the lever brought
forward, the disc put in with the hand, the lever reversed, and the
micrometer screw carefully adjusted. A number of readings is taken,
and an average struck. Supposing this to be = — 2.045° (z.e., the zero
mark for the present inclination of the polariser rods), the number is
to be deducted from the original reading ; thus, + 0.955 — (— 2.045) =
0.955 + 2.045 = 3.0.
If the urine was examined in a tube two decimetres long, then
2 [a], = 3.0%, and [«], = 1.5.
[«], being the specific rotating power for grape-sugar (C,H,,0,), is
in this case = + 52.5°.
52.5 for 100 grms. in 100 ce.
100
grms. I 100 ee.
2.5
1 for
, 100 x 1.5 i
1.5° for ————— orms. in 100 ce.
52-5
The percentage of sugar in the case taken would therefore be
] dS 5 )
100 Xx 1.5
52-5
Care should be taken throughout the observation that the position
of the lamp is not altered, otherwise varying results are obtained.
= 2.85 per cent.
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CARBOHYDRATES —CHOLURIA. 287
During the whole process, therefore, the same position of the lamp and
instrument must be maintained, and all readings should be taken con-
tinuously with one filling of the platinum cage.
By carefully observing these precautions, very accurate results may
be obtained.
The instrument will serve also to show whether a liquid has the power of
rotating light or not. In the latter case, the zero-point of the disc stands in the
same lateral position to the zero-point of the vernier as the second pointer to the
zero-point of the segment connected with the polariser (right or left); the devia-
tion of the zero-point of the disc from that of the vernier being half as great as
the deviation of the two rods.
2. Levulosuria.—Fruit-sugar is found sometimes in conjunction with
grape-sugar in the urine (K. Zimmer, Seegen).82_ The latter will then
yield all the reactions of grape-sugar, including that with phenyl-
hydrazin. It may happen under such circumstances that a specimen
of the urine examined with the polarimeter will fail to rotate polarised
light to the right, or may even rotate it to the left; and from this fact
the presence of levulose may be inferred.
3. Lactosuria.— Milk-sugar occurs in the urine of women who are
nursing.” Its recognition can be effected only by separation from the
fluid (Hofmeister). An effort has been made with the phenyl-hydrazin
method to transform this body in the urine into phenyl-lactosazon
(v. Jaksch *§*), but as a test the expedient has not succeeded.
According to Jischer, the presence of milk-sugar may he inferred if,
while no result is obtained with the phenyl-hydrazin and the fermenta-
tion tests, evidence of sugar.is given by Trommer’s and Nylandeyr’s
tests.
4. Dextrin.—Dextrin has been seen in the urine of diabetes (L.
Reichard *§°), where it seemed to take the place of grape-sugar. In such
cases Reichard found that the urine behaved with Trommer’s test in
all respects like a solution of dextrin, the originally blue fluid becoming
first gradually green, then yellow, and sometimes dark brown.
5. Animal Gum.—Landwehr ?*6 has recently found in the urine a
carbohydrate presenting a close analogy to members of the gum series.
To this he has given the name of “animal gum,” and he believes that
it is a normal constituent of the fluid. The methods for its detection
and isolation will be found in the original contribution on the subject.
The statements there made are confirmed by Wedenski.28"
Amongst other carbohydrates occasionally present in health and disease
are maltose (Le Nobel, v. Ackern?*), and a left-rotatory body observed
by Leo and Kiilz 28° in diabetic urine.
III. Choluria.—Of the bile constituents, the biliary acids and _ pig-
ments chiefly concern us here. although cases previously reported by others, and
amongst them by Sfolvis,24 would appear to be instances of this con-
dition. [ (Uro)hematoporphyrin, like urobilin, may exist in the urine
partly in the form of a chromogen, which becomes a pigment on oxida-
tion. (Halliburton).*5| Viewed by reflected light, the urine is opaque
and almost black—or in a thin layer, brownish-red. The colour is
unchanged by boiling. It is, or may be, free from albumin, since
hematoporphyrin does not contain albumin. When diluted and treated
with HCl the characteristic spectrum (Hoppe-Seyler*?°) may be seen.
This exhibits four absorption-bands, viz., two, narrow and faint, situated,
one between C and D, the second between D and £ but nearer to £,
and two broad and dark bands, of which one overlaps D to the red
end of the spectrum, while the other lies between / and F. These
* latter may alone be visible, and are alone evidence of hematoporphyrin.
To detect this substance chemically, about 30 cc. of the urine are taken
and treated with alkaline solution of barium chloride; the mixture is
filtered and the precipitate washed first with water and afterwards with
absolute alcohol ; the precipitate while still wet is rubbed up in a mortar
with alcohol and hydrochloric acid, allowed to stand for a while and
then heated in the water-bath. The solution thus obtained, if hemato-
porphyrin be present, should have a reddish colour, and when filtered
and examined with the spectroscope, the filtrate should give the two
absorption-bands of hematoporphyrin (Salkowski). The clinical signifi-
cance of this state is not yet fully known. [MacMunn **" and Le Nobel 2?8
have described it in Addison’s disease, acute rheumatism, pneumonia,
measles, pericarditis, typhoid, meningitis, and other diseases.] In some
people it follows the use of sulphonal.*”?
[Hematoporphyrin derived from the blood by the action of sulphuric
acid and (uro)hematoporphyrin derived from urine differ in their
spectra. MacMunn has recently found a pigment, which he regards as
intermediate between the two, in three specimens of urine. These
urines were of a deep Burgundy-red colour, free from albumin, and on
the addition of H,SO, showed the spectrum of acid hematoporphyrin.**°]
VI. #ther-Sulphurie Acids and their Derivatives (Indigo-
Blue, Indigo-Red, Skatol, Phenol, Parakresol, Pyrocatechin, Hydrochinon)
and the Aromatic Oxy-Acids.
(a.) Indicanuria.—Indigo-blue (indigo, indigotin) as such, is rarely
present in the urine, usually in’decomposed urine, and hardly ever so
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294 THE URINE.
plentifully as to impart its colour to the fluid. It may always, however,
be obtained from urine as a product of the decomposition of salts of
indoxyl-sulphuric acid (potassium indoxyl-sulphate).*1
Indol, a regular product of bacterial putrefaction of albumin (see
p. 202), is the basis of indican (indoxyl-sulphuric acid).**? It is oxidised
to indoxyl within the system, and by combination with the sulphuric
acid present forms indoxyl-sulphuric acid. The decomposition of in-
doxyl-sulphuric acid yields, besides indigo-blue, other substances of
similar character, such as indirubin ; but to these no practical interest
attaches in the present state of our knowledge.***
With reference to the clinical import of indicanuria, it must be borne
in mind that the quantity of indoxyl-sulphuric acid formed varies
in health with the food ingested, and it is increased especially by
animal diet. ¢
Apart from this, an undue proportion of indican in the urine is a fact
of pathological interest, and there are certain diseases in which indoxyl-
sulphuric acid is regularly produced in excess.
It was formerly believed that starvation and wasting diseases were
attended with the separation of indican (Senator **+) ; but more recent
observation #85 has shown that this is dependent on the fact that in
such diseases albuminous putrefaction takes place in the alimentary
canal, and in consequence there is an increased production of indol, the
antecedent of indican. The presence of indican in the urine is very
often a sign of intestinal putrefaction, and its quantity in certain cases
varies with the activity of that process.**° It may also accompany the
decomposition of albumin in other cavities. Thus, in a case of pleurisy
with abundant unhealthy exudation, the author has found a profusion
of indican in the urine, and when this manifestation arises in the course
of peritonitis, it may be taken as an evidence of the character of the
disease and of the formation of putrid pus. [Hochsinger *3” has recently
studied this subject in connection with infants. He found that the
urine of new-born children was free from indican, and in healthy infants
it occurs only in traces. It becomes more abundant in intestinal dis-
orders and is always most so when these are attended by acute
diarrhcea.*88 Tuberculosis, whether affecting the intestinal tract or
not, was always accompanied by profuse indicanuria. Hochsinger
attributes the condition to decomposition of milk-albumin in the in-
testinal tract. |
Large doses of thymol were followed by an increased production of indican
(Bohland).**9
In general, therefore, the appearance in the urine of larye quantities of
indican implies that abundant albuminous putrefaction is progressing
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ESTIMATION OF INDICAN. 295
actively in some part of the system. Caution must be observed in further
narrowing the inference as to diagnose a gangrenous suppuration, for
instance, since in simple constipation a notable indicanuria will very
often arise.
It may be remarked here that the deep brown colour which usually
belongs to urine rich in indican is not due directly to the presence of
indoxyl-sulphuric acid, but depends upon the higher oxidation products
of indol which accompany it. These bodies bear to indoxyl-sulphuric
acid the same relation that the brown, green, or black colouring matters
of carbolic urine do to phenol-sulphuric acid.
Detection of Indican.—The methods employed for this purpose pro-
ceed upon the principle of splitting up the indoxyl-sulphates of the
urine, and obtaining from them a coloured product—indigo-blue.
Jafés Test.*°—A few cc. of the urine are treated with an equal
quantity of hydrochloric acid, and, drop by drop, a solution of some
hypochlorite is added by means of a glass pipette, and shaken up with
the fluid. The chromogen formed by decomposition of indoxy]-sulphuric
acid is oxidised into indigo-blue. Care must be taken that hypochlorites
are not in excess, since this would alter and bleach the indigo-blue.
Stokvis **1 recommends the admixture of a little chloroform in the
process, with the object of dissolving the indigo-blue as it forms. The
chloroform solution then takes a blue colour [and the colouring-matter
is obtained as a deposit after evaporation. Albumin if present should
be removed before performing this test, since it forms a blue colour
with hydrochloric acid (Ha/liburton).*4”]
Obermayer *° has suggested a useful modification of Jafé's test. The
urine is treated with 1 in 5 solution of sugar of lead, which, however,
must not be in great excess, filtered through dry paper, the filtrate mixed
with an equal bulk of fuming HCl containing 1 to 2 parts in 500 of ferric
chloride solution, and then’ thoroughly shaken for.one to two minutes.
The indigo-blue formed is then taken up with chloroform.
Weber's Test.°44—Thirty ce. of urine are mixed with an equal quantity
of hydrochloric acid, 1-3 drops of dilute nitric acid added, and the
mixture boiled. The fluid assumes a dark colour. If allowed to cool
and then shaken up with ether, the presence of indigo-blue is shown by
the formation of a blue froth on the surface, while the ether exhibits
a rose or violet tint. [MacMunn uses chloroform instead of ether,
and examines the violet fluid with the spectroscope, which shows
an absorption-band before D (indigo-blue), and another after D (indigo-
red), This method is preferable to Jaffé’s for the detection of small
quantities of indigo, which are destroyed by the hypochlorite (Hadld-
burton).*# |
Quantitative Estimation.—The methods of Jaffé and Salkowshki are
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296 THE URINE.
the most useful. Their principle is the same as that of the tests for
the presence of indican.
Salkowshi’s 4 Colorimetric Process is perhaps the best. A rough
analysis is first effected by determining the quantity of chlorinated lime
solution with which indigo forms in greatest abundance. If in this way
it is found that the urine contains much indican, 2.5—5 cc. are diluted
with water to 10 cc., while, if there be but little indican present, 10 ce.
of undiluted urine are taken as the basis of the experiment. In either
case an equal quantity of hydrochloric acid is added, and that propor-
tion of chlorinated lime solution which was found in the preliminary
reaction to be required. The mixture is then neutralised with caustic
soda, and carbonate of soda added to make it alkaline. The indigo-blue
which forms is collected in a filter, and then washed with water until it
no longer exhibits an alkaline reaction, when it is dried and repeatedly
extracted by heating with chloroform until the latter ceases to colour
with it. The chloroform extract is then, by the addition of chloroform,
made up to a quantity expressed by a round number of ec. placed in a
glass vessel with parallel sides, and the intensity of its colour compared
with that of a freshly prepared chloroform solution of indigo-blue of
known strength.*4* To one or other of these, as required, more chloro-
form is added, until their tint is adjudged equal. From the known
constitution of the standard the quantity of indigo-blue derived from
the urine (2.5-5 or 10 cc.) taken may be also known, and its percentage
may be readily calculated.
From the urine passed in twenty-four hours under ordinary conditions
of diet 5-20 merms. of indigo-blue can be obtained on an average.
Indigo-Red.—There is now no doubt (Rosin *$) that indigo-red (indi-
rubin) as well as indigo-blue occurs in the urine. It is formed together
with indigo-blue when a urine rich in indican is boiled with nitric acid
(O. Rosenbach’s test). For its detection Rosin renders the urine alkaline
with sodium carbonate, and then extracts the indigo with ether. The
inferences which Ros?n has drawn from the presence of this body in the
urine are questioned by other observers, and Rosenbach’s *#9 test cannot
be taken as evidence of anything except that the urine contains abun-
dance of the indigo antecedent.
There are certain other aromatic derivatives of the urine which will
engage our attention here, both because they are chemically allied to
indoxyl-sulphuric acid, and also because pathologically their production
is apt to coincide with the manifestation of that substance.
().) Skatoxyl-Sulphuric Acid.—This body results from the skatol of
the feces (Brieger).°° It is assumed that skatol, by a process analogous
to that undergone by indol, is oxidised to skatoxyl within the body,
appearing in the urine as skatoxyl-sulphuric acid. It is probable that
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ESTIMATION OF ATHER-SULPHURIC ACID. 297
the red colour which develops in the urine in the presence of acids is to
some extent due to decomposition products of this substance.**!
(c.) Parakresol- and Phenol-A:ther-Sulphuric Acid.—The other mem-
bers of the aromatic group which occur in human urine in combina-
tion with sulphuric acid are phenol (carbolic acid), parakresol, pyro-
catechin, and hydrochinon. To the latter we shall have need to refer
again. The methods by which these bodies may be detected are highly
interesting and clinically instructive.
Salkowski*°? has shown that the urine of patients suffering from
ileus and peritonitis, in addition to a large percentage of indican, con-
tains also a considerable proportion of phenol-forming substance, and
Brieger’s *°° experiments have proved that the elimination of the ante-
cedent of indigo (indoxyl-sulphurie acid) on the one hand, and that
of the phenol-producing substances (phenol, parakresol-ether-sulphuric
acid) with the aromatic oxy-acids on the other, bear to one another no
constant relation as to activity ; and that author found that in diphtheria,
searlatina, and facial erysipelas phenol was formed in greatly increased
quantity, whilst in typhoid, relapsing and intermittent fevers, small-
pox, and meningitis it could be obtained but very sparingly from the
urine. These statements are borne out by others.*°4
Again, in all cases where albuminous putrefaction is actively pro-
gressing in the intestine or other organs, in addition to the salts of
indoxyl-sulphuric acid phenol is increased in the urine, and in general,
together with phenol, the other members of the aromatic group become
evident in connection with pulmonary gangrene, putrid bronchitis, foetid
pleuritic exudation, and decomposition generally throughout the body.
Detection of Ather-Sulphurie Acids.—For this purpose the urine is
first treated with barium chloride in excess to precipitate simple sul-
phuric acid and then boiled with hydrochloric acid. If zther-sulphuric
acid be present, it is decomposed with the formation of the uncombined
acid. This combines with the barium present to form sulphate of
barium, and a white precipitate is deposited.
The quantitative estimation of the phenols (phenol, parakresol) is
conducted in the manner to be described at p. 299, and their presence
may be determined by the tests given at p. 161 and p. 202. It must be
mentioned, however, that the investigations of Rumpf*®° have shown
that an accurate quantitative analysis cannot be made by any of the
methods hitherto in use. For the comparative investigation of these
substances the original work of Brieger *°° may be consulted.
Quantitative Estimation of Asther-Sulphuric Acid.—The percentage
of this body in the urine may be best determined by Bauwmann’s 7
method as modified by Salkowshi.?°§
To 200 cc, of urine is added a like quantity of alkaline barium
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298 THE URINE.
chloride solution (two parts saturated solution of baryta, and one part
of solution of chloride of barium saturated in the cold). The mixture
is allowed to stand for some minutes and then passed through a thick
filter which has been carefully dried. Of the filtrate, which must be
perfectly clear, 100 cc. ave taken and rendered strongly acid with ro ce.
of hydrochloric acid (sp. gr. 1.12), then boiled and heated on the water-
bath until all the precipitate which forms has settled. The beaker may
be heated on an iron plate coated with asbestos, and allowed to remain
till its contents are cold. The precipitate is next collected and placed
on a filter of Swedish paper which has previously been washed with
dilute hydrochloric acid, and care must be taken that the filter is not
allowed to empty itself entirely during the process. With the aid of a
glass rod protected with a ring of india-rubber, and rinsing with boiling
water, the entire precipitate is placed on the filter, and is there washed
with boiling water until the filtrate which passes through fails to give
a precipitate with dilute sulphuric acid, thus showing the absence
of free chloride of barium. Should it happen that the fluid passing
through the filter is turbid, this may be due to the presence of soluble
substances, as phenols-produced. by the decomposition of the compound
acids. To ascertain their character in this case, the cloudy filtrate
is placed in a beaker on the water-bath heated to boiling-point, when,
if the turbidity be due to phenols, these pass off in vapour and leave
the fluid clear. Where, on the other hand, the appearance is caused
by the barium precipitate having passed through the filter, the turbidity
will not be removed in this way, and the experiment is spoiled. The
precipitate is next washed with boiling alcohol, and finally with ether,
and together with the filter-paper placed upon a platinum crucible of
known weight and heated for a long time. After this the platinum
crucible is raised to a white heat, allowed to cool, and then weighed
again. The calculation is made as follows :—233 parts by weight of
sulphate of barium correspond to 98 parts by weight of sulphuric acid
(H,SO,), and consequently the quantity of sulphuric acid in 100 ce. of
the urine may be computed by the formula—
ce 98 x M = 0.4206 x M
233
Where
w = the quantity of sulphuric acid required.
M = the quantity of barium sulplate found.
ll
If the object be to determine the total quantity of the sulphuric acids
(simple and compound), so as to find out their respective proportions in
the urine, the latter is filtered. Another too ce. are taken and treated
with 10 ce. of hydrochloric acid (sp. gr. 1.12), then boiled for fifteen
C
c
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ESTIMATION OF PHENOLS—PYROCATECHIN. 299
minutes and chloride of barium solution added in excess. The remain-
der of the process is that described above. The difference between the
total quantity and that of ether-sulphuric acids obtained expresses the
proportion of simple sulphuric acid in the urine.
For the methods of estimating sulphur when present in the urine in
other forms see pp. 323, 327.
Quantitative Estimation of Phenols.—The phenols (phenol and para-
kresol) which have passed over in the distillation of a known quantity
of urine previously acidulated are estimated in the form of tribromo-
phenol by Landolt’s method, with the precautions suggested by Bawmann
and Brieger.*°9
One-fourth of the urine passed in twenty-four hours is mixed with
one-fifth its bulk of hydrochloric acid and distilled. Distillation is
continued until the distillate ceases to colour with bromine water, after
which it is filtered. All the fluid which has passed through—including
that tested during the process—is now treated with bromine water
until a permanent yellow colour is attained. The precipitate is allowed
to settle for two or three days, when it is separated on a filter which
has been weighed and carefully dried over sulphuric acid; it is then
washed with bromine water and dried over sulphuric acid in the dark
until it has acquired an approximately constant density. It is then
weighed on the filter, and the difference between the result and the
weight of the filter recorded expresses that of the tribromo-phenol
formed. From this the quantity of carbol in the urine may be esti-
mated thus :—331 parts by weight of tribromo-phenol correspond to
94 parts by weight of carbol, and the following formula results :—
— 94 =
e==* x M=0,2839 x M
331 59
Where
the quantity of carbol required.
the quantity of tribromo-phenol found.
I
av
M
This method may also be employed for the analysis of vomited matters in cases
of carbolic acid poisoning (compare p. 161).
J. Munk has computed that the quantity of phenols excreted with
the urine averages 0.017 to 0.051 grm. in the twenty-four hours. For
purposes of more accurate analysis it is important to determine the
quantity of indoxyl-sulphuric acid and ether-sulphuric acids eliminated
in the manner already indicated (p. 295), and to remove the analogous
substances generated in intestinal decomposition by means of a calomel
purge. °6°
(d.) Pyrocatechin —This body, like the others, occurs in the urine
only in combination with sulphuric acid ; and it is if not an invariable,
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300 THE URINE.
at all events a very frequent constituent of that fluid.**! The urine
containing it is characterised by the fact that it is colourless when
passed, but becomes dark after exposure to the air; and the change
is expedited by the addition of caustic potash. When boiled with
hydrochloric acid, it becomes a powerful reducing agent. An ammo-
niacal solution of silver exposed to it will quickly deposit metallic silver
in the cold.
These properties, however, are not sufficient to determine the presence
of pyrocatechin. To do this it must be isolated, and the following
method is the best for the purpose.*°? The urine is evaporated to one-
fourth its volume on the water-bath, filtered, and the filtrate boiled
with excess of sulphuric acid. It is then allowed to cool and repeatedly
shaken up with ether, the ethereal extracts collected, the ether dis-
tilled off, the residue neutralised with carbonate of baryta, and again
extracted with ether. Pyrocatechin passes over in the ethereal extract,
and when the ether is distilled off, it remains as a more or less pure
crystalline substance. If the character of the latter is not sufficiently
apparent, it may be re-crystallised from benzol in the form of prisms
belonging to the tetragonal system. If some of these be dissolved in
water in a watch-glass and a few drops of a very dilute solution of per-
chloride of iron be added, an emerald-green colour develops, and this
changes to violet on the addition of a little ammonia.?®
(e.) Hydrochinon.—It has been ascertained by Bawmann and Preusse °*4
that hydrochinon appears in the urine after carbolic acid poisoning,
and these authors believe that to its presence the dark colour of that
fluid after the exhibition of carbolic acid is due. It is always in the
form of ether-sulphuric acid in the urine, and the process for its detec-
tion is the same as that for pyrocatechin.*
The crystals of hydrochinon belong to the rhombic system, and they
crystallise readily from their solution in toluol.
According to Baumann and Preusse,?6> when rapidly heated in an
open test-tube, hydrochinon forms violet fumes, which condense as an
indigo-blue sublimate, and in the application of this property we possess
a very sufficient test for its presence.
(f.) The Aromatic Oxy-Acids.—The aromatic oxy-acids which have
been proved to exist in the urine are paroxyphenyl-acetic acid, paroxy-
propionic (hydroparacumaric) acid,*6” paroxyphenyl-elycolic acid,3% and
oxyamygdalic acid,*°° to which must he added uroleucic (trioxyphenyl:
propionic) acid (Kirk, Wolkow, and Baumann *) and homogentisic
(dioxyphenyl-acetic) acid. In view of the significance which the re-
searches of Wolkow and Baumann have conferred upon these . latter
substances, there will be need to refer to them separately undér the
head of Alkaptonuria. i
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AROMATIC OXY-ACIDS—ALKAPTONURIA. 301
Detection of the Aromatic Oxy-Acids.—Twenty cc. of urine are treated
with hydrochloric acid, and heated for some time on the water-bath to
expel the volatile phenols. It is then allowed to cool, and repeatedly
extracted with ether. The ethereal extract is: shaken up with a weak
solution of carbonate of soda. The oxy-acids are taken up by the
latter, whilst the phenols present are retained by the ether. The
alkaline solution is now acidulated with sulphuric acid and extracted
with ether. The latter is allowed to evaporate, and the residue dis-
solved in water is submitted to Millon’s test (p. 258). A red. colora-
tion shows the presence of aromatic oxy-acids.
In a similar manner an approximate quantitative estimation of these
bodies may be effected.271
VII. Alkaptonuria.—Although the substances with which we have
to deal under this heading belong properly to the aromatic series, and
are oxy-acids, the special clinical importance which attaches to them
makes it convenient to adopt Baumann’s classification, and treat them
apart. By the term alkaptonuria is meant the condition in which the
uroleucic acid of A7zrk and the homogentisic acid of Wolkow and Bau-
mann occur in the urine. There is no doubt that the urine in certain
cases (see p. 300) contains these acids in addition to pyrocatechin.
Bedeker * gave to a substance resembling these, which he dis-
covered in the urine; the name of alkapton. A similar substance
was discovered by Hbstein and J. Miiller*"? very abundantly present
in a child’s urine, and Fiirbringer and Fleischer *"? have obtained
evidence of such in cases of phthisis. The urine has characters very
similar to those conferred upon it by the presence of pyrocatechin (see
p- 299). Baumann and Wolkow believe that the production of the
acids in question is due to an anomalous metabolic process of life-long
continuance, by which the tyrosin (paroxyphenylamidopropionic acid) of
the system is perverted, probably by the action of some definite micro-
organism. For the method of recognising homogentisic acid the reader
is referred to the very interesting treatise of Bawmann and Wolkow.?™
The condition of the urine known as alkaptonuria may be said to exist
when the urine answers the description given at p. 300, thus showing
that it contains a large amount of pyrocatechin.
VIII. Inosituria.—Inosite occurs in small quantity in the urine in
cases of diabetes insipidus and in albuminuria. For its detection it
must be separated from the urine. To this end Cooper-Lane’s ?"* method
is the best. According to Magneune,™ inosite is obtained as hexa-
hydrobenzol.
IX. Melanuria.—The urine of persons suffering from pigmented
tumours sometimes contains a substance to which the name of melanin
has been given, but of which the chemical constitution is not yet sufti-
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302 THE URINE.
ciently established. It is sometimes held in solution, and more rarely
suspended in the form of small granules. It very seldom happens that
the fluid has a dark colour when passed, but it generally blackens in-
tensely when submitted to oxidising agents (sulphuric and hydrochloric
acids and ferric chloride). This fact would point to the conclusion
that the body in question is not melanin, but a chromogen—melanogen
—analogous to that which precedes the formation of urobilin. Such
urine turns dark on exposure to air. The pigment can be partially
separated from the urine by means of acetate of lead or perchloride of
iron. It is insoluble in cold alcohol, ether, and acetic and dilute mineral
acids. It is soluble in boiling concentrated mineral acids, in boiling
lactic and acetic acids, in concentrated solutions of caustic potash and
soda, and in ammonia. It contains iron, sulphur, and nitrogen. The
most sensitive test for the presence of melanin is the addition of bromine
water (Zeller),°° which causes the urine to deposit a yellow precipitate,
which gradually blackens.
More recent experience has shown that a fairly concentrated solution
of perchloride of iron serves well to detect its presence (v. Jaksch,
Pollak)?" A few drops of this reagent will cause the fluid to turn
grey ; and if more be added, a precipitate of phosphates falls, carrying
the colouring-matter with it, and again dissolves with an excess of the
solution.
Sodium nitro-prusside with caustic potash and acetic acid gives a deep
blue colour (Thormdhlen),?"8 which depends probably on the formation
of soluble and insoluble Berlin-blues (v. Jassch).
In connection with this subject the reader may refer to the opinion of Kruken-
berg 7 and Salkowski*®° (see p. 316), that in Weyl’s test for kreatinin boiling with
acetic acid similarly produces Berlin-blue.
The latter, however, cannot always be obtained by the action of the
nitro-prusside salt on melanin isolated from the urine, and the reaction
must ot be regarded as a test for melanuria, or only when other tests
(and especially that with perchloride of iron) have shown the presence
of melanin or melanogen. Moreover, the Berlin-blue reaction can be
obtained in urine which is free from melanin. Thus, in the case of
children suffering from prolonged constipation, it has been had at the
same time that the fluid was rich in acetone or diacetic acid and
indoxyl-sulphuric acid (v. Jaksch), and in a case of diabetes by Dresch-
feld,**! when its nature and the presence of the substances just named
were probably established. It would appear, therefore, that in these
conditions also a body is present which gives Berlin-blue with nitro-
prusside compounds. Possibly this is indol. Investigations with that
body derived from a preparation of picrate of indol gave the same result
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MELANURIA—ACETONURIA. 303
(v. Jaksch), The practical significance of this condition is greatly
limited by the fact that the urine may contain a large quantity of
melanin in wasting diseases, whilst that derived from individuals
suffering from melanotic cancer or sarcoma may be entirely free from
it. Senator **? has recently confirmed this view by a series of clinical
observations. Nevertheless, as an adjunct in diagnosis, the tests given
are of undoubted utility.?8
X. Acetonuria.—Normal urine contains traces of acetone (phy-
stological acetonuria, v. Jaksch **+), but this body occurs in excessive
proportion under certain morbid conditions (pathological acetonuria).
In association with diseases we may distinguish (1) febrile acetonuria ;
(2) diabetic acetonuria; (3) acetonuria accompanying certain forms of
cancer independently of inanition; (4) acetonuria of starvation; (5)
the production of acetone in psychoses; (6) acetonuria as an expres-
sion of auto-intoxication ; (7) acetonuria in derangements of digestion.**°
The commonest of these forms is febrile acetonuria. It does not belong
especially to any~particular fever.**° In connection with diabetes the
appearance of acetone in the urine indicates an advanced stage of the
disease, but does not otherwise affect the prognosis. Of greater con-
sequence 38’ are those cases in which much acetone is found in connection
with grave symptoms of cerebral irritation, less often of depression.
Acetonuria existing alone (auto-intoxication with acetone) tends to a
favourable termination (v. Jaksch).°88 Finally, it should be noticed that
recent researches have shown that an abundance of nitrogenous food
tends to the production of acetonuria.
Detection of Acetone.—A rough test for acetone is that of Legal. A
quantity of the urine (several cc.) is treated with a few drops of a
freshly-made and somewhat concentrated solution of sodium nitro-
prusside, and with a moderately strong solution of caustic soda or
potash. The fluid develops a red colour, which rapidly disappears, and
if acetone be present, gives place to purple or violet-red on the addition
of a little acetic acid. In the absence of acetone the purple-red tint
does not form on the addition of acetic acid.
For purposes of greater accuracy it is necessary to distil the urine, and
to apply to the distillate the tests presently to be described. To do this,
one-half to one litre of the urine may be taken, and a little phosphoric
acid may be placed with it in the retort to prevent the evolution of
gases. Of the distillate 10-30 cc. may be taken and tested with—
(1.) Lieben’s Test.—To several cc. a few drops of iodo-potassic iodide
solution and caustic potash are added. Jf more than a trace of acetone
be present, an abundant precipitate of iodoform crystals is deposited.
This test is very reliable, and will serve even for the detection of traces
of acetone.
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304 THE URINE.
(2.) Reynolds’ Test.—This depends on the property which acetone
possesses of promoting the solution of recently-formed mercuric oxide.
It is conducted as follows :—The yellow precipitate (mercuric oxide)
obtained by the reaction of mercuric chloride with an alcoholic solution
of caustic potash is added to the distillate from the urine, which is then
filtered, and to the clear filtrate sulphide of ammonium is cautiously
added. If acetone be present, some of the mercuric oxide will have dis-
solved and a black ring (sulphide of mercury) forms at the plane of
contact with the ammonium sulphide.
Legal’s Test, already described, may be applied also to the urinary
distillate, but it is less to be relied upon than the others, since parakresol,
which also passes over in distillation, exhibits a similar reaction.**?
Quantitative Estimation of Acetone.—This may be effected by v.
Jaksch’s method as modified by Nenchi.3°° Very good results are
obtained by the process first devised for scientific purposes by Mes-
singer,**! applied to the investigation of urine by Huppert,**? and rendered
available for clinical use by v. Engel and Devoto.**? It is conducted
thus: The urine is first examined by Legal’s test, and, according to the
result, 20-50, or at most roo cc., are placed in a flask and made up to
100 ce. with distilled water and 2 cc. of a 50 per cent. acetic acid solu-
tion. This flask is connected by a long glass tube with the cooler, in
front of which is a distillation flask, and in front of that a bullet
apparatus filled with urine. Distillation is carried on until 7;ths of the
original volume of the fluid have passed over. A portion of the residue is
submitted to Lieben’s test, and if this shows the presence of acetone, the
result must be rejected and the process commenced over again after the
addition of more distilled water. To the distillate 1 cc. of dilute (1 in 8)
sulphuric acid is added and the mixture distilled. The second distillate is
poured into a flask of 1 litre capacity fitted with a polished glass stopper,
and, also, for distillation purposes, with a doubly perforated cork, and
having a bullet apparatus full of water in front of it. When distilla-
tion is completed, the flask is closed with its glass stopper and the fluid
carefully titrated according to Huppert’s directions with {5th normal
iodide solution and ‘5th normal hyposulphite solution. These solutions
being used, 1 cc. of the iodo-solution corresponds to 0.967 mgrm. of
acetone. The researches which v. Engel has pursued by this method
have greatly extended our previous knowledge concerning the secretion
of acetone, and they have also established the facts on a secure basis.
XI. Diaceturia.—By the term diaceturia is meant the condition
in which diacetic acid appears in the urine. It is always pathological,?%
and occurs in diabetes (Gerhardt) and fevers (v. Jaksch, Deichnuiller,
Sedfert), and also idiopathically as a form of auto-intoxication. It is
most common in children as a concomitant of fever,**> and is then gene-
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DIACETURIA—LIPACIDURIA. 305
rally devoid of serious significance, but in adults it is a symptom of
grave import. In febrile and diabetic states the development of diacet-
uria commonly forebodes the advent of coma.
Urine holding diacetic acid is always rich in acetone, and in presence
of perchloride of iron develops a Bordeaux-red. This property, how-
ever, does not serve to distinguish the presence of the former body,
since it belongs equally to a number of substances which are apt to
exist in the urine.#% For its detection the following process may be
adopted.
To the urine a fairly-concentrated solution of perchloride of iron is
cautiously added, and if a phosphatic precipitate forms, this is removed
by filtration and more of the perchloride of iron solution supplied. If
the Bordeaux-red colour appears, one portion of the urine is boiled,
whilst another is treated with sulphuric acid and extracted with ether.
If now the urine which has been boiled shows little or no change, whilst
the perchloride of iron reaction in the ethereal extract is no longer
evident after 24-48 hours; and if at the same time (on testing the
urine directly and its distillate) it is found to be rich in acetone, the
condition may be inferred to be that of diaceturia.
XII. Lipaciduria.—By this term is meant the condition in which
volatile fatty acids are found in the urine (v. Jaksch,?" v. Rokitanshy °°).
These bodies: occur there in traces normally, especially formic, acetic,
and butyric acids ; and they may be derived from healthy urine in con-
siderable quantity by the use of oxidising agents.?"® They are also a
product of alkaline fermentation.
As a manifestation of disease, on the other hand, they are often
present in quantity in the simple urine. Thus, in the urine of fevers,
of hepatic diseases affecting the proper structure of the liver, and in
diabetes, formic, acetic, butyric, and recently also propionic acid have
been detected.
There is no special diagnostic significance attaching to this condi-
tion; in general, it is determined by the same causes which produce
febrile acetonuria.
For the detection of fatty acids the urine is distilled with phosphoric
acid, and the distillate carefully neutralised with carbonate of soda,
evaporated to dryness on the water-bath, the residue extracted with
boiling alcohol, filtered, again evaporated, dissolved in water, and the
solution submitted to the tests mentioned at p. 201. The principal
reactions are shortly recapitulated here.
1. A little of the urine is treated with sulphuric acid and alcohol. An odour of
acetic zether indicates the presence of acetic acid.
2. To another portion perchloride of iron is added. The specimen assumes a
red tint, which disappears on boiling, and a rusty precipitate remains.
U
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306 THE URINE.
3. The addition of nitrate of silver causes a white precipitate, which rapidly
blackens if formic acid be present.
With reference to the appearance in the urine of other organic acids, see
PP. 336, 337:
XIII. Lipuria.—Small quantities of fat are often seen in the urine of
chronic nephritis with a very fatty state of the kidney (see pp. 229, 247),
in phosphorus-poisoning,*! and diabetes mellitus. Fat in large propor-
tion was found by Hbstein 4°? in a remarkable case of pyonephrosis.
Fat is also a common manifestatation in chyluria, and it is a physio-
logical constituent of the urine of pregnant women.
Its presence is sufficiently apparent. The urine containing it is
usually very turbid, and clears when shaken up with ether. The fatty
particles may be separated by means of Stenbeck’s sedimentator (see p. 218).
It is apt also to hold globules of fat, which are easily recognisable by their
powerful refracting properties ; and it is not uncommon for this substance
to occur in the form of needles, as it does in the feces (p. 196), especially
in connection with chronic nephritis and septiceemia.?™
XIV. Chyluria.—By this term is meant the simultaneous appearance
at intervals of fat and albumin in the urine, apart from the manifesta-
tion of other morbid constituents, such as casts, renal epithelium, We.
The sediment, however, usually contains red and white blood-corpuscles
in small numbers. ;
The urine under these circumstances tends to form coagula of fibrin
on standing, and occasionally it gelatinises throughout. Hitherto
chyluria has been met with almost exclusively in the tropics, and in
persons who have lived there for a long time, and it has been shown
by Waucherer and Lewis (p. 58) to depend upon the invasion of the
urinary tract by Filaria sanguinis hominis. The embryo of this parasite
is generally to be found in the urine; and the chemical investigations
of Grim 44 make it appear that in the majority of cases the abnormal
condition of the urine is due to unnatural communications between the
lymphatics and urinary passages affected by filaria. The subject, how-
ever, needs further elucidation, inasmuch as chyluria is occasionally
observed in persons who have never lived in the tropics.4%
Langgaard *° has detected large quantities of cholesterin in the urine
in a ease of chyluria.
XV. Oxaluria.—It has been stated already that oxalic acid occurs
in healthy urine, but it is subject to very great increase in certain
morbid states, and the condition is then called oxaluria.
Oxalates may remain in solution in the urine, and it is important to
be able to determine absolutely the quantity of oxalic acid present as
such. This can be done by a modification of Neubauer’s method (Fiir-
bringer and Czapek).4
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OXALURIA—ESTIMATION OF OXALIC ACID. 307
Quantitative Estimation of Oxalic Acid, Neubauer’s Method.**—The
urine passed within twenty-four hours is accurately measured, and treated
first with calcium chloride and ammonia, then with acetic acid until it
has a slightly acid reaction, and afterwards a little alcoholic solution of
thymol is added to restrain the development of micro-organisms. The
mixture is allowed to stand for some time, when the white precipitate
which forms is separated on a filter, and (together with the latter) is
placed in hydrochloric acid, gently heated, the fluid filtered off, and the
filter washed with water until it has no longer an acid reaction. The
collected filtrate is evaporated to a small bulk in a capsule on the
water-bath, then placed in a strong glass cylinder, and the capsule in
which it was evaporated is washed with dilute hydrochloric acid and
water, the washings being added to the fluid in the cylinder. Ammonia
solution is then poured upon the surface of the latter, and the whole is
tinted with a few drops of tincture of litmus. The mixture is allowed
to stand for a considerable time. The precipitate which has formed
is obtained on a so-called ash-free filter, the ash constituent of which
has previously been accurately ascertained, and the oxalate (of lime)
which adheres to the walls of the cylinder is removed on a glass rod
guarded with an india-rubber ring, and added to the precipitate on the
filter. The latter is next freed from chlorine by washing with water,
and rinsed with acetic acid. The filter is then dried, and ignited
on a platinum crucible, which is heated to a constant weight in the
blow-pipe flame. By this means oxalate of lime is changed into lime.
Now as 56 parts of lime correspond to go parts of oxalic acid, the
quantity of the former obtained when multiplied by 1.6071 shows the
quantity of oxalic acid in the urine taken.*”°
In healthy urine the amount of oxalic acid passed in twenty-four
hours is 0.02 grm. (Liirbringer).
An excess of oxalic acid is occasionally found in diabetes, and espe-
cially when the proportion of sugar diminishes (vicarious oxaluria).*!
Oxaluria is also known as an affection swt generis (oxalic acid diathesis,
idiopathic oxaluria), (Cantand).4™
It must be admitted that our knowledge of this condition as a clini-
cal symptom is very defective, but the author’s experience induces him
to adopt the conclusion of J. Beybie*? and Cantani, that there are
certain complaints, characterised by pains in the back and loins and
attended with rapid emaciation, in which the only objective symptom
besides is an excessive elimination of oxalic acid with the urine.
Neidert *? observed in a complaint with nervous symptoms more than
0.5 grm. of oxalic acid per litre of wine; and Kisch ‘+ found in nine
cases of extreme lipomatosis only one in which there was an increase of
0.040 grm. in the litre.
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308 THE URINE.
XVI. Cystinuria.—This is a condition of rare occurrence, and
clinically of little importance, since it is only accidentally by the forma-
tion of calculi that it gives rise to trouble. It is usually chronic in its
course. It should be mentioned that Hbstein #9 has found cystin con-
currently with albumin in the urine of acute articular rheumatism
(comp. p. 243).
The researches of Stadthagen, Brieger, v. Udransky, and Baumann #6
have shown that such urines also contain diamines, and in particular
putrescin, cadaverin, and a diamin which is isomeric with the latter.
These bodies occur at the same time in the feces of such patients
(p. 205), while both urine and feces of healthy persons are free from
them. It is possible that they originate in a special form of intestinal
infection, are absorbed from the alimentary canal, and eliminated to-
gether with cystin in the urine.
XVII. The Urie Acid Diathesis.—Although the deposition of a
very abundant sediment of urates in the urine does not warrant the
inference that uric acid is excreted in excess, there is no doubt that there
are certain processes in the system, the chief evidence of which is such
an increase in the elimination of uric acid, and it is important to possess
the means of estimating this condition.
Many methods have been devised for this purpose, as those of Fokker
and Salkowski, and in recent years by Haycraft,#" Czapek, and JW.
Camerer.18 That of Fokker,“ as modified by Salkowshi,?° depends
upon the comparative insolubility of urate of ammonia. Those of £.
Salhowshi *?! and of E. Ludwig #2 are based on the estimation of the
almost insoluble double silver salt of uric acid.
Ludwig's process has the advantage that it can be carried out con-
pletely in twelve to fourteen hours, and it is further serviceable as a
qualitative test for uric acid in the other secretions, and in the blood
as well as in the urine.
For its application the following solutions are needed :—
1. An Ammoniacal Silver Solution.—This is prepared by dissolving
26 grms. nitrate of silver in distilled water, and adding ammonia until
the brown precipitate thrown down at first is again dissolved. The
fluid is made up to a litre, placed in a well-stoppered flask, and pro-
tected from the light.
u. A Magnesia Mixture.—A hundred grms. of crystallised magnesium
chloride are dissolved in water, and a large excess of ammonia added,
and then ammonium chloride until the precipitate (magnesium hydrate)
is entirely dissolved. The fluid so derived should be tolerably clear.
It is made up to a litre and placed in a stoppered bottle till required.
il. Solution of Sodium or Potassium Sulphide.—Fifteen grms. of
caustic potash or ro erms. of caustic soda are dissolved in.a litre of
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ESTIMATION OF URIC ACID. 309
water, and one-half of the fluid is saturated with sulphuretted hydro-
gen, after which the other half is added to it. The potash or soda
used must be entirely free from nitrates and nitrites, and to this end
it is well to use caustic soda prepared from metallic sodium.
A hundred or 200 ce. of urine are measured off in a dry glass cylinder
and carefully poured into a beaker of 200-300 cc.
capacity. Ten or 20 ce. (according as 100 or 200 ce. 2
of urine has been taken) each of solutions i. and ii.
are mixed together in a measure-glass, and ammonia a)
is slowly added until the precipitate is dissolved. The
clear fluid is then poured from the cylinder in which
the urine was measured and added to the latter in the
beaker-glass, and the mixture stirred for some time.
The precipitate which forms is allowed to stand for
half an hour or an hour, after which it is placed with
the fluid on a filter, and two or three, times the quan-
tity of water, to which a little ammonia has been added,
is supplied. For this purpose Ludwig employs an aspi-
rator, but it is not necessary, since filtration proceeds
rapidly enough without it.
The precipitate and the filter together are placed in
the beaker, and ro or 20 ec. (according to the quantity
of urine taken) of solution iii., diluted with an equal
quantity of water, is heated to boiling in a flask, added to
the precipitate in the beaker, and the mixture frequently
stirred, 40 ec. of boiling water supplied, and the mix-
ture heated over a flame until it begins to boil. It is
repeatedly stirred while allowed to cool, and passed
through a filter, which is afterwards washed two or
three times with boiling water and collected in a large
capsule. The filtrate is treated with hydrochloric acid
until it has a feebly acid reaction, and is then concen-
trated on the water-bath to a volume of 10-15 ce.
Uric acid begins to separate at this point in crystals,
which are often of a beautiful white colour.
The best plan is to continue evaporating, without regard to
the quantity of fluid remaining, until the point is reached
when uric acid begins to separate from the hot solution.
The fluid is now allowed to cool for an hour, when F!. 132.—Ludwig’s
f 7 . Filter (actual size).
the separation of uric acid will be completed. The
precipitate is brought upon a Ludwig's filter arranged with glass-wool.
This instrument consists of a glass tube about 14 em. long and 2 em.
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310 THE URINE.
in diameter in its upper point, growing rapidly narrower below, and
constricted to little more than capillary calibre at a point 4 cm. from
its lower end (fig. 132). The lower end is cut off obliquely. The tube
is packed from the point of constriction upwards as far as the beginning
of the broad part with glass-wool, which is best introduced by means of
a slender glass rod, and in such a manner that the obstruction is densest
below, and less compact as it proceeds upwards.
To facilitate this, the glass-wool with which the funnel is to be blocked may be
previously moistened with a little ether.
The author prefers asbestos to glass-wool. It answers the purpose well
and does not irritate the skin.
The upper end of the instrument is closed with a ground-glass
stopper.
When arranged with glass-wool as described, the whole is dried at 110°
C., allowed to cool, and weighed.
The filter is fixed in a suitable support, and the fluid with the uric
acid precipitate is placed upon it. The filtrate is used to wash out
the uric acid from the capsule in which it was formed, and this is
repeated until no trace of the uric acid is left in the latter, the whole
having been placed on the filter. Finally, the latter is washed repeatedly
with a little water, and best by means of an aspirator, after which the
filter. and precipitate together are dried at 100° C. They are then
allowed to cool, and small quantities of bisulphide of carbon added in
three portions of about 2 or 3 cc., the bisulphide of carbon removed by
the addition of ether, and the filter dried at 110° C. until it attains
a constant weight. The difference between this weight and that of the
filter as previously ascertained expresses the amount of uric acid in the
quantity of urine taken. The dried filter containing the uric acid may
be conveniently weighed by placing it in the scale upon a little triangular
glass support of known weight and hollowed into a suitable angle, in
which the thin end of the filter rests. The disturbing oscillation of the
latter in the scale-pan may be prevented in this way.
It may be remarked that Ludwig’s process has the advantage over the
other methods referred to that by its means several observations can be
made in one day.
A healthy adult excretes o.2-1.0 grm. of uric acid with the urine in
twenty-four hours. The quantity is increased in health by an abundant
animal diet, and pathologically in fever, leukemia (Fleischer and Penzoldt,
Rohland and Schurz), pernicious anemia, and in diseases of the heart
and lungs with obstructed respiration.4#4 A series of observations which
the author has made with the Salhowshi-Ludwig method in a case of
diabetes gave the quantity of uric acid excreted as between 0.9400 and
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URIC ACID—UREA. 311
1.4814 grm., and this quantity was not diminished by the administration
of alkalis.
The excretion of uric acid is diminished in a number of chronic
affections, such as nephritis, gout (after the acute paroxysm), diabetes,
and chronic arthritis. A diminution was also found by v. Bamberger #
in a case of progressive muscular atrophy. Salkowski and Spilker °°
have observed that taking alkali internally is followed by a fall in the
amount of uric acid in the urine ; and in sick children the use of alcohol
has a similar effect (v. Jaksch).427
Finally, we sometimes meet with a condition in which, with emacia-
tion and certain subjective symptoms, as hypochondriasis, &c., is asso-
ciated an enormous increase in the elimination of uric acid as the only
objective manifestation, and such cases undoubtedly constitute what is
called the uric acid diathesis. 48
XVIII. Urea.—By far the greater part of the nitrogen taken in with
the food is eliminated as urea. It must not, however, be forgotten that
there are in the urine other nitrogenous compounds, such as uric and
hippuric acids, amido- and other acids, and ammonia salts, but the great
bulk of nitrogenous waste is removed in the form of urea. Of this
body 32-40 grms. are daily excreted by a healthy man, but its quantity
varies considerably under physiological, and still more under morbid
conditions.
Amongst diseases, fever and diabetes are attended with increased
elimination of urea. [Prout has described a morbid condition which
he calls azoturta, and which he ascribes to an excessive formation of
urea. | On the other hand, this is diminished in chronic affections
accompanied by malnutrition and in diseases involving the proper struc-
ture of the liver, where it is elaborated (Schréder).
The quantity of urea excreted is lessened by taking alcohol in the case of
children (v. Jaksch).“° On the other hand, there is an increased excretion of
urea in children during the febrile period of lobar pneumonia (v. Jaksch).4}
Bernabei #3" has observed a diminished excretion (hypoazoturia) as a constant
occurrence in chronic alcoholism.
Variations in the output of urea are an expression of changes in nitro-
genous metabolism generally, and as such possess the highest clinical
interest. It would be well if we could measure the quantity of that
body in the urine at any given time, but the processes by which this
can be done are not available for clinical purposes.
An approximate estimate of the quantity of urea excreted in the
course of twenty-four hours may, however, be effected by Hiifner’s #°
method. In this the urea is decomposed by means of alkaline hypo-
bromites, and the nitrogen given off as a gas is collected, whilst the
carbonic acid combines with caustic soda present. The apparatus
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312 THE URINE.
required is represented in the accompanying figure. It consists of a
cylinder of stout glass of 100 cc. contents (B), expanding at its middle,
and connected below by means of a binder and tight-fitting tap with a
smaller tube (A), also of glass, which holds about 5 cc. It is important
that the capacity of the latter, which serves to receive the urine,
together with that of the perforation in the tap, shall be accurately
Fic. 133.—Hiifner’s Apparatus for Estimation of Urea.
known. To this end the apparatus is carefully washed with water,
rinsed out with alcohol, and dried. The tap is opened, and mercury
poured into the lower vessel so as to overflow into the upper one. ‘The
tap is now closed, the overflow of mercury above it poured off, and the
contents of a removed and weighed in a vessel whose own weight is
known. The result divided by the sp. gr. of mercury (13.59) gives the
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ESTIMATION OF UREA. 313
cubie contents of the tube a. This must be verified by repeating the
process, and if the capacity ascertained should vary each time, the mean
must be taken. It should be calculated to three places of decimals.
In cases where the method of weighing cannot be conveniently carried out,
the capacity of the vessel destined to hold the urine may be ascertained with
great accuracy thus :—This portion of the apparatus is filled with a watery solu-
tion of some aniline dye which is not taken up by chloroform, the apparatus
washed out with chloroform and the tinted water together with the chloroform,
in which little or none of the dye dissolves, is placed in an accurately graduated
burette. The chloroform is allowed to settle and the quantity of the aniline
fluid in the burette is read off. This process should be gone through at least
three times, and the mean is taken of the ascertained results, which, however,
usually agree well.
The remaining parts of the apparatus are a glass bowl (c¢) fitting by a
caoutchoue stopper in its bottom upon the upper extremity of B, and a
glass tube 30-40 cm. in length, 2 cm. wide, and accurately graduated in
0.2 em. units of capacity.
A rough estimate of the proportion of urea is formed either by previous
analysis, or, better, by inference from the sp. gr. of the urine, and the
‘latter diluted in such a way that a specimen shall contain not more than
1 per cent. urea. The vessel a, whose capacity is accurately known, is
filled by means of a long funnel with urine, the well-greased tap closed,
and the bulbous vessel B washed well with water, so as to remove all
trace of urine from its surface. Another tube, about half a metre long,
may be interposed between the upper end of B and the bowl (c), with
the object of prolonging the contact between the column of urine and
the hypobromite, and so securing its complete decomposition.
A fresh solution of hypobromite is then made in the following man-
ner :—1o0o germs. of caustic soda are dissolved in 250 cc. of water, the
mixture allowed to cool, and 25 cc. of bromine added. The solution
must be freshly prepared for use, withheld from the light, and kept in
a cool place. The concentrated fluid so prepared gives better results
than the more diluted reagent formerly in use (Pfliiger and Schench).434
With the vessel c in position, B is entirely filled with the above solution,
and a concentrated solution of common salt is poured into c to a depth
of rem. The graduated tube p is likewise filled with the common salt
solution, care being taken to exclude air-bubbles, and inverted in c over
the tapering extremity of B, which projects into the solution of common
salt contained in that vessel. It is fixed by a clamp in this position.
Distilled water may be substituted for the salt solution.
The tap is now opened. The relatively heavier hypobromite solution
sinks, and as it does so a rapid evolution of gas takes place and lasts
for 15-20 minutes. The nitrogen formed collects in the graduated tube,
and when it has ceased to be given off, the latter is closed with the
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314 THE URINE.
thumb and, still inverted, placed in a cylinder of pure water. It is
there held with a clamp, and is depressed as much as possible for a
space of fifteen minutes. After that it is raised with wooden forceps
until the fluid in the tube and that in the cylinder stand at the same
level. The volume of contained gas is then read off, and the barometric
pressure and temperature are noted at the same time. i
From the volume of nitrogen obtained in this manner the weight in
‘orammes of the urea taken may be deduced by the following formula :—
v(b-')
ae 354-3. 760 (1 + 0.00363t)
Where
G = weight of urea in grammes.
as
t
) = barometric record.
volume of gas generated (in cc.).
temperature.
}’ = tension of water-vapour at temperature ¢.
The percentage of urea is expressed by the product of G x 100
divided by the volume of urine analysed. The number 354.3 is sub-
stituted in the equation for 372.7, since it has been found that from
t grm. of urea the total quantity of nitrogen, namely, 372.7 cc., is
never obtained in this way, and that the number chosen more aptly
represents the fact.
The value of 0’ will be found in Bunsen’s tables, from which the
following figures are extracted.“° They express in millimetres the
tension of water-vapour at the corresponding temperatures, which are
those most commonly existent :—
oC. . . 9.165\14°C. . . 11.908) 18°C. . . 15.357] 22°C. . . 19.659
u°C. . . 9792/15°C. . . 12.699 | 19°C. . . 16.346] 23°C. . . 20.888
WAP. 5 Mowat GSP Ch 5 5 eESAS || or, 5 6 Were ian, . . aaa
1 Cm eal LOZ 177 Chee 4 a2 aoe Caen lS: 405) 0251 Canes 550
To carry on-such investigations uninterruptedly at least two sets of
apparatus should be available. The researches of Pfiiger®° and his
pupils have shown that the results obtained are not entirely accurate,
but sufficiently approximate. The method has the advantage over
others presently to be described, that it can be carried out quickly.
Moreover, the object of a clinical investigation is less often to ascer-
tain the precise quantity of urea than to determine its variations at
different times, and this purpose the method admirably fulfils.
Huppert ®" has shown that by this process one can ascertain approxi-
mately the total amount of nitrogen excreted in the urine, provided
that the uncorrected number representing the amount of nitrogen, as
obtained by Hiifner’s method, be multiplied by 1.136. In the case of
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ESTIMATION OF UREA—KREATININ. 315
a febrile urine the factor is 1.18. Recently a number of other apparatus
of the same kind have been employed.#28 That of Lange seems specially
serviceable,*9
The quantitative estimation of urea may also be effected by Liebig’s
titration method, as modified by Pfitiger. It will be found described
at length in the systematic works of Huppert, Hoppe-Seyler, and Leube-
Salkowsht.° The method of Morner and Sjoqvist*“ is also a good one,
but the figures derived by it are a little too high.
To estimate exactly the total quantity of nitrogen obtainable from the
urinary products other methods are needed, as those of Will-Varrentrapp
and J. Kjedahl.“2 It is often desirable to determine the amount of
urea with reference to the total excretion of nitrogen, and this may be
done by the application separately of Morner’s and Kjedahl’s methods.
The qualitative tests for urea are described in the chapter on Blood
(p. 69). In connection with urine they possess but little practical
interest.
XIX. Kreatinin. —-In addition to the substances mentioned at
p- 321, human uwrine contains certain other-nitrogenous organie com-
pounds, by means of which nitrogen is also eliminated from the system.
Amonest these are betain, hypoxanthin (sarkin), xanthin, xanthokrea-
tinin, kreatin, and kreatinin. The occurrence of these substances is,
with the exception of the last, without clinical significance at present.
The interest attaching to the separation of kreatinin is of a very sub-
ordinate kind, and it will suffice to state a few facts concerning its
production, detection, and clinical import. For information about the
other substances named the reader may consult the books of reference
already mentioned.
The formation of kreatinin has been shown to be intimately associated
with the decomposition of ruscle-substance, and the quantity produced
is in direct relation to the amount of flesh-meat consumed as food,
and, under certain circumstances, to the muscle-waste within the body.
Under these circumstances muscle contains kreatin, which is changed
into kreatinin as it passes through the body.
This is to be borne in mind when a clinical inference is drawn from
the observation of an increase or diminution of the quantity of kreatinin
secreted. Hitherto such inferences as were possible have had but a
limited application to the purposes of diagnosis. They are insufficiently
based, and rest for the most part on the experience of individual cases.
According to Neubauer,#* the quantity excreted by a healthy man is
about 1 grm. According to Pouwchet,** it is 1 grm. in the case of the
male, 0.75 grm. in that of the female, while kreatinin is altogether
absent from the urine of sucklings. This point, however, is contested
by Gocco.”
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316 THE URINE.
An increase in the output of kreatinin has been observed in acute
diseases of all kinds while attended with fever, and in diabetes (Senator),
and a diminution in chronic nephritis and diabetes insipidus, in convales-
cence after acute diseases, in chlorosis, aneemia, tuberculosis, and maras-
mus,*" and as a consequence of insufficient feeding.45
Kreatinin is a base which forms highly characteristic compounds with
acids, such as phosphotungstic and phosphomolybdic, hydrochloric and
sulphuric, and with salts of the heavy metals.
Qualitative Vests—Kreatinin may be detected directly in the urine
by the methods of Weyl # and Jafé.#°
Weyl’s Test.—For the application of this test the urine should be
freed from acetone by distillation (p. 303). A freshly prepared and
very dilute solution of nitroprusside of soda and caustic potash is
added. If kreatinin be present, the fluid will take a beautiful red
colour (like that produced in Legal’s test for acetone), which soon dis-
appears, and does not return with the further addition of acetic acid.
Jagés Test.—A fairly concentrated solution of picric acid and a little
caustic potash are added to the urine. If the fluid be heated, the
presence of kreatinin will be shown by the appearance of a beautiful
red coloration. Acetone and grape-sugar yield a similar reaction.
Picrie acid with caustic potash alone gives a slight red colour.
Quantitative Estimation.—Kreatinin forms with zine chloride a double
salt of slight solubility, and this property is made the basis of the
quantitative method, which was first devised by Mewbauer #! and modi-
fied by Salkowshi.4°?
Two hundred ce. of urine are mixed with a little milk of lime until
the fluid has an alkaline reaction. This is to precipitate phosphoric
acid. A solution of calcium chloride is added until a precipitate ceases
to form. The fluid is allowed to stand for half an hour, after which
the precipitate is filtered off and repeatedly washed with water, and
the filtrate and washings (a¢idulated with a little sulphuric acid) are
evaporated on the water-bath to a syrupy consistence. To the residue
is added 50-100 cc. of 78 per cent. alcohol; the mixture is well stirred
and allowed to stand in the cold for several (6-8) hours; then it is
filtered, and to the filtrate (which, if alkaline, must be rendered acid
with acetie acid) 10-15 drops of an alcoholic solution of zinc chloride
are added. The latter is prepared by adding alcohol to a concentrated
solution of zine chloride until a density of 1.2 is attained. After the
lapse of two or three days the precipitate is brought upon a filter of
known weight, and the filtrate as it passes through is constantly
returned to wash the vessel which contained the precipitate. When
all the precipitate has been brought upon the filter in this way, it is
washed with go per cent. alcohol until the filtrate shows but slight
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ESTIMATION OF KREATININ—PTOMAINES. 317
opalescence with silver nitrate; after which it is dried to a constant
weight at roo° C. One grm. kreatinin-zinc-chloride corresponds to
0.6242 grim. kreatinin. The amount of kreatinin in the quantity of
urine taken may therefore be known by multiplying the quantity of
kreatinin-zine-chloride obtained by 0.6242.4%
Kreatin, which is closely related to kreatinin, does not occur as such in the
urine, but it is readily formed from kreatinin in alkaline fluids. Hence it follows
that alkaline urine should not be employed clinically for the quantitative estima-
tion of kreatinin.
In addition to kreatinin a number of basic substances have recently
been isolated from urine by precipitation with phosphotungstic acid
(Thudichum **), such as urochrome, urotheobromin, omichol, and reducin.
The physiological action of these substances is not yet known.
Salomon * has proved that hypoxanthin is a normal constituent of
urine. Future researches will show in what relation it stands to cer-
tain diseases, or to the putrefaction bases presently to be described.4°6
XX. Ptomaines (Putrefaction Bases) in the Urine.—It would
appear from the investigations of Powchet 1°" that healthy urine contains
traces of certain toxic substances of an alkaloid character, and according
to the researches of Bouchard,#® Lépine, and Guerin,®® these bodies
are more abundant under morbid conditions. They were found by
A, Villiers *° as an invariable manifestation in measles, diphtheria, and
pneumonia ; and in the urine of cholera A. G. Pouchet #1 discovered an
alkaloid which was not identical with that observed by him in the feces
of the same disease (see p. 205). Feltz *°? found similar bodies in the
urine of cancer patients, and Lépine +? in that of pneumonia. Roges and
Gaume ** observed that the toxic property of the urine was lessened in
the febrile period of pneumonia (retention of potash salts ?). Bouchard *
discovered that human urine acted as a poison when injected within the
veins of animals (rabbits), and he referred the effects to various sub-
stances, among which were animal alkaloids. For the detection of the
urinary alkaloids the following method has been adopted by Tanret,
Bouchardat, and Cardier #8 ;—
To the urine which has been acidulated with acetic acid a solution of
the iodide of mercury and potassium is added. The precipitate, which
contains the alkaloids, is readily distinguished from those of other
substances, as albumin, mucin, and uric acid, obtained with the same
reagent, by its solubility in alcohol at a warm heat.
Ch. Bouchard rendered the urine alkaline with caustic soda, and
derived a poisonous body as an ethereal extract.
Pouchet fixed the alkaloid by combination with tannic acid, and
subsequently precipitated it with oxide of lead from alcoholic solution.
The methods adopted by the other observers mentioned above differed
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318 THE URINE.
much as to details. They will be found described at length in the
original communications. That of Brieger (p. 158) serves best for the
detection of animal alkaloids in the urine. In some cases, however, it
is important that the urine be previously concentrated in vacuo. Should
no result be obtained with this, Gautier’s 467 method may next be tried.
Finally, the Stas-Otto method may be applied to the same purpose.
(See p. 158.)
The diamines of the urine may be precipitated as benzoyl compounds,
and best by the action of benzoyl chloride and caustic potash. Bav-
mann and Udransky 8 succeeded in separating several basic derivatives,
amongst them cadaverin (pentamethylendiamine), putrescin (tetramethyl
diamine), and a small quantity of a third diamine, from the urine of a
patient with cystinuria and vesical catarrh (see p. 308). Normal urine
was found to be free from these bodies. The author has been for some
time engaged in observing the occurrence of similar poisonous bases in
the urine of health and disease, and he has found that normal urine and
that of some diseases, notably typhoid, pneumonia, leukemia, cystic
pancreas, and Weil’s disease,#°? hold such only in very small quantity.
He would venture to make some suggestions for the benefit of those who
are engaged with similar researches. In the first place, it would be well
to follow the example of Brieger, Baumann, and v. Udransky, and with-
hold the name of alkaloids from the bodies (diamines) alluded to, which
are derived from the system under morbid conditions, because all that
have been recognised as yet are simply diamines, and because none yet
examined exhibit the characteristic property of alkaloids, namely, the
pyridin radicle. Next, it would be desirable to discriminate between
the physiological bases of the urine (kreatinin, reducin, &c.), which belong
normally to the fluid, and those which are associated only with certain
diseased states. It is not intended to imply that the physiological bases
cannot under any circumstances give rise to the symptoms of disease
or of poisoning. (See below.) Experience is not wanting to make it
seem in the highest degree probable that the retention, and still more
the increased formation, of such physiological products in certain dis-
eases may induce symptoms of the gravest character, and greatly imperil
the life of the patient.
Again, it would appear that in certain acute affections specific sub-
stances of a toxic character, not observable in normal urine, may be
excreted with that fluid. Undoubtedly the matter is somewhat obscure.
The author’s views may be stated as follows. It is possible to dis-
tinguish :—
(1.) Clinical (morbid) symptoms depending upon the retention of
the physiological bases (and under this heading would come uremia)
and certain of the symptoms of obstruction (retention-toxicosis).
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ANIMAL ALKALOIDS—FERMENTS. 319
(2.) Clinical symptoms, referable to the presence of basic products,
which are formed in the system (blood, &c.) in disease and eliminated
with the urine (noso-toxicosis). [Bruschettini*™ has conveyed tetanus
to animals (rats and rabbits) by injecting the urine of patients suffering
from that disease—a fact which would make it appear that the poison
of tetanus is eliminated by the urine. ]
(3-) Clinical symptoms which are caused by the formation of toxic
basic substances from morbid matter, such as pathological fluids lodged
in certain parts of the system. Such bases are absorbed, and then give
rise to manifestations of severe poisoning. Under this heading would
come the collective symptoms of ammoniemia (see p. 77), and others
which follow the absorption of gangrenous pus (auto-toxicosis). The
latter are sometimes characterised by the presence of guanin,*? and it
is probable that the formation of toxalbumins has much to do with
them. These may readily be detected by the methods of Brieger and
Fraenkel.+?
(4.) Clinical symptoms, and consequently morbid types, induced by
the action of toxic bases taken into the system with the food, such as
the poison of sausages and cheese, p. 158 (exogenic toxicosis).
These distinctions are based partly upon clinical observation and
partly upon experiments on animals. They will serve as a scheme for
the further elucidation of this very important subject.
If we have dwelt at some length on the result of observations which
are not yet completed, we have done so because we believe that the
careful investigation of the urine in this direction will throw light
upon the nature of some diseases which are at present not sufficiently
understood,
XXI. The Ferments of the Urine.—The appearance in the
urine of a body resembling pepsin was long ago established by ».
Briicke.** Sahli, Leo, Gehrig, Stadelmann, and Patella + made similar
experiments, and confirmed the presence of pepsin in the urine. It has
been asserted that trypsin is also an occasional constituent of that fluid,
though some observers, Leo, Stadelmann, and Grriitzner,*® have failed to
find it.
With reference to the pepsin ferment of the urine, clinical interest
attaches to it from the fact that it is absent in typhoid and carcinoma
of the stomach,*”" and according to some observers (Mya, Belfanti #78) in
nephritis.
For the detection of pepsin Sahl’s method (adapted from those of
y. Wittich and Griitzner) may be employed. It is founded upon the
property which, as v. Wittich originally observed, blood fibrin possesses
of readily absorbing that body from solutions. To this end a little
pure fibrin is placed in the urine and allowed to rest there several
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320 THE URINE.
hours. It is then removed, placed in dilute hydrochloric acid (.2 per
cent.), and the mixture kept at a temperature of 30-4o° C. Any
pepsin present is precipitated on the fibrin, and the latter is slowly
digested in the acid fluid.
Diastatic ferment also is said by Hovoltschiner and Rosenberg to occur
in urine.479 The researches of Breusing *° and observations made by
the author tend to show that the ferment in question is in many cases
not diastase, but an amylolytic substance. At the same time it must be
stated that the author has frequently determined the presence of diastase
by the usual.methods, both in health and disease. So, too, Leo #8! has
found diastase both in healthy and in morbid urine.
Milk-curdling ferment is occasionally present in the urine (Hovolt-
schiner,*®? Boas,*83 Helwes).
As to whether the urine contains a ferment capable of decomposing
urea into carbonic acid and ammonia, opinions differ. On the one
hand, Musculus+8+ believes that he has isolated such a ferment, but
Leube*® has sought for it in vain in urine which was actually under-
going ammoniacal fermentation. 4°
B. Inorganic Substances.—The inorganic constituents of the
urine are for the most part salts of hydrochloric, sulphuric, and phos-
phoric acids, to which must be added carbonates, silicates, nitrates and
nitrites, and sulphuretted hydrogen.
1. Chlorides.—The chlorides of sodium, potassium, ammonium, and
magnesium are found in the urine, and of these we are chiefly con-
cerned with chloride of sodium. Of this salt 10-15 grms. are voided
by a healthy man in twenty-four hours; but its quantity is greatly
influenced, even in disease, by the supply of salt taken as food.
It is increased by an abundant diet and as a consequence of condi-’'
tions which determine the retention of chlorides within the system ;
and diminished in fevers, and notably in croupous pneumonia.487 The
elimination of chloride of sodium has also been observed to be less in
cases of chronic nephritis, and sometimes in certain diseases of the
stomach (Gluzinsh?).4§
Detection of Chlorides.—The urine is treated with nitric acid, and a
solution of nitrate of silver added. A caseous precipitate soluble in
ammonia, insoluble in nitric acid, shows the presence of chlorides.
Quantitative Estimation of Chlorides.—Mohr’s method is to treat the
urine with chromate of potash, and gradually add nitrate of silver,
when all the chlorine combines with the silver to form silver chloride,
and the occurrence of a-red precipitate (chromate of silver) marks
the end of the reaction. The details of the process will be found in
works on urinary chemistry. Saliowshi’s ° modification of Volhard’s 49
method is to be preferred.
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ESTIMATION OF CHLORIDES. 321
When to a solution of nitrate of silver acidulated with nitric acid is
added some of a solution of sulpho-cyanide of ammonium, a curdy
white precipitate forms, and this, like chloride of silver, is insoluble in
nitric acid, soluble in ammonia. If the fluid also contains a ferric salt,
a blood-red colour (ferrocyanide) forms at the moment when the last
of the silver is precipitated. If now the sulpho-cyanide of ammonium
solution is of a known degree of concentration, it is possible to deter-
mine the quantity of silver present by noting the point at which the
red coloration takes place. To apply this principle for gauging chlorides
in solution to the fluid containing them, a silver solution of a definite
degree of concentration is added in excess, and that portion of it which
is not precipitated as chloride of silver is measured in the manner indi-
cated above.
The following solutions are needed in the process :—
1. Pure nitric acid of 1.2 sp. gy.
u. Concentrated solution of double sulphate of ‘ron and ammonia free
From chlorine. It is necessary that this be free from chlorine, and if
not already so, it must be purified by crystallisation.
ili. Nitrate of silver solution of definite strength. The chemically pure
crystalline salt is dissolved in water in the proportion of 29.075 grms.
to the litre. '© while Penzoldt®™ and Petri *'8 dissent from it.
Ehrlich obtains the reaction, not with dia-benzol-sulphonic acid itself,
but with sulphanilic acid. Fifty cc. hydrochloric acid are made up to
1ooo ce. with water and sulphanilice acid added to saturation. To 200
ce. of the mixture 5 cc. of a 4 per cent. solution of sodium nitrite are
added, and the resulting fluid is added to the urine in equal parts.
Ehilich*®™ has recently recommended that five to six times the volume
of absolute alcohol should be added to the fluid to be tested, and the
reagent, prepared as above, then added drop by drop to the filtrate.
Normal urine gives a yellow colour, while the urine of fever patients,
&e., turns scarlet.°° The author’s experience would induce him fo dis-
claim for this test any clinical importance whatever, and he would especially
enjoin the necessity of avoiding inferences based upon the appearance of
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THE URINE IN DISEASE. 329
the reaction indicated. He believes that the colour when obtained is
always due to the presence of acetone, and he prefers to regard the pro-
cess rather as an uncertain indication of that body than as a test for
anything else.°21
It will be seen from this brief statement that a careful analysis of the
urine will serve to make evident the details of acute processes earlier
and more readily than the methods formerly at our disposal. Other
lines of investigation are appropriate to certain acute affections ; thus,
for instance, in pneumonia the presence of chlorides will be sought.
II. The Urine in Disorders of the Circulation (Congestion).
—Under such conditions the urine in its physical characters closely
resembles that of fever. It is diminished in quantity, of acid reaction,
and high sp. gr. (1.025-1.035). It commonly deposits urates.
Chemically it may be distinguished from fever urine hy—
(1.) The absence of acetone and diacetic acid.
(2.) The presence of albumin in greater quantity.
Microscopically, and especially when the congestion is chronic, the
urine exhibits some leucocytes and altered red blood-corpuscles, often
also hyaline casts and cylindrical aggregations of urates (see p. 224,
fig. 94), waxy and a few granular casts and renal epithelium. Such
constituents indicate secondary changes in the kidney of a chronic
inflammatory character.
[The Urine of Phthisis.—Hale-White**? has pointed out that the urine of
phthisis exhibits two peculiarities. Such urine remains acid for a very long
time, occasionally for several months, and contains few bacilli, but a large pro-
portion of yeast-like organisms. The persistence of acidity is probably due to
a form of acid fermentation. ‘The urine, when kept for a long time, turns very
dark in colour, some specimens becoming quite black. The cause of this change
is not known.]
III. The Urine in Diseases of the Urinary Organs.
1. Renal Affections. .
(a.) Acute Nephritis.—In this disease the urine is at first diminished
in quantity—s5o0o0-800 ce. or less being passed in twenty-four hours—
of acid reaction, and high sp. gr. (1.015-1.025). The sp. gr. rarely
attains to so great a height as in the urine of congestion. It ranges in
colour from blood-red to that of a watery extract of meat, and the
presence of blood-pigment in considerable quantity may be determined
by Heller’s test or by spectroscopic examination. In the latter case, if
the urine be. fresh, the characteristic bands of methemoglobin may be
visible.
Chemical analysis shows large quantities of albumin.
Microscopical investigation of the sediment affords the clue to the con-
dition. It exhibits—
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339 THE URINE.
(1.) Red blood-corpuscles in variable proportion. These are for the
most part altered, and present the appearance of washed-out discs
(phantom corpuscles).
(2.) Some leucocytes. These are always less numerous than the
phantom cells just mentioned.
(3.) Epithelium. Chiefly small polyhedral uninuclear cells from the
urinary tubules, with a few others derived from the renal pelves and
bladder.
(4.) Casts. These are (a) formed of blood-corpuscles ; (4) formed of
leucocytes ; (¢) formed of renal epithelium; (@) hyaline, more or less
thickly beset with epithelial cells and red or white blood-corpuscles.
Such. are the microscopical constituents of the sediment at the
outset of an acute nephritis, as in the first and second days of the
nephritis of scarlatina and erysipelas. They alter their character as
the disease progresses, and after the lapse of a few days, and side by
side with those described, appear the metamorphosed casts, granular and
waxy, We.
When in the course of chronic nephritis an acute exacerbation takes
place, the urine possesses a similar character to that described above.
But, as before, the description applies with full force only to the earlier
period of the attack. If death from uremia or cedema of the lungs
does not ensue, the physical characters of the urine tend gradually to
return to those of health. It is more abundant, the contained blood
grows less, and then a light flesh-water tint alone declares the existence
of acute nephritis. Albuminuria becomes less marked, and finally ceases
with the approach of health. The other signs, recognisable only by
means of the microscope, disappear with, or shortly after, the cessation
of the albuminuria. It must be borne in mind that to justify the
diagnosis of nephritis the formed material of the urine must be present
in considerable quantity.
The occurrence of micro-organisms has been noticed at p. 235.
(v.) Chronic Nephritis.—The urine is normal in quantity, or some-
what lessened (1200-1500 ee. daily), acid, and of normal sp. gr. It
usually contains a very considerable proportion of albumin. Micro-
scopically the sediment is very variable in character, but renal epithelium
is never absent, and the cells are often fatty. There are metamorphosed
casts of different kinds, especially granular casts, and hyaline casts
covered with blood-corpuscles or renal epithelium (p. 226). These are
of special importance in diagnosis.
The occurrence of casts composed of fatty matter or pyeriendl with
fat-erystals indicates advanced fatty degeneration of the renal. tissue
(p. 229).
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CONTRACTED AND AMYLOID KIDNEY. 331
It occasionally happens that, with all the symptoms of chronic nephritis
present, no trace of casts or epithelium can be found in the urine. This occurs
most often in long-standing and very chronic cases. Schrwald**3 has called
attention to the occasional absence of casts from the urine of nephritis, and
believes that this is to be accounted for by their solution by pepsin (see p. 319) in
acid urine. To guard against this, he suggests that the urine should be allowed
to stand only for a short time and at a low temperature. To obtain the deposit
by means of the sedimentator would undoubtedly add an element. of certainty.
Glaser °** has shown that, as the result of moderate indulgence in alcohol, the
non-albuminous urine of healthy persons may contain abundance of leucocytes
and casts of all kinds. These he ascribes to irritation of the kidney by alcohol.
In conclusion, it may be stated that in rare cases of chronic nephritis the urine
is altogether normal.
(c.) Contracted Kidney.—The quantity of urine is very greatly in-
creased—4oo0o to 5000 ce. being passed in the twenty-four hours. Its
reaction is acid and sp. gr. low (1.008-1.012 and less). In this respect,
however, exceptions are not uncommon. The author has met with
cases in which the quantity of the excretion was diminished and the sp.
gr. proportionally increased. It is pale in colour, and contains but little
albumin, sometimes only a mere trace. The sediment is usually scanty,
and, when examined with the microscope, exhibits generally but a few
hyaline and some granular casts
It is to be observed that even those cases in which only a trace of albumin is
to be found (small red kidney of &ibbert) often run a particularly unfavourable
course.
(¢.) Amyloid Kidney.—In this condition the urine presents charac-
ters which are for the most part similar to those of contracted kidney,
that is to say, it is increased (though sometimes normal) in quantity, of
acid reaction, and low sp. gr. As a rule, however, it contains more
albumin.
Microscopical examination of the sediment shows hyaline casts in
comparative abundance and some epithelium. The microscopical ap-
pearances, however, are subject to much variety, and the author has
observed cases which were hardly to be distinguished from those of
chronic nephritis. The amyloid reaction (iodo-potassic-iodide and sul-
phuric acid, &c.) with the casts cannot be depended upon, since, on the
one hand, it is often obtained when the post-mortem appearances show
no amyloid degeneration of the kidneys, and, on the other, it is absent
in many cases where the symptoms (enlarged spleen and liver, &c.) point
to this condition.
(e.) Ureemia.—The urine in cases where the symptoms of uremia
supervene is always rich in albumin, and microscopically resembles
that of nephritis. It is scanty in a degree that sometimes amounts to
anuria, and even when greatly reduced in quantity, we often find that
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332 THE URINE.
its sp. gr. is still below the healthy standard. Again, the quantity
excreted may remain unaltered, but the sp. gr. in such cases is always
greatly reduced.
When the urine is of this character, it would seem to hold poisonous
bases in smaller quantity than ordinarily.52°
What has been said here applies only to typical forms of renal disease. The
appearances are modified according to the various anatomical perversions of the
kidney structure upon which they depend.
Investigations which the author has made as to the character of the
urine of children suffering from nephritis show that the important con-
stituents of the excretion, urea, uric acid, sulphuric and phosphoric
acid, are constantly diminished in quantity. In adults, according to
Miinzer, the urea is less, and the total elimination of nitrogen is always
reduced.5*6
2. Pyelitis Caleulosa.—The urine passed during the paroxysms
of this affection is diminished in quantity, contains mucin in abundance,
blood and pus in variable proportions, and concrete masses of uric acid
or urates. After the paroxysms the urine is passed in great abundance.
It is then pale in colour and of low sp. gr., and exhibits probably a
flocculent precipitate of mucin. Persistent polyuria is common. When,
as commonly happens, the condition is complicated with catarrh of the
ureter and bladder, a more or less abundant purulent sediment forms
independently of the attack.
According to J. Fischi,°*" the urine at the commencement of this
disease always contains casts, both hyaline and granular, and this
authority regards their presence as of great importance in the differ-
ential diagnosis of pyelitis and cystitis. In addition, there occur plugs
of cylindrical form composed of conglomerated white blood-corpuseles.
These are probably derived from the renal pelves, and indicate an exten-
sion of the processes to the kidney proper, or pyelonephritis. When
the latter. condition is established by the appearances of pyelitis, then
the presence of nephritis, and granular casts, renal epithelium, &c., may
be observed.
In a case which was under the author's care, investigation of the urine dis-
closed a remarkable appearance. ‘The patient was a woman with renal calculus
causing pain, The urine held abundance of carbonate and sulphate of calcium
and triple-phosphate, and in it were long spiral bodies of large size, which
macroscopically, microscopically, and chemically exactly resembled Curschmann’s
spirals. There was no pus. ‘he condition was probably an affection of the
ureter analogous to enteritis membranacea, and it might be appropriately called
ureteritis membranacea. These membranous bodies continued to be discharged
for some days.
8. Cystitis.—In uncomplicated cystitis the urine is generally pale,
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CYSTITIS—TUBERCULOSIS. 333
of normal sp. gr., and has an acid reaction, unless when alkaline fermen-
tation takes place within the bladder. In the latter case it is turbid,
and deposits on standing a more or less abundant deposit of fat-laden
and swollen leucocytes and triple-phosphate crystals. Microscopically,
moreover, pus cells and epithelium of various forms are to be seen.
Amongst the latter, certain cells from the deeper layers of the mucous
lining, provided with one or two finger-shaped processes, are especially
noticeable (see p. 219). In connection with ichorous or hemorrhagic
cystitis, red blood-corpuscles and pigment masses appear in the urine.
The complication of cystitis with an affection of the ureter cannot be
determined by chemical and microscopical investigation, but its presence
must be diagnosed from the existence of the other clinical symptoms.
Schnitder 8 has observed that the urine in cases of cystitis often
contains a bacillus, pure cultivations of which, when transferred to the
bladder of animals (rabbits), give rise to symptoms of the disease.°?
Similar indications may be produced by a purulent urethritis, and
confusion in this respect is to be guarded against.
The condition which has been designated as ammonizmia, and which depends
upon the absorption of ptomaines from the bladder, is often, but not always,
accompanied with cystitis. In this connection the urine, when freshly voided, is
undergoing alkaline fermentation (see p. 217).
4, Tuberculosis of the Urinary Organs.
(a.) Tubercular Ulceration. — Chemically and microscopically the
urine in this condition resembles that of cystitis or pyelitis. It is
pale, of normal sp. gr. and quantity, contains a variable proportion of
albumin, and an abundant sediment, which consists principally of
swollen and fat-laden ‘pus-cells. The diagnosis must rest chiefly upon
the recognition of tubercle-bacillus by the methods described in con-
nection. with the examination of the sputum (p. 104). In chronic
tubercular affections the micro-organism is to be seen in great abund-
ance in the urine, as in the specimen represented in fig. 108, and, as
in this case, it tends to cohere in groups shaped like the letter S (comp.
p- 236). The precise localisation of the affection must rest upon other
grounds.
(b.) Miliary Tuberculosis.—In this affection the urine is often un-
changed. It is apt, however, to contain blood at intervals, and may
be distinguished from nephritis by the absence of casts and renal epi-
thelium. Tubercle-bacilli are never to be found in considerable quantity
in the sediment.*
5. Calculus and Tumours of the Bladder.—These are to be
suspected when copious intermittent hemorrhages take place, and
when the blood which is passed with the urine separates from it and
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334 THE URINE.
is deposited in a thick layer at the bottom of the receiving vessel. The
subjective symptoms, pain, &c., are usually sufficiently distinctive (see
p- 250).
6. Catarrhal Urethritis.—The urine in catarrhal urethritis is
altogether unchanged, except that. the first flow contains pus. The
affection is rarely met with. Bockhart**! ascribes it to infection with
non-specific vaginal secretion.
7. Gonorrhzal Urethritis.—The appearances are the same as in
simple urethritis, but pus is usually very copious. It would appear
that in all cases, while the infection is recent, specific micro-organisms,
gonococci, are to be found. These were discovered by Weisser. They
are diminutive roll-shaped cocci, aggregated in large groups, which often
closely pack the exfoliated epithelium cells of the urethra and cover
Fic. 134.—Gonococci of Urethritis (eye-piece I1I., objective, oil-immersion y;, Zezss).
their surface (Weisser, Bumm, Bockhart).°*2 More recent experience
tended at first to lessen the clinical significance of these forms (v. Zeissi,
Hartdegen, Wendt),®*? since bodies altogether resembling gonococci
have been found to be present in the genital tract under the most dis-
similar conditions. The researches of Wertheim 4 in Schauta’s clinic,
however, have quite lately established their specific character beyond
any doubt. Aceording to Rous,°* the supposed gonorrheal microbe
may be distinguished from other forms by the fact that it does not stain
with Gram’s method. C. Schiitz’s®6 process is as follows :—The pre-
pared cover-glasses are placed in a semi-saturated solution of methylene-
blue holding 5 per cent. carbolic acid, and left in it for 5-10 minutes.
They are then removed and washed in distilled water, to which acetic acid
has been added in the proportion of five drops of the dilute acid to 20 ce.
of water. After this they are given the contrast-stain in a very dilute
solution of safranin. This method furnishes good specimens, but there
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URETHRITIS— HEPATIC DISEASE. 335
is no reason to prefer it to staining with carbol-fuchsin, by which the
specimens figured here were obtained. Fig. 134 represents gonorrheal
pus from a case of old infection ; fig. 135 shows gonococci from a pre-
paration of Dr. Kolisko, made with the pus two days after the infecting
coitus.®°7 The occurrence of gonococci threads and hyaline epithelium
occurring in the urinary sediment of this condition is worthy of notice.®**
IV. The Urine in Diseases of the Alimentary Canal.—
Diseases of the alimentary canal, for the most part, do not specially
affect the urine pathologically ; but in general it may be stated, that
where they are attended with increased albuminous decomposition
within the intestine, that fluid is apt to contain a large amount of indi-
can. Carcinoma of the stomach with ulceration is occasionally attested
by the appearance of peptone in considerable quantities (Matxner). In
@.” o©&
y ea?
No G oh ZX 5
@ w & @
— SO i
mm >
CO ; ag
So" @@ e
Fic, 135.—Gonococei (two days after infection).
chronic catarrh of the stomach, and especially in dyspepsia, the acidity
of the urine is apt to be much lessened.
V. The Urine in Hepatic Affections.—It may be stated in
general that in all diseases which seriously involve the proper struc-
ture of the liver, the excretion of urea is diminished, and even in certain
severe forms (acute yellow atrophy) entirely suppressed (Schultzen
and Riess).°°9 It is then to some extent represented by other nitro-
genous metabolites which appear in the urine as leucin and tyrosin *4°
(comp. p. 244), and together with these certain non-nitrogenous sub-
stances. Oxyamygdalic acid (Schultzen and Riess, Réhmann**), lactic
acid, and the volatile fatty acids are often eliminated, as in cancer and
syphilis affecting the liver (v. Jaksch).>#
Diseases which cause an obstruction to the flow of bile are attended
with the presence of bile-pigments in the urine (see p. 288).
In atrophic cirrhosis the latter is scanty, rich in urates, and almost
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336 THE URINE.
or entirely devoid of biliary colouring-matters, but often contains a
high percentage of urobilin. In hypertrophic cirrhosis it is often quite
normal in quantity, sometimes increased, and exhibits abundance of
bile-pigment.
The appearance of sugar and albumin in connection with disease of
the liver is too uncertain to be of service in diagnosis. According to
Kraus and Ludwig,°* the ingestion of carbohydrates (grape-sugar) when
the liver is diseased is attended by glycosuria. The knowledge of this
fact, however, is of little use since glycosuria belongs equally to other
conditions, as diabetes insipidus, cystic pancreas, &c. Indeed, the
chemical constitution of the urine in hepatic disease generally exhibits
much variety.°+#
VI. The Urine in Diabetes Mellitus. —In this disease the urine
is pale and clear, and in colour often inclines to green. Its quantity
is enormously increased, as much as 12-15 litres being passed in twenty-
four hours, sp. gr. high, ranging from 1.030-1.050. It is usually rich
in the indigo-forming substance, and invariably contains a greater or
less proportion of grape-sugar (p. 273). Towards the close of the
disease albumin in considerable quantity is apt to make its appearance
(Stokvis).°4° Exceptional cases of diabetes are met with in which the
quantity of urine is not increased, and its sp. gr. is even lowered. When
diabetes is complicated by acute disease, the excretion of sugar may
entirely cease, as has been pointed out by &. v. Engel in a contribution
from the author’s clinic.
The author has met with one case of diabetes mellitus, in the practice of
Professor Nothnagel, in which the urine contained much acetone, and showed a
sp. gr. of 1.003. It.was also found to hold more than 0.3 per cent. sugar in
solution.
Other substances that are occasionally to be found in the urine of
diabetes are acetone in large quantity, diacetic acid, and a number of
other organic acids, such as f-oxy-butyric acid,°#” fatty acids,48 We.
[The urea of diabetic urine is in excess of the normal—uric acid is un-
affected or diminished (Zaylor). Ammonia, according to Stadelmann,
is present in large quantity, but it is neutralised and the urine remains
acid in consequence of the $-oxy-butyric acid which it contains. ]
In view of the fact that B-oxy-butyrie acid occurs in the. urine of
diabetes, and of other conditions, as febrile states, some notice of the
method of detecting that body is called for. The following method by
Kiilz is the best.o4? The grape-sugar in the urine is fermented with
yeast, the fluid filtered, and the filtrate concentrated to a syrupy con-
sistence. The latter is mixed with its own bulk of concentrated
sulphuric acid, the mixture distilled, and the distillate collected in a
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DIABETES—AN MIA. Bae
test-glass. If 8-oxy-butyric acid be present, crystals of a-crotonic acid
separate on cooling from the contents of the test-glass, and may be
recognised by determination of their melting-point (72° C.). Should
no such crystals form in the process, the distillate is shaken up with
zther, and the crystals which deposit on evaporation of the ether are
tested to ascertain their melting-point.
[The researches of Stadelmann and others point to B-oxybutyric acid as the
toxic agent in diabetes. It yields diacetic acid on oxidation, and this breaks
up into CO, and acetone.]
Diabetic urine contains other carbo-hydrates, fruit-sugar,°®? dextrin,
&c. According to Kiilz,°°! casts occur at the commencement of diabetic
coma.
VII. The Urine in Diabetes Insipidus.—Marked polyuria is the
characteristic symptom. Sixteen to twenty litres may be passed in the
day. The urine is clear and almost colourless, of greatly reduced sp. gr.
(1.0001~-1.004). It contains neither albumin nor sugar, although it
sometimes yields a small proportion of indican and inosite.
VIII. The Urine in Anemia.—The fluid is pale, of low sp. gr., and
neutral or alkaline in reaction. [Though pale when passed it sometimes
turns a deep red colour on the addition of nitric acid (Zaylor). This
depends on the presence of a chromogen (see p. 214).] In the later
stages of a severe anemia albumin may be found, whilst at the same
time, except for a few hyaline casts, tissue elements are entirely absent
from the sediment (Bamberger’s hematogenic albuminuria).
[The urine of pernicious anemia is of low sp. gr. and very highly
coloured. It contains (1) pathological urobilin ; (2) granules of blood
pigment, microscopically ; (3) excess of iron. These characters are of
549
much importance in diagnosis (Hunter).5°2
According to Hunter, the elimination of iron by the urine, while diminished in
chlorosis, is greatly increased in pernicious anzemia. He estimates the daily out-
put as follows: In health, 5.6 mgrms. ; in chlorosis, 1.7 mgrm.; in pernicious
anemia, 32.2 mgrms. The same observer has found diamines in the urine of
this disease.>°3]
B55
In leukemia the elimination of uric acid is increased.*54 Pyrus 555 has
observed leucin, and lactic acid is also found in the urine.*5* The
urine is rich in nucleo-albumin,°*” but never contains peptone.
It will be convenient here to describe the method by which the lactic
acid may be detected.
Detection of Lactic Acid.The urine is evaporated on the water-bath
to the consistence of a syrup and extracted with alcohol. After the
alcohol is distilled off or evaporated, the residue is extracted with ether,
the ether distilled off, and the residue dissolved in water. To the
Y
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338 THE URINE.
solution a little basic acetate of lead is added. It is then filtered, the
filtrate treated with sulphuretted hydrogen, again filtered, and finally
digested on the water-hath. Lactic acid remains behind in the form of
a syrup. From this the zine salt may be obtained by the addition of
carbonate of zinc. It may be recognised by its microscopical appearance
(small prisms), or chemically by the proportion of water and of zine
respectively which result from its decomposition.
Colasanti and Moscatelli®® assert that sarcolactic acid appears in the urine
normally after great bodily exertion. AHcuss*° failed to detect lactic acid in the
urine either of health or in osteomalacia.
IX. The Urine of Toxie States.
1. Poisoning with Acids.—Poisoning with strong mineral acids—
nitric, sulphuric, and hydrochloric—is generally followed by the appear-
ance of blood and albumin in the urine. The symptoms, however, are
often very transient. Toxic nephritis may ensue, and this especially
when sulphuric acid was the poison. The urine is then scanty, of high
sp. gr. and acid reaction. Chemically and microscopically, it presents
the characters of that of acute nephritis (see p. 329). In every case of
poisoning with acids which the author has had an opportunity of observ-
ing, the urine possessed the property of dissolving cupric sulphate in
alkaline solution, and reducing it when subsequently boiled, whilst at the
same time the most sensitive tests besides gave no indication of sugar.
2. Poisoning with Alkalies.— After poisoning with caustic potash,
which may be taken as the type of this condition, the urine passed
during the first few hours contains albumin, invariably in severe cases,
but very often also when the symptoms are slight. Its chemical and
microscopical characters at the same time are not otherwise those of
nephritis. Its reaction is feebly acid, seldom neutral, very rarely
alkaline. It possesses the reducing property in a marked degree; while
no evidence of sugar can be obtained with the phenylhydrazin reaction
and other tests. Where the toxic agent has heen chlorate of potash,
acute nephritis is apt to follow. ‘The detection of this salt in the urine
may be effected by the method described at p. 152.
3. Poisoning with Metals and Metalloids.
(a.) Lead Salts.—In acute lead-poisoning, especially when attended
with colic, large quantities of albumin are often transitorily present in
the urine ; more frequently still a true renal albuminuria, due to secondary
nephritis, occurs. The presence of lead may be determined directly by
the method described in connection with the vomit (see p. 152).
(v.) Salts of Mercury.—The urine in mercurial poisoning, after the
lapse of a few hours, contains a large proportion of albumin, and very
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POISONING WITH METALS. 339
often blood. The symptoms of nephritis are usually sooner or later
developed. This is especially true of poisoning with corrosive sub-
‘imate.
Mercury may be detected in the same manner as in the vomit (p. 153),
or in the urine Firbringer’s process may be employed,* or, better still,
Ludwigs method.
Five hundred ce. of urine are acidified with hydrochloric acid (1-2 cc.) in a
beaker and heated to 50-60° C. Three grms. of granular zine or finely-divided
copper are then placed in the fluid, which is shaken up for half a minute. The
metal is then allowed to settle, the supernatant fluid poured off, and the sedi-
ment obtained upon a filter, where it is well washed with boiling water, and dried
at 60° C. The powdered metal is then placed in a tube of hard glass, of 8-10
mm. diameter, closed at one end, covered with a plug of asbestos, upon which
again is put a layer some 5-6 cc. deep of granular oxide of copper ; then another
asbestos plug, and, finally, another layer of granular zinc, which has been pre-
viously dried and well heated. When the tube is filled in this way, it is drawn
out to capillary calibre at a point some millimetres behind the last asbestos plug,
and a bulbous expansion is made at the end. ‘The cupric oxide is first heated to
a dull red, the layer of zinc to a lesser degree, and, finally, the powdered metal
containing mercury.
The mercury is deposited as a metallic powder in the capillary tube. The
latter is then broken off above the last of the asbestos rings by letting water drop
on it; a few particles of metallic iodine are placed in the first part of the
tube while still hot, and the other expanded end of the capillary is connected
with an aspirator (Béhm’s air-pump serves best). ‘The iodine vapour impinges
on the mercury, and mercuric iodide forms, and is easily distinguished by its
colour.*#4
Wolf and Nega*® have employed a modification of this process. Organic
matter is first removed by hydrochloric acid and chlorate of potash, and copper
as a thin foil is introduced to receive the metal (mercury) instead of granular
zinc or powdered copper. The method is said to be very satisfactory. That of
Al¢*66 is still more simple. Winternitz**? has devised a method for the quanti-
tative estimation of mercury in the urine.
Almén’s*®3 method is the following :—About 300 cc. of the urine to be tested
are taken, a little caustic soda and some sugar added, and the mixture boiled.
The phosphatic sediment which falls carries the mercury with it. When it has
entirely settled, the fluid is decanted off, the sediment dissolved in hydrochloric
acid, and a piece of fine copper or brass wire placed in the fluid, which is then
maintained at a moderate heat for an hour and a half. After this the wire is
removed, boiled in alkaline water, and dried with blotting-paper. It is then
placed in a glass tube of small calibre, which is broken a few millimetres in front
of the wire, fused at the end, and heated over a small flame. The mercury sub-
limes, and is deposited in small globules, which can be readily recognised with
the microscope. The reagents employed in the process should be previously
tested for such mercury as they may themselves contain (see p. 153).
(c.) Salts of Copper.—In poisoning with copper salts, the urine is
always reduced in quantity. It usually contains albumin, and very often
also blood. As to whether acute nephritis can originate in this way,
some doubt exists. Experiments on animals would seem to favour the
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340 THE URINE.
assumption. To detect the poison in the urine, the method described at
p- 154 will serve.
(d.) Arsenic.—In acute arsenical poisoning albumin and sometimes
blood in considerable quantities appear in the urine. In one case the
author has observed all the signs of acute nephritis. The urine pos-
sesses the reducing property, but sugar cannot otherwise be made evi-
dent. The effect on the urine of chronic arsenic-poisoning is but little
understood. Albuminuria would seem occasionally to occur in this
connection.
For the detection of arsenic, see chapter on the vomit (p. 154).
(e.) Phosphorus.—At the outset of a case of phosphorus-poisoning the
urine is not notably changed as to quantity or sp. gr. Later it contains
albumin, but not usually in considerable quantity, occasionally blood,
and very commonly casts of different kinds. The presence of peptone
has repeatedly been recorded (Gerhardt, Maixner, v. Jaksch). Biliary
acids and colouring-matters are also met with, and Schultzen and Riess
have detected sarcolactic acid. In a case which recently came under
his notice, the author obtained an appreciable quantity of fatty acids
from 300 ce. of the fluid. Tyrosin and leucin are rarely present, as is
the case in acute yellow atrophy ofthe liver. Fat has been found in
large quantities in the urine of phosphorus-poisoning.°® The elimina-
tion of urea has been reported as exceeding or falling short of the healthy
standard in different cases.
In a case of severe phosphorus-poisoning under the author’s care the output of
urea estimated as nitrogen was, on the first day (of twenty-four hours) after the
poisoning 5.6028 grms., on the second day 7.9946 grms., on the third day 16.0406
grms., and on the fourth day 10.2458 grms. The patient was at once submitted
to rigorous treatment, and ultimately recovered. It will be observed that the
accident was followed immediately by a diminished elimination of urea, which
again exhibited a notable increase. Observations by Dr. Miinzer, the author's
assistant, which will shortly be published, furnish valuable information on the
subject of metabolism in connection with phosphorus-poisoning. With his per-
mission, it may be stated here that the urine contains an enormous increase of
ammonia, side by side with a falling off in the quantity of urea and of the nitro-
genous excretion. Uric acid was normal. These results were obtained by the
investigation of two fatal cases.
4. Poisoning with Alkaloids.
(a.) Morphia.—In acute poisoning with morphia the urine is com-
monly found to contain sugar. In chronic morphinism, again, it has a
powerful reducing action, and sugar may sometimes be found with other
tests (see p. 273). [The reducing property depends upon the presence of
glycuronic acid (Halliburton.] For the detection of morphia in the urine
the method described at p. 156 may be adopted. It must be borne in
mind, however, that morphia does not appear in the urine in all cases of
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POISONING WITH ALKALOIDS—WITH CARBOLIC ACID. 341
morphia poisoning or morphinism, and its absence does not prove that the
alkaloid has not been taken. The researches of Donath®” have shown
that it may disappear entirely within the system.
(b.) Nicotin.—The toxic effects of nicotin are not associated with any
special changes in the character of the urine. For the detection of the
alkaloid see p. 157.
(c.) Atropin.—Little that is definite is known of this condition.
Atropin may be isolated from the urine in the same manner as that
described in connection with the vomit (p. 157). As a test for its
presence a little of the urine may be placed in an animal’s eye, and the
mydriatic effect watched for. This will be obtained, according to de
Ruitter and Donders,*™! when the urine contains the alkaloid in the
proportion of one part to 130,000 of water. In cases of poisoning with
deadly nightshade berries (Atropa belladonna), the urine has a peculiar
fluorescence (A. Paltauwf*"?), due to the presence of scopoletin. This
does not occur in poisoning with the pure alkaloid, and in certain cir-
cumstances it affords an indication as to the source of the poison.
(d.) Ptomaines (Exogenic Toxicosis).—The phenomena of poisoning
with ptomaines need further investigation. In a case (of sausage-
poisoning) which was recently under the care of Professor Nothnagel;
albuminuria and the signs of nephritis supervened. Subsequent experi-
ence has convinced the author that kidney trouble regularly occurs in
the later stages of ptomaine-poisoning.
5. Poisoning with Ethylic Aleohol.—Chronic alcohol-poisoning
appears to produce nephritis and arterio-sclerosis.°"? In the acute condi-
tion the poison can be found only as the merest trace in the urine.°4
To recognise its presence the urine must be distilled by means of a
steam-bath, and the distillate treated in the manner described at p. 161.
6. Chloroform-Poisoning.—In this condition the wrine is gene-
rally of high sp. gr. It often contains a trace of albumin and some
sugar [or glycuronie acid (Halliburton).| According to Kast and Mester,°”
the urine after the prolonged administration of chloroform contains an
organic sulphur compound and urobilin, and is highly toxic.* For the
detection of chloroform the urine is distilled by means of a steam-bath
to prevent frothing, and the first drops of the distillate are submitted to
Hoffmann’s or Vitali’s test (see p. 161). The results obtained in this way
are equally useful with those of Maréchal’s method.?™
7. Carbolic Acid-Poisoning.— When large quantities of carbolic
acid have been administered through the mouth or absorbed from a
wound, the voided urine assumes a dark-green colour, which changes
to black on standing. This colour is due to the presence of hydro-
chinon, a derivative of phenol, which, while still within the system, is
in part transformed into coloured oxidation products (Baumann and
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342 THE URINE.
Preusse).*"* Pure phenol is never present, but even in the severest
cases is found only in combination with sulphuric acid (p. 297). Hence
a violet coloration with
the characteristic reaction of carbolic acid
solution of perchloride of iron—cannot be obtained with the urine.
The latter contains a small quantity of albumin, and commonly also
hemoglobin (p. 271). A further evidence of the condition depends
upon the diminished proportion of simple sulphuric acid which it con-
tains. When chloride of barium is added to healthy urine acidulated
with acetic acid, an abundant precipitate of barium sulphate falls; but
when from any cause the quantity of sulphuric acid in the uncombined
form is lessened, this precipitate fails, or is represented by a mere tur-
bidity. If now in this case the urine be filtered and boiled with hydro-
chloric acid, so as to decompose the phenol-sulphurie acid (see p. 297),
with the reproduction of simple sulphuric acid a copious precipitate of
barium sulphate forms.
Inasmuch as phenol-sulphuric acid is normally a constituent of the
urine, it serves but little purpose in cases of carbolic acid-poisoning to
attempt an estimate of the phenol which passes over as tribromo-phenol
(see p. 299) in the process of distillation. A better plan is to determine
the relative proportion of simple and compound sulphuric acid present
(see p. 323). If it be found that the latter is increased while the first
is diminished, and if at the same time such affections as promote the
elimination of vther-sulphuric acids (active albuminous decomposition)
can be excluded, this is strong presumptive evidence of carbolic acid
poisoning.
The same method will serve for the detection of all the aromatic
substances which appear in the urine as ether-sulphuric acids in cases
of poisoning or after the administration of drugs.
8. Poisoning with Nitro-Benzol and Aniline.
(a.) Nitro-Benzol.—In cases of poisoning with this substance, the
urine has the odour of nitro-benzol, and generally contains a substance
which has the property of rotating polarised light to the left, and of
reducing cupric sulphate in alkaline solution.*”
().) Aniline.—The recorded observations of cases of poisoning with
aniline show that the character of the urine varies considerably. It is
usually dark in colour and highly concentrated (Grandhomme).®° In
one instance (Fr. Miller 1) it was free from sugar, albumin, and blood,
and exhibited the reduction phenomenon in a marked degree. A®ther-
sulphuric acids were notably increased. An ethereal extract was found
to contain aniline by its yielding a violet colour in presence of solution
of chloride of lime (see p. 162). Muller is of opinion that this substance
is in part eliminated as paraamido-phenol-sulphuric acid.
9. Poisoning with Carbonic Oxide Gas.—The urine passed in
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DETECTION OF DRUGS. 343
this condition invariably contains grape-sugar**? (see p. 273), and an
uncertain proportion of albumin. The quantity of sugar varies directly
with the intensity of the poisoning.
V. THE DETECTION OF CERTAIN DRUGS IN THE URINE.
1. Iodoform and Salts of Iodine and Bromine.—After the
exhibition of iodoform, whether internally or by outward application
iodides and iodates may be detected in the urine. So too with iodine
when applied externally as the tincture, or taken by the mouth as iodide
of potassium, it may be readily recognised in that fluid.
To test for iodine. the urine is treated with a little fuming nitric
acid or chlorine water, and shaken up with chloroform. If a salt of
iodine be present, the metal is set free, and dissolves in the chloroform,
with the formation of a red colour.
The quantitative estimation may he effected best by Harnach’s>*
method, in which all the iodine is converted into palladium iodide.
Iodine appears in the urine very shortly after it has been taken into the
system. A quarter of an hour will suffice for its manifestation there.
Bromine salts, when very abundant, may be detected thus :—The
urine is treated with chlorine water, and shaken up with chloroform,
when bromine dissolves in the latter, with the production of a yellow
colour. It will usually be found necessary, however, to evaporate the
urine previously, then to incinerate it carefully, and to test the colour
less watery extract from the ash in the manner described above.°*+
2. Salicylates—Salol and Betol.—Salicylates also very quickly
pass into the urine. The latter then exhibits a remarkable reducing
power, and yields a violet colour in presence of solution of perchloride
of iron. This reaction depends partly upon the presence of salicylic
acid and partly upon that of salicylurie acid, into which the latter is
changed within the system. This reaction is not readily prevented by
boiling. The body on which it depends is taken up by ether from
acidified urine, and can be detected in the ethereal extract by means
of solution of perchloride of iron. The reaction, unlike that of diacetic
acid (see Diaceturia), does not disappear on standing. It is well in
testing for it to precipitate the phosphates with solution of perchloride
of iron and filter, and then test the filtrate with more of the reagent.
The exhibition of salol (phenyl-ether of salicylic acid) imparts a
similar character to the urine, which also on standing acquires a tint
varying from dark-green to black, like that following the use of car-
bolic acid.
The use of betol (naphthalol, salicylate of B-naphthol-ether) does not
impart any special colour to the urine, which, however, yields the per-
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344 THE URINE.
chloride of iron reaction. Both salol and betol appear in the urine as
sulphuric acid combinations (v. Jaksch).>*
3. Quinine, Kairin, Antipyrin, Thallin, Antifebrin, and
Phenacetin.
(a.) Quinine.—This alkaloid is said by Kerner *%* to be eliminated as
dioxyquinin. It renders the urine dark. For its detection a large
quantity of the fluid is taken, treated with ammonia, and shaken up
with ether. The latter is then distilled off or evaporated, and quinine
remains in the residue. It is dissolved in acidulated water, and the
addition of chlorine water and ammonia causes an emerald-green tint to
develop.
(b.) Kairin.—Under the influence of this drug the urine acquires a
brown colour, which becomes brownish-red with solution of perchloride
of iron. The substance upon which this reaction depends may be
extracted with ether from acidified urine. The reaction in the ethereal
extract remains even after the lapse of weeks. The addition of strong
acids to the urine destroys the reaction, and it is, moreover, impaired
by prolonged boiling. According to v. Mering,°* kairin is eliminated
as kairin-potassium sulphate.
(c.) Antipyrin imparts a darker tint to the urine, which gradually
becomes a purple-red when treated with perchloride of iron. If the
urine be acidulated and extracted with ether, a substance is obtained
which colours brown with perchloride of iron. This reaction is gradually
lost after the lapse of a few days. It is impaired, but not destroyed,
by boiling the urine. It is destroyed by the addition of acids. Esti-
mation of the quantities of simple and of ether-sulphuric acids in
appropriate instances has shown that antipyrin is eliminated as a sul-
phuric acid combination (v. Jaksch).
(d.) Thallin.—The urine after the administration of thallin is usually
a brownish-green when viewed in bulk, greenish in a thin layer.
Treated with perchloride of iron, it presently exhibits a purple-red tint,
which, after the lapse of four or five hours, if undisturbed, passes into
a brownish-red. If a little mineral acid be added and the fluid be
shaken up with ether, the latter takes up a substance which colours
brown-red with perchloride of iron. The coloration does not vanish
when the specimen is allowed to stand, but rather becomes more
marked, When the pure thallin urine is shaken up with ether, the
ethereal extract contains a body which colours green with perchloride
of iron (thallin).°% The tint in this case disappears on prolonged
standing. The red colour obtained with perchloride is lost by boiling
for a few seconds. It is likewise destroyed by mineral acids. Thallin
is partly eliminated in the form of chinanisol.
(e.) Antifebrin.—-The physical character of the urine is unaffected
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CHRYSOPHANIC ACID. 345
even by large doses of antifebrin. Chemically it has been ascertained
by F. Miiller that it contains more than the normal proportion of
ther-sulphuric acids; and this is accounted for by the supposition that
antifebrin is changed within the system to paraamido-phenol-sulphuric
acid. Where the drug has been exhibited in large quantities, it may
be recognised in the urine (F. Miiller 8°) thus :—The fluid is boiled with
one-fourth its bulk of strong hydrochloric acid, and when it has cooled,
a few ce. of a 3 percent. solution of carbolic acid is added, and then a
few drops of a solution of chromic acid. If paraamidophenol be present,
the specimen develops a red colour, which gives place to blue on the
addition of ammonia.
For the detection of antifebrin Yvon” recommends the following
method :—The urine is shaken up with chloroform, and the residue from
the extract is heated with a little mercurous nitrate. If antifebrin be
present an intense green coloration takes place. When antifebrin has
been separated from the urine, as by shaking it up with ether and
acid, it can also be recognised by the addition of chloroform and caustic
potash. Antifebrin also is excreted for the most part in combination
with sulphurie acid (fr, Miiller, Morner, v. Jaksch). According to
Morner,°*! this body is in part oxidised to acetylparaamidophenol within
the system, and eliminated as ether-sulphurie acid.
(f.) Phenacetin (acetphenetidin).—The colour of the urine is un-
affected by this body, even in large doses. It rotates polarised light
to the left (glyeuronic acid combination, Fr. Miller”), and exhibits
the paraamidophenol reaction described above. It contains no free
phenacetin, but the presence of phenetidine may be shown by changing
it into its diazo compound, which then yields a purple coloration with
naphthol or yellow with phenol (Jfiller). The process is as follows :—
To a specimen of the urine two drops each of hydrochloric acid and of
sodium nitrite solution (1 per cent.) are added. The further addition
of an alkaline watery solution of a-naphthol and a little caustie soda
causes a beautiful red colour to develop, and this passes into violet if
hydrochloric acid be supplied. Under the same conditions phenol gives
a citron-yellow in alkaline and a rose colour in acid solution. When
large doses of the drug have been taken, the urine gradually takes a
brown-red tint in presence of perchloride of iron solutions and oxidising
substances, changing slowly to black on standing for a long time. Ac-
cording to Ubaldi,°°? the ingestion of phenacetin is attended by an
increase in the amount of combined sulphuric acid in the urine.
4. Chrysophanie Acid.—The administration of infusion of senna
or of preparations of rhubarb imparts a reddish-brown colour to the
urine, which may be present in the freshly-voided fluid or develop on
standing. This gives place to red on the addition of alkalies at ordinary
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340 THE URINE. Y
temperatures. When boiled with alkalies the resulting phosphatic sedi-
ment is not red, but yellow; and if dissolved in acetic acid the solution
also colours yellow, changing to violet on exposure to the air; in this
respect differing from the precipitate of blood-pigments, which is also
soluble in acetic acid, but gradually bleaches when exposed.
5. Santonin.—Santonin taken internally colours the urine yellow,
which again gives place to red on the addition of alkalies. Its presence
may be discriminated from that of rhubarb (Afunh:) °*+ from the fact that
the red colour developed by the latter in presence of alkalies, though
permanent, is rapidly destroyed by reducing agents (granular zinc,
sodium amalgam), whilst that due to santonin persists under like cir-
cumstances. Chrysophanic acid is precipitated with baryta water. The
precipitate is red and leaves a colourless filtrate. The latter is yellow
if santonin be present. The addition of alkaline carbonates turns the
urine red, rapidly if it contain rhubarb, very slowly and gradually in the
case of santonin.
G. Hoppe-Seyler®” has suggested the following method for the dis-
crimination of chrysophanic acid and santonin :—The urine is treated
with caustic soda and extracted with amylie alcohol. If the colouring
matter of santonin be present, it passes over with the alcohol, and the
specimen is decolorised. The colouring matter of chrysophanic acid
derived from the exhibition of rhubarb or of senna is little or not at all
taken up by amylic alcohol in presence of the alkali.
6. Tannin.—When tannin has been taken medicinally in large
doses, the urine turns dark-green with solution of perchloride of iron.
7. Naphthalin.—Naphthalin in large doses causes the urine to
assume, especially on standing for a long time, a dark tint, like that
due to carbolic acid.
According to Penzoldt,°"’ a dark-green colour develops rapidly in
presence of concentrated sulphuric acid.
8. Copaiba Balsam.—Copaiba balsam in the urine yields a red
colour with hydrochloric acid, changing to violet when heated. If
ammonia or caustic soda be added to the urine, a light-brown colour
with a blue fluorescence develops (Ei/lefsen).5°7
When boiled with an acid the urine gives a precipitate which is
soluble in alcohol.
It may be mentioned here that after the use of oil of turpentine the
urine sometimes gives a precipitate with acids. It has also a charac-
teristic odour of violets.
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CHAPTER VIII.
INVESTIGATION OF EXUDATIONS, TRANSUDATIONS,
AND CYSTIC FLUIDS.
Fiuip may be effused into any of the cavities of the body as a conse-
quence of inflammation or of disturbances in the circulatory system.
Under appropriate circumstances a portion of such fluid may be
drawn off by puncture or in some other way, or a spontaneous opening
may occur, and in either case the fluids so obtained may be submitted
to examination. In this way much useful information may be secured
for the purposes of diagnosis. A question arises at the outset as to
whether the fluid is an inflammatory product (exudation), or the result
of impediment to the circulation, or derived from the degeneration of
certain organs. (transudation).
A.—EXUDATIONS.
An exudation may be purulent, sero-purulent, putrid, hemorrhagic,
or serous, All such fluids, with the exception of the last two, imply,
of course, an inflammatory origin. Upon its other characters, and
especially upon the nature of the tissue elements which it contains,
more precise inferences may be based in the case of any one of them.
1. Purutent Exupations.
I. NAKED-EYE APPEARANCES.—Pus (bonum et laudabile) is
a turbid fluid of varying consistence and high sp. gr., with an alkaline
reaction, and ranging in colour from grey to a greenish-yellow. It
may accumulate in natural cavities (exudations), or be effused amongst
the tissues (phlegmon), or, finally, it may be secreted from the surface
of a wound. On standing in a cool place, it separates into two layers,
the upper of which is of a light-yellow colour and tolerably transparent,
and the lower opaque from the deposit of pus-cells. It is often brown
or brownish-red from admixture with blood. Putrid pus can always
be discriminated by its naked-eye properties. It is thin, green, or
brownish-red, and emits an extremely penetrating odour of indol and
skatol.
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348 EXUDATIONS
II. MICROSCOPICAL CHARACTERS.
1. White and Red Blood-Corpuscles and Epithelium.— When
pus is submitted to microscopical examination, it discloses a multitude
of cells which entirely resemble white blood-corpuscles. When derived
from a perfectly fresh specimen, these cells exhibit the contractile pro-
perty, and the mahogany coloration obtained with solution of iodine
and iodide of potassium or ammonium attests the presence of glyco-
gen. This reaction is obtained best with fresh pus from the surface
of a wound. The dead cells are shrunken and very granular, or may
appear as decomposed or decomposing particles of protoplasm.
In addition to this, giant pus-corpuscles and fat-laden cells are occa-
sionally observed. No special significance attaches to their presence.
They have been seen in the pus from an abscess of the gum (Boettcher 1),
in hypopyon (Bizzozero?), and in the contents of suppurating ovarian
cysts (v. Jaksch).
Some red blood-corpuscles are nearly always present in freshly-secreted
pus, and when blood in considerable quantity has been effused and after-
wards its elements disintegrated, the discharge may be more or less
amply tinged by admixture with blood-pigment or hematoidin crystals.
Fatty particles and globules are seldom wanting, either free or com-
bined with the protoplasm of the cells. The epithelium elements are
comparatively few. In cancerous exudation from the pleural cavity
vacuolated epithelial and fatty endothelial cells are commonly to be
met with.
2. Fungi.—Modern research® has established the fact that the
formation of pus in animal organisms is effected almost entirely through
the agency of micro-organisms, and that such bodies can nearly always
be detected in the discharge with the aid of the staining methods (p. 377)
which the recent advances of science have placed within our reach, where
the microscope alone fails to disclose their presence.
Important experiments upon animals+ have shown also that suppura-
tion may be caused by certain chemical substances, as cadaverin, croton
oil, &c., independently of micro-organisms ; and it is possible that the
human system may be similarly affected by them.
1. Micrococci.—Micrococci of varying form and size are very often
to be seen in fresh pus.° Fig. 136, which represents the appearance of
a specimen taken from a pleural exudation and stained by Gram’s
method, affords an appropriate illustration, They are usually arranged
in chains (Streptococci), occasionally in pairs (Diplococci).
Passet,® proceeding on Koch’s method, has cultivated no less than
eight different forms of fungi from pus. When suppuration has con-
tinued for a long time in a cavity excluded from the air, micro-organisms
are sometimes wanting in the pus. Bréeger™ has observed Staphylo-
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FUNGI—BACILLUS OF TUBERCLE. 349
coccus pyogenes aureus and Streptococcus pyogenes in pus from a
woman with puerperal fever. The presence of micro-organisms hitherto
mentioned is evidence of suppuration in the course of septic processes
(comp. p. 47). Bujwid® lately made the interesting discovery that the
effect of grape-sugar upon the tissues is to promote the development of
Staphylococcus aureus by diminishing their resistance, and so to favour
the formation of pus. The tendency of diabetics to undergo suppurative
processes, so long a matter of clinical observation, is explained in this
way.
A blue colour has occasionally been observed on the surface of suppurating
wounds. This is produced by colonies of Bacillus pyocyanogenus or of a fungus
resembling it. The colouring-matter has been isolated from such pus in combina-
tion with hydrochloric acid.1°
7
a if
0%
*
Nery
Rg
O sO ‘s
Fic. 136.—Cocci from an Empyema, prepared by Giam’s method (eye-piece III., objective
Zeiss oil immersion ,!;; Abbe's mirror and open condenser).
The detection of pathogenic fungi in pus is a point of great im-
portance.
2. Tubercle - Bacillus.—The tubercle-bacillus has often been dis-
covered in tubercular pus,!! but the author has sometimes failed to find
it even in the fresh discharge. Its presence, of course, is conclusive as
to the nature of the disease, but its absence does not imply that no
tubercle is present. It would appear that under certain conditions the
bacillus rapidly disappears from fresh discharges (Metschnihof}).
8. Bacillus of Syphilis.—The bacillus discovered by Lustgarten ! in
the pus of syphilis affords a valuable indication of this disease ; but
caution must be observed in identifying it, since Alvarez and Tavel 4
have shown that certain secretions, as the smegma preputiale and
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350 EXUDATIONS.
vulvare, are apt to contain forms which closely resemble the venereal
microbe. Such forms are to be discriminated by the behaviour of
stained preparations in presence of alcohol. In the case of the bacillus
of syphilis, these are with difficulty and very slowly bleached by alcohol,
whilst the microbe of smegma readily loses its colour under the action
of that substance.
An important addition to our knowledge of the bacillus of syphilis
was recently made by Kamen, who found the micro-organism in the
sputum of a child of nine years. The character of Lustgarten’s bacillus
hag been much questioned of late, and others have regarded certain
cocci as the specific excitants of syphilis (Kassowitz, Hochsinger, Disse,
Taguchi).
For the detection of the bacillus of syphilis Lustgarten 1 proceeds as
Fic. 137.—Actinomyces Granules in Glycerine from Actinomycosis of Pleural Cavity
37 y' y
(eye-piece II., objective IV., Hartnack).
follows :—The cover-glass preparation is immersed in an Ehrlich-Weigert
gentian-violet fluid for 12-24 hours at the ordinary temperature. It
is then removed, rinsed for some minutes with absolute alcohol, and
placed for ten seconds in a 14 per cent. solution of permanganate of
potash, after which it is treated with a watery solution of pure
sulphurous acid, and finally washed with water. Should it happen
after this that the preparation still shows colour, it is again placed in
permanganate of potash for three or four seconds, and afterwards in
sulphurous acid until all colour has disappeared, the remainder of the
process also being repeated. It is to be noted that other microbes,
both pathogenic and innocuous, are stained by Lustgarten’s process as
well as that of syphilis.
De .Giacomi}® has suggested a method which is very serviceable for
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ACTINOMYCES. Sw
the detection of the bacillus of syphilis. In this the dried cover-glass
preparation is warmed for some minutes in an aniline-water fuchsin
fluid, then washed with water to which a few drops of perchloride of
iron solution have been added, and finally decolorised in a concentrated
solution of that salt. The bacillus then remains of a red colour, while
all other micro-organisms are bleached.
Fic. 138.—Actinomyces from a Case of Actinomycosis of Pieural Cavity (eye-piece III.,
objective, oil immersion j};, Reichert ; compressed).
4. Actinomyces.—This parasite was first discovered by Bollinger!” in
cattle, and afterwards in man by Ponfick 8 and Israel." In the former
it gives rise to tumours of considerable size, but in man its proliferation is
usually associated with chronic inflammation and the production of pus.
It would appear from numerous communications that have been made
in recent years that actinomycosis is a disease of very wide distribution,
Fic. 139.--Actinomyces from Peritoneum (eye-piece III., objective, oil immersion 5, Reichei't,
unstained preparation).
and that amongst its symptoms is a severe form of angina, till lately
obscure, to which the name of angina Ludovici has been given.2°
[It usually affects the intestinal?! tract, but primary actinomycosis of the
apices of the lung has been met with,” and six cases °3 have been recorded in
which the disease had its seat in the brain. One of these by Dr. Orlow™ is of
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352 EXUDATIONS.
exceptional interest. Anderson” of Nottingham has lately recorded a case
of actinomycosis of the face and neck, which was successfully treated by
operation. ]
The pus of this disease is thin, viscous, and somewhat tenacious, and
discloses to the naked eye small nodules of a grey or yellow colour, and
about the size of a poppy-seed. Under a low power of the microscope
these particles appear as a dense bunch-like aggregation of spherules,
which under a higher magnifying power are seen to consist of pear-
shaped, and radially arranged masses, which have a considerable refrac-
tive power (figs. 138, 139). Towards the centre of such masses the
individual elements diminish in size and fade into a fine network of
ramifying fibres. If one of the nodules be bruised, it shows in the first
place numerous detached club-shaped forms, having a radiating disposi-
tion toward the periphery (fig. 138), and passing gradually at the centre
into a sort of detritus ; and in addition to these are a variety of other
objects, club-shaped and of indeterminate appearance (degeneration types
of the fungus), lying apart.
There was for a long time much doubt as to the botanical character
of Actinomyces. Recently, however, it has been established 7° that it
belongs to the class of fission-fungi, being a fission-alga (Cladothrix).
The characteristic club-shaped bodies must be regarded as degeneration
forms of the fungus. In unstained microscopical preparations they
may be seen sometimes to fade into the central fine network, and even
occasionally to be enclosed in its meshes (fig. 139). [C@rookshank**
believes that actinomyces is a fungus intermediate between the fission-
and the higher fungi ; and Dr. W. Hill °$ refers it to the Basidiomycetes. |
With the aid of staining methods (Gram’s is the best) the individual
threads of the network are readily distinguishable. They present a
jagged or undulating contour, and result from the cohesion of a series
of minute spherical organisms, connected together by a remarkably
delicate envelope. The centre, to which all the constituent threads of
a group converge, is occupied only by a very dense network of this
formation (fig. 140).
The pear-shaped bodies above alluded to may be more clearly defined
by staining with Wezgert’s*® process. For this purpose a solution is
made by adding together zo cc. absolute alcohol, 5 cc. concentrated
acetic acid, and 40 ce. of distilled water, and to the mixture so much of
the so-called French extract of litmus as will give the fluid a dark-red
colour, remaining ruby-red after repeated filtering (Wedl’s®° litmus
solution). In this solution the cover-glass preparations are allowed to
remain for an hour or so, then lightly rinsed with alcohol, and placed
for two or three minutes in a 2 per cent. gentian-violet fluid, which
should be boiled before use, and filtered after cooling.
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BACILLUS OF GLANDERS. 353
If the specimen be now examined, it will be found that whilst the
central’mass of Actinomyces is colourless, the fungus threads are
stained a ruby-red. Baranski*! advocates staining with picro-carmine.
In most cases, however, the character of this fungus can be determined
by a simple microscopical examination. The physical qualities of the
pus, and the discovery in it of groups of Actinomyces or the club-
shaped degeneration forms of the parasite, are points which will aid the
diagnosis. In particular cases it may be necessary to resort to Gram’s
staining method, and to observe the minute structure of the ultimate
threads of the fungus, as noticed above (comp. p. 352). Bujwid *? has
obtained pure cultivations of actinomyces by means of Buchner’s** method
(p. 388). Seen with the naked eye, these bear a close resemblance to
cultivations of tubercle-hacillus.
Fic. 140.—Preparation from same case as last, stained by Gram's method (eye-piece IV.,
objective, oil immersion j,, Zeiss ; Abbe's mirror and open condenser).
5. Bacillus of Glanders.—The specific micro-organism may be found
in the pus from the ulcerated nasal passages in glanders. The method
deseribed in connection with the examination of the blood (p. 46) will
serve for its recognition here.
Another method has recently been suggested (Loffler).°4 An aniline-
-water-gentian-violet fluid or a concentrated alcoholic solution of methylene-
blue may be employed, and immediately before use it is added to its
own bulk of a (1: 10,000) solution of potash. In the fluid which results
the cover-glass preparation is immersed for five minutes. It is then
removed and placed for a second in a 1 per cent. solution of acetic acid,
tinged slightly yellow with oo-tropeolin. By means of another mix-
ture, containing two drops of concentrated sulphurous acid and one of a
5 per cent. solution of oxalic acid in ro ce. of water, the alkaline stain-
ing fluid may be decomposed and the preparation freed from colour. In
this way the micro-organisms are very beautifully stained.
The bacillus of glanders may also infest the pus from an abscess.
In any case, its character may usually be sufficiently determined in
stained specimens by means of the microscope. When necessary, how-
ever, all doubt may be removed by observing the result of inoculating
Z
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354 EXUDATIONS.
animals with the microbe. In the intermediate process of cultivation
certain characteristic properties are disclosed. When the various other
micro-organisms which are nearly always present in the pus have been
eliminated by Koch’s method (p. 385), the pure plate-cultivation crop
made in nutrient agar-agar at 37° C. has the appearance of a greyish-
white drop. The pure cultivation-product, when inoculated upon
animals, as the mouse or guinea-pig, induces glanders. When engrafted
on the potato and kept at a temperature of 35° C. the bacillus forms,
in two or three days, a thin greasy coating of a brown colour. In
coagulated blood-serum at a low temperature it develops after two or
three days in the form of small scattered transparent drops which have
a colour very much the same as that of the serum. ‘The fungus is
readily cultivated in glycerine agar-agar *° and in nutrient milk-peptone.*¢
When allowed to rest for some time longer, the cultivations are said to
develop spores, but this point is not established (Bawmgarten).37
6. Bacillus of Anthrax.—Opportunity occasionally offers of exa-
mining the pus derived from a carbuncle in anthrax. The specific
micro-organism is that described at p. 42. nN XY o 2e6
' Fic, 141.—Bacilli of Tetanus (pure cultivation). Compensation eye-piece VIII., objective oil-
immersion ,, Zeiss (from Koch).
9. Bacillus of Influenza.—R. Pfeifer has found in the sputum, and
cultivated, a definite micro-organism, which he believes to be charac-
teristic of influenza. By Kitasato*? it was cultivated to the fifth gene-
ration in glycerine-agar, and Canon ** has detected a similar fungus in
the blood of those infected with the disease, and afterwards by means
of cultivation-experiments established its identity with the bacillus of
Pfeifer and Kitasato. Although the micro-organism has not yet been
found in pus, it will be described here, both because its discovery was
announced too late to notice it in its proper place in this book, and
also because it doubtless exists in the pus of those infected with
influenza.
According to Pfeiffer, the bacilli have the form of very minute rods
of about the same thickness as those of mouse-septicemia. They stain
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PROTOZOA—VERMES—CRYSTALS. 357
well in Léffler’s methylene-blue fluid when heated (see p. 41), and also
in dilute Ziehl-Neelsen fluid (p. 106). They do not stain with Gram’s
method. On glycerine-agar solidified obliquely, after twenty-four hours
they develop the appearance of drops of water which require a lens to
make them visible. The colonies remain separate. For the detection
of the bacillus in the blood, according to Canon, the latter is spread on
a cover-glass and dried in the usual way ; the cover-glass preparation is
treated for at least five minutes with absolute alcohol, and is then put
for three to six hours to stain in Chenzinshy’s eosin-methylene-blue fluid
(see p. 57).°+
It is probable that the pathogenic micro-organisms of pus include
others besides those mentioned here. Reference may be made espe-
cially to the interesting observations of Eppinger,®® concerning a new
cladothrix which has been found in abscesses.
3. Protozoa.—Little is known as yet as to the presence of these
parasites in pus. Kiinstler and Pitres®® found numerous large spores
with ten to twenty crescentic corpuscles in the pus from the pleural
cavity of a man. These bodies closely resembled the coccidia which
occur in the bodies of mice (comp. pp. 89, 180). Litten *" observed cerco-
monads in the puncture-fluid, derived probably from the lungs. Masse 8
has reported the presence of amcebe in the pus from a hepatic abscess.
4. Vermes.—Filaria have been observed occasionally as occurring
in the pus of tropical abscess of the liver.*® In temperate climates also
abscesses result from an invasion of hydatids, and in such cases the
pus contains entire echinococcus cysts, or fragments of the membrane
and hooklets. Babesiu® found filaria in the gastro-splenic omentum.
They were probably the same as G'rassi’s®! Filaria inermis. With
these should be mentioned the bodies resembling filaria which Sarcani °?
reports as found by him in the suppurating parotid of a woman.
5. Crystals.
1. Cholesterin.—Crystals of cholesterin are very rarely to be found in
fresh pus—more commonly in that derived from cold abscesses, and most
abundantly in foetid discharges and in suppurating ovarian cysts. For
their character and recognition the reader is referred to pp. 111, 203, 249.
2. Hematoidin.—This body exhibits the same variety of form here
as in the sputum, the urine, and the feces (pp. 111, 195, 241). Its
presence invariably points to a previous hemorrhage. It is specially
abundant in the case of suppurating hydatid cysts.
3. Fatty Needles.—These are of very many shapes and forms, occur-
ring sometimes singly, and sometimes in groups and clusters. They are
the outcome of a degenerative process, and show that the pus in which
they are found has been long formed. Very perfect margarin needles
may be obtained from gangrenous pus (fig. 142).
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358 EXUDATIONS.
4, Triple Phosphate.—Crystals of triple phosphate are a common
constituent of the pus (see p. 248). Crystals of carbonate and of phos-
phate of lime are also met with, and most commonly in foetid pus.
III. CHEMICAL EXAMINATION OF THE PUS.—lIt rarely hap-
pens that much aid accrues to diagnosis from the chemical examination
of the purulent discharges. The albuminous substances which may
commonly be recognised are serum-albumin, globulin, and especially
peptone (Hofmeister) in large quantity. The latter is derived from
the cells, not from serum. For the means of detecting these bodies the
reader is referred to p. 255.
Fresh pus always contains glycogen, and traces of grape-sugar are
seldom wanting. In testing for the latter, the pus should be boiled
with an equal weight of sodium sulphate, to free it from albumin,
filtered, and the filtrate treated in the manner previously described
(p. 274).
In cases of jaundice the pus may contain bile-pigments and biliary acids.
Considerable quantities of nuclein, fats, cholesterin, and a number
of inorganic salts, notably phosphate and chloride of sodium (Miescher,
Naunyn °°), are constantly to be found.
In three specimens of pleuritic exudation which he has investigated
the author found abundance of acetone, and it would appear from a
private communication of Professors Baumann and Batimler that that
body is commonly a constituent of pus. In another specimen sub-
mitted to him by Dr. R. Paltauf, whose attention had been attracted
by the evident odour of acetone, it was found by the author to be plen-
tifully present; and the researches of others have shown that acetone
is frequently present in large proportion in exudation fluid. Feetid
pleural exudation often contains sulphuretted hydrogen. The method
for its detection is described at p. 327. There, as in certain forms of
hydrothionuria, fungi possessing the property of liberating sulphuretted
hydrogen may be isolated from the fluid.
Guttmann > found indigo-producing substances in exudations. The
author has repeatedly established the presence of fatty acids,—acetic,
formic, and butyric acids. Pus contains further a trace of uric acid and
several xanthin bases. Much interest attaches to the occasional presence
of guanin (v. Jaksch).©
2. Sero-Purutent Exupations.
Sero-purulent closely resemble the purulent discharges in their chemi-
cal, physical, and morphological character. They are distinguished
chiefly by the relatively smaller proportion of extractives which they
yield. They invariably point to antecedent inflammation.
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PUTRID, HAZ MORRHAGIC, AND SEROUS EXUDATIONS. 359
3. Purrip Exupations.
Discharges of this character are brown or brownish-green in colour,
and have a penetrating and disagreeable odour. Their reaction is
usually alkaline. Microscopically they exhibit much-shrunken leuco-
cytes and an abundance of crystals, chiefly of fat, and of cholesterin
and hematoidin in lesser proportion. They also contain a profusion of
fission-fungi of different kinds (see fig. 136).
4. H&morrHacic Exupations.
A hemorrhagic exudation contains an abundance of red blood-cor-
puscles, and often also a considerable quantity of dissolved hemoglobin.
Endothelial cells loaded with fat are almost invariably to be found,
and when these occurring in pleuritic fluid exhibit the glycogen re-
action in a marked degree, they favour the assumption of carcinoma
Fic. 142.—Pus from Putrid Empyeina (eye-piece III., objective 8a, Reichert).
(Quincke).®8 A positive diagnosis upon this point results from the
further discovery of cancer-cells.
In the absence of determinate (specific) elements, as cancer-cells,
tubercle-bacillus, &c., no very definite conclusion can be drawn from
the hemorrhagic character of the discharge, since many different pro-
cesses may be associated with the effusion of blood. Still, in the case
of pleuritic fluid, where scurvy and cancer of the pleura can be excluded,
the appearances would point to tuberculosis.
5. Serous Exupations.
Fluids of this class are almost quite clear and more or less deeply
tinged yellow; they coagulate on standing (for twenty-four hours),
and yield a clot which is usually rich in fibrin, Microscopically they
exhibit scattered red blood-corpuscles in usually fairly good preserva-
tion, but sometimes much attenuated, a number of leucocytes, some
fatty globules and endothelial cells, separately or in groups. In addi-
tion to these are sometimes cells ranging from 7-30 u in diameter, and
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360 EXUDATIONS.
formed of very small droplets. These may contain two or three large
cavities (Bizzozero).®
There is reason to believe that micro-organisms very frequently
infest the serous exudations, but the subject calls for further elucida-
tion. It would appear, at any rate, that fungi occur oftener in them
than in the transudations which so closely resemble them in their
physical and chemical properties. The fluid obtained from the pleural
cavity in tubercle of the pleura with breaking down of tissue may
contain the specific bacillus of. that disease. In cases, however, where
no discharge of tubercular matter has taken place into the pleural
cavity, the tubercle-bacillus will not be found.
Cholesterin crystals occur in serous discharges of old standing.
Chemically, serous exudation fluid contains serum-albumin and globulin,
but no peptone. Sugar in small quantity is invariably present,’? and
acetone from time to time. A notable fact is the frequent or perhaps
invariable occurrence of uric acid in exudations of this kind.
The density of the fluid is clinically a fact of much consequence.
It may be estimated by means of a pycnometer, or with an accurate
aérometer, regard being had at the same time to conditions of tempe-
rature. The sp. gr. will usually be found to exceed 1.018 (Reuss).™
6. CHyLous ExuDATIONS.
Peritoneal exudation is commonly characterised by the abundance
of fatty matter which it contains. This also is especially true of dis-
charges depending upon obstruction of the thoracic duct.
The appearance of chyle, however, is sometimes misleading, since it
has been shown that this character belongs in general to pathological
fluids of low sp. gr., especially to such as owe their origin to passive
congestion (Ff. A. Hoffmann).’?
Boulengier*? draws a distinction between chylous and chyliform
exudation, limiting the first of these terms to the case in which chyle
is actually discharged into the peritoneal cavity, while the second im-
plies only that the fluid has the properties of chyle. Chylous effusion
is very rich in fat. A specimen of chylous pericardial fluid was found
by Hasebroek “+ to contain 10 per cent. of the latter.
For the discrimination of the different forms of pleuritic effusion, the
bacteriological evidence is of much importance. Thus the absence of
micro-organisms points to a tubercular origin when the exudation is
purulent ; sero-fibrinous exudations are also usually free from fungi, and
cases of empyema occur in which only Staphylococcus pyogenes is found.
Exudations occurring in the course of pneumonia often exhibit Frenkel’s
pneumonia-coccus, and such have generally a favourable termination.
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TRANSUDATIONS. 361
In general it is a difficult task to determine whether a particular
fluid effused into one of the cavities of the body is due to inflamma-
tion (exudation) or to simple obstruction (transudation). In such
cases a probable conclusion may be based upon the specific gravity
of the fluid (Méhu, A. Reuss)."® A further point of interest in this
connection is the fact that inflammatory fluids are relatively rich in
fibrin (for the estimation of this body see p. 270), and in dry residue
products."7
B.—TRANSUDATIONS.
Transudation fluids may be serous, sanious, or, in rare instances,
chylous. Their sp. gr. is in general lower than that of inflammatory
effusion into the same cavity. They are always alkaline,” and for the
most part of a yellow colour.
Microscopically they exhibit but few tissue elements—fewer than, but
in other respects similar to, those of serous exudation. It should be
noted that in serous pleuritic effusion a large quantity of endothelium
is often detached. This must not be taken to imply endothelial pro-
liferation in a new growth (carcinoma), unless blood be also present,
when such an inference acquires additional support." Chemically,
transudation products exhibit much albumin, and generally sugar.5?
For the detection of the latter the process detailed at p. 274 may be
employed. They are always free from peptone.
Such fluids are distinguished from exudations chiefly by their low
sp. gr. and the difficulty with which they coagulate. The distinction,
however, is not easy to make in many instances.*!
The author would observe that in six specimens of transudation fluid and serous
exudation, which were entirely free from blood-corpuscles and dissolved blood-
pigment, he succeeded in separating no small quantity of urobilin. This body
is commonly to be found in transudations and exudations, and uric acid is always
present in them. In the transudation from a case of cirrhosis of the liver Mosca-
telli recently found allantoin.®? For the detection of uric acid the process de-
scribed at p. 71 may be applied.
C.—CONTENTS OF CYSTS.
The physician has often to decide whether a particular specimen of
fluid withdrawn from the body by aspiration or puncture is inflamima-
tory in its origin or due to passive congestion, and finally whether it
is derived from a cyst. Such a question is least apt to arise in explora-
tion of the pleural cavity, but in connection with abdominal symptoms
it is frequently very urgent to be able to give a definite answer. And
this is not always easy ; at times, indeed, it is impossible.
The cysts with which we have to do in this way are hydatid and
ovarian cysts, and, in rare instances, cystic kidney and pancreatic cysts.
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362 CYSTIC FLUIDS.
1. Hydatid Cysts.—The fluid obtained by puncture from a hydatid
cyst is clear, alkaline, and usually of low sp. gr., 1.006-1.010. It con-
tains a small quantity of a reducing substance (grape-sugar), very
little albumin, and abundance of inorganic salts, as sodium chloride.®
Succinic acid and inosite have also been detected. The microscopical
appearances are very characteristic. Amongst these are the hooklets
(see also p. 109) and portions of echinococcus membrane, so readily dis-
tinguished by its transverse striation and uniformly granular inner
surface (p. 109, fig. 61). Scolices may also be seen, and are known by
the two circles of hooklets and four suctorial discs on the anterior aspect
(head) and the sack-like hinder part, which is separated from the head
by an annular constriction. If the cysts have suppurated or be filled
with blood, as sometimes happens, chemical examination will usually
throw but little light upon their character. An absolute diagnosis is
possible only when hooklets or shreds of membrane have been seen in
the fluid. Consequently it is well to receive the latter in a conical glass,
and to carefully examine the sediment for these bodies.
Hydatid cysts often contain hematoidin crystals (see p. 196).
2. Ovarian Cysts.—The fluid obtained from ovarian cysts is re-
markably variable in its character.
It is generally to be distinguished from inflammatory and congestion
fluids by its high sp. gr., which ranges from 1.020 to 1.026. Its
reaction is alkaline, and it has little tendency to coagulate.
It is further marked by the great abundance of tissue débris which
it contains, and, from the nature of the cells which preponderate,
information may be drawn as to the kind of cyst from which it has
been taken.
Instances, however, occur in which the fluid from an ovarian cyst
shows nothing by which it may be known from that of ascites, and,
exceptionally, it has a sp. gr. even lower than that of a transudation
fluid. According to Schatz, Gusserow, and Westphalen,8* a low sp. gr.
with little albumin points to a cyst of the broad ligament.
When hemorrhage has taken place into the cyst, its contents may
vary in colour from red to a chocolate-brown, and be very turbid. The
microscopical examination of ovarian fluid shows a very variable quan-
tity of red and white blood-corpuscles, and many forms of epithelium,
squamous, columnar, and ciliated (fig. 143, a, 0, c). These cells, how-
ever, are rarely well preserved, but are for the most part far advanced in
fatty degeneration, and often with difficulty recognisable. Colloid con-
cretions (fig. 143, 7), in all probability derived from epithelium, are
invariably found in the so-called colloid cysts.
Certain forms of ovarian cysts may be readily differentiated by a
microscopical examination of their contents. Thus in dermoid cysts
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OVARIAN CYSTS. 363
may be seen, besides squamous epithelium, hairs, and crystals—choles-
terin, fatty, and hematoidin. Chemical investigation, too, throws
much light upon the character of an ovarian fluid. It will be found
as a rule to contain albumin, and always metalbumin (paralbumin),
and it is this body principally which renders it turbid and stringy
(Hammarsten).®
To Test for Metaliumin.—The fluid is mixed with three times its
bulk of alcohol and allowed to stand for twenty-four hours, when it is
filtered, the precipitate squeezed out, and suspended in water, which
is again filtered. The filtrate is opalescent and has the following
characters :—(a.) On boiling it becomes turbid, but does not form a
precipitate. (%.) No precipitate forms with acetic acid. (c.) Acetic
acid and ferro-cyanide of potassium render the fluid thick and impart
Fic. 143.—Contents of an Ovarian Cyst (eye-piece III., objective 8a, Reichert).
a, Squamous epithelinm cells; b. Ciliated epithelium cells; c. Columnar epithelium celis;
d, Various forms of epithelial cells; ¢. Fatty squamous-epithelinm cells; f. Colloid
bodies ; g. Cholesterin crystals.
to it a yellow tint. (d.) Millon’s reagent, on boiling, yields a bluish-
red;colour. (e.) Concentrated sulphuric and glacial acetic acid yield a
violet colour (Adamkiewicz). (f.) Huppert *®® has pointed out that when
the fluid containing metalbumin is boiled with sulphuric acid it yields
reducing substances, and this he regards as one of its most characteristic
properties. It must be noted that metalbumin is a constituent of other
pathological fluids besides that of an ovarian cyst. These cysts, and
especially dermoid cysts, also hold a considerable quantity of cholesterin
in solution. Cystic fluids have been frequently shown to contain dias-
tatic ferment in appreciable quantity.‘
8. Cystic Kidney.—In all cases where a sufficient specimen can be
obtained, the fluid from a cystic kidney (hydronephrosis) may be at
once identified on the ground of its chemical properties and microscopical
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364 CYSTIC FLUIDS.
appearances. An important point is the presence of renal epithelium,
and this should be carefully sought for. Then the determination of
urea and uric acid in large quantity indicates a connection with the
kidney ; but it must not be forgotten that these bodies occur more or
less plentifully in ovarian cysts, or may be supplied to them when they
communicate with the urinary tract by an abnormal channel.
It has been said that for the purpose of diagnosis the greatest signifi-
cance attaches to the presence of epithelium from the urinary tubules ;
and inasmuch as this usually occurs very sparingly in the fluid from a
cyst, the latter after removal by puncture should be allowed to settle
and the sediment carefully examined. Such of the clinical symptoms
of cystic kidney as call for notice here are very various. P. Wagner *§
observed that the urine is often scanty, Albuminuria and intermittent
hematuria, symptoms of sufficiently vague import, also occur.
4. Pancreatic Cysts.—The fluid from a pancreatic cyst is of low
sp. gr.—tr.oro-1.012 (Karewshi®), 1.022 (Hofmeister), 1.028 (v.
Jaksch )—and usually, though not always, has an admixture of blood.
In the author’s experience the blood-pigment is in the form of methe-
moglobin. There is also present abundance of cholesterin. Of proteids
there is serum-albumin ; rarely mucin is found. Metalbumin is absent.
The fluid also contains diastatic ferment, but the fact has by itself no
weight in diagnosis, since that body is very frequently met with else-
where (see p. 205). It is only when the sugar resulting from its action
is found to be maltose that any significance attaches to its presence
(see p. 287).
Such a fluid has the property of digesting albumin without the addi-
tion of acid, and it is this property which lends itself chiefly to the
purpose of diagnosis. -To test it, according to Boas,” the fluid may be
added to milk, and after precipitation of the casein the biuret test is
applied. If the reaction is obtained, the fluid is shown to have the
peptonising property, and it may be inferred that it is derived from the
pancreas, since no other cystic fluid is known to dissolve albumin in
alkaline solution. Of less moment is the property of such fluids to
emulsify fat and to disengage carbon dioxide gas on the addition of
acids. The importance of the characters here described is in most cases
greatly impaired by the fact that the larger and the older the cyst, the
less do its contents exhibit the physiological peculiarities of the pan-
creatic juice (Wolfler).° It follows that where the clinical symptoms
point to a cyst of the pancreas, it is not admissible to reject the inference
on the ground that the fluid is devoid of the tryptic character, and to
this extent the diagnostic value of these chemico-physiological observa-
tions is necessarily curtailed.
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SECRETIONS FROM FISTULA. 365
D.—THE SECRETIONS FROM FISTULZ.
Where these consist of a purulent, or simply serous fluid, discharging
through an unnatural outlet, their diagnosis may be based upon the
considerations already dealt with under the headings Transudations and
Exudations. A greater, or at least, at present, a more physiological
interest attaches to the appearances in those cases where fluids are dis-
charged by an unnatural opening, which might be assumed to communi-
cate with the intestine, because the fluid closely resembles the intestinal
fluid in its physiological properties, while fuller investigation shows that
it is derived from cavities lined by secreting glandular epithelium.
The author has analysed the secretion from a case of this kind which
Professor Woljfler observed and operated upon. The fluid had an acid
reaction, and contained albumose and peptone in considerable quantity,
pepsin, and a ferment which changed maltose into grape-sugar; no
diastatic ferment.”
The maltose employed in this research gave Trommer’s reaction only very
faintly (see p. 274). When it acted upon the secretion at 40° C., both Trommer’s
and Nylander’s tests gave positive results.
Small quantities of free hydrochloric acid were perhaps also present
—the Congo-red and benzo-purpurin tests gave feeble results—but there
was no sugar, urea, bile-pigment, or urobilin. Of inorganic salts there
were chlorides.
From this statement it appears that the fluid in many of its characters
resembled the mixed secretion of the intestinal tract.
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CHAPTER IX.
THE SECRETIONS OF THE GENITAL ORGANS.
I. THE SEMINAL FLUID.
1. Naked-Eye Appearances of the Semen.—The seminal fluid
is a thick, white, and somewhat opaque fluid, of slightly alkaline reac-
tion. It is tolerably tenacious, and resists the pressure of the cover-
class. It owes this property to the presence in it of a gelatinous
substance, which, under the microscope, appears to be hyaline, and
encloses innumerable cavities of various sizes. The semen has a peculiar
odour, which is derived, according to Fiirbringer,! from the prostatic
fluid, and depends upon the large proportion*of compounds of Schreiner’s
base (zethylenimin) (see p. 110) which it contains.
2. Microscopical Examination of the Semen.—The sperma-
tozoa, which are to be seen in great numbers in the semen, are thread-
like bodies about 50 wu in length, and provided with a head 4.5 » long,
and compressed in one plane, so as to appear club-shaped when seen
from the side. They exhibit very lively movements, but their motility
is rapidly destroyed by the addition of water, drying, &c. They are
present only in semen and in fluids with which the latter is mixed, and
obviously they may possess a great interest in the diagnosis of certain
morbid conditions. It may happen that the physician will have to
examine the semen to settle a question of sterility. A persistent
absence of spermatozoa (azoospermia) will show that the individual is
incapable of procreation, and this may occur whilst the other signs of
sexual power are retained. Of forty cases of sterile marriages, Kehrei?
found that azoospermia was the cause in fourteen. It is very impor-
tant to distinguish the persistent condition from the temporary absence
of spermatozoa, which occurs as a result of excessive and repeated inter-
course. Under such circumstances the fluid ejaculated consists almost
entirely of prostatic secretion (Pirbringer).°
In addition to spermatozoa, the semen exhibits certain cells—large
and small, finely granular testicle-cells, with one or more nuclei—some
columnar and squamous epithelium, a few large round hyaline bodies,
lecithin corpuscles, and stratified masses of amyloid substance, which
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THE SEMEN. 367
are finely granular within, and usually enclose a central kernel—these
are derived from the prostatic secretion ; and, finally, a few leucocytes—
which usually have two nuclei—and spermatic crystals. Some red
blood-corpuscles may also be seen.
Certain pathogenic micro-organisms, and especially tubercle-bacillus, may be
present in the secretion from the genital tract. They are usually discharged with
the urine. The seat of the disease may be determined in such cases by other
signs, as swelling of the testicle and epididymis, &c. (comp. p. 236).
In some pathological conditions the semen may be coloured a chocolate-
brown from the presence of a quantity of amorphous blood-pigment.
This happens especially in old people and in persons who have often
suffered from orchitis.
A very particular interest attaches to the spermatic crystals. In their
appearance and chemical properties they very closely resemble the
Fic. 144.—Microscopical appearance of the semen (human) eye-piece III., objective 8a, Reichert.
a. Spermatozoa; b. Columnar epithelium cells; ¢c. Bodies enclosing lecithin granules ; d.
Squamous epithelium cells from the urethra; d’. Testicle cells; e. Amyloid corpuscles ;
J. Spermatic crystals ; g. Hyaline globules.
crystals which have been already described as occurring in the blood,
sputum, and feeces (see p. 110). iirbringer has shown that while the
basic compound is derived from the prostatic fluid, the phosphoric acid
combined with it is furnished by the other component of the semen—
the spermatic or testicular secretion. The crystals form immediately
and in great abundance, when a 1 per cent. solution of ammonium
phosphate ([NH,],HPO,) is added to the pure prostatic fluid, and their
presence in large numbers, therefore, under all circumstances, indicates
prostatorrhcea (see p. 366).
It follows, therefore, that such crystals are not characteristic of the
semen, and the admixture of that secretion with some fluid or in a dried
discharge can be established only on the discovery of spermatozoa.. For
this purpose, when dried, they must be dissolved out in water from the
discharge containing them.
3. Chemical Examination of the Semen.—But little informa-
tion can be derived in this way. According to Mvescher, the funda-
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368 SECRETIONS OF THE GENITAL ORGANS.
mental constituent of spermatozoa is nuclein. Globulin and serum-
albumin have been found in the semen, and it is very rich in inorganic
substances. Posner‘ asserts that albumose is also present.
IIl.—_SECRETIONS OF THE SEXUAL ORGANS OF THE FEMALE.
1. Mammary Secretion (the Milk).—During the entire period of
gestation, and especially from the third month of pregnancy onwards,
a thin, whitish, and more or less turbid fluid may be obtained by pressure
from the breast. This is a fact of great importance, and the existence
of such a secretion is by itself strong evidence of pregnancy.
The fluid in question, when examined microscopically, presents in
the first place a great number of strongly refractive bodies of very
irregular size. These are called colostrum-corpuscles; they are fatty
Fic. 145.—Colostrum of a Woman in Sixth Month of Pregnancy (eye-piece III.,
objective 8a, Reichert).
in character, and are usually aggregated in groups. In addition to
these are to be seen a few leucocytes and some epithelial cells from the
inner surface of the ducts.
Immediately after confinement the colostrum-corpuscles disappear
from the milk, and eight or ten days after parturition are no longer
to be found. Cerny® supposes that colostrum-corpuscles are lymphoid
cells whose function it is to take up and alter the unused milk-globules,
which they then transfer from the acini of the gland to the lymphatics.
In their place is seen a profusion of fatty globules of irregular dimen-
sions, and together with these certain particles (Hoppe-Seyler) which
consist of casein and nuclein.
In diseases of the breast, and especially in cases of abscess and
inflammation during suckling, the milk is apt to exhibit an inter-
mixture of leucocytes.
Micro-organisms occur in the secretion in connection with certain morbid
states. Thus Escherich® found fungi in the milk of a woman suffer-
ing from septicemia, and these on cultivation proved to be pathogenic.
Pathogenic Staphylococci have also been isolated by Koch’s cultivation-
process from the milk of a woman with facial erysipelas (Karlinsiz).”
Similarly the author has detected micro-organisms, and especially cocci,
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VAGINAL SECRETION. 369
which stained by Gram’s method, in the milk of a patient with puerperal
septicemia.$ Further observations on the presence of fungi in human
milk have been published by Mf, Kohn and H. Newmann.®
From observations which the author has made, it would seem probable
that tubercle-bacillus also is occasionally present. The matter deserves
further notice.
The milk of some of the lower animals has been known to be infested by non-
pathogenic micro-organisms (Bacillus cyanogenus and Micrococcus prodigiosus),
from which it may derive an abnormal blue or reddish tint (Ncelsen, Hueppe).!”
The chemical constitution of the milk varies under different condi-
tions both of health and disease. The milk of sick women is generally
less rich in fat, and the proportion of lactose is diminished. Neither
bile-pigments nor biliary acid have yet been satisfactorily demonstrated
in the secretion of jaundice (v. Juksch).1! The albuminous constituents
of human milk are serum-albumin, casein, and nuclein. In also contains
milk-sugar and fats. For the detection and estimation of the latter, the
method described for the same purpose in the chapter on urine may be
employed. Special processes for the quantitative analysis of the milk
may be found in Hoppe-Seyler’s work.
The examination of the milk of wet-nurses is a point of practical
interest for the physician. It should be tested carefully as to its naked-
eye and microscopical characters, and in all cases chemically analysed.
In addition to this, information may be derived from the employment
of the bacteriological methods. And it is highly expedient that the
milk, whether of healthy or diseased women, should be submitted,
wherever possible, to Koch’s plate-cultivation processes, so as to ascer-
tain the absence of fungi.
2. Vaginal Secretion.—This, under ordinary circumstances, is a
thin fluid with an acid reaction. It contains a few large leucocytes,
each with a single nucleus, and squamous epithelium cells, which, for
the most part, are covered with microbes. In vaginal catarrh the
number of leucocytes is greatly increased, and some red blood-corpuscles
may be visible.
In cases of ulcerating carcinoma implicating the vagina or the vaginal
portion of the uterus, a copious foetid discharge takes place, and in this
the characteristic large cells of cancer may be found (fig. 146).
Hausmann detected fatty needles in the vaginal mucus.
Among the parasites which have been found in this situation are :—
1. Yeast and Fission-Fungi.— Various fungi belonging to these classes
infest the vagina. Thrush-fungus vegetations also have been seen there.
The vaginal secretion normally (Winter’*) and during confinement
(Déderlein and Samschin }*) contains fission-fungi, as, e.g., Staphylo-
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370 SECRETIONS OF THE GENITAL ORGANS.
coccus pyogenes albus, aureus, and citreus. Finally, it is sometimes
important to examine the secretion for tubercle-bacillus and gonococci
by the prescribed methods.
2. Trichomonas Vaginalis.—This parasite is an infusorium of oval
shape, and about 10 # in length. It has a long caudal appendage, three
flagella, and a lateral row of cilia.
Of the chemical constitution of the vaginal mucus little is known. It
has been said to contain trimethylamin (Hilger).
Fic. 146.—Preparation of Vaginal Secretion in a Case of Cancer of the Cervix Uteri
(eye-piece I1I., objective 8a, Reichert).
3. The Uterine Secretion.
1. Menstruation.—At the outset of menstruation there is an increased
discharge of vaginal secretion. Later on there is mixed with this an
abundance of red blood-corpuscles and prismatic epithelial cells laden
with fat from the interior of the uterus. The proportion of blood-cells
begins to diminish after a few days, and leucocytes preponderate towards
the close of the period. At this time also epithelium and a large quan-
tity of fatty detritus are discharged.
2. The Lochia.—The fluid discharged during the first few days after
parturition is thin and of a red colour. In addition to red and white
blood-corpuscles it exhibits uterine and vaginal epithelium. Later,
whilst the red corpuscles diminish in number, the leucocytes and epithe-
lium increase, and the discharge assumes a grey or even white colour.!°
Microbes are always plentifully present, even in the absence of septi-
cemia. According to Déderlein,” healthy lochia are free from fungi,
while in disease he found them without exception to contain Strepto-
coccus pyogenes. These statements are confirmed by Thomen.!8
A point of special importance in diagnosis is the examination of the
uterine secretion for the pathogenic fungi, to which reference has been
already made. ‘The secretion may be removed for the purpose by means
of a tampon.
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CHAPTER X.
METHODS OF BACTERIOLOGICAL ‘RESEARCH.
THE great practical importance which this subject has acquired of late
makes it necessary that the physician should be familiar with the pro-
cesses for ascertaining the presence of micro-organisms.
In all cases where micro-organisms may be the exciting cause of
disease, his first task will be to detect them in the secretions or natural
fluids by means of the appropriate methods for staining them.
When this is done, it remains in many instances to discover the
micro-organisms in particular situations, cells or tissues, so as to exclude
a mere misleading coincidence.
Further, the micro-organisms are to be cultivated outside the system 5
so that, where their morphological character and their behaviour to
staining substances are not sufficiently distinctive, the requisite infer-
ences may be drawn from their mode of growth and development.
Finally, it is possible by experiments upon animals to settle definitely
whether the transmission of a pure cultivation of the micro-organisms
will produce symptoms more or less closely resembling those attributed
to their agency in man.
The staining methods at our disposal and the perfection of our optical
instruments in many cases render the detection of micro-organisms easy,
but their cultivation and the transferring of them to animals is often
very difficult. Thus in the case of many diseases, micro-organisms have
been discovered under such circumstances as to leave no doubt that
they were the exciting cause, while every effort towards their cultiva-
tion and transmission to animals has failed of success. This, however,
has been achieved in the case of a number of pathogenic fungi, as, for
instance, the bacilli of glanders, anthrax, tubercle, cholera, leprosy, and
probably of typhoid fever.
It is no longer necessary for diagnosis to pursue the inquiry in every
instance through its entire course (detection, cultivation, and transmis-
sion to animals); but in some diseases, as tuberculosis, it is sufficient
to note the characteristic effect of staining substances. In others,
again (as relapsing fever and, occasionally, anthrax), a simple micro-
scopical examination will serve, without the application of staining
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372 METHODS OF BACTERIOLOGICAL RESEARCH.
processes. In doubtful cases of anthrax, the diagnosis may be settled
securely by the direct transmission of the blood to animals,
With reference to Asiatic cholera, the mere detection of the fungus
in the stools is never sufficient, but it must be isolated by Koch’s
cultivation methods, when it will be recognised by its mode of growth.
With the progress of science we may learn to know a definite fungus
as the cause of each of the infectious diseases; but even then, when
all the conditions indicated above have been complied with, our labour
will not have ended. It will remain to extend our acquaintance with
the life-history of the parasites, so as to determine the sources of
nitrogen and of carbon and the inorganic salts upon which they depend
for their growth. It is only when this is done that a secure foundation
will be laid for a system of rational therapeutics.1
A short account will be given here of the methods employed in such
researches. It will naturally begin with a description of the apparatus,
and in the first place of the microscope.
I._THE MICROSCOPE.
The shape, size, and adjuncts of the body or stand of the microscope
itself are in general of little moment. Habit will determine, in most
cases, whether the tube used shall be worked by a screw or with the
hand. . For the examination of plate-cultivations, however, the former
will be chosen. Neither is it essential that the stand should be jointed,
but it is absolutely necessary that tt be faultless in its construction. It
must also be capable of adjustment for use with the most powerful objectives,
and with an Abbe’s condenser or equivalent arrangement.
The stage must be sufficiently large and firm, and the opening in it
as large as possible, so that a plate-cultivation, for instance, may be
inspected easily with a low power.
For bacteriological investigations, as has been already observed, an
Abbe’s or other condenser adjusted movably to the microscope-stand
is needed. The principle of such an instrument is this: The rays of
light reflected from the mirror of the microscope are passed through
the principal axis of a lens interposed between the mirror and the
objective in such a direction that they fall upon the object, which thus
receives a cone of light as highly concentrated as possible. If narrow
diaphragms be introduced between the mirror and the collecting lens,
an illumination of the image is obtained similar to, but probably some-
what more intense than, that where narrow cylindrical diaphragms are
used. The edges of the image are in all cases well defined, even in
unstained preparations, and such a condenser may be employed with
advantage for histological work. If the diaphragms be removed and
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THE MICROSCOPE—LENSES. 373
an open-condenser light consequently employed, the outlines disappear
and become entirely undistinguishable (Koch).2 Under these circum-
stances nothing else can be distinctly made out with uncoloured pre-
parationus. With stained preparations, however, it is far otherwise,
and in this lies the valuable application of the open-condenser light as
discovered by Koch. The outlines, in so far as they depend for their
appearance on a distinction in the refractive properties of the object
(corresponding to a structural difference amongst its parts) and those
portions which are but lightly stained, are lost to view, while the
deeply-stained particles, as the coloured nuclei of cells (granulations),
and especially fungi coloured with aniline or other dyes, become more
exquisitely defined. In this way micro-organisms may readily be seen
and recognised, even when very sparsely present in a preparation. he
apparatus 1s indispensable for bacteriological research.*
In addition to a suitable stand and a condenser, good objectives are
needed.
First a weak objective, magnifying about 60 to 80 diameters, for the
inspection of plate-cultivations; and in addition it is very advanta-
geous to have a good powerful dry objective. There are many objects,
as fresh blood, fresh milk, or fresh pus, for the examination of which
immersion-lenses are not suitable. For such purposes Zeiss’s lenses F
or D, or Reichert’s 84, may be recommended. With these, especially
if a condenser be also used, many bacteriological preparations, as those
of tubercle-bacillus from the sputum, may be adequately investigated.
For very delicate preparations, and in particular where minute details
of structure are to be made out, an immersion-system is needed. The
water-immersion systems, formerly much in use, have been superseded
of late by the oil-immersion (homogeneous immersion) lenses made by
Stephenson and Abbe and Zeiss, which are to be preferred on account
of the better definition and clearness of the image which they produce.
Instead of water, there is interposed between the front lens of the
objective and the object (cover-slip), a fluid having the same refractive
index as glass. For this purpose a mixture of fennel- and castor-oils
may be used. Reichert employed with his lenses a mixture of vase-
line and olive-oil, which has the advantage of being odourless, and of
penetrating less readily within the lenses. At present concentrated
cedar-oil is most in use. Such a system has the further advantage
that it does not require correction-collars to be used, as do dry lenses,
and that powerful eye-pieces may be employed with it. It is very
* The best results are obtained with the instruments supplied by Hartnack (Pots-
dam), Seibert and Kraft (Wetzlar), Leitz (Wetzlar), and especially by Zeiss (of Jena).
CO. Reichert of Vienna supplies with his little microscopes IV. and V. a condenser
which is very suitable for clinical purposes.
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374 METHODS OF BACTERIOLOGICAL RESEARCH
advantageous also to place a drop of oil on the under surface of the
slide which carries the object, between this and the collecting lens of
the condenser.
Fic. 147. GesLicrchenus Stand No. IL.b., with draw-tube, rack-and-pinion fine adjustment,
and Abbe’s condenser.
Of less moment is the choice of an eye-piece. In general, for every
form of investigation, except bacteriological research, eye-pieces of low
magnifying power should be taken. For the rest, the eye-pieces II.
Digitized by Microsoft®
THE MICROSCOPE. B75
and V. as supplied by the firms of Reichert and Zeiss will serve for
all cases. The periscopic eye-pieces of Seibert and Krafft are very
excellent.*
An objective of crown- and flint-glass was first adopted by Dv. Schott
of Jena. It is an admirable contrivance, and has become indispensable
for many purposes, as in photographing micro-organisms, where a well-
defined achromatic outline is required. Zeiss has given such the name
of apochromatic objectives. The corresponding compensation eye-pieces
Ca
A ‘ fe
kK ‘n rE
A ail cee TMT
il “ 1 Oh f
mil ui iM em =
ws =
hn an
te
HUN
‘i
al
Fic. 148.—Abbe’s Condenser, as made hy Zeiss. Natural size, side view. Sp. mirror.
should be used with them. Their chief advantage lies in the fact that
they give a clear and well-defined image with eye-pieces of greater
streneth than could formerly be used. Apochromatic objectives of
* The author has for many years employed an instrument made by Reichert, and
he has found it to serve well in every kind of microscopical work, histological and
bacteriological. Its parts are as follows :—Eye-pieces II. and IV., objectives 4, 8a,
and oil-immersion 74, ; a small stand with condenser (Abbe’s) and cylinder-diaphragm.
Its price was 207 florins without the oil-immersion, which cost 107 florins. Very
good and inexpensive systems of lenses are also made by Plossl of Vienna.
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376 METHODS OF BACTERIOLOGICAL RESEARCH.
excellent construction are supplied by Reichert. The images of the
most delicate objects obtained with Reichert’s homogeneous immersion
objective of 2 mm. focal length, and even with the working eye-piece
12, are clear and distinct in their smallest details. There is one dis-
advantage attending the use of these lenses. They need a finer
adjustment than the usual mechanism affords, and the image becomes
indistinct with the slightest movement of the instrument. It has then
IZ
a
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{MW
nw
E\\
SSS
ae
Leet enna |
toss k%
Fic. 149.—Abbe’s Condenser as above, showing the collecting system of lenses.
d. Iris diaphragm.
to be focussed anew. ‘This defect is apt to produce misleading appear-
ances, and it must be admitted that the otherwise excellent apochro-
matic objectives supplied by Zeiss are so far in need of improvement.
[For bacteriological work, it is convenient to have a microscope with
a stand to which an Abbe’s condenser can be fixed under the stage.
Fig. 147 shows a convenient form made by Reichert of Vienna. Other
makers furnish somewhat similar stands. Abbe’s condenser is placed
under the stage, and the tube of the microscope is provided with a
DETECTION OF MICRO-ORGANISMS. 377
“revolver” or ‘“nose-piece,” to which lenses of different magnifying
powers are fixed.
In an Abbe’s condenser (fig. 148) the illuminating apparatus is a
condenser system of very short focus (the section of the lenses is shown
in fig. 149), which collects the light reflected by the mirror (Sp)—the
plane side of the mirror being used—into a cone of rays of very large
aperture, and projects it on the object. For ordinary work the cone
of light is reduced by means of diaphragms, the most convenient form
being that known as the “iris diaphragm,” which can be adjusted to
any size (fig. 149, d). Oblique illumination can be obtained by placing
the diaphragm eccentrically, which is done by means of the rack-and-
pinion movement (e).
When very exact definition is required, apochromatic lenses are
employed. They are expensive, but the objectives are so constructed
as to secure the union of three different colours of the spectrum in one
point of the axis. The images projected by them are nearly equally
sharp with all the colours of the spectrum. As there is very great
concentration of light by these objectives, they permit of the use of
very powerful eye-pieces, thus giving high magnifying power with rela-
tively long focal length. A series of compensating oculars are used
with these lenses. The eye-pieces of extremely low power are called
“searchers,” while the ordinary or working eye-pieces, beginning with
a magnifying power of 4, are classified as 4, 8, 12, 18, and 27. With
these eye-pieces great magnifying power is obtained, partly by the lens,
but also by the ocular used. ]
II. THE DETECTION OF MICRO-ORGANISMS.
In many cases the object to be examined may be placed under the
microscope without preparation of any sort. The characteristic micro-
organisms will then become visible. This is so with the spirillum of
relapsing fever, anthrax-bacilli in the blood, &c. For the most part,
however, special processes are necessary for the detection of micro-
organisms. The details of some of the processes for the prepara-
tion of specimens have been gone into in the chapters on the Blood,
Sputum, &c., which the reader will consult for information concerning
them.
It will not be out of place if we give here a brief summary of the
methods in use, and point out the particular purposes to which each is
applicable. The principles upon which all of them are based were
worked out by Koch, Hhrlich, and Weigert ; and almost every day some
new process or a modification of the old familiar methods is made
known. It would far exceed the limits of this book to attempt an
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378 METHODS OF BACTERIOLOGICAL RESEARCH.
account of all the methods which have been suggested, and the various
modes of applying them. We shall confine ourselves to what has
appeared in the more important and systematic essays dealing with the
subject. Those of Giinther*? and Unna,* especially the latter, com-
prise an accurate and exhaustive account of the methods for staining
fungi. Particularly good results in the staining of micro-organisms in
sections, which, however, lies beyond our province, have been obtained
with Kiihne’s® processes. They have been. tested by Rille, a pupil of
the author, and have been found most valuable for dry cover-glass
preparations as well. The methylene-blue method® and Kiihne’s"
modification of Gram’s method (staining with alcoholic solution of
Victoria-blue) are very serviceable in the examination both of sections
and of the secretions.
In the examination of the blood and secretions for pathogenic micro-
organisms it is in general best to proceed with the use of basic aniline
dyes as described at p. 40. Should it happen that no result is obtained
in this way, greater certainty may be secured with Ldfler’s method
(p. 41), which is especially suitable for detecting the bacilli of typhoid
fever and glanders, and, finally, with Gram’s method (p. 41). All the
fungi hitherto discovered stain with this, except the bacilli of typhoid
and cholera, and gonococct. The bacillus of hen-cholera is also un-
affected by it.
Guinther's method (p. 45), is very serviceable for staining the spirillum
of relapsing fever. The investigation of the blood and secretions for
tubercle-bacillus should be carried out precisely in the manner laid down
by Koch and Lhrlich (p. 105). Staining with basic aniline dyes serves
well for the detection of fungi in the buccal cavity, the nasal secretion,
and the gastric contents ; but for examining the buccal secretion Gram’s
or Giinther’s method may also be adopted with advantage, since they
render visible the very delicate Spirocheete buccalis (p. 81) and capsulo-
cocci.
In searching for the fungi of the alimentary canal, pathogenic and non-
pathogenic, all the processes hitherto mentioned should be employed
where a thorough investigation is aimed at, and the observer should not
forget to add a little iodo-potassic-iodide solution to a drop of the fiuid
under examination (see p. 171).
In examining the urine, the best results are secured with Gram’s or
Friedlander’s method (p. 108). By their aid the author has detected in
various specimens of urine from persons both in health and disease an
unexpected profusion of different forms of fission-fungi.
The micro-organisms which occur in pus stain most readily with Gram’s
method, or its modification already referred to (Victoria-blue). Liffler’s
and Friedlinder’s methods are applicable to the same purpose.
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CULTIVATION OF MICRO-ORGANISMS. 379
To stain the spores of micro-organisms a preparation is made in the
manner indicated at p. 40, but exposed for a longer time to the heat.
It may be passed through the flame about ten times (Hueppe).8 When
this is done the bacilli lose their staining properties, whilst the spherical
objects, if they consist of spores, take up colouring-matter. It is still
better to employ the process of double staining. The preparation is first
stained in a hot Ziehl-Neelsen fuchsin solution, then decolorised with
nitric acid, and again stained with methylene-blue. The spores then
appear red and the bacilli blue.? :
Special processes have been devised for the purpose of defining the
flagella which some bacteria present. These have been worked out by
Lofier, Kiinstler, Newhaus, and Trenkman2® As a mordant Loffler
employs a fluid composed as follows: solution of tannin (tannic acid 20
parts, water 80 parts) ro cc. ; a cold saturated solution of ferric sulphate,
5 ec.; watery or alcoholic solution of fuchsin, methyl-violet or wool-
black, r ce. The staining-fluid is neutral saturated anilin-water-fuchsin
solution. The method of proceeding will be described here. The cover-
glasses are heated with concentrated sulphuric acid, washed with water
and then with a mixture of alcohol and ammonia in equal parts, and
afterwards polished with a cloth which should be free from grease.
They are then brought in contact with a platinum needle carrying a
particle of the pure cultivation, and the latter is spread out finely and
divided upon their surface, after which they are allowed to dry in the
air. They are next grasped between the fore-finger and thumb of the
observer and passed through the flame of a lamp. 394, 404,
415, 423.—Quincke, see (117).—Laache, see (123).
16 Muir, Journal of Anatomy, xxvi. p. 393.
1 Neubert, St. Petersburger med. Wochenschr., xiv. No. 32, 1889; Dehio, ibid.,
Xvi. 1, 1891.
18 Kraepelin, Neurologisches Centralblatt, No. 3, 1890.
129 F, Miiller, Charité-Annalen, xiv. 253, 1889.—A. Klcin, Wiener klin. Wochen-
schr., iv. 721, 745, 1891.—v. Noorden, Charité-Annalen, xvi. (sep. pub.).
130 Block, Diss. Stettin, 1871.—Grawitz, Virchow’s Archiv, lxxix. 546, 1877, and
Ixxxi. 355, 1880 —Lichtheim, Zeitschr. fiir klin. Medic., vii. 140, 1884.
131 Kitasato, Zeitschr. f. Hygiene, vii. 225, 1889.
132 Koch, Cohn’s Beitriige zur Biologie der Pflanzen, ii. 429, 1877 ; and Mittheilun-
gen aus dem kaiserlichen Gesundheitsamte, i. 1, 1881.—Zhrlich, see (93).— Weigert,
Centralbl. fiir die medic. Wissensch., ix. 609, 1881 ; and Berl. klin. Wochenschr.,
XV. 241 and 261, 1877.
133 See Daland, Fortschr. der Med., ix. 824, 1891.
134 Scheurlen, Centralbl. f. Bakteriol. u. Parasitenkunde, viii. 257, 1890.
13 Ehrlich, Zeitschrift fiir klin. Med., ii. 710, 1881.
136 Lifler, Mittheilungen aus dem kais. Gesundheitsamte, ii. 439, 1884.
137 Gram, Fortschritte der Medicin, ii. 186, 1884.
138 Weigert, Fortschritte d. Medicin, v. 228, 1887.
139 Pollender, Mikroskopische und mikrochemische Untersuchung des Milzbrand-
blutes, sowie tber Wesen und Cur des Milzbrandes. Casper’s Vierteljahrshcrift
fiir gerichtliche und 6ffentliche Medicin, viii. 103, 1855.—Brauel/, Virchow’s
Archiv, xi. 132, 1857, and xiv. 32, 1858.—Davaine, Compt. rend. de l’Académie des
Sciences, lvii. 220, 1863.
140 Bollinger, V. Ziemssen’s Handbuch, iii. 544, 2nd edit. For exhaustive in-
formation, see Wilhelm Koch, Milzbrand und Rauschbrand, 1886. Deutsche
Chirurgie, 9. Lief.—Baumgarten, Jahresbericht iiber die Fortschritte in der Lehre
von den Mikro-organismen, &c., i. 52, 1886; ii. 124, 1877; ili. 101, 1888.—Fliigge,
Die Mikro-organismen, &c., 2nd edit., Leipzig. 1880.
141 2. Koch, Cohn’s Beitriige zur Biologie der Pflanzen, ii. 277 and 429, 1877.—R.
Koch, Wundinfectionskrankheiten, Leipzig, 1878; and Mittheilungen aus dem
kaiserlichen Gesundheitsamte, i. 49, 1881.
12 Eppinger, Wiener med. Wochenschr., xxxviii, Nos. 37, 38, 1888.—R. Paltauf,
Wiener klin. Wochenschr., Nos. 18-26, 1888, where a fullaccount of the literature
on the subject will be found.
18 Obermeyer, Centralbl. fiir die medic. Wissenschaften, xi. 145, 1873; also for
further information consult v. Jaksch, Wiener medic. Wochenschr., xliii. 120, 159,
and 186, 1884.—Fliigge, see (141).
144 Sarnow, Der Riickfallstyphus in Halle a. 8. im Jahre 1879-81. Inaugural
Dissertat. Leipzig, 1882.
145 Karlinski, Fortschritte d. Medicin, viii. 161, 1891.
U6 Sacharof, Baumgarten’s Jahresbericht, iv. 314 (ref.), 1889.
M7 Giinther, Fortschritte der Medic., iii. 755, 1885. :
48 Weichselbaum, Wiener med. Wochenschr., xxxiv. 333 and 365, 1884.
149 Meisels, Wiener med. Wochenschr., xxxiv. 1149 and 1187, 1884.
150 Lustig, Wiener med. Wochenschr., xxxiv. 430, 1884.—Sticker, Centralbl. fiir
klin. Med., vi. 441, 1885.—Doutrelepont, Deutsche medic. Wochenschr., xi. 98, 1885.
—Riitimeyer, Centralbl. fiir klin. Med., vi. 353, 1885.
151 Tiebmann, Lo Sperimentale, xlv. 30, 1891.
132 Ehrlich and Guttmann, Berliner klin. Wochenschr., 124, 1891.
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396 BIBLIOGRAPHY.
153 Hamerle, Prager med. Wochenschr., xvi. 106, 1891.
14 Lofler, Arbeiten aus dem kaiserl. Gesundheitsamte, i. 141, 1836.
155 Lofler and Schiitz, Deutsche medic. Wochenschr., ix. 52, 1882.
156 [srael, Berl. klin. Wochenschr., xx. 155, 1883. For exhaustive information
as to the older and more recent literature on the subject, see Fliigge (140), and
Baumgarten, Jahresb., ii. 181, 1887; iii. 156, 1888; iv. 154, 1889; v. 226, 1890.
17 ~Weichselbaum, Wiener medic. Wochenschr., xxxv. Nos. 21-24, 1885.
8 Meisels, Wiener med. Wochenschr., xxxvi. 759, 1886.
19 Riitimeyer, Centralbl. fiir klin. Med., viii. 145, 1887.—Neuhauss, Berlin. klin.
Wochenschr., xxiii. 89 and 389, 1886.
160 Janowski, Centralbl. f. Bakteriol. u. Parasitenkunde, v. 657, 1889.
161 VY, Noorden, Minch. med. Wochenschr., xxxiv. No. 3, 1887.
162 Orthenberger, Munch. med. Wochenschr., xxxv. Nos. 49 and 50, 1888.
3 Sanger, Deutsche med. Wochenschr., xv. No. 8, 1889.
164 Weichselbaum, Wiener med. Wochenschr., xxxviii. Nos. 35 and 36, 1888.
165 4, x. Liselsberg, Wiener klin. Wochenschr., iii. 731, 1890.—Levy, Centralbl. f.
klin. Med., x. 65, 1890.—Brunner, Wiener klin. Wochenschr., iv. 392, 1891.
166 4. y, Rosthorn (oral communication).
167 Crookshank. An investigation into the so-called “‘ Hendon Cow Disease,” in
its relation to scarlet-fever in man. Trans. Patholog. Society, 1888, printed
separately in pamphlet form.
168 Crookshank, op. cit.
169 The account was published in Reports xv. and xvi. of the Local Government
Board, in the “Transactions of the Epidemiological Society,” New Series, vol. v.,
“Proceedings of the Royal Society,” vol. xlii., and in “ Nature,” No. 919, vol. xxxiv.
170 Bareggi, Gaz. Lomb., viii. p. viii— Babes, Virchow’s Archiv, ex. 562, 1888.
W1 Nikolaier, Deutsche med. Wochenschr., x. 842, 1884. —Rosenbach, Archiv fiir
klin. Chirurgie, xxxiv. 306, 1886.—/Hochsinger, Centralbl. fiir Bacteriol. und Para-
sitenkunde, ii. 145 and 177, 1887.—Beumer, Zeitschr. fiir Hygiene, iii. 242, 1888. —
Peiper, Centralbl. fiir klin. Medic., viii. No. 42, 1887.—V. Hiselsberg, Wiener klin.
Wochenschr., i. 232, 259, 1888, where exhaustive references to the literature on
the subject are given.
i” Brieger, Untersuchungen iiber Ptomaine, pt. iii. p. 89, Berlin, 1886 ; Berlin.
klin. Wochenschr., xxv. 311, 1886 ; and Deutsche med. Wochenschr., xiii. 303,
1887 ; Virchow’s Archiv, exii. 549, 1888.
173 Nissen, Deutsche med. Wochenschr., xvii. 775, 1891.
M4 A, Bruschettini, Riforma Med., April 11, 1892.
7% Kitasato, Archiv f. Hygiene, vii. 225, 1889.
7% Belfanti and Pescarolo, Centralbl. fiir Bacteriologie und Parasitenkunde, iv.
514, 1888 ; Bawmgarten, Jahresbericht, iv. 230, 1889; v. 201, 1890.
17 Klebs, Die allgemeine Pathologie, &c., pt. i. p. 144. Jena, 1887.
v8 Laveran, Comptes rendus, xcv. 87, 1882.
Marchiafava and Celli, Fortschritte der Medic., i. 573, 1883 ; and iii. 339 and
787, 1885. For further literature—Laveran, Richard, Councilman, and Abbot—see
Baumgarten, i. 153, 1885 ; also Schelling, Centralbl. f. Bacteriol. u. Parasitenkunde,
x. 570 (ref.), 1891.
180 See O. Rosenbach, Berliner klin. Wochenschr., xxviii. 840, 1891.
181 Gerhardt, Zeitschr. fiir klin. Med., vii. 372, 1884.
182 Golgi, Centralbl. f. Bacteriologie und Parasitenkunde, i. 346, 349, 1887;
Fortschritte der Medicin, 82, 1889.—Metschnikoff, Centralbl. f. Bacteriol. u. Para-
sitenkunde, i. 624, 1887.—Chenzinsky, ibid. iii. 457, 1888.—¥For later literature
see Baumgarten’s Jahresbericht, iv. 230; v. 201, 1890.—Osler, British Med.
Journal, xii. 556, 1887.——-Shattuck, Boston Med. and Surg. Journal, cxviii. 450,
1888.—Evans, Brit. Med. Journal, No. 1426, 897, 1888.
BS
a
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CHAPTER I.—THE BLOOD. 397
183 Dyer, Proc. Roy. Soc., May 28, 1$91.—Fenton Evans, ibid., February 12,
18y1.
184 Councilman, Centralbl. fiir Bacteriologie und Parasitenkunde, ii. 377. 1887.
Fortschritte der Medicin, vi. 449, 500, 1888.
185 Mosso, Centralbl, fiir Bact. und Parasitenk., ii. 17, 1887.
186 [. Pfeiffer, Zeitschr. fiir Hygiene, ii. 397, 1887.
187 Yommasi-Crudeli, Centralbl. f. Bact. und Parasitenk., i. 349, 1887.
188 Schiavuzzi, ibid., i. 203, 1887.—F. Cohn, ibid., ii. 363, 1887.
189 Danilewsky, Gisuimenal fiir die med. vyecenneneit XXV. 737 and 753, 1886;
Centralbl. f. Bacteriol. u. Parasitenkunde, ix. 397, 1891.
19 Grassi and Feletti, see (191).—Celli and Sanfelice, Fortschritte d. Med., ix.
449, 1891.
19 Laveran, see (178).—Marchiafava and Celli, Riforma Medica (sep. pub.),
April 1890: Berliner klin. Wochenschr., xxvii. 1010, 1890; Fortschritte der
Medicin, ix. 283, 1891.—(olgi, Sulla infezione malarica, Torino, 1886; Beitrage
zur pathologischen Anatomie, &c., vii. 649, 1890; Fortschritte der Medicin, vii.
81, 1889; Zeitschr. f. Hygiene, x. 136, 1891.—Celli and Guarnieri, Fortschritte
der Medicin, vii. 521, 561, 1889.—Grassi and Calandraccio, Centralbl. f. Bacteriol.
u. Parasitenkunde, vii. 396, 430, 1890.—(rassi and Feletti, ibid., ix. 403, 430, 461,
1891; X. 430, 481, 517, 1891.—Canalis, Giornale medico del. R. Esercito e della R.
Marina, Rome, 1889; Fortschritte d. Med., viii. 286, 325, 1890.—R. Paltauf,
Wien. klin. Wochenschr., iii. 24, 47, 1890.—Quincke, Mitth. f.d. Verein Schleswig-
Holsteiner Aerzte, 1890.—Dolega, Fortschritte d. Med., viii. 769, 809, 1890;
Verhandl. d. Congresses f. innere Medicin, ix. 518, 1890.—P. Lehn, Berliner
klin. Wochenschr., 26, 292, 1890; Zeitschr. f. Hygiene, viii. 78, 90, 1890; tio-
logische u. klin. Malariastudien, Berlin, 1890, which has an exhaustive re-
ference to the literature.—Chenz ae see the Russian translation of this book by
Prof. V'schudnowsky, p. 120, St. Petersburg, 1890, which also has an excellent figure
of the Plasmodium malariz.—Rosenbach and Rosen, Deutsche med. Wochenschr.,
xvi. 325, 1890.—V. Jaksch, Prager med. Wochenschr., xv. 40, 1890. See also
Hochsinger, Wiener med. Presse, xxxii. 658, 1891.—Mannaberg, Centralbl. f. klin.
Med., xii. 513, 1891.—Z. Malachowshi, ibid., 601, 1891.—Baumgarten’s Jahresbericht,
iv. 306, 1889 ; v. 425, 1890.—Bein, Charité-Annalen, xvi. 181, 1891.
192 Dock, Fortschritte der Med., ix. 187, 1891 ; Medical News, 1891.—C. Spener,
Centralbl. f. Bacteriol. und Parasitenkunde, x. 554 (ref.), 1891.
193 Hehir, Lancet, May 28, 1892.
194 Golgi, Fortsch. der Med., 7, Pl. I.—Plehn; Celli, and Guarnieri, Fort-
schritte der Med., Pl. III. fig. 15.
195 Golgi, ibid.
196 Golgi, ibid.
197 Golgi, Zeitschr. f. Hygiene, x. 136, 1891.
18 Golgi, l.c.
199 Celli and Marchiafava, Berliner klin. Wochenschr., xxvii. 1010, 1890.
200 Celli and Guarnieri, l.c., Pl. IIIa.
201 Compare the striking observations made by Danilewski, op. cit., p. 398.
2022 See also O. Hertel and C. v. Noorden, Berliner klin. Wochenschr,, xxviii.
(sep. pub.), 1891.
203 V, Jaksch, see (191).
204 Chenzinsky, in Prof. Tschudnowsky’s translation of this book, p. 420, St.
Petersburg, 1890.—Plehn, Atiol. and klin. Malariastudien, Berlin, 1890.—Mala-
chowski, Grassi, and Feletti, see (191).
205 Hochsinger, see (191).—Paltauf (oral communication).
206 Loef, Centralbl. fiir Bacteriologie und Parasitenkunde, ii. 353, 1887,—Pfeiffer,
ibid., ii. 126, 1887.
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398 BIBLIOGRAPHY.
*07 See Leuckart’s classical work : Die menschlichen Parasiten und die von ihnen
herriihrenden Krankheiten, Leipzig, i. 617, 1865; also LZ. K. Schmarda, Lehrbuch
der Zoologie, i., Vienna, 1871; and B. Hatschek, Lehrbuch der Zoologie, Jena,
1888.
708 Bilharz and C. Th. V. Siebold, Zeitschrift fiir wissenschaftliche Zoologie, iv.
59, 72, and 454, 1853; and Bilharz, Wiener medic. Wochenschr., vi. 49, 1856. For
further literature, see Meissner, Schmidt’s Jahrbiicher, clxv. 289, 1875 ; clxxxix.
84, 1881; cxciii. 30, 1882.
£09 Cobbold, Lancet, ii. 1877.
10 Ringer and Patrick Manson, Med. Times and Gazette, July 2, 1881.
"ul Leuckart, 1.c., ii. 628, 1876.—Meissner, Schmidt’s Jahrbiicher, clxv. 289, 1875 ;
clxxxix. 81, 1881 ; cxciii. 29, 1882.
“12 Lewis, Lancet, i. No. 2. 1873; and the same in Centralbl. fiir med. Wissen-
schaft, xi. 335, 1873; xiii. 771, 1874. “On a hematozoon inhabiting human
blood,” Calcutta, 1872; Deutsches Archiv f. klin. Med., xii. 540, 1873; xv. 613,
1874.
213 Bourne, Brit. Med. Journal, No. 1429, p. 1050, 1888.
"14 Meissnér, Schmidt’s Jahrbiicher, clxv. 289, 1875.
215 John Guitéras, Philad. Med. News, April 1886; Fortschritte der Medicin,
iv. 974, 1886.
16 Myers, Wykeham, Centralbl. fiir Bacteriologie und Parasitenkunde, ii. 761,
1887.
217 Stephen Mackenzie, Lancet, ii. 398, 1881.—Patrick Manson, op. cit.—Scheube,
Festschrift fiir E. Wagner, p. 242, Leipzig, 1888.—Lanceraux, Gazette des Hépi-
taux, lxi. 630, 1888.
18 See Hoppe-Seyler, Medic.-chem. Untersuchungen, Tiibingen, 1867-70.—
Schneider, Wiener medic. Wochenschr., xvii. No. 14, 99, 102, 1868.—Preyer, Die
Blutkrystalle, Jena, 1871.—Hoppe-Seyler, Physiol. Chemie, Berlin, 375-399, 1881.—
Rollett, Hermann’s Handb. der Physiol., iv. Bd. i. p. 38, 1880.—Zandois and
Stirling's Text-book of Physiology, p. 22, 4th edit., 1891.
19 Teichmann, Zeitschr. fiir ration. Med., iii. 375, 1853, and viii. 141, 1857; also
Funke, ibid., N. F., i. 185.
220 Hoppe-Seyler, 1.c., Medic.-chem. Untersuchungen, p. 44.
221 Nencki and Sieber, Archiv fur experiment. Pathol. u. Pharmakol., xviii. 401,
1884; xx. 325, 1886; xxiv. 430, 1888.
222 Hoppe-Seyler, Berichte der deutschen chem. Gesellschaft, vii. 1066, 1874.
3 (. le Nobel, Centralbl. fiir die med. Wissensch., xxv. 305, 1887; and Archiv f.
die ges. Phys., xl. 501, 1887.
24 Maly, Centralbl. fiir die medic. Wissensch., ix. 849, 1871; and Liebig’s An-
nalen, clxiii. 77, 1872.
25 Virchow, Virchow’s Archiv, i. 379, 1847.
26 Latschenberger, Sitzungsberichte der k. Akademie (Vienna), xcvii. 2, 1888
(pub. sep.).
27 Hoppe-Scyler, Physiol. Chemie, p. 391. Berlin, 1881.
228 Jaderholm, Zeitschr. fiir Biologie, xiii. 193, 1877.
29 See Bohm, Ziemssen’s Handbuch, xv. 158, 2nd edit., 1880.—Lewin, Lehrbuch
der Toxikologie, p. 23. Wien, 1885.—Hoppe-Scyler, Virchow’s Archiv, xi. 288,
1857.—For additional information, see Husemann’s Handb. der Toxikologie.—4A.
Jéderholm, Die gerichtlich-medicinische Diagnose der Kohlenoxydvergiftung,
1876.
230 Hoppe-Seyler, Virchow's Archiv, xili. 104, 1858.—Otto, Anleitung zur Aus-
mittlung der Gifte, p. 246, 6th edit., 1884.
231 FB, Salkowski, Zeitschrift fiir physiolog. Chemie, xii. 227, 1888.
232 Kuniyost Katayama, Virchow’s Archiv, cxiv. 53, 1888.
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3 Kunkel, Sitz. d. phys. med. Gesellschaft zu Wiirzburg, ix., Sitzung vom 28
April 1888.—A. Wetzel, Inaug. Diss., Wiirzburg, 1889.
*44 Rubner, Archiv f. Hygiene, x. 155, 1890.—Dreser, Archiv f. experimentelle
Pathologie u. Pharmakologie, xxix. 119, 1891.
*5 Hoppe-Seyler, Physiolog. Chemie, op. cit., p. 386.
36 Lewin, Virchow’s Archiv, lxxiv. 220, 1878; and Lehrbuch der Toxikologie,
p. 48.
*37 Preyer, Centralbl. fiir die medic. Wissenschaft, v. 259 and 273, 1867.
238 Hoppe-Seyler, Physiolog. Chemie, l.c., p. 385.
*39 Marchand, Virchow’s Archiv, lxxvii. 488, 1879.
*40 Stokvis, Archiv fiir experiment. Pathologie und Pharmakologie, xxi. 169,
1886.—A. Bokai, Deutsche med. Wochenschr., xiii. 42, 1887.
*4l Marchand, Archiv fiir experim. Pathol. und Pharmakol., xxiii. 273, 347, 1887.
—Cahn, ibid., xxiv. 180, 1887.
242 Lenhartz, Deutsch. med. Wochenschr., xiii. 9, 1887.—Hammer, Prager med.
Wochenschr., xiii. 275, 1888.—Dittrich, Archiv f. experiment. Pathol. u. Pharma-
kol., xxix. 247, 1891.
*43 Hoppe-Seyler, Physiolog. Chemie, p. 476.
44 Gf. Hayem, Compt. rend., cii. 698, 1886.—Fr. Miiller, Deutsche med. Wochen-
schr., xiii. 27, 1887.
24 Filehne, Archiv fiir experiment. Pathologie, ix. 329, 1878.—Lewin, Virchow’s
Archiv, lxxvi. 443, 1879. ;
+46 See Ponjfick, Verhandlungen des Congresses fiir innere Medicin, ii. 205, 1883.
—Stadelmann, Archiv. fiir experiment. Patholog. und Pharmakol., xv. 337, 1882;
Xvi. 118, 225, 1884.—Afanassiew, Zeitschr. fiir klin. Med., vi. 281, 1883.
47 Thudichum, Journal fiir prakt. Chemie, civ. 257, 1868.—Maly, Jahresbericht
fiir Thierchemie, xi. 126, 1882.—Ch. A. MacMumnn, Maly’s Jabresbericht fiir Thier-
chemie, xi. 210, 1882.—C. Vierordt, Zeitschrift fiir Biologie, x. 21 and 399, 1874.
248 PR. v. Jaksch, Verhandl. des Congresses f. innere Med., x. 353, Wiesbaden,
1891.
“49 1, Hering, Prager. medic. Wochenschrift, xi. 97, 1886.
250 Maschek, ibid., xi. 185 and 197, 1886.
°51 Hoppe-Seyler, Handb. der physiol. u. patholog.-chem. Analyse, 5th edit.,
421, 1885.
252 Hoppe-Sceyler, ibid., p. 432.
253 F. Ludwig, Wiener medic. Wochenschrift, xxxi. 122, 1881.—V. Jaksch, Zeitschr,
fiir klin. Medic., vi. 413, 1883.
254 Devoto, Rivista clin. archivio italiano de clin. med., xxx, 11 (pub. sep.),
1891.
*55 Picard, Virchow’s Archiv, xi. 189, 1857.
236 H, Schiff, Berichte der deutsch. chem. Gesellschaft, x. 773, 1877.
27 LT. v. Udransky, Zeitschy. f. physiol. Chemie, xii. 355, 377, 1888.
258 Hoppe-Seyler, Handbuch, p. 140.
259 Haycraft, from Gamgee, quoted by Ralfe, Clin. Chem., p. 87.
260 V, Schréder, Archiv f. experiment. Patholog. u. Pharmakol., xv. 375, 1882.
761 4, B. Garrod, Med. and Chirurg. Trans., xxxi. 183, 1848; xxxvii. 49, 1854;
The Nature and Treatment of Gout, Schmidt’s Jahrbiicher, cx. 124, 1861.
262 Abeles, Medicinische Jahrbiicher, ii. 497, 1887.
263 Salomon, Charité-Annalen, v. 137, 1880; Zeitschr. f. physiol. Chemie, ii. 65,
1878.
264 R. v. Jaksch, Zeitschr. f. Heilkunde, xi. 415, 18go.
*65 _Hoppe-Seyler, Handbuch, pp. 142 and 419.
266 R, v, Jaksch, Zeitschr. f. Heilkunde, xi. 438, 1890.
267 R, v, Jaksch, ibid., xi. 424.
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p.
400 BIBLIOGRAPHY.
68 J, Horbaczewski, Sitzb. d. k. Akad. Wien, c., pt. iii., 1891.
69 Claude Bernard, Legons sur le Diabéte. Paris, 1877.
*70 Abeles, Zeitschr. f. physiol. Chemie, xv. 495, 1891.
+1 Y. Jaksch, Zeitschr. fiir. klin. Medic., xi. 20, 1886.
272 Pavy, Ralfe, Clin. Chem., p. 88.
73 Claude Bernard, Beaunis, Nouv. Elements de Physiol., 3rd ed., p. 138, 1888.
74 Seegen, in Pfluger’s Archiv, xxxiv. 1884; xxxvii. 1885 ; xxxix. 1886.
75 Hoppe-Seyler, Physiolog. Chemie, 1.c., p. 430.
76 Freund, Wiener medic. Blatter, viii. 268 and 873, 1885; and Matray, ibid., p.815.
°77 Trinkler, Ceutralbl. f. d. med. Wissenschaft, xxviii. 498, 1890.
278 Salomon, Deutsche med. Wochenschr., iii. 92, 421, 1877.—v. Frerichs, Zeitschr.
klin. Med., vi. 33, 1885; Ueber Diabetes. Berlin, 1884.
79 Gabritschewsky, Archiv f. experiment. Pathol. u. Pharmakol., xxviii. 272, 1891-
80 Freund, Wiener medic. Jahrbiicher, i. 335, 18386.
81 Baumann and v. Udransky, Berichte der deutsch. chem. Zeitschr., xxi. 2744,
1888. Compare Chapter on Urine.
282 V. Jaksch, Zeitschr. fiir. klin. Medic., xi. 307, 1886.
°83 J/oppe-Seyler, Handbuch der physiolog. und patholog. chemischen Analyse,
1.¢., p. 103.—Berlinerblau, Archiv fiir experiment. Patholog. und Pharmakolog., xxiii,
333, 1887. See Chapter on Urine.
284 Hougouneng, Maly’s Jahresbericht, xvii. 430, 1888.
85 Hoppe-Seyler, op. cit., p. 399.
*6 Pettenkoffer, Annalen der Chemie u. Pharmacie, lii. 90, 1844.
*87 Mylius, Zeitschr. fiir physiolog. Chemie, xi. 492, 1887.
"88 L. v. Udransky, see (257).
*89 Mackay, Archiv fiir experimentelle Pathol. u. Pharmakol., xix. 269, 1885.
80 On the subject of cholemia, see Ponfick, v. Ziemssen’s Handb., vol. viii. pt. i.
p. 12, edit. of 1880.
*91 R. v. Jaksch, Verhandl. des Congresses f. innere Med., x. 353, 1891.
292 Silbermann, Archiv fiir Kinderheilkunde, viii. 401, 1887.
°93 Harveian Oration, Royal Coll. Physicians, 1888, British Med. Journal.
54 Ch. Bouchard, Compt. rend., cii. 669, 727, 1127, 1886; and Lecons sur les
Auto-intoxications dans les Maladies. Paris, 1887.
*9 Horbaczewski, Wiener Med. Jahrbiicher, 389, 1883.
296 V. Jaksch, Zeitschr. fiir klin. Med., xiii. 350, 1888.—Peiper, Virchow’s Archiv,
exvi. 337, 1889.
*7 R. v. Jaksch, Zeitschr. f. Heilkunde, xi. 433, 1890.
*“8 VY. Jaksch, Ueber Acetonurie und Diaceturie. Berlin, 1885.
*99 R. Wanach, Inaugural Dissertation. St. Petersburg, 1888.
300 Schenk, Anatom.-physiol. Untersuchungen, p. 10. Vienna, 1872.
3. Freund, Wiener medic. Wochenschr., xxxvii. 10, 40, 1887.
30° _Hoppe-Seyler, Handbuch der physiolog. und pathol. chem. Analyse, l.c., p. 316
and 423.—Rollett, Hermann’s Handb, der Physiol., vol. iv. pt. i, p. 124.—Landois
and Stirling, 4th edit., 1891.
393 VY. Limbeck, Grundriss einer klin. Pathol. des Blutes. Jena, 1892.
Ea)
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CHAPTER II.
THE BUCCAL SECRETION.
1 Heidenhain, Hermann’s Handbuch, v. 1, 1883; Maly, ibid., v. 2, 1881; as also
Sticker, No. 297 of Volkmann’s Clinical Series, Leipzig, 1887 ; Die Bedeutung des
Mundspeichels in physiologischen und pathologischen Zustiinden. Berlin, 1889.
* W. D. Miller, Die Mikro-organismen der Mundhihle, p. 54, 60. Leipzig, 1889.
* Lewis, Lancet, ii. 513, 1884.—Miller, Deutsche medic. Wochenschr., xi. 138 and
843, 1885.
4 Vignal, Archives de Physiologie, viii. 325, 1886, and x. 285, 1887, where also
abundant references will be found. See also Le 7h. David, Les Mikrobes de la
Bouche. Paris, 1890.
° D. Biondi, Zeitschr. fiir Hygiene, ii. 194, 1887.
° W. D. Miller, Inaug. Diss., Berlin, 1887; Schmidt’s Jahrbuch, cexvii. 122, 1888.
7 Miller, Centralbl. fiir Bacteriologie und Parasitenkunde. i. 47, 1887.
8 Miller, Die Mikro-organismen der Mundhohle, p. 206.
® Lifler, Mittheilungen aus dem Kais. Gesundheitsamte, ii. 480.—Vetter, Cen-
tralbl. f. klin. Med., xi. 11, 321, 1890.—H. Mery and P. Boulloche, Fortschritte der
Medicin, ix. 851, 1891.—Sanarelli, Schmidt’s Jahrbiicher, ccxxxii. 125, 1891.
0 Friinkel, Deutsche med. Wochenschr., xiv. 443, 1888.
1 fiilz, Zeitschr. fiir Biologie, xxiii. 321, 1887.
™ Colosanti, Maly’s Jahresbericht, xix. 72, 1890.
8 H, Schliesinger, Virchow’s Archiv, cxxv. 146, 350, 1891.
4 Griess, Berichte der deutschen chem. Gesellschaft, xi. 624, 1878.
1 [. Weiss, Centralbl. f. klin. Med., xi. 807, 1890.
16 J, Schramm, Berl. klin. Wochenschr., xxiii. 843, 1886.
W Salkowski, Virchow’s Archiv, cix. 358, 1887.
18 Ralfe, Clin. Chem., p. 176.
19 See Maly, Hermann’s Handbuch, l.c., v. 2, 8.
“0 Fleischer, Verhandlungen des Congresses fiir innere Med., ii. 119, 1883.
1 Boucheron, Compt. rend., 1881.
2 Rosenbach, Centralbl. f. klin. Med., xii. 145, 1891.
8 Ralfe, Clin. Chem., p. 177.
2 Samuel Fenwick, The Saliva as a Test for Functional Disorders of the Liver,
London, 1887.
°5 EB. Friinkel, Virchow’s Archiv, cxiii. 484, 1888.
°6 Frithwald, Jahrbuch f. Kinderklinik, xxix. 200, 1889.—Ze Th. David, Les
Mikrobes de Ja Bouche, p. 161, 1890.—H. Ranke, Jahybuch f. Kinderheilkunde,
xxvii. 309, 1888.
*7 See Kehrer, Ueber den Soorpilz, Heidelberg, 1885, where is given a full
account of the literature of the subject.—Baumyarten, Jahresbericht itiber die
Fortschritte in der Lehre von der pathog. Mikro-organismen, i. 145, 1885 ; ii. 330,
1886 ; iii. 318, 1887; iv. 303, 1888; v. 420, 1889.—Fliigge, l.c., p. 119.
°8- A. Freudenberg, Centralbl. fiir klin. Medicin, vii. No. xl., 1886.
*) Rees, A. de Bary, Vergleichende Morphologie und Biologie der Pilze, p. 405.
Leipzig, 1884.
30 Grawitz, Virchow’s Archiv, lxx. 566, 1877, and Ixxiii. 147, 1878.
31 Plaut, Baumgarten’s Jahresbericht, &c., l.c., i. 149, 1886.
32 Baginsky, Deutsche medic. Wochenschr., xi. 866, 1885.
33 Klemperer, Centralbl. fiir klin. Medic., vi. 849, 1885.
31 Fliigge, l.c., p. 119.
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402 BIBLIOGRAPHY.
3 Plaut, Centralbl. fiir Bacter. und Parasitenkunde, i. 527, 1887 (ref.).
°6 Hauser, Deutsches Archiv fiir klin. Med., xlii. 127, 1887.
“7 Miller, Die Mikro-organismen der Mundhoble, p. 54.
38 Zopf, Die Spaltpilze, p. 103, 1886.
39 Schech, Miinchner med. Wochenschr., xxxiv. 254, 1887.
40 Roth, Wiener med. Presse, xxviii. 897, 1887.
41 Dickinson, Lumleian Lectures, 1888.
2 Roux and Versin, Baumgarten’s Jahresbericht, iv. 234 (ref.), 1889; v. 215
(ref.), 1890.—Zarniko, Centralbl. f. Bacteriol. u. Parasitenkunde, vi. 153, 178, 224,
1889.—Spronck, Wintyens, and van den Brink, Centralbl, f. d. med. Wissensch.,
xXvili. 363 (1890).—Aolisko and Paltawf, Wiener klin. Wochenschr., ii. 147, 1889.
—Escherich, Centralbl. f. Bacteriol u. Parasitenkunde, vii. 8, 1890; Piidiatrische
Arbeiten, p. 302, Berlin, 1890.—A'lein, Centralbl. f. Bacteriol. u. Parasitenkunde,
vii. 489, 521, 1890.— Beck, Zeitschr. f. Hygiene, viii. 434, 1890.
43 Lofler, Mittheilungen aus dem kaiserlichen Gesundheitsamte, ii. 421, 1884;
and Centralbl. fiir Bacteriologie und Parasitenkunde, ii. 105, 1887 (ref.) ; vii. 528,
1890.
4G. v. Hofmann Wellenhof, Wiener med. Wochenschr., xxxviii. Nos. 3 and 4,
1888 (Supplement).
4 Brieger and Fraenkel, Berliner klin. Wochenschr., No. ii. 1890.— Wassermann and
Proskauer, Deutsche med. Wochenschr., xvii. 585, 1891; other references to the
literature are given in Baumgarten’s Jahresbericht, iv. 234, 1889; v. 211, 1890.
46 Baginsky, Archiv f. Kinderheilkunde, xii. 421, 1891.
47 Peters, Berlin. klin. Wochenschr., xxv. 420, 1888.
48 Th. Hering, Zeitschr. fiir klin. Med., vii. 358, 1884.
49 0. Chiari, Revue mens. de Laryngologie, No. 10 (Sup.), 1887.—See also Decker
and Sezfert, Sitz.-ber. der phys.-med. Gesellschaft. Wiirzburg. II. Sitz., Jan. 7,
1888.
CHAPTER IIL
THE NASAL SECRETION.
1 L. Weibel, Centralbl. f. Bacteriologie und Parasitenkunde, ii. 465, 1887.
2 See Reimann, Baumgarten’s Jahresbericht, iii. 417, 1888 (ref.).
3 Notinagel, Wiener med. Blatter, Nos. 6, 7, 8, 1888.
4 FE. Frénkel, Virchow’s Archiv, xciv. 499, 1882.
° Hajek, Baumgarten’s Jahresbericht, iii. 416, 1888 (ref.).
6 Lowenberg, Deutsche medic. Wochenschr., xi. 6, 1885.
7 Tost, Deutsche medic. Wochenschr., xii. 161, 1886.
8 Lowenberg, ibid., xii. 446, 1886.
® H. v. Schritter and Winkler, Beitrag zur Pathologie der Coryza. Vienna, 1890.
0 Schubert, Archiv fiir klin. Medic., xxxvi. 162, 1885 ; Berliner klin. Wochenschr.,
No. 39, 1889.
1 Proskauer, Zeitschr. f. Ohrenheilkunde, xxi. 311, 1891.
2 B. Friinkel, v. Ziemssen’s Handbuch, iv. 1, 189, 2nd edit., 1879.
B Leyden, Deutsche med. Wochenschr., xvii. 1085, 1891.
14 Sticker, Zeitschr. f. klin. Med., xiv. 8, 1888.
1 Levy, Berliner klin, Wochenschr., xxviii. 816, $45, 1891.
16 Q, Chiari, Wiener medic. Wochenschr., xxxv. 1397 and 1461, 1885.—Scifert,
Sitzungsberichte der Wiirzb. phys.-med. Gesellschaft, 1885, 14th session; and
Volkmann’s Sammlung klin, Vortriige, 204.
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CHAPTER IV.—THE SPUTUM. 403
CHAPTER IV.
TH SPUTUM.
1 For an exhaustive account of the literature on this subject up to the year 1855,
see A. Biermer, Die Lehre vom Auswurfe, Wiirzburg, 1855; and for later contri-
butions, von Ziemssen’s Handbuch (the chapter on Diseases of the Lungs and
Bronchi), also Troup, The Sputum: its Diagnostic and Prognostic Significations,
1888. Further recent literature will be referred to in the text.
2 H. Kossel, Zeitschr. fiir klin. Medicin, xiii. 152, 1888.
Krinig, Verhandl. des Congresses f. innere Med., x. 407. Wiesbaden, 1891.
Gabritschewsky, Deutsch. med. Woch., Oct. 22, 1891.
See Biermer, p. 50.
Henle and Bihlmann, see Biermer, p. 34.
See Friedlinder, Untersuchung iiber Lungenentziindung, 1873.—Amburger,
Petersburger med. Wochenschr., xii. 13, 1876.—Hcitler, Wiener med. Wochenschr.,
XXvii. 1185 and 1219, 1877.—Hichhorst, Lehrb. der physikal. Untersuchung innerer
Krankh., i. 381, 1886, 2nd edit.—7roup, The Sputum, 1888, pp. 207-211.
8 Bizzozero, l.c., p. 202.
» Virchow, Virchow’s Archiv, vi. 562, 1854.
W Panizza, Archiv fiir klin. Medic., xxviii. 343, 1881.
1 Buhl, Lungenentziindung, Tuberculose, Schwindsucht. Munich, 1872.
12 Guttmann and Smidt, Zeitschr. fiir klin. Medic., iii. 124, 1881.
3 Troup, The Sputum, p. 210.
14 FA, Hoffmann, Archiv f. klin. Med., xlv. 252, 1889.
15 Sommerbrodt, Virchow’s Archiv, lx. 165, 1872; Berliner klin. Wochenschrift,
xxvi. 1025, 1889.
16 Lenhartz, Deutsche med. Wochenschr., xv. 1039, 1889.
7 Kronig, Charité-Annalen, xv. 227, 1890.
18 Leyden, Virchow’s Archiv, liv. 328, 1872.
19 Curschmann, Archiv fiir klin. Medic., xxxii. 1, 1883. Further, Ungar and
Curschmann, Verhandl. d. Congresses f. inn. Med. Wiesbaden, i. 162, 192, 1882.
20 OQ. Vierordt, Berlin. klin. Wochenschr., xx. 473. 1883. V. Jaksch, Centralbl.
fiir klin. Medic., iv. 497, 1883. Pel, Zeitschr. fiir. klin. Medic., ix. 29, 1885. 4.
Sanger, Festschrift zur Eroffnung des neuen allgemein Krankenhauses zu Ham-
burg. Eppendorf, 1889 (sep. pub.).
1 Lewy, Zeitschr. f. klin Med., ix. 522, 1885.
2 T'roup, Edin. Med. Journ., Dec. 1885 ; ‘The Sputum,” 1888.
2 Wovdez, Wiener klin. Wochenschr., iv. 41, 1891.
*3 Ozermak, ibid., iv. 378, 1891.
2t Fr, Miiller and Schmidt, see Leyden, l.c.—Gollasch, Fortschritte der Medicin,
vii. 361, 1889.—Fink, Inaug. Dissert., Bonn, 1890.
“5 Leyden, Deutsche med. Wochenschr., xvii. 1085, 1891.
26 4, Hiiber, Zeitschr. f. klin. Med., xvii. 341, 1890.
27 Friedreich, Virchow’s Archiv, ix. 613, 1856; x. zor and 507, 1856; and xxx.
388, 1864.
:8 Virchow, Virchow’s Archiv, ix. 557, 1856.
2 Lichtheim, Berlin. klin. Wochenschr., xix. 129 and 147, 1882; and Zeitschr.
f, klin. Medic., vii. 140, 1884.
30 Schiitz, Mittheilungen aus dem kaiserlichen Gesundheitsamte, ji. 208, 223
(for full bibliography on the occurrence of moulds in diseased lungs, 1884).—Pan-
sini, Virchow’s Archiv, cxxii. 424, 189o.
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404 BIBLIOGRAPHY.
3! Paltauf, Virchow’s Archiv, x. 543, 1885.—Lindt, Archiv fiir experim. Pathol.,
XX1. 269, 1886.—Zoss, Centralbl. f. Bacteriol. u. Parasitenkunde, ix. 506, 1891.
3° Virchow, Virchow’s Archiv, ci. 401, 1856.—Friedreich, ibid., xxx. 390, 1864.
See Falkenheim, Archiv fiir experiment. Pathologie, xiv. 339, 1885.
Fischer, Deutsches Archiv fiir klin. Medic., xxxvi. 344, 1885 (with further
notices).— Hauser, Deutsches Archiv fiir klin. Medic., xlii. 127, 1888.
*® Pansini, Virchow’s Archiv, cxxii. 424, 1890.
36 Leyden and Jaffé, Deutsches Archiv fiir klin. Medic., ii. 488, 1867.
37 R. Koch, Erster Congress fiir intern. Medicin, Wiesbaden, i. 56, 1882; Ber-
liner klin. Wochenschr., xix. 21, 1882; Mittheilungen aus dem kais. Gesund-
heitsamte, ii. 1, 1884, Berlin.
38 The literature on the tubercle bacillus has increased greatly of late years.
Here it miust suffice to refer the reader to Fliiqge, l.c., p. 15 ; Weichselbaum, Cen-
tralbl. fiir Bacteriologie und Parasitenkunde, iii. 496-750, 1888 ; and Baumgarten,
Jahresbericht, iv. 158, 1889 ; v. 247, 1890.
39 Lutz, Monatshefte fiir prakt. Dermatol. Erganzungsheft, i. 77, 1886.—Amau,
Baumgarten’s Jahresbericht, iii. 170 (reference), 1888; compare also Biedert and
Sigel, Virchow’s Archiv, xcviii. 91, 1884, and Biedert, Berliner klin. Wochenschr.,
Xxill. 713, 1886.
# See Cornil and Babes, 1.c., p. 584.—Hiippe, l.c., p. 54.—LHdgar Crookshank, An
Introduction to Practical Bacteriology, p. 162, London, 1886.—Fliigge, l.c., p. 208.
4. Neelsen, Baumgarten’s Jahresbericht iiber die Fortschritte in der Lehre von
den pathogenen Mikro-organism., i. $5, 1886.
*® Czaplewski, Centralbl. f. Bacteriol. u. Parasitenkunde, viii. 685, 1890.—Fréinkel,
Berliner klin. Wochenschr., xxi. 195, 1884; Deutsche med. Wochenschr., xviii.
552, 1887. See Giinther, Wiener klinische Wochenschr., i. 292, 1888.—Biedert,
Berliner klin. Wochenschr., xxiii. Nos. 42, 43, 1886; xxiv. 30, 1887.
8 Gabbett, Lancet, April 1887.
4 VY. Jaisch, Prager med. Wochenschr., xiv. 210, 1891.—JZitten, Wiener klin.
Wochenschr., iv. 415, 1891.
® Kiihne, Centralbl. f. Bacteriol. u. Parasitenkunde, viii. 293, 1890.
4 Gibbes, Pract. Pathol. and Morbid Histol., p. 118; and Lancet, May 5, 1883.
4” Kiebs, Archiv fiir experimentelle Pathol., iv. 420, 1875.
48 Eberth, Deutsches Archiv fiir klin. Medic., xxviii. 1, 1881.
4% Koch, Mittheilungen aus dem kaiserlichen Gesundheitsamte, i. 46, 1881,
Berlin.
°° Fricdlénder, Fortschritte der Medicin, i. 716, 1883; and Virchow’s Archiv,
Ixxxvii. 319, 1882. See also Cornil and Babes, 1.c., 349.—Crookshank, l.c., p. 133.—
Baumgarten, Jahresbericht, i. 10-17, 1886; ii. 70, 1887; iii. 33, 1888; iv. 42, 1889;
Vv. 52, 1890.—Fliigge, |.c., p. 343-
1 Friedlinder, Fortschritte der Medicin, iii. 757, 1885.
* A. Friinkel, see (108).
3 Weichselbaum, see (109).
*4 Baumgarten, Jahresbericht, i. 142 (reference), 1886; also ibid., ii. 311, 1887;
iii. 309, 1888; iv. 286, 1889; v. 395, 1890.
» J. Isracl, Klinische Beitriige zur Kenntnis der Actinomykose des Menschen.
Berlin, 1885.
8 Jekinowitsch, Centralbl. £. Bacteriol. u. Parasitenkunde, v. 352 (reference), 1889.
7 Kuschew, ibid., v. 353 (reference), 1889.—R. Paltauf, Anzeiger der k.k. Gesell-
schaft der Aerzte in Wien, No. 6, Feb. 15, 1886.
8 Deichler, Zeitschrift fiir wissenschaftl. Zoologie, xliii, Part i., 1886; xlviii.
303, 1889.
® Afanussiew, St. Petersburger Wochenschr., xii. 322, 331, 339, 347, 1887.
0 Smtschenko, ibid., xiii. 193, 203, 1888,
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5. Kannenberg, Virchow’s Archiv, lxxv. 471, 1879; and Zeitschr. fiir klin. Medic.,
i. 228, 1880.
6 Bichhorst, Lehrbuch der physik. Untersuchungsmethoden, i. 406, 2nd edit.,
1886.
68 Hochsinger, Wiener med. Blatter, x. 20, 21, 1887.
Manson, see Chap. i. (210).
Leyden, Virchow’s Archiv, liv. 324, 1872.
Schreiner, see Chap. i. (86).
Ladenburg and Abel, Berichte der d. chem. Gesellschaft, xxi. 758, 1888.
Compare 4. W. v. Hofmann, ibid., xxiii. 3297, 3723, 1890; W. Majert and
A. Schmidt, ibid., xxiii. 3718, 1890.
6 Friedreich, see (27). — Zenker, Schmidt’s Jahrbiicher, clxxii. 284 (reference),
1876.
0 Bizzozero, l.c., p. 150.
1 Troup, l.c.
7 Virchow, Virchow’s Archiv, i. 395, 1847.—Fricdreich, ibid., xxx. 380, 1864.—
Schultze, ibid., 1xi. 130, 1874.
73 Biermer, ibid., xvi. 545, 1859; and l.c., p. 55.
™ Leyden, Volkmann’s Sammlung klin. Vortrage, 114 and 115.
> Black, Schmidt's Jahrbiicher, cv. 305 (reference), 1860.
Leyden, Virchow’s Archiv, lv. 239, 1872; and Ixxiv. 414, 1878.
7 R. Fischer, Jahresbericht fiir Thierchemie, ix. 361 (reference), 1879.
73 Fiirbringer, Deutsches Archiv fiir klin. Medic., xvi. 499, 1875.
% Ungar, ibid., xxi. 435, 1878.
80 HT. Kossel, see (2).
81 See also Devolo, Rivista clinica, xxviii. (sep. pub.).
2 Hoppe-Seyler, Handb. d. physiol. u. pathol.-chem. Analyse, p. 414, 5th edit.
83 Peters, Prager medic. Wochenschr., iv. 5, 1864; Schmidt’s Jahrbiicher, exxiii-
277 (reference), 1864.—Leyden and Jaffé, Deutsches Archiv fiir klin. Medic., ii.
499, 1867.
4 Biick, Dissert., Wiirzburg, 1888.—Jacobson, Dissert., Berlin, 1889.
8 Hirschler and Terray, Wiener med. Presse, xxxi. 648, 747, 1890.
86 Saiomon, Maly’s Jahresbericht, viii. 55 (reference), 1879.
8 Filchne, Aus den Sitzungsberichten der physikal.-medic. Societit in Erlangen,
Sittings of 11th June and roth Dec. 1877.—Stolnikow, Petersburger medic. Woch-
enschr., No. 8, 1878.—Stadelnunn, Zeitschr. f. klin. Med., xvi. 128, 1889.
88 Escherich, Deutsches Archiv fiir klin. Medic., xxxvii. 196, 1885.
89 V. Bamberger, Wiirzburger medic. Zeitschr., ii. 333, 1861.—Renk, Zeitschr. fur
Biologie, xi. 102, 1875.
90 Lumniczer, Wiener med. Presse, xix. 666, 711, 750, 791, 811, 1888.
% Lobisch and v. Rokitansky, Centralbl. f. klin. Med., xi. 1, 1890.
Hv. Frisch, Wiener medic. Presse, xxiv. 1437, 1469, 1883.
% Gabritschewsky, Deutsch. med. Wochenschr., Oct. 22, 1891.
% Cf. Leyden, Zeitschr. fiir klin. Medic., viii. 375, 1885.—Jichtheim, Fortschritte
der Medic., i. 1, 1883.—Brchmer, Die Aetiologie der chronischen Lungenschwind-
sucht, &c. Berlin, 1885..—G. Sée, Die bacillire Lungen-Phthise, German edit. by
Dr. M. Salomon, Berlin, 1886.
9 Robert Koch, Deutsche med. Wochenschr., xvi. 1029, 1890.
9 V, Jaksch, Verhandl. des Congresses f. in. Med., x. 82. Wiesbaden, 1891.
97 Biedert and Siegel, Virchow's Archiv, xcviii. 91, 1884.
98 Nothnagel, Berl. klin. Wochenschr., i. 273 and 283, 1864.
99 Rosenbach, Berl. klin. Wochenschr., xii. 645, 1875.
10 Zopf, Spaltpilze, p. 59, 3rd edit. Breslau, 1885.
101 Renz, Schmidt’s Jahrbiicher, cxxiii. 278, 1864.
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as
406 BIBLIOGRAPHY.
102 Lower, Berl. klin. Wochenschr., i. 335, 1864.
103 Feuerstock, Fortschritte der Medic., i. 456 (reference), 1883.
104 Pansini, Virchow’s Archiv, cxxii. 424, 1890.
105 A. Frénkel, Zeitschr. fiir klin. Medic., x. 401, and xi. 437, 1886.
106 Weichselbaum, Wien. med. Wochenschrift, xxxix. 1301, 1339, 1367, 1886.
107 Newmann, Zeitschrift fiir klin. Medic., xiii. 73, 1888.
108 Frdnkel, Zeitschrift f. klin. Med., xi. 437, 1886.
109 Weichselbawm, see above (106).
WW Friénkel, Deutsche med. Wochenschr., xii. No. 13, 1886.
M1 Pio Fou and Bordoni-Uffreduzzi, Zeitschrift fiir Hygiene, iv. 67, 1888.
12 Weichselbaum, Fortschritte der Medicin, v. Nos. 18 and 19, 1887; and Wiener
klin. Wochenschr., i. 573, 595, 659. 1888.
13 Goldschmidt, Centralblatt f. Bacteriologie und Parasitenkunde, ii. 649, 1887.
114 Yor further notices of pneumonia cocci :—Seifert, Berichte der Wiirzburger
medic. Gesellschaft, 1884.—Platonow, Mittheilungen aus der med. Klinik zu
Wiirzburg (Gerhardt), p. 221, Wiesbaden, 1885.—Matray, Wiener allgem. medic.
Zeitung, xxxi. 217, 1886.—Fliigge, l.c., p. 204.—Baumgarten, Jahresbericht, i. 9,
1886; ii. 54, 1887; iii. 33, 1888; iv. 53, 1889; v. 52, 18900.—Weichselbaum, Cen-
tralbl. f. Bacteriologie u. Parasitenkunde, i. 553, 587, 1887.—Knauthe, Schmidt’s
Jahrb., ccoxi. 28, 1886 —Dippe, ibid., ccxiii. 35, 1887.—Wolf, Wiener medic.
Blatter, x. 10-14, 1887.—Baumgarten, Lehrbuch der pathologischen Mythologie,
i. 236, Brunswick, 1890.—Levy, Archiv f. experimentelle Pathol. u. Pharmakol.,
xxix. 139, 1891.—Pansini, Virchow’s Archiv, cxxii. 424, 1890.
5 Kannenberg, see (61).
16 Stadelmann, l.c., p. 127.
uu” Bonome, Deutsche med. Wochenschr., xii. 932, 1886.
es Hirschier and Terray, Wien. med. Presse, xxxi. 698, 747, 1890. 1
9 Bouveret, Schmidt’s Jahrbiicher, ccxxvii. 152 (reference), 1890.
120 Merkel, Ziemssen’s Handbuch, i. p. 501, 2nd edit.
CHAPTER V.
GASTRIC JUICE AND VOMIT.
1 On the physiology of this subject, see Maly, Chemie der Verdauungssafte
und Verdauung, Hermann’s Handb. der Physiologie, v. 2, p. 37; Hoppe-Seyler,
Physiolog. Chemie, l.c., p. 47, Verdauung, p. 175.
2 Abelous, Comptes rendus, cviii. 310, 1889.
3 Compare also Wasbutski, Archiv f. experiment. Pathol. u. Pharmakol., xxvi.
133, 1889.—Leubuscher, Zeits. f. klin. Med., xvii. 474, 1890.—Kast, Maly’s Jalires-
bericht, xvii. 271 (reference), 1890.— Strauss and Wurtz, Archiv de Med. experi-
ment., Schmidt’s Jahrbiicher, ccxxv. 119 (reference), 1890; Hamburger Centralbl.
f. klin. Med., xi. 425, 1890.—Kabrhel, Archiv f. Hygiene, x. 382, 1890.
4 Jaworski, Centralblatt fiir klin. Medic., vii. 849, 1886.
5 Leube, Ziemssen’s Handb. der spec. Pathol. und Therapie., vii. 2; also Volk-
mann’s Sammlung klin. Vortriige, No. xii. p. 496 ; Archiv fiir klin. Medic., xxxiii.
I, 1883.
® See Maly, Hermann’s Handbuch, l.c., v. 2, p. 41.
? Schiitz, Zeitschr. fiir Heilkunde, v. 4o1, 1884.
8 Ewald and Boas, Virchow's Archiv, ci. 325, 1886, and civ. 271, 18°8.
® See also Ritter and Hirsch, Zeitschr. fiir klin. Medicin, xiii. 1888.— Jaworski,
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CHAPTER V.—GASTRIC JUICE AND VOMIT. 407
Archiv f. klin. Med., xxxiii. 227, 1883.—Other methods are given in the Russian
translation of this book by Profs. V'schunowsky, Jawein, and Pruriz, p. 426.
10 Edinger, Deutsches Archiv f. klin. Med., xxix. 555, 1881.
1 Spéith, Minch. med. Wochenschrift, xxxiv. 51, 1887.—.J. Czyrmianski, Thera-
peutische Monatshefte, i. 265, 1887.
12 Boeci, Moleschott's Untersuchungen der Naturlehre, xiv. 437, 1891.
18 Sahli, Correspondenzbl. f. Schweizer Aerzte, xxi. (sep. pub.), 1891.—Giinsburg,
Deutsche med. Wochenschr., xv. No. 41, 1889.
4 Huppert and Schiitz, Zeitschr. fiir physiolog. Chemie, ix. 577, 1885; and
Schiitz, see (7).
1 Schumburg, Virchow’s Archiv, xcvii. 260, 1881.
16 Boas, Centralblatt fiir die med. Wissenschaften, xxv. 417, 1887.
W Raudnitz, Prag. med. Wochenschrift, xii. 24, 1887.
18 Johnson, Zeitschrift fiir klinische Medicin, xiv. 240, 1888.
19 Boas, ibid., xiv. 249, 1888.
*Y Klemperer, ibid., xiv. 280, 1888.
“1 @. Rosenthal, Berliner klin. Wochenschr., xxvi. No. 45, 1888.
22 Johannessen, Zeitschr. f. klin. Med., xvii. 304, 1890.
3 Sandberg, Schmidt's Jahrbiicher, ccxxiii. 256 (reference), 1889.
24
See Catrin, Arch. gén., xix. 455, 584, 1887.
> Reichmann, Berl. klin. Wochenschr., xix. 606, 1882 ; xxi. 768, 1884; and xxiv.
12-16, 1887.—Sahli, Corresp.-Blatt der Schweizer Aerzte, xv. 1885, quoted by
Riegel.—L. Schiitz, Prager medic. Wochenschr., x. 173, 1885.—Van der Velden,
Tagebl. der 58. Versamml. deutsch. Naturforscher, 437, 1885, Strassburg.— Riegel,
Deutsches Archiv fiir klin. Medic., xxxvi. 427, 1885 ; and Zeitschr. fiir klin. Medic.,
xi. 1, 1886.
*6 Riegel, Deutsche med. Wochenschrift, xii. 52, 1886 ; and Zeitschrilt fiir klin.
Medicin, xii. 434, 1887.
7 Korezynski and Jaworski, Deutsche med. Wochenschrift, xii. 829, 856, 872,
1886.
*8 Reichmann, l.c., see (25).—Riegel, Deutsche med. Wochenschrift, xiii. 637,
1887.— Sticker, Miinchener, med. Wochenschrift, xxxiii. 32, 33, 1886.
*9 Boas, Deutsche med. Wochenschrift, xiii. 519, 548, 577, 1887.—Honigmann,
Miinch. med. Wochenschrift, xxxiv. 951, 972, 994, 1887.
*0 For the estimation of acid, see £. Ludwig, Medicinische Chemie, p. 118
Wien-Leipzig, 1885.
31 Bwald, Klinik der Verdauungskrankheiten, ii. 18, 1888. Berlin.
32 Teo, Centralbl. f. d. med. Wissenschaft, xxvii. No. 27, 1889; Diagnostik
der Krankheiten der Verdauungsorgane, p. 92. Berlin, 1890.
33 Leo, Diagnostik, p. 114, 1890; Archiv f. d. ges. Physiol., xlviii. 614, 1891.
344A. Loffmann and A. Wagner, Centralbl. f. klin. Med., xi. 713, 1890.—Lco,
ibid., xi. 865, 1890.
35 Kossler, Zeits. f. physiol. Chemie, 1891.
36 See R. Miller, Schmidt’s Jahrbiicher, clxxi. 113. 1876; clxxix. 113, 1878;
and cxcii. 65, 1881.—Muly, Chemie der Verdauungssafte und der Verdauung.
Hermann’s Handb. der Physiol., v. 2, l.c., p. 59.
37 Mohr, Zeitschr. fiir analytische Chemie, xiii. 321 (reference), 1874.
38 Zwald and /oas, see (8).
39 Witz, Zeitschr. fiir analyt. Chemie, xv. 108 (reference from Pharm. Centyral-
halle, p. 94, 1875), 1876.—Hilger, Zeitschr. fiir analyt. Chemie, xvi. 116 (reference
from Pharm. Centralhalle, xvii. 257), 1877.
40. Maly, Zeitschr. fiir physiol. Chemie, i. 174, 1877.—Van der Velden, Zeitschy.
fiir physiol. Chemie. iii. 25, 1879; Deutsches Archiv fiir klin. Medic., xxiii. 369,
1879; xxvii. 186, 1880.
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408 BIBLIOGRAPHY.
41 Kost, Dissertation, Jahresbericht iiber die Leistungen und Fortschritte der
gesammten Medicin, xxviii. 136 (reference), 1888.
2 Hwald, see (31).
43 Boas, Deutsche med. Wochenschr., xiii. 852, 1887.
44 Bourget, Revue médicale de la Suisse romaine (sep. pub.), 1888.
4° Koster, Likare forenings forhandlingar, xx. 355.—Hammersten, Maly’s Jahres-
bericht fiir Thierchemie, xv. 287 (reference), 1886.
46 Héssclin, Miinch. med. Wochenschr., xxxiii. 93, 1886.— Riegel, see Alt, Central-
blatt fiir klin. Medicin, ix. No. 3 and No. 13 (sep. Supplement), 1888.— Pettenkofer, Annal. der Chemie, xxv. 95, 1884.
® Vanlair and Masius, Centralbl. f. die medic. Wissensch., ix. 369, 1871.
7 Virchow, Virchow’s Archiv, lii. 558, 1871.
8 Fichhorst, l.c., p. 240.
® Nothnagel, l.c., p. 185.
1 Litten, Berl. klin. Wochenschr., xxv. 292, 1888.
1 Loos, Prager med. Wochenschr., xiv. 579, 1890.
2 See also Kitagawa, Zeitschr. f. klin. Med., xviii. 9, 1890.
13 Virchow, Virchow’s Archiv, v. 278, 1853.—Nothnagel, l.c., p. 96.
4 Q, Kitagawa, Inaug. Dissert. Wiirzbure, 1889.
1 Nothnagel, l.c., p. 90.
16 Compare also Avtagawa, Inaug. Dissert. Wiirzbure, 1890.
7 Vignal, Diastatic Ferments, 1889.
18 MacFadycan, Internat. Congr. of Hygiene, Lancet, Aug. 15, 1891.
19 Wyss, Verhandl. der 7. Versammlung der Gesellsch. f. Kinderheilkunde, vii.
149, 1888. Compare also Levy, Archiv f, experiment. Patho]. u. Pharmakol.,
xxix. 148, 1891.
20 Uffelmann, Deutsches Archiv fiir klin. Med., xxiv. 437 (447), 1881.
21 See Mayer, Gahrungschemie, p. 93. Heidelberg, 1879.
2 Nothnagil, 1.c., p. 113.—Brieger, Zeitschr. fiir physiol. Chemie, viii. 306,
1884.— Ufielmann, see (20).—Lscherich, Fortschritte der Med., iii. 515, 547, 1885;
and Die Darmbacterien des Siiuglings, &c., Stuttgart, 1886; Centralbl. f. Bacter.
u. Parasitenk., i. 705, 1887.—Bienstock, Zeitschr. fiir klin. Med., viii. 1, 1884.—
Stahl, Verhandl. des Congresses fiir int. Med., iii. 193, 1884.—A isl, Fortschr. der
Med., iv. 144 (ref.), 1886.—Miller, Deutsche med. Wochenschr. xi. 138, 843,
1886.—Sucksdorf, Baumgarten’s Jahresb., iii. 420 (ref.), 1888.
23 Prazmowski, Untersuch. iiber die Entwicklungsgeschichte u. Fermentwirkung
einiger Bacterienarten. Leipzig, 1880.
24 Koch, Ueber den Infectionsorganismus der Cholera. Berliner klin. Wochen-
schr., XXi. 477, 493, 509, 1884; Deutsche medic. Wochenschr., x. 499, 519, 1884;
Baumgarten, Jahresber., i. 109, 1885; ii. 290, 1887 ; iii. 278, 1888; iv. 261, 1889 ;
v. 365, 1891; Cornil and Babes, |.c., p. 467 ; Crookshank, l.c., p. 1373; Fliigge, l.c.,
Pp. 344.
°5 Neuhauss, Centralbl. f. Bacteriol. u. Parasitenkunde, v. 81, 1889.
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CHAPTER VI.—THE FACES. 413
°6 Lofler, Centralbl. f. Bacteriol. u. Parasitenkunde, vi. 224, 1889; vii. 639,
1890. See also Frénkel and Pfeiffer, Mikrophotographischer Atlas, fig. 96.
7 HHueppe, Fortschr. der Med., iii. 619, 1885.
*8 Babes, Virchow’s Archiv, xcix. 148, 1885.—Vandyke Carter, Lancet, ii. 405,
1884.—Wicati and Mietsch, Deutsche med. Wochenschr., ix. 361, 1884; and
Archives de Physiol. normale et pathol., xii. 72, 1885.—Van Ermengen, Recherches
sur le Microbe du Choléra asiatique, Paris, 1885; Deutsche Wochenschr., xi.
499, 1885 ; New Investigations on the Cholera Microbes, trans. by Dr. R. Kukula,
1886 ; see further Pfeiffer for exhaustive references ; Deutsche med. Wochenschr.,
xii. Nos. 5, 6, 7, 8, 9, 13. 14, 1886; Rossbach, v. Ziemssen’s Handb., 3rd edit., vol.
ii. p. 32, 1886; Riedel, Die Cholera, Entstehung, Wesen und Verhiitung dersel-
ben. Berlin, 1887.
*9 Schottelius, Deutsche med. Wochenschr., xi. 213, 1885; see also Di Vestea,
Centralbl. fiir Bacter. und Parasitenk., ii. 320 (ref.), 1888.
30 Bitter, Baumgarten’s Jahresber., ii. 299 (ref.), 1886.—Rietsch, Centralbl. fiir
Bacter. und Parasitenk., ii. 654, 1887.
31 Poehl, Berichte der deutschen chem. Gesellsch., xix. 1161, 1886.—Bujwid,
Zeitschr. f. Hygiene, ii. 52, 1887; and Centralbl. f. Bacter. und Parasitenk., iii.
169, 1888 ; iv. 494, 1888. For further literature see Dunham, Zeitschr. f. Hygiene,
ii. 337, 1887 ; Ali-Cohen, Fortschr. der Med., No. 17, 1807 ; for Zéislein, Jadassohn,
consult Bujwid, l.c., p. 70.
®2 Brieger, Deutsche med. Wochenschr., xiii. 305, 469, 1887.
3 Salkowski, Virchow’s Archiv, cx. 366, 1888.
34 Kitasato, Zeitschr. f. Hygiene, vii. 519, 1889.
35 Oantant, Deutsche med. Wochenschr., xii. 89, 1886.
36 Brieger, Berliner klin. Wochenschr., xxiv. 817, 1887.
7 Powchet, Compt. rend., xcix. 847, 1884.
38 Finkler, Tagblatt der Magdeburger Naturforscherversammlung; Deutsche
med. Wochenschr., x. 36, 1884; Tagblatt der 58 Versamml. deutsche Natur-
forscher und Aerzte zu Strassburg, p. 438, 1885,—Finkler and Prior, Ergiinzungs-
hefte zum Centralbl. fiir allgem. Gesundheitspflege, i., Pts. 5 and 6, 1885.
39 V. Hovorka and Winkler, Baumgarten’s Jahresbericht, v. 367 (reference), 1890.
40° Deneke, Deutsche med. Wochenschr., xi. 33, 1885.
41 Lberth, Virchow’s Archiv, 1xxxiii. 486, 1881.
#2 Klebs, Archiv fiir experiment. Path. und Pharmak., xii. 231, 1880; xiii. 381,
1881.—Eppinger, Klebs’ Handb. der patholog. Anatomie, Pt. vii., edit. by Prof.
Eppinger, 1880.
43 Koch, Mittheil. aus dem kaiserl. Gesundheitsamte, i. 45, 1881.—Meyer, Inaue.
Dissert. Berlin, 1881.—Friedldnder, Verhandl. der Berl. physik. Gesellsch., 1881.
—Gaffky, Mittheil. aus dem kaiserl. Gesundheitsamte, ii. 372, 1884.—Further con-
sult Cornil and Babes, 1.c., p. 419; Crookshank, 1.c., p. 1743 Fliigge, 1.c., p. 198;
Baumgarten’s Jahresber., i. 100, 1886; ii. 150, 1887 ; iii. 233, 1888; iv. 142, 1889;
v. 189, 1890.
4 Friinkel and Pfeiffer, Mikrophotographischer Atlas, pl. 46.
4 Gafky, l.c., p. 384.
46 Birch- Hirschfeld, Schmidt's Jahrb., ccxv. 288, 1887; and Archiv fiir Hygiene,
vii. 342, 1888. :
47 Buchner, Centralbl. fiir Bacter. und Parasitenk., iv. 353, 385, 1888.—P/fwil,
ibid., iv., 769, 1888.
48 Pfeiffer, Deutsche med. Wochenschr., xi. 500, 1885.
49 Chantemesse and Widal, Archives de Physiol. &c., ix. 217, 1887.
50 Holz, Zeitschr. f. Hygiene, viii. 143, 1890.
51 Grancher and Deschamps, cited by Holz.
52 Néggerath, Fortschritte d. Med., vi. 1, 1888.
oo
2
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414 BIBLIOGRAPHY.
°3 Kitasato, Zeitschr. f. Hygiene, vii. 515, 1889.
>4 Compare also Heim, Miinchener med. Wochenschr., xxxvi. 408. 1889.—
Petruschky, Centralbl. f. Bacteriol. u. Parasitenkunde, vi. 660, 1889.—Karlinski,
ibid., vi. 65, 1889.—Janowski, ibid., viii. 167, 193, 230, 262, 417, 449, 1890.
°> Babes, Centralbl. f. klin. Med., xii. 682 (ref.), 1891.—Cassedebat, Centralbl. f.
med. Wissensch., xxviii. 678 (ref.), 1890.—Uffelmann, Berliner klin. Wochenschr.,
xxviii. 858, 1891.
6 F. Frankel and M. Simmonds, Centralbl. fiir klin. Medic., vi. 737, 1885 ; and
Die iitiologische Bedeutung des Typhus-bacillus. Leipzig, 1886.—C. Seitz, Bacteriol.
Studien z. Typhus-atiologie. Munich, 1886.
57 Beumer and Peiper, Zeitschr. fiir Hygiene, i. 489, 1886; and ii. 110, 1887. See
further Strotinin, ibid., i. 465, 1886.—EZ. Frankel and M. Simmonds, ibid., ii. 138,
1887. — Dreyfuss-Brissac, Gaz. hebdomadaire, xxiv. 434 (ref.), 1887.
°8 Beumer, Deutsche med. Wochenschr., xii. No. 28, 1887.—Brouardel and Chante-
messe, Centralbl. f. Bacter. u. Parasitenk., iii. 144 (ref.), 1888. — Kowalski, see Seitz,
ibid., ii. 681, 724, 751, 1887.—Ali-Cohen, Baumgarten’s Jahresb., iii. 149 (ref.), 1888.
' 59 Lichtheim, Fortschr. der Med., ii. 1, 1883.
60 See R, Leuckart, vol. i. Pt. i, 2nd edit., p. 221, 1879-86.
6. Nothnagel, l.c., p. 110, where further references will be found.
Grassi, see Bizzozero, l.c., p. 134.
63 VY. Jaksch, Wiener klin. Wochenschr., i. 511, 1888.—Z. Cohen, Deutsche med.
Wochenschr., xvii. 853, 1891.
64 Lésch, Virchow’s Archiv, Ixy. 196, 1875.
6 Lambl, Prager Vierteljahresschr., xi. 1, 1859; and further see Nothnagel, p. 110.
66 Kartulis, Virchow’s Archiv, xcix. 145, 1885; Centralbl. f. Bacteriol. u. Para-
sitenkunde, ix. 365, 1891. See ref. (174).—J/asswiten, Centralbl. f. Bacteriol. u.
Parasitenkunde, vi. 451 (reference), 1889.—Osler, ibid., vi. 736, 1890.—Dock, Texas
Medical Journal (sep. pub.), 1891.
687 Dressler, see Leuckart, tst edit., p. 740.—Gubler, ibid., 2nd edit., 279. — Kjellberg,
Virchow’s Archiv, xviii. 527, 1860.— Himer, see Leuckart, l.c., p. 278.
88 Podwyssoki, Centralbl. f. Bacteriol. u. Parasitenkunde, vi. 736, 1889.
69 Lambl, l.c., p. 51, and plate 1, fig. 2.
7% Davaine, Traité des Entozoaires, vi. Paris, 1860.—Marchand, Virchow’s
Archiv, lxiv. 293, 1875.—Zunker, Deutsches Archiv f. prakt. Med., i. 1878.
1 Grassi and Schewiakof, Zeitschr. f. wiss. Zoologie, xlvi. 143, 1888.
” Erich Miillcr, Verbandl. des biologischen Vereines zu Stockholm (sep. pub.),
1890.
73 Grassi, see Leuckart, l.c., p. 964 and 968.
74 Perroncito, Centralbl, f. Bacter. u. Parasitenk , ii. 738, 1887; Archives ital. de
Biologie, ix. (sep. pub.); x. (sep. pub.); Giorn. d. R. Acad. di Medicina (sep. pub.),
1887.
7 VY, Jaksch, Wiener klin. Wochenschr., i. 511, 1888.
76 Marchand, see (70).—Zunker, see (70).
77 Malmsten, Virchow’s Archiv, xii. 302, 1857.
78 Stieda, Virchow’s Archiv, xxxvi. 285, 1866.—G@raziadei and Perroncito, see
Bizzozero, l.c., p. 189.—A. Ortmann, Berliner klin. Wochenschr., xxviii. 814, 1891.
See also Mittercr, Inaug. Dissert.
79 VW. Jakseh, 1.c., p. 512.
80 See Leuckart, Le., 2nd edit., p. 513.
81 Tbid., p. 617.
82 Tbid., p. 832.
83 Grassi, Centralbl. f. Bacter. u. Parasitenk., i. 97, 1887; and Grassi-Calandruccio,
ibid., ii. 282, 1887.—Comini, ibid., ii. 27 (ref.), 1887.
% Bilharz, see Leuckart, l.c., p. 833.—Grassi, Comini, Calandruccio, see (83).
62
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CHAPTER VI.—THE F.ZCES. 415
Perroncito and Airoldi, Gazetta degli Ospidali (sep. pub.), 1888.—Ors?, Sei casi di
Tenia nana (sep. pub.) ; Senna, Gazetta med. Lombard (sep. pub), 1889.
8 Ranson, see Crassi, l.c., p. 285.
86 Leidy, Parona, see Leuckart, l.c., p. 998.
87 Grassi, Centralbl. f, Bacter. u. Parasitenk., i. 257, 1887.
88 4. Hoffmann, Jahrb. f. Kinderheilk., xxvi. Pts. iii. and iv. (sep. Sup.), 1887.—
Kriiger, St. Petersburg. med. Wochenschr., xii. 341, 1887.—Brandt, Centralbl. f,
Bacteriol. u. Parasitenk., v. 99 (ref.), 1889.
89 Grenet, see Leuckart, l.c., p. 841.
® Grassi, Centralbl. f. Bacteriol. u. Parasitenk., i. 257, 1888.
1 Leuckart, l.c., p. 864.
® Runeberg, Deutsches Archiv f. klin. Med., xli. 304, 1887.—Rayher, ibid., xxxix.
31, 1886.—Lichtheim, Verhandl. des Congresses fiir innere Med., vi. 85, 1887.—
Schapiro, Zeitschr. f. klin. Med., xiii. 416, 1888.—Fr. Wiiller, Charité-Annalen, xiv.
p. 9 (sep. pub.).
%3 See Leuckart, l.c., p. 930.
EEN Mijen@l, NWGE, oh yin
% Cf. Bérenger Féraud, Lecons cliniques sur les Tenias de l’Homme. Paris, 1888,
% F, Heller, Aerztl. Bericht des Wiener Allgem. Krankenhauses, p. 262, 1857.
% Leuckart, l.c., 2nd edit., vol. i. Pt. iii. pp. 1 and 589.
% Biermer, Schweizer Zeitschr. f. Heilkunde, ii. 381, 1865.—Bostroem, Deutsches
Archiv fiir klin. Med., xxxiii. 557, 1882.—Buaclz, Berliner klin. Wochenschr., xx.
234, 1883.
99 Bizzozero, l.c., p. 182.
100 Baelz, see (98).
101 See Bizzozero, 1.c., p. 182.
102 See Poirier, Centralbl. fiir Bacter. u. Parasitenk., ii. 186 (ref.), 1888.
3 Leuckart, l.c., 1st edit., vol. ii. p. 156.
104 Tutz, Centralbl. f. Bacter. u. Parasitenk., iii. 553, 584, 616, 1888.
105 Kartulis, ibid., i. 65, 1887.
106 Devaux, Progrés médicale, xv. 415, 1887.—Hogg, Brit. Med. Journ., No. 1438,
122, 1888.
107 #nystein, Prager med. Wochenschr., xvi. 498, 1891.
108 See Lutz, Centralbl. f. Bacter. u. Parasitenk., ili. 681, 713, 744, 1888.
109 Leuckart, l.c., vol. ii., 1st edit., p. 351.
10 Thid., p. 411.
11 Perroncito, see Meissner, Schmidt's Jahrb., clxxxix. 85, 18$1.—Calandruccio,
Centralbl. f. Bacter. u. Parasitenk., i. 665 (ref.), 1887.
12 Menche, Zeitschr. fiir klin. Med., vi. 161, 1883.—Mayer, Centralbl. f. klin.
Med, Nos. 9 and 16, 1885 ; and Vélkers, Berliner klin. Wochenschr., xxii. No. 36,
1885.—Sahli, Deutsches Archiv fiir klin. Medic., xxxii. 421, 1883.—Leichtenstern,
Centralbl. fiir klin. Med., vi. 195, 1885 ; and Deutsche med. Wochenschr., xi. Nos.
29 and 30, 1885; xii. Nos. 11, 12, 13, 14, 1886; xiii. 565, 594, 620, 645, 669,
691, 712, 1887 ; and Ernst, ibid., xiv. 291, 1888.—Béumler, Correspondenzbl. d.
Schweizer Aerzte, i. 1885.—Seifert and Fr. Miiller, Centralbl. f. klin. Med., vi.
27, 1885.
Us Firket, Académie royale de Belgique, viii. No. 12, 1884.
4 Seifert, Verhandl. der physik.-med. Gesellsch. Wiirzburg, xxi. (N. F.), No.
6, 1888.
15 See Lutz, R. Volkmann’s Sammlung, Nos. 255, 256, 1885.
16 Lancet, Oct. 21, 1887.
7 Sonsino, Lancet, Feb. 22, 1890.
us Leuckart, l.c., p. 460.
19 /yni, Berliner klin. Wochenschr., xxiii. 614, 1886.
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416 BIBLIOGRAPHY.
120 Leuckart, 1.c., p. 512.
121 See Meissner, l.c., p. 88; also Bizzozero, l.c., p. 185.—Seifert, Verhandl. des
Congresses fiir int. Med., ii. 337. Wiesbaden, 1881.
zero, 1.C., p. 185.
13° Leuckart, 1.c., p. 952.—Grassi, Centralbl. f. Bacter. u. Parasitenk., ii. 413
(ref.), 1887.
M4 Joseph, ibid., ii. 533 (vef.), 1887.
125 Rembold, Wiener med. Presse, xix. 373 (ref.), 1888.—Zampa, Centralbl. f.
Bacter. u. Parasitenk., iv. 371 (ref.), 1888.—Hohn, Prager med. Wochenschr., xvi.
107, 1891.
1°6 Finlayson, Brit. Med. Journ., June 8, 1889.
17 Leichtenstern, Deutsche med. Wochenschr., xii. 175, 1886.—Nothnagel, l.c.,
p. 198.
128 Uffelmann, Deutsches Archiv f. klin. Med., xxiv. p. 452.
129 Nothnagel, 1.c., p. 193.
180 Gerhardt, Zeitschr. fiir klin. Med., vi. 78, 1883.
131 Qesterlein, Mittheil. aus der medic. Klinik in Wiirzburg, i. 1, 1885.
182 Stadelmann, Deutsches Archiv fiir klin. Med., xl. 372, 1887.
133 [/felmann, 1.c., p. 450.
134 By, Miller, Zeitschr. fiir klin. Med., xiii. 45, 1887.
135 Uffelmann, l.c., p. 446.
1386 See also Baginsky, Die Verdauungskrankheiten der Kinder., p. 230. Tiibin-
gen, 1884.
137 Hoppe-Seyler, Handbuch der physiol. und pathol. chem. Analyse, l.c., p. 505.
138 Thid., l.c., p. 339.
139 Thid., l.c., p. 507.
10 VY. Jaksch, Zeitschr. fiir physiol. Chemie, x. 536, 1886.
11 Brieger, Berichte der deutschen chem. Gesellsch., x. 1027, 1877.
12 Thudichum, Journ. of Chem. Soc., viii. p. 400.
13° Brieger, see (141).
14 Wegscheider, Ueber die normale Verdauung der Siuglinge. See Hoppe-Scyler,
l.c., p. 338.
U5 Brieger, see (147).
6 Nencki, Berichte der deutschen chem. Gesellsch., viii. 723, 1875.
14” For further statements regarding these bodies see Kiihne, Ber. der deutschen
chem. Gesellsch., viii. 206, 1875 ; Nencki, ibid., viii. 336, 722, 1517, 1875; Brieger,
ibid., x. 1027, 1877; Nencki, Zeitschr. fiir physiol. Chemie, iv. 371, 1880; Brieger,
ibid., iv. 414, 1880; A. Bayer, Ber. der deutschen chem. Gesellsch., xiii. 2339,
1880; Vappeiner, ibid., xiv. 2382, 1881; EZ. Salkowski, Zeitschr. fiir physiolog.
Chemie, viii. 417, 1884; #. and W. Salkowshi, ibid., ix. 8, 1885.
48 Hoppe-Seyler, Lehrbuch der physiol.- und pathol.-chem. Analyse, p. 114.
U9 Schulze in Benedikt, l.c., p. 25.
10 Miiller, Zeitschr. f. klin. Med., xii. 52, 1887.
D1 Hoppe-Seyler, op. cit., p. 96. Compare R. Benedikt, Analyse der Fett, &c.
Berlin, 1889. This work, which deals with the fecal fats, may also be usefully
consulted on various other special points.
132 Miiller, l.c., p. 113.
13 Compare Benedikt, p. 181 and 212.
4 Benedikt, l.c., p. 72.
5 Miiller, l.c., p. 48.
16 Miiller, l.c., p. 112.—Muzzi, Maly’s Jahresbericht, xix. 285 (reference), 1889.
1” Meéhu, Journ. de Pharm, et de Chim., Aug. 1878 ; Maly’s Jabresbericht, viii.
269 (ref.), 1879; and L’Urine normale et patholog., p. 49. Paris, 1880.
458 Hoppe-Seyler, op. cit., p. 329.
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CHAPTER VI.—THE FACES. 417
9 Senator, Berliner klin. Wochenschr., v. 251, 1868.—Stefano, Gazetta degli
Ospedali, 1883.
160, Hammarsten, Lehrbuch der physiol. Chemie, p. 183. Wiesbaden, 1891.
161 Pouchet, see (37).—Rose, Zeitschr. f. physiol. Chemie, xvi. 192, 1892.
1 VY. Udransky and Baumann, Zeitschr. f. physiol. Chemie, xiii. 362, 1889.—
Stadthagen and Brieger, Berliner klin. Wochenschr., xxvi. 344, 1889.
163 V. Jaksch, Zeitschr. f. physiol. Chemie, xiii. 116, 1887.
164 Hoppe-Scyler, op. cit., p. 317.
16 See Hoppe-Scyler’s admirable grouping, op. cit., p. 326.
166 Widerhofer, see (2).
67 Escherich, Fortschritte der Med., iii. 515 and 547, 1885.
168 Baginsky, Zeitschr. fiir physiol. Chemie, xii. 434, 1888.
1689 Bizzozero, 1.c., p. 195.
1 Zweifel, Archiv £. Gynakol., vii. 474, 1875.—Hoppe-Seyler, op. cit., p. 340.
M71 Wegscheider, see (144).
172 Nothnagel, see (1).
"3 Heubner, Ziemssen’s Handb., ii. 508, 2nd edit., 1886.
M4 Hlava, Centralbl. fiir Bacter. und Parasitenk., i. 537, 1887.—Aartulis, ibid.,
iii. 745, 1888.
™5 Klebs, l.c., p. 203.—Chantemesse and Widal, see Cornil, Bull. de Acad. de
Méd., lii. 6, 1888; Schmidt’s Jahrbiicher, ccxix. 239 (ref.), 1888; Baumgarten’s
Jahresbericht, iv. 236 (reference), 1889, where also Michelsohn has some critical
remarks.
76 ©, Schmid, Charakteristik der epidem. Cholera, &c. Leipzig, 1850. See
Hoppe-Seyler, Physiol. Chemie, p. 358.
7 Pel, Centralbl. fiir klin. Med., viii. 297, 1887.—Ze Nobel, Archiv fiir klin.
Med., xliii, 285, 1888.
M8 Vogel-Bicdert, Lehrb. der Kinderkrankheiten, 9th edit., p. 115. Stuttgart,
1887.
19 Berggriin and Katz, Wiener klin. Wochenschr., iv. 858, 1891.
CHAPTER VII.
THE URINE.
1 For the Physiology of the subject, see Heidenhain, Hermann’s Handb. der
Physiologie, v. 1, 279, 1883; also Landois and Stirling, Text-Book of Physiology,
p. 479, 4th ed., 1891.
2 Wollheim de Fonseca, Maly’s Jahresbericht, xix. 187 (reference), 1890.
3 Glum, Diss., Centralbl. f. med. Wissensch., xxviii. 243 (reference), 1890.
4 For the special Chemistry of the subject, see Huppert, Neubauer, and Vogel, Anlei-
tung zur qualitativen und quantitativen Analyse des Harns, 9th edit., Wiesbaden,
1891 ; Leube and Salkowski, Die Lehre vom Harn, Berlin, 1882; Lébisch, Anleitung
zur Analyse des Harns, Wien, 1883; Hoppe-Seyler, Handb. der physiol.- und pathol.-
chemischen Analyse, p. 340, 5th edit., Berlin, 1885; Z. Zaache, Harn Analyse fiir
prakt. Aerzte, Leipzig, 1885; further, consult W. Zuelzer, Lehrb. des Harnanalyse,
Berlin, 1880; C. Fr. W. Krukenberg, Grundriss der medic.-chem. Analyse, Heidel-
berg, 1884; Leo Liebermann, Grundziige der Chemie des Menschen, Stuttgart,
1885 ; Tappeiner, Anleitung zu chemisch-diagnostischen Untersuchungen am Krank-
enbette, 2nd edit., Munich, 1888; Seifert and Miller, Taschenb. der medic.-klini-
schen Diagnostik, 4th edit., Wiesbaden, 1888; Schotten, Kurzes Lehrbuch der
2D
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418 BIBLIOGRAPHY.
Analyse des Harns, Leipzig ; 0. Vierordt, Diagnostik interner Krankheiten, p. 334,
Leipzig, 1888; Roberts, Pract. Treatise on Urinary and Renal Diseases ; Halli-
burton, Text-Book of Chemical Physiology and Pathology, London, 1891 ; MacMunn,
Clinical Chemistry ; Proc. Roy. Soc., No. 208; Journ. of Phys., x., Nos. 1 and 2.
> Lanect, i., 1890, p. 481.
6 Compare Dujardin-Bcaumetz, Schmidt’s Jahrbiicher, ccxxviii. 152 (reference),
1890.
7 (. Vierordt, Zeitschr. fiir Biologie, x. 21 and 399, 1874.—MacMunn, Clin.
Chem., p. 104; id, Maly’s Jahresbericht, xx. 201 (ref.), 1891.
8 Leo Liebermann, Maly’s Jahresber. fiir Thierchemie, xv. 447 (ref.), 1886.
® £, Baumann and C. Preusse, Du Bois-Reymond’s Archiv, 245, Jahrgang 1879-
10 Fagge, Principles and Pract. of Med., ed. 1891, ii., p. 644.
1 Mott, Pathol. Trans., lx. 127; Lancet, March 1889.
2 Hunter, Practitioner, Aug. 1888 ; Lancet, Oct. 1888.
8 Hale-White, Brit. Med. Journ., May 21, 1892.
MM Halliburton, Chemic. Physiol., 1891, p. 712.
Quincke, Zeitschr. fiir klin. Med., (sup. vol.), vii. 21, 1884.
16 See Sticker and Hiibner, Zeitschr. fiir klin. Med., xii. 114, 1887; v. Noorden,
Archiv fiir experim. Pathol. und Pharmakol., xxii. 325, 1887; and O. 7. Rongstedt,
Maly’s Jahresbericht, xx. 196 (reference), 1891.
W Hale- White, Brit. Med. Journ., May 21, 1802.
18 Huppert, Neubauer, Vogel, l.c., p. 19.
19 F. and L. Sestini, Die landwirthschaftlichen Versuchsstationen, Pts. ii..and
iii., 1890.
© Huppert, Neubauer, Vogel, l.c., p. 433; and Ott, Zeitschr. fiir physiolog.
Chemie, x. 1, 1885.
*1 F, Taylor, Pract. of Med., 2nd edit., p. 705.
2 Compare Glaser, Deutsche med. Wochenschr., xvii. 1193, 1891.
3 #. Salkowski, Deutsche med. Wochenschr., xiii., No. 16 (sep. Supplement), 1888.
4 V. Jaksch, Prager med. Wochenschr., xvi. 210, 1891.—Litten, Wiener klin.
Wochenschr., iv. 416, 1891. Rohrbeck of Berlin and Wrana of Prague have con-
structed similar apparatus.
>> Compare Senator, Berliner klin. Wochenschr., xxviii. (sep. pub.), 1891.
26 (laser, see (22).
7 Vitali, Maly’s Jahresbericht, xviii. 326 (reference), 1890.—Compare also £.
Briicke, Monatshefte fiir Chemie, x. 129, 1889.
8 Bizzozero, l.c., 2nd edit., p. 260.
29 Richhorst, Lehrb. der physikal. Untersuchungs-methoden innerer Krankheiten,
and edit., pt. ii. p. 336. Compare also Lehrbuch der Gewebelehre, by C. Toldt,
pp. 493 and 503, Stuttgart, 1884.
30 Vigla, Quevenne, L’Espérience, No. 12, 1837, and Nos. 13, 26, 27, 1838. See
Nasse, Schmidt's Jahrbiicher, xxxiv. 356 (ref.), 1842. Rayer, Traité des Maladies
des Reins, ii., 1840.
3. Simon, Johannes Miiller’s Archiv fiir Anat., Physiol. und wissenschaftl.
Medicin, p. 28, plate ii. fig. 4, 1843.—-Nasse, Schmidt’s Jabrb., xxxiv. 356 (ref.),
1842.
#2 Henle, see C. Pfeufer, Zeitschr. fiir rationelle Med., i. 61 and 68, 1844.
33 Glaser, see (22).
*4 Rovida, J. Moleschott, Untersuch. zur Naturlehre des Menschen und der
Thiere, xi. 1; xi. 182, 1867. é
* Nothnagel, Deutsches Archiv fiir klin. Med., xii. 326, 1874.
* Burkart, Die Harncylinder, l.c., p. 44.—Vischl, Prager Vierteljahrsschr.,
cxxxix. 27, 1878.
“7 Leube, Zeitschy. fiir klin. Med., xiii. 6, 1887.—For further information see 0.
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CHAPTER VII.—THE URINE. 419
Bayer, Archiv fiir Heilk., ix. 136, 1868.—Scnator, Virchow’s Archiv, lx. 476, 1874
It. Wagner, v. Ziemssen’s Handb., vol. ix. p. 47, 3rd edit., 1882.— Knoll, Zeitschr
fiir Heilk,, iii. 148, 1882.—Fiirbringer, Die Krankheiten der Harn.- und Geschlechts-
organe. Braunschweig, p. 20, 1884.—Burkart, Die Harncylinder, 1884.—Knoll,
Zeitschr. fiir Heilk., v. 289, 1884.
*8 Martini, Archiv fiir klin. Chirurgie, xvi. 157, 1884.
* V. Jaksch, Deutsche med. Wochenschr., xiii., Nos. 40 and 41, 1888.
* Compare Loos, Jahrb. f. Kinderheilkunde, xxx. (sep. pub.), 1890.
4. Rindfleisch, Lehrb. der pathol. Gewebelehre, p. 438. Leipzig, 1875.—Lany-
hans, Virchow’s Archiv, Ixxvi. 85, 1879.
® Rovida, see (34); also Weisgerber and Perls, Archiv fiir experiment. Patho-
logie, vi. 113, 1877.—Posner, Virchow’s Archiv, 1xxix. 361, 1880.—Voorhove, ibid.,
Ixxx 247, 1880.—Singer, Zeitschr. fiir Heilk., vi. 143, 1885.—Kobler, Wiener klin.
Wochenschr., iii. 531, 574, 576, 577, 1890.
#3 Nothnagel, see (35).
44 Henle, see (32).
4 M. Huppert, Virchow’s Archiv, lix. 395, 1874.
46 Leube, Zeitschr. fiir klin. Med., xiii. 7, 1887.
47 Compare R. v. Hoesslin, Miinchener med. Wochenschr., No. 45 (sep. pub.),
1888.
48 ZT. Thomas, Archiv fiir Heilkunde, xi. 130, 1870.
49 Bizzozero, 1.c , p. 225.
” S. Pollak and Térik, Maly’s Jahresber., xvi. 458 (ref.), 1887 ; and Archiv fiir
experim. Pathol. und Pharmakol., xxv. 87, 1888.
5l Rovida, 1.c., p. 8.—Kobler, see (42).
52 Ribbert, Centralbl. fiir die med. Wissensch., xix. 305, 1880.
°3 Knoll, see (37).
“4 EB. L. Mayer, Virchow’s Archiv, v. 199, 1853.
°° ‘Huppert, see (45).
*6 Heitzmann, Wiener med. Bliitter, Nos. 24 and 25, 1890.
7 Leube, Zeitschr. fiir klin. Med., iii. 233, 1881.
°8 Miquel, Bulletin de la Société Chim. de Paris, xxxi. 392, 1879, and xxxii. 126,
1879 (see Huppert, l.c., p. 183).—V. Jaksch, Zeitschr. fiir physiol. Chemie, v. 398,
1881.—Leube, Virchow’s Archiv, c. 540, 1885.—Billet, Comptes rendus, c. 1252,
1885.—C. Fliigge, l.c., p. 169.—V. Limbeck, Prager med. Wochenschr., xii. 189, 198
206, 215, 1887.
59 Roberts, On Bacilluria, Int. Med. Congress, ii. 157-163. London, 1881.—
Schottelius and Reinhold, Centralbl. fiir klin. Med., viii. 635, 1886.
60 Fischer, Berliner klin. Wochenschr., i. 18, 1864.—Teufel, ibid., i. 17, 1864. ~
61 Cramer, Zeitschr, fiir klin. Med., vi. 54, 1883.—Albertoni, Maly’s Jahresbericht,
xix. 466 (reference), 1890.
62 Kannenberg, Zeitschr. fiir klin. Med., i. 506, 1880.—Litten, ibid., iv. 191, 1882.
3 Fehleisen, Die Aetiologie des Erysipels. Berlin, 1883.
64 Martini, see (38).—Litten, Zeitschr. fiir klin. Med., ii. 452, 1881.—Senetz,
Petersburger med. Wochenschr., No. 46, 1883.
65 Weichselbaum, Wiener med. Wochenschr., xxxiv. 241, 1885.
66 Lustgarten and Mannaberg, Vierteljahrschr. fiir Dermatologie und Syphilis,
xiv. 905, 1887; and Mannabery, Centralbl. fiir klin. Med., ix., No. 30, 1888;
Zeitschr. f. klin. Med., xviii. 223, 1890.
67 Letzerich, Zeitschr. fiir klin. Med., xiii. 33, 1888 ; xviii. 528, 1891.
68 Mircoli, Centralbl. fiir Bacteriol. und Parasitenk., iii. 336 (ref.), 1888.
69 Neumann, Berliner klin. Wochenschr., xxv., No. 7-9, 1888. Statements will
be found here also as to the occurrence of tubercle bacilli, the spirilla of relapsing
fever, kc.
Eos
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420 BIBLIOGRAPHY.
7” Karlinski, Prager med. Wochenschr., xv. 437, 452, 1890.
71 Philipowicz, Wiener med. Blatter, xxxiv. 673 and 710, 1885.
72 Kannenberg, see (62).
73 Leube, Sitzungsber. der physik.-med. Akad. Erlangen, Dec. 11, 1882.—osen-
stein, Centralbl. fiir med. Wissensch., xxi. 65, 1883.—Babes, ibid., xxi. 129, 1883.
—Shingleton Smith, The Lancet, ii. 942, 1883,—ZJrsai, Wiener med. Presse, 1141
and 1173, 1884.—Benda, Deutsche med. Wochenschr., x. 154, 1884.—Kreske,
Miinchener med. Wochenschr., xxxiv. Nos. 30, 31, 1887.
+ Philipowicz, see (71).
7 Cf. Braatz, Petersburger med. Wochenschr., xiii. 119, 127, 1888.
76 Leube, see (57).
? Hassall, The Lancet, ii. 21, Nov. 1859. Schmidt's Jahrbiicher, cix. 157 (ref.),
1861.
78 Balz, Berliner klin. Wochenschr., xxiii. No. 16, 1883.
7) Hatch, The Lancet, i. 875, 1887.
80 Mosler, Deutsche med. Wochenschr., xiii. 507, 1887.
1 Leuckart 1.c., p. 390.—Cannon, The Lancet, i. 6, 1887.
Scheiber, Virchow’s Archiv, ]xxxii. 161, 1884; see also Oerley, Die Rhabditiden
und ihre medic. Bedeutung. Berlin, 1886.
83 2. Peiper and Westphal, Centralbl. fiir klin. Med., ix. 145, 1888.—Baginsky,
Deutsche med. Wochenschr., xiii. 604, 1888.
a
nt
ie)
82
§ Maly’s Jahresbericht, xvi. 469 (ref.), 1887.
8 Fiirbringer, Archiv fur klin. Med., xviii. 143, 1876.
86 Kussmaul, Wirzburger med. Zeitschr., iv. 64, 1863.
87
Lbstein, Archiv fiir klin. Med., xxiii. 115, 1879.
Holm, Journal fiir prakt. Chemie, c. 142, 1867.
G. Stdédeler, Annalen der Chemie und Pharmacie, cxxxii. 323, 1864.
Hoppe-Seyler, Handb. d. physiol. u. pathol.-chem. Analyse, l.c., p. 245.
" Leyden, Zeitschr. fiir klin. Med., ii. 471, 1881.
* Foltanek, Wiener klin. Wochenschr., ii. 15, 1889.—Rosenheim, Zeitschy. f.
klin. Med., xv. 447, 1889.
® Fritz, Zeitschr. fiir klin. Med., ii. 471, 1881.
Stein, Archiv fiir klin. Med., xviii. 207, 1876.
W. Valentiner, Centralbl. fiir med. Wissensch., i. 913, 1865.—Fiirbringer,
Archiv fiir klin. Med., xx. 321, 1877.
% See Huppert, l.c., p. 167.
” Tiebig, see Huppert, l.c., p. 168.
% J. Miiller, Zeitschr. f. analytische Chemie, xii. 234 (ref.), 1873.
® Krukenberg, Chem, Untersuchungen zur wissensch. Medicin, pt. ii. p. 128.
Jena, 1888.
100 H, Bence Jones, Chem. Centralbl., xiii. 847, 2 (ref.), 1868.
1! Piria, Liebig’s Annalen, Ixxxii. 251, 1852.—Staedeler, ibid., cxvi. 57, 1860.
102 Scherer, Journal fiir prakt. Chemie, Ixx. 406, 1857.
“8 R. Hoffmann, Liebig’s Annalen, 1xxxvii. 124, 1857.—L. Meyer, ibid., cxxxii.
156, 1864.
i! C. Wurster, Centralblatt fiir Physiologie, i., No. 9 (sep. Supplement), 1887.
1 Hoffmeister, Liebig’s Annalen, cxxxix. 6, 1877.
16 Scherer, Journal fiir prakt. Chemie, 1xxix. 410, 1857.
7 Frerichs, Wiener med. Wochenschr., iv. 465, 1854.—Schultzen and Ricss,
Annal. des Charité-Krankenhauses, xv.—Pouchet, Maly’s Jahresber. fiir Thier-
chemie, x. 248 (ref.), 1880. —A. Frénkel, Berliner klin. Wochenschr., xv. 265, 1878.
—Blendermann, Zeitschr. fiir pbysiol. Chemie, vi. 234, 1882.—A. Trsai, Maly’s
Jahresber. fiir Thierchemie, xiv. 451 (ref.), 1885.
18 Prus, ibid., xvii. 435 (ref.), 1888.
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CHAPTER VII.—THE URINE. 421
109 See also Feser and Friedberger (whose observations refer to horse’s urine),
Maly’s Jahresb. fiir Thierchemie, iv. 231 (ref.), 1875.
0 F, Taylor, Pract. of Med., 2nd edit., 701.
11 Ord, Colloids and Crystallisation, Lond., 1879.
2 Holm, see (88).
U3 Ord, Proc. Pathol. Soc., Brit. Med. Journ., May 21, 1892.
"4 Ord, Berliner klin. Wochenschr., xv. 365, 1878.—. Chiari, Prager med.
Wochenschr., xiii. 541, 1888.
> Fr, Miiller, Berliner klin. Wochenschr., xxvi. 889, 1889.
U6 Senator, Internationale Beitrige zur wissench. Med., Festschrift, Rudolph
Virchow gewidmet zur Vollendung seines 70 Lebensjahres, iii. (sep. pub.). Berlin,
1891.
7 Frerichs, Die Bright’sche Nierenerkrankung und deren Behandlung. Bruns-
wick, 1851.— Voyel, Virchow’s Handbuch der spec. Pathol. und Therapie, vi. 2,
709. Erlangen, 1865.—U/tzmann, Wien. med. Presse, xi. 82, 1870.
us Leube, Virchow’s Archiv, Ixxii. 145, 1878.—Fiirbringer, Zeitschr. fiir klin.
Med., i. 346, 1889.—Senator, Die Albuminurie. Berlin, 1882.—@C. Posner, Berliner
klin. Wochenschr., xxii. 654, 1885 ; Virchow’s Archiv, civ. 497, 1886; and Archiv
fiir Anat. und Physiol. (physiol. Abtheil.), 1888. Compare Mulfatti, Intern.
Centralbl. f. d. Physiol. u. Pathol. der Harn- und Sexual-organe, i. 266, 1889.
19 VY. Noorden, Deutsches Archiv fiir klin. Med., xxxviii. 3, 205, where will be
found also very exhaustive and exact references to the literature on the subject
of physiological albuminuria.
120 Leube, Zeitschr. fiir klin. Med., xiii. 1, 1887.—H. Winternitz, Zeitschr. f-
physiol. Chemie, xv. 189, 1891.
Ll Grainger Stewart, On Albuminuria, 1888, p. 19.
122 Anschiitz, Die Destillation unter vermindertem Drucke im Laboratorium.
Bonn, 1887.
123 Stirling, The Lancet, ii. 1157, 1887.—Ringstedt, Schmidt’s Jahrbiicher, ccxxv-
141 (ref.), 1889.—Heubner, Festschrift zu Henoch’s 70 Geburtstag, p. 26. Berlin,
1890.— Washburn, Centralbl. f. klin. Med., xi. 786, 1890.
124 Payvy, Lancet, i. 711, 1888.
12 Moxon, Guy’s Hospital Reports, 1878.
126 Fagge, see Taylor, Med., p. 791.
127 Taylor, Pract. of Med., 2nd edit., p. 790.
128° Falkenheim, Deutsches Archiv fiir klin. Med., xxxy. 446, 1884.
129 Huchard, L’?Union Médical, 58.
130 Haig, Brit. Med. Journ., Jan. 11, 1891.
131 Wirchow, Gesammte Abhandl. zur wissensch. Med., 846, 1856. Compare
Clinical Lectures on Important Symptoms. On Albuminuria, by (Grainger
Stewart, Edinburgh, 1888.
132 Bright, Report of Medical Cases, 1827 and 1831.
133 Christison, Ueber die Granular-Entartung der Niere, trans. by J. Mayer,
with remarks by Rokitansky. Vienna, 1841.—Rayer, Traité des Maladies des Reines,
ii., 1840.—Frerichs, Die Bright’sche Nierenerkrankung und deren Behandlung, 1851.
—Traube, Ueber den Zusammenhang von Herz- und Nieren-krankheiten. Berlin,
1856. For exhaustive notices, see £. Wagner, v. Ziemssen’s Handbuch der spe-
ciellen Pathol. und Therapie. Leipzig, 1882.
134 Kauder, Archiv fiir experiment. Pathol. und Pharmakol., xx. 411, 1886.—
Pohl, ibid., xx. 246, 1886.
135 Compare A. Csatdry, Archiv f. klin. Med., xlvii. 159, 1890.
136 Mf. Huppert, Virchow’s Archiv, lix. 305, 1874.
137 Schreiber, Archiv fiir experim. Pathol. und Pharmakol., xix. 237, 1885, and
xx. 85, 1886.
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138 Singer, Prager med, Wochenschr., xii. 9, 1887.—Kobler, Wiener klin.
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139 Leyden, Zeitschr. fiir klin. Med., iii. 161, 1881.
WH, Lorenz, Wiener klin. Wochensch., i. 119, 1888.
141 VY, Bamberger, Wiener med. Wochenschr., xxxi. 145 and 177, 1881.
12 Bull, Berliner klin Wochenschr., xxiii. 717, 1886.—Mareau, Revue de Méd.,
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klin. Med., xii. 168, 1887.—Caufield, Med. News (sep. issue), 1887.—G. Johnson,
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143 -V, Jaksch, Deutsche med. Wochenschr., xiv., Nos. 40 and 41, 1888. Compare
also Loos, Jabrbiicher f. Kinderheilkunde (sep. pub.), 1890; and &. v. Engel,
Prager med. Wochenschr., xv. 615, 189c.
144 See Kinnicr, Centralbl. fiir klin. Med., vii. 772 (ref.), 1886.
45 Falkenheim, see (128).
16 Merley, De Albuminurie intermittente cyclique ou Maladie de Pavy. Paris,
1887.
17 See F’. Rose, Annal. der Physik und Chemie, xxviii. (104), 132, 1833.
M8 J. F. Heller, Archiv fiir physiol. und pathol. Chemie und Mikroscopie, v. 161,
1852.
9 Heynsius, Pfliiger’s Archiv, x. 239, 1875.
159 Clin. Soc. Trans., xix. p. 339.
151 Hindenlang, Berliner klin. Wochenschr., xviii. 205, 1881.
152 Penzoldt’s Hltere und neuere Harnproben, 2nd edit. Jena, 1886.—V. Noorden,
see (119).
153 Fiirbringer, Deutsche med. Wochenschr., xi. 467, 1885.
14 G, Johnson On the Various Modes of Testing for Albumin and Sugar, p. 6.
London, 1884.
9 M. Jaffe, Zeitschy. fiir physiol. Chemie, x. 399, 1886.
198 See Huppert, Neubauer, and Vogel, 1.c., p. 121.
197 Liebermann, Centralbl. fiir die med. Wissensch., xxv. 321 and 450, 1887.—
C. Wurster, Centralbl. fiir Physiol., i., No. 9 (sep. issue), 1887.—L. Salkowski,
Zeitschr. f. physiol. Chemie, xii. 215, 1889.
158 See Huppert, Neubauer, and Vogel, l.c., p. 71.
19 Schick, Prager med. Wochenschr., xv. 306, 1890.
160 Zouchlos, Wiener allgem. med. Zeitung, No. 1, 1890.
161 4, B. Cohen, Maly’s Jahresbericht, xviii. 116 (ref.), 1888.
182 G. Roch, Pharmaceutische Centralhalle, 549, 1889.—J. A. Macwilliam, Brit.
Med. Journ., No. 1581, 837, 1891.
163 Macwilliam, l.c., p. 840, 1891.
164 See also Jolles, Wiener med. Presse, xxxi. 825, 1890.
165 Devoto, Zeitschr. f. physiol. Chemie, xv. 474, 1891.
166 See Huppert, l.c., p. 554.
187 Roberts, Lancet, i. 313, 1876.—Stolnikow, Petersburger Wochenschr., xii.,
1876; Maly’s Jahresber. fiir Thierchemie, vi. 148 (ref.), 1887.—J. Brandbery,
Upsala Likare forh., 15.—Hammarsten, Maly’s Jahresber. fiir Thierchemie, x. 265
(ref.), 1881 ; see also Laache, l.c., p. 78.
168 Zaache, l.c., p. 79.
169 Hammarsten, Maly’s Jahresb., x. 265 (ref.), 1881, and xiii. 217 (ref.), 1884.
1 Guttmann, Berliner klin. Wochenschr., xxiii. 117, 1886.
™! COzapek, Prager med. Wochenschr., xiii. 128, 1888.
1” Sokolow, Maly’s Jahresb., xvii. 223 (ref.), 1888.—Th. Geisler, Berlin. klin
Wochenschr., xxvi. 1111, 1889.
3 Christensen, Virchow’s Archiv, cxv. 128, 1889.
4 Th. Geisler, see (172).
Ss
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CHAPTER VII.—THE URINE. 423
% Noel Paton, Schmidt’s Jahrbiicher, ccxxii. 4 (ref.), 1889.
% Huppert and Zdhot, Zeitschr. f. physiol. Chemie, xii. 467, 1888.—ZdhoF,
ibid., xii. 484, 1888.
1 Hofmeister, ibid., iv. 253, 1880; v. 66, 127, 1881; vi. 51, 1881; Prager med.
Wochenschr., v. 321, 335, 1880.
"8 Hofmeister, see (177).—Maianer, Prager Vierteljahrschr., cxliv. 75, 1879.—V.
Jaksch, Prager med. Wochenschr., v. 292 and 303, 1880; vi. 61, 74, 86, 133, 143.
1881 ; and Zeitschr. f. klin. Med., vi. 413, 1883.
8 VY. Jaksch, Zeitschr. f. klin. Med., vi. 413, 1883.
189 Maianer, ibid., viii. 234, 1884.
181 Pacanowski, ibid., ix. 429, 1885. See also Kottnitz, Centralbl. f. d. med.
Wissensch., xxix. 513, 1891 ; and Loeb, ibid., xxix. 577, 1891.
1 Fischel, Archiv £. Gynikologie, xxiv. 27, 1884. Compare, however, Thomson,
Deutsche med. Wochenschr., xv. 899, 1889 ; and Kottnitz, ibid., xv. 900, 1889.
183 Grocco, Sulla Peptonuria, di nuovo sulla Peptonuria. Milan, 1883-84.—Secchi,
Maly’s Jahresber., xvii. 444 (ref.), 1888.—0. Brieger, Inaug. Dissert., Breslau,
1888.—Katz, Wiener med. Blitter, xiv., Nos. 45, 46, 48, 50-52 (sep. pub.), 1890.
184 Pochl, Maly’s Jahresber., xvii. 432 (ref.), 1888.
18 Mya and Belfanti, Centralbl. f. klin. Med., vii. 729. 1888.
> Hofmeister, see (177).—Devoto, Zeitschr. f. physiol. Chemie, xv. 465, 1891.
187 HT, Huppert, l.c., p. 189, 8th edit.
18 J, A. Schulter, Maly’s Jahresber., xvi. 228 (ref.), 1887.
18 Maixner, Zeitschy. f. klin. Med., xi. 342, 1886.
199 Devoto, see (186); Rivista clin. Archivo italiano di clin. Med., p. 30 (sep.
pub, ), 1891.
11 VY, Jaksch, Zeitschr. f. physiol. Chemie, xvi. 243, 1892.
12 §. Martin, quoted by Halliburton, p. 787.
18 Macwilliam, British Med. Journ., Jan. 16, 1892.
14 Kiihne and Chittenden, Zeitschr. f. Biologie, xix. 159, 1883; xx. 11, 1884;
and xxii. 409, 1886.—Miihne, Verhandl. des naturhistor. medic. Vereines zu
Heidelberg, Nos. i., iii, p. 286.—Herth, Monatshefte f. Chemie, v. 266, 1884.
1% Senator, Die Albuminurie im gesunden und kranken Zustande, p. 9. . Berlin,
1882.—Ter Gregoriantz, Zeitschr. f. physiolog. Chemie, vi. 537, 1882.—V. Jaksch,
Zeitschr. f. klin. Med., viii. 216, 1884.
196 Loeb, Archiv f. Kinderheilk., ix. 53, 1887 ; x. 212, 1889.
1%” Heller, Berliner klin. Wochenschr., xxvi. 1038, 1889.
8 Kahler and Huppert, Prager med. Wochenschr., xiv. 33, 35, 45, 1889.
199 Képpner, Archiv f. Psychiatrie, xx. 825, 1889.
200 ©, Posner, Berliner klin. Wochenschr., xxv., No. 21, 1888.
*0l_ Thormihlen, Virchow’s Archiv, cviii. 322, 1887.
202 Kiihne and Chittenden, .p. 278.
203 Maguire, Brit. Med. Journ., ii. 1886, p. 543.
204 Senator, quoted by Halliburton, 1.c., p. 783.
205 Kauder, see (134).
206 Pohl, see (134); see also A. Csatdry, (135).
207 Halliburton, l.c., p. 783.
208 Huppert, l.c., p. 277.
209 Heller, Wiener med. Zeitschr., i. 48, 1859; Schmidt’s Jahrbiicher, civ. 39
(ref.), 1859.
210 See Huppert, l.c., p. 302.
ll Rosenthal, Virchow’s Archiv, ciii. 516, 1886.
212 Thid., l.c.
13 Almén, see Hammersten, Lehrbuch d. physiol. Chemie, p. 336. Wiesbaden,
1891.
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A424 BIBLIOGRAPHY.
24 Neisser, Centralbl. f. med. Wissenchaften, xix. 545, 1881.
Zur Nieden, Berliner klin. Wochenschr., xviii. 705, 1881.
216 Langer, Prager med, Wochenschr., xvi. 389, 391.
217 Rosenbach, Berliner klin. Wochenschr., xvii. 132, 151, 1880.—Zhrlich,
Zeitschr., f. klin. Med., iii. 383, 1881.—Boas, Archiv f. klin. Med., xxxii. 355,
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Zeitschr. f. klin. Med., xiii. 163, 1888.—J. S. Bristowe and S. M. Copemann,
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28 Taylor, Pract. of Med., p. 787.
219 Hoppe-Seyler, Physiolog. Chemie, l.c., p. 862.
Compare Lewin and Posner, Centralbl. f. die med. Wissensch., xxv. 353,
Halliburton, l.c., p. 777-
22 Compare Huppert, Anleitung zur Analyse des Harns, Lc., p. 279.
3 Fr, Miiller, Mittheilungen aus der med. klinik in Wiirzburg, i. 266, 1885.
Obermayer, Centralbl. f. klin. Med., xiii. 1, 1892.
Ls, Fischer, Berichte d. deutschen chem. Gesellschaft, xxiii. 2114, 1890. I
cannot forbear drawing the reader’s attention to these reports, which are of the
highest medical interest.
25 V. Briicke, Vorles. uber Physiologie, i. 375, 2nd edit. Wien, 1875.
~6 Wedenski, Zeitschr. f. physiol. Chemie, xiii, 112, 1888.—L. v. Udrdnsky,
Berichte d. naturforsch. Gesells. in Freiburg, xi. 183.—Moritz, Archiv f. klin.
Med., xlvi. 252, 1890.—Gaube, Maly’s Jahresbericht, xix. 225 (ref.), 1890.
7 G, Johnson, Brit. Med. Journal, April 9, 1892.
28 G, S. Johnson, Proc. Roy. Soc., xliii. pp. 493, 554.
9 Morse, Schmidt's Jahrbiicher, ccxxii. 22 (ref.), 1889.
230 Méhu, Maly’s Jahresber., viii. 188 (ref.), 1888.
304 Taylor, Pract. of Med., p. 784.
“31 W, M. Ord, Centralbl. f. d. med. Wissensch., xxviii. 94 (ref.), 1890.
22 Halliburton, l.c., p. 793-
33 V, Jaksch, Zeitschr. f. klin. Med., xi. 20, 1886.
#4 Moritz, Miinchener med. Wochenschr., Nos. 1 and 2 (sep. pub.), 1891.—
Kraus and Ludwig, Wiener klin. Wochenschrift, iv. 855, 1891.
285 Worm-Miiller, Pfliiger’s Archiv, xxxvi. 172, 1885.
+86 Moore, Lancet, ii. 1884; and Heller, Archiv f. Mikroskopie und mikroskop.
Chemie, i. 212 and 292, 1844.
87 Hoppe-Scyler, Berichte der deutschen chem. Gesellsch., iv. 346, 1871.
238 T'rommer, Annal. der Chemie und Pharmacie, xxxix. 360, 1841.
Compare Jastrowitz, Deutsche med. Wochenschr., xvii. 253, 292, 1891.
Pavy, see F. Taylor, l.c., p. 776.
Worm-Miiller, Pfliiger’s Archiv, xxvii. 107, 1882.
242 Moritz, Deutsches Archiv f. klin. Med., xlvi. 260, 1890; see also (234).
43° Leube and Salkowski, l.c., p. 223.
24 Finhorn, Virchow’s Archiv, cil. 263, 1885.
“4 Halliburton, 1.c., p. 99, 793-
46, Fischer, Berichte der deutschen chem. Gesellsch., xvii. 579, 1884.
V. Jaksch, see (232).
348 JTirschl, Zeitschr. f. physiol. Chemie, xiv. 383, 1890.—Havelburg, Centralbl. f.
klin. Med., xi. 89, 1891.
249 Geyer, Wiener med. Presse, xxx. 1686, 1889.—Moritz, Archiv f. klin. Med.,
xlvi, 264, 1890.—Luther, Inaug. Dissert., Berlin, 1890.
20 Hirschl, 1.c., p. 387.
21 §. Kobrak, Inaug. Dissert, Breslau, 1887. — Rosenfeld, Deutsche med.
Ss
23
240
241
24
a
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CHAPTER VII.—THE URINE. 425
Wochenschr., xiv. 451, 479, 1888.—Pollatschek, ibid., xiv. 354, 1888.—Hirschl,
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*2 Bottger, Journal f. prakt. Chemie, lxx. 432, 1857.
23 FB, Salkowski, Centralbl. f. d. med. Wissensch., xxiii. 433, 1885.
*4 See Huppert, Neubauer, and Vogel, 1.c., 8th edit., p. 168.
*» Nylander, Zeitschrift £. physiol. Chemie, viii. 175, 1884.
*8 Penzoldt, l.c., p. 16; see also R. Jahreis, Beitrige zur Untersuchung des
Harns auf Eiweiss und Zucker. Inaug. Dissert, Erlangen, 1886.
*7 M. Rubner, Zeitschr. fiir Biologie, xx. 397, 1884.
28 Penzoldt, see (152).
9 Laache, l.c., p. 111.—Penzoldt, 1.c., p. 16.
°60 G. Oliver, Bedside Urine Testing.
*81 Johnson, 1.¢., p. 367.—Thiéry, Progrés médical, xiv. 633, 1886.
*62 Th. Weyl, Schmidt’s Jahrbiicher, ccxii. (ref.), 1886.
*63 Penzoldt, Berliner klin. Wochenschr., xx. 201, 1883.
“1 VY. Jaksch, Mittheil. des Wiener Docteren-collegiums, x. 1884.
*6 Salkowski, Virchow’s Jahresber., xix. 148, 1884.
66 H. Molisch, Sitzungsber. der kais. Akad. der Wissensch. (Wien), xciii. ii. 912,
1886; and Centralbl. f. die med. Wissensch., xxi. 49, 1887.
*67 Seegen, Centralbl. f. die med. Wissensch., Nos. 44 and 45, 1886.
*8 Mylius, Zeitschr. f. physiol. Chemie, xi. 492, 1887.—I”. Udrdnsky, ibid., xii.
381, 1888.
*69 -V. Briicke, Wiener med. Wochenschr., viii. 337, 1858.—Seegen, Archiv f.
Physiol., v. 375, 1872.—Abeles, Centralbl. f. die med. Wissensch., xvii. 33 and 209,
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270 Baumann and v. Udrinsky, Berichte der deutsch. chem. Gesellschaft, xxi.
2744, 1888.
“71 Luther, l.c., p. 12.—Roos, Inaug. Dissert., Freiburg, 189r.
7 Fehling, Annal. der Chemie und Pharmacie, Ixxii. 106, 1848; cvi. 75,
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73° Teube and Salkowshi, 1.c., p. 231.
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7 Salkowski, l.c., p. 232.
276 Munk, Virchow’s Archiv, cv. 63, 1888.
+7 F, Taylor, Medicine, p. 777.
*78 Roberts, he Lancet, i. 21, 1862.
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bericht, xix. 224 (ref.), 1890. For other similar apparatus, such as that by
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*81 For details regarding the construction of the Polarimeter, see Hwppert,
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282 K, Zimmer, Deutsche med. Wochenschr., ii. 329, 1876.—Secgen, Centralbl. f.
die med. Wissensch., xxii. 753, 1884.
283 De Sinety, Maly’s Jahresber. fiir Thierchemie, iii. 134 (ref.), 1874.—Hempel,
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101, 1877.—Johanovsky, Archiv f. Gyniikologie, xii. 448, 1877.—Kaltenbach, Zeitschr.
f. physiol. Chemie, ii. 360, 1877.—Ney, Archiv f. Gynikologie, xxxv. 239, 1889.
24 V, Jaksch, Zeitschr. f. klin. Med., xi. 25, 1886.
285 F. Reichard, Pharm, Zeitschr. f. Russland, xiv. 45 (see Aiilz, Maly’s Jahresber.,
v. 60, 1876).
286 Tandwehr, Centralbl. f. die med. Wissensch., xxiii. 369, 1885.
7 Wedenski, Zeitschr. f. physiol. Chemie, xiii. 127, 1888.
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426 BIBLIOGRAPHY.
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84 Salkowski, Zeitschr. f. physiol. Chemie, iv. 134, 1880.
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34 B. Salkowskt, ibid., 302.—Huppert, l.c., p. 310.—Stokvis, Med. Tidschr. voor
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*85 Baumaun, Zeitschr. f. physiol. Chemie, x. 123, 1886.
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°87 Hochsinger, Wiener med. Presse, xxxi. 1570, 1618, 1890. Deutsche med.
Wochenschr., No. 12, 1891.
338 Compare also Kast and Boas, Miinchener med. Wochenschr., xxxv. 55, 1888
89 Bohland, Deutsche med. Wochenschr., xvi. 1040, 1890.
340 Jaffé, Pfliiger’s Archiv, iii. 448, 1870.
341 See Senator, Centralbl f. die med. Wissensch., xv. 257, 1877.
32 TTalliburton, 1.c., p. 744.
43° Obermayer, Wiener klin. Wochenschr., iii. 176, 1890.
344 Weber, Zeitschr. f. anal. Chemie, xviii. 634, 1879 (see Archiv. der Pharm.,
cexiii. 340, 1879).
“45 Talliburton, l.c., p. 744.
346 Salkowski, Virchow’s Archiv, ]xviii. 407, 1876.
47 Gand L. Kriiss, Colorimetrie und quantitative Spectral-analyse von Ham-
burg. Leipzig, 1891.
348 Rosin, Centralbl. f. klin. Med., 505, 1889; Virchow’s Archiv, cxxiii. 1891.
349 Rosenbach, Berliner klin. Wochenschr., xxvi. 1490, 1889; xxvii. 581, 1890.—
Boginsky, Archiv f. Kinderheilkunde, xiii. 312, 1891.—#. Salkowski, Berlin. klin.
Wochenschr., xxvii. 202, 1889.—2. A. Ewald, ibid., xxvi. 953, 1889.—Abraham,
ibid., xxvii. 385, 1891.— Rwmpel and Mester, Centralbl. f. klin. Med., xii. 527 (ref.),
18901.
350 Brieger, Zeitschr. f. physiol. Chemie, iv. 414, 1880.
351 Brieger, Zeitschr. f. klin. Med., iii. 468, 1881.—WMester, Zeitschr. f. physiol.
Chemie, xii. 130, 1888.
352 7, Salkowski, Centralbl. f. die med. Wissensch., xiv. 818, 1876.
353 Brieger see (351).
354 Hoppe-Seyler, Zeitschr. f. physiol. Chemie, xii. 1, 1887.—Poehl, Petersburger
med. Wochenschr., xii. 423, 1887.—Kast and Boas, Miinch. med. Wochenschr.,
XXxv. 55, 1888.
35 Rumpf, Zeitschr. £. physiol. Chemie, xvi. 220, 1892.
356 Brieger, see (351).
- 337 Baumann, Zeitschr. f. physiolog. Chemie, i. 71, 1878.
358 7, Salkowski, Virchow’s Archiv, ]xxix. 551, 1880; and Zeitschr. f. physiolog.
Chemie, x. 346, 1886.
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428 BIBLIOGRAPHY.
89 H, Landolt, Ber. der deutschen chem. Gesellsch., iv. 771, 1871.—Baumann
and Brieger, Zeitschr. fiir physiolog. Chemie, iii 149, 1879 ; and Ber. der deutschen
chem. Gesellsch., xii. 804, 1879.
360 Baumann, Zeitschr. f. physiol. Chemie, x. 129, 1886.
361 Baumann, Pfliiger’s Archiv, xiii. 63, 1875 ; and Zeitschr. f. physiolog. Chemie,
vi. 183, 1882.
62 See Huppert, Vogel, Neubauer, l.c., p. 76.
3683 W. Ebstein and J. Miiller, Virchow’s Archiv, Ixii. 554, 1873; 1xv. 394, 1875.
°64 Baumann and Preusse, Du Bois-Reymond’s Archiv f. Anat. u. Physiol., 245,
1879.
#65 Huppert, l.c., p. 78.
365 Baumann and Preusse, Zeitschr. f. physiol. Chemie, iii. 157, 1879.
#67 Baumann, Berichte d. deutschen chem. Gesellschaft, xii. 1450, 1879; Cxxxiii.
79, 1880; Zeitschr. f. physiol. Chem., iv. 304, 1880.—Z. and ZH. Salkowski, Berichte
d. deutschen chem. Gesellschaft, xii. 1438, 1879.
368 Huppert, l.c., p. 151.
369 Schultzen and Riess, see Huppert, l.c., p. 151.
%70 Kirk, see Huppert, l.c., p. 152.—Wolkow and Baumann, Zeitschr. f. physiol.
Chemie, xv. 228, 1891.
*71 Baumann, Zeitschr. f. physiolog. Chemie, iv. 311, 1880.
“72 Boedeker, Zeitschr. f. rat. Med., vii. 130, 1857. —Zbstein and J. Miiller,
Virchow’s Archiv, 1xii. 554, 1873; lxv. 394, 1875.— Fiirbringer, Berliner klin.
Wochenschr., xii. 313, 1875.—Flei cher, ibid., xii. 529, 547, 1875.
*3° Wolkow and Baumann, l.c., p. 252.—Araske and Baumann, Minchener med.
Wochenschr., xxxviii. 1, 1891.
374 Cooper Lane, Ann. d. Chemie und Pharmacie, cxvii. 118, 1861 (contributions
from Prof. C. Boedecker’s laboratory).
*7 See Huppert, l.c., p. 102.
“6 Zeller, Archiv f. klin. Chirurgie, xxix. 9, 1884.
“7 V, Jaksch, Zeitschr. f. physiol. Chemie, xiii. 385, 1889.— Pollak, Wiener med.
Presse, Xxxix. 1473, 1515, 1556, 1889.
*78 Thormiihlen, Virchow’s Archiv, cviii. 317, 1887.
*79 Krukenberg, Maly’s Jahresber., xiv. 60 (ref.), 1885 ; and Chem. Untersuch.
in wissenschaftl. Med., Pt. ii. p. 128. Jena, 1888.
80 Salkowski, Zeitschr. f. physiol. Chemie, ix. 127, 1884.
#81 Dreschfield, Schmidt’s Jahrb., ccxili. 213 (ref.), 1887.
82 Senator, Charité-Annalen, xv. (sep. pub.), 1890.
*85 See Liselt, Prager Vierteljahrsschr., lix. 190, 1858, and lxx. 87, 1862; A.
Pribram, ibid., lxxxvili. 16, 1865; Dressler, ibid., ci. 68, 1869; Ganghofner and
Ptibram, ibid,, cxxx. 77, 1876; £. Wagner, Berliner klin. Wochenschr., xxvii. 431,
1884 ; Paneth, Archiv f. klin. Chirurgie, xxviii. 179, 1884; K. 4. H. Mirner, Zeit-
schr. f. physiol. Chemie, xi. 66, 1886; Mura, Virchow’s Archiy, cvii. 250, 1887 ;
Brandi and L. Pfeiffer, Zeitschr. f. Biologie, xxvi. 348, 1890.
*4 VY. Jaksch, Ueber Acetonurie und Diaceturie. Berlin, 1885.—De Boeck and
A, Slosse, De la Présence de l’Acetone dans 1’ Urine aliénés, &c., 1891.
885 Lorenz, Zeitschr, f. klin. Med., xix. 19, 1891.
*86 Baginsky, Archiv f. Kinderheilkunde, ix. 1. 1887.
“7 V, Jaksch, Zeitschr. f. klin. Med., x. 362, 1885.—Jujinger, Wiener klin.
Wochenschr., i. 367, 1888.—S. West, Maly’s Jahresbericht, xix. 418 (ref.), 1890.—
Pawinski, Berliner klin. Wochenschr., xxv., No. 50, 1888.—Lorenz, l.c., p. 54.
88 Rosenfeld, Deutsche med. Wochenschr., No. 40, 1885.—Zphraim, Inaug.
Dissert., Breslau, 1885.—Honigmann, Inaug. Dissert., Breslau, 1886.—Jufe, Inaug.
Dissert., Wiirzburg, 1886.
“89 For the other reactions of acetone, see v. Jaksch, Ueber Acetonurie und
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Diaceturie, lc., p. 21; also Lorenz, l.c., p. 21.—Men Taniguti and L. Salkowski,
Zeitschr. f. physiol. Chemie, xiv. 476, 1890.
*0 V, Jaksch, Zeitschr. £. physiol. Chemie, vi. 541, 1882.—Nencki, see Pawinski
(387).
*. Messinger, Bericht. d. deutsch. chem. Gesellsch., xxi. 3366, 1888.
*2 Huppert, 1.c., p. 470.
*8° R. v. Engel, Prager med. Wochenschr., xvi. 247, 1891.—Devoto, Rivista clinica,
Archivio italiano di clinica Medica, xxx. (sep. pub.), 1891.
“4 V. Jaksch, Ueber Acetonurie und Diaceturie, l.c., p. 101.
*% WV. Jaksch, Zeitschr. f. Heilkunde, iii. 34, 1882.—Schrack, Jahrbuch f. Kinder-
heilkunde, xxix. 411, 1889.
%6 V. Jaksch, ibid., p. 116.
37 VY. Jaksch, 58 Versammlung deutscher Naturforscher und Aerzte in Strass-
burg, Sept. 1886; Zeitschr. f. klin. Med., xi. 307, 1886; Zeitschr. f. physiol.
Chemie, x. 536, 1886.
98 V7. Rokitansky, Wiener med. Jabrb., ii. (No. 1), 205, 1887.
*99 VV. Jaksch, see (397).
4 Salkowski, Centralbl. f. d, med. Wissensch., xxvi. No. 38, 1888 ; and Zeitschr.
f. physiol. Chemie, xiii. 265, 1889.—Ken Taniguti, ibid., xiv. 980, 1890.
41 2, Schiitz, Prager med. Wochenschr., vii. 322, 1882.
402 See (87).
#3 See also Rassmann, Centralbl. f. d. med. Wissensch., xix. 567 (ref.), 1881.
Grim, Langenbeck’s Archiv, xxxii. 511, 1885.
Brieger, Zeitschr. f. physiol. Chemie, iv. 407, 1880.—A. Huber, Virchow’s
Archiv, evi. 126, 1886.—Rossbach-Goctze, Verhandl. des Congresses f. innere Med.,
vi. 212, 1887.—Kisch, Deutsche med. Wochenschr., xii. 39, 1886.—Francotte,
Schmidt’s Jahrb., cexiii. 145 (ref.), 1887.
46 Tanggaard, Virchow’s Archiv, lxxvi. 545, 1879.
47 Fiirbringer, Archiv f. klin. Med., xviii. 154, 1876.—Czapcek, Zeitschr. f. Heil-
kunde, ii. 345, 1881.
48 See Huppert, l.c., p. 494.
409 For other methods for the determination of oxalic acid in the urine, such as
those by Schultzen and Buchheim, see Leube and Salkowski, l.c., p. 118; W. Mills,
Virchow’s Archiv, xcix. 305, 1885; Salkowski, Zeitschr. f. physiol. Chemie, x. 120,
1886; Nickel, ibid., xi. 189, 1887.
10 Fiirbringer, Archiv f. klin. Med., xvi. 516, 1875.
41. Cantani, Oxalurie, Germ. transl. by Hahn. Berlin, 1880.
42 Beybie, Schmidt's Jahrb., lxvii. 52 (ref.), 1850.
Neidert, Miinchener med. Wochenschr., xxxvii. 590, 1890.
Kisch, oral communication.
Ebstein, Deutsches Archiv fiir klin. Med., xxiii. 138, 1878, and xxx. 188, 1882 ;
further see A. Niemann, Deutsches Archiv f. klin. Med., xviii. 223, 1876; Loebisch,
Liebig’s Annalen, clxxxii. 231, 1876; Steffenhagen, Virchow’s Archiv, c. 416, 1885.
416 Stadthagen and Brieger, Berliner klin. Wochenschr., xxvi. 344, 1889.—V.
Udrinsky and E. Bawmann, Zeitschr. f. physiol. Chemie, Ixxv. 77, 1890.
47 See A. Hermann, Zeitschr. f. physiol. Chemie, xii. 496, 1888.
Czapek, ibid., xii. 502, 1888.—Camerer, Zeitschr. f. Biologie, xxvi. $4, 1889.
49 Fokker, Pfliiger’s Archiv, x. 153, 1875; xlv. 389, 1889.
0 2. Salkowski, Virchow’s Archiv, Ixviii. gor, 1876 ; Zeitschr. f. physiol. Chemie,
xiv. 31, 1890.
#1 #. Salkowski, Leube, and Salkowski, 1.c., p. 96.
+2 7. Ludwig, Wiener med. Jahrb., 597, 1884.
423 Fleischer and Penzoldt, Deutsches Archiv f. klin. Med., xxvi. 401, 1880,—
Rohland and Schurz, Pfliiger’s Archiv f. Physiologie, xlvii. 469, 1890.
404
405
413
4
4
415
418
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430 BIBLIOGRAPHY.
+4 Cf. Stadthagen, Virchow’s Archiv, cix. 390, 1887.
#5 VY, Bamberger, Oesterr. Zeitschr. f. prakt. Heilkunde, vi. 7, 1860.
#26 Salkowski, Virchow’s Archiv, cxvli. 570.
“27 Y, Jaksch, Der Weingeist als Heilmittel, Wiesbaden, 1890.—See also ZL.
Thomas, Anleitung zur qualitativen und quantitativen Analyse des Harns, 9th edit.,
p. 237. Wiesbaden, 1890.
#28 Compare also A. J/aig’s Harnsiiurestudien, and G. Hofman, Prager med.
Wochenschr., xiv. 329, 1889.
£9 Prout, Taylor's Med., p. 699.
430 VY, Jaksch, l.c., p. 32.
431 V, Jaksch, Zeitschrift zu E. Henoch’s 70 Geburtstag, Berlin, 1890.—JZ. Thomas,
ley) pr 221;
482 Bernabei, Centralbl. f. klin. Med., x. (ref.), 1889.
433 Liifner, Zeitschr. f. physiol. Chemie, i. 350, 1877; and Jacobj, Zeitschr. f.
analyt. Chemie, xxiv. 307, 1885.
434 Pfliiger and Schenck, Pfliiger’s Archiv, xxxviii. 325, 1886; Schenck, ibid.,
xxxviii. 511, 1886; and Z. Salkowski, Zeitschr. f. physiol. Chemie, x. 110, 1886.
485 Bunsen, Gasometrische Methoden, 2nd edit., p. 357, 1877.
436 Pliiger, see (434).
“7 Huppert, l.c., p. 531.
438 Méhu, Urine normale, &c., l.c., p. 136.
439 G, Lange, Pfliiger’s Archiv, xxxvii. 45, 1885.
40° Huppert, l.c., p. 504.—Hoppe-Seyler, l.c., p. 363.—Leube-Salkowski, l.c. p. 58.
4 Morner and J. Sjoqvist, Skandinay. Archiv f. Physiol., ii. 438, 1891.
42 Will-Varrentrapp, see Leube-Salkowshi, l.c., p. 58.—J. Kjedahl, Zeitschr. f.
analyt. Chemie, xxii. 336, 1883.
43° Neubauer, Annal. der Chemie und Pharmacie, cxix. 27, 1861.
444 Pouchet. Maly’s Jahresber., viii. 247 (ref.), 1881.
445 Grocco, La Creatinina in Urine normali et patologiche. Perugia, 1886.
46 Senator, Virchow’s Archiv, lxviii. 422, 1876.
447 See Thomas, Neubauer, and Vogel, Pt. ii. p. 583. Wiesbaden, 1890.
48° Baldi, Maly’s Jahresbericht, xix. 132 (ref.), 1890.
49 Th, Weyl, Ber. der deutschen chem. Gesellsch., xi. 217, 1878.
450 Jafé, Zeitschr. f. physiol. Chemie, x. 399, 1886.—Colasanti, Maly’s Jahres-
bericht, xix. 132 (ref.), 1890.
#1 Neubaucr, Annal. der Chemie und Pharmacie, cxix. 33, 1861.
42 Salkowski, see Leube and Salkowski, Die Lehre vom Harn, p.111. Berlin, 1882.
43 Taniguti and Salkowski, Zeitschr. f. physiol. Chemie, xiv. 471, 1890.
#4 Thudichum, Compt. rend., cvi. 1803, 1888.
45 Salomon, Zeitschr. f. physiol. Chemie, xi. 410, 1887.
46 Wor exhaustive information relative to these and other xanthin bodies, see
Huppert, l.c., p. 200 and 551; G. Bruhns, Zeitschr. f. physiol. Chemie, xiv. 533, 1890.
47 4. G. Pouchet, Comptes rendus, xcvii. 1560, 1883, and c. 361, 1885.
#8 Ch, Bouchard, Comp. rend. Soc. Biolog., 604, 1882; 665, 1884; see Maly’s
Jahresber., xii. 55, 1883, and xiv. 216, 1885.
49 Lépine and Guerin, Revue de Médicine (Sup.), 1885.
460 4, Villiers, Comptes rendus, c. 1246, 1885.
461 4, G. Pouchet, see (457).
462 Feltz, Maly’s Jahresbericht, xvii. 433 (ref.), 1888.
463° Lépine, Centralbl. f. klin. Med., xi. 12 (ref.), 18g90.— Lépine and Aubert, Comptes
rendus (sep. pub.), July 1885.
464 Roges and Gaume, Centralbl. f. klin. Med., xi. 12 (ref.), 1890.
45 Bouchard, Legons sur les Autointoxications dans les Maladies, Paris, 1887 ;
and Comptes rendus, cvi. 1582, 1888.
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466 Tanret, Bouchardat, and Cardier, see Huppert, l.c., p. 220.
467 Gautier, Maly’s Jahresbericht, xvi. 523 (ref.), 1887.
468 VY. Udrdnsky and Baumann, see Chap. v. (164).
469 Kerry and Kobler, Wiener klin. Wochenschr., iv. 525, 1891. — Griffiths,
Fortschritte der Medicin, x. 112 (ref.), 1872.
40 Y. Jaksch, Wiener klin. Wochenschr., iii. 1011, 1890.
Bruschettini, Riforma med., April 11, 1892.
V. Jaksch, Zeitschr. f. Heilkunde, xi. 440, 1890.
43 Brieger and Frénkel, Berliner klin. Wochenschr., No. 11 (sep. pub.), 1890.—
Brieger, Zeitschy. f. klin. Med., Supp. to vol. xvii. 253, 1890.
44 V. Briicke, Sitzungsber. der kais. Akademie, Vienna, xliii. 618, 18Sr.
4 Sahli, Pfliiger’s Archiv, xxxvi. 209, 1885.—Jco, ibid., xxxvii. 223, 1885.—
Gehrig, ibid., xxxviii, 38, 1885.—Stadelmann, Zeitschr. fiir Biologie, xxiv. 226,
1887 ; xxv. 208, 1888.—Schnapauff, Maly’s Jahresbericht, xix. 199 (ref.), 1890.—
Patella, Schmidt’s Jahrbiicher, ccxvii. 117 (ref.), 1888.
46 Griitzner, Miinchener medic. Wochenschr., xxiv. 946, 1887.
47 Teo, Verhanal. d. Congresses f. in. Med., vii. 364, 1888.
478 Mya and Belfanti, Centralbl. fiir klin. Medicin, vii. 729, 1886.
479 Hovoltschiner, Virchow’s Archiv, civ. 42, 1886.— Rosenderg, Dissertation,
Tiibingen, 1890.
480 Breusing, ibid., cvii. 186, 1887.
481 Teo, see (477).
482 Hovoltschiner, see (479).
43° Bous, Zeitschr. fiir klin. Medicin, xiv. 264, 1888.—Helwes, Pfliiger’s Archiv,
xiii, 384, 1888.
484 Musculus, Pfliiger’s Archiv, xii. 214, 1875.—Miquel, Berichte d. deutschen
chem. Gesellschaft, xxiii. 702 (ref.), 1890.
45 Teube, Virchow’s Archiv, c. 540, 1885.
486 Compare Benderky, Virchow’s Archiv, cxxi. 554, 1890.
487 Redtenbacher, Wien. med. Zeitschr., 373, 1850. See L. Thomas, Neubauer, and
Vogel (2), 549, 1885.—WHeller, Heller’s Archiv, i. '23, 1844.—F. Réhmann, Zeitschr.
fiir klin. Med,, i. 513, 1886.
#8 Gluzinski, Berl. klin, Wochenschrift, xxiv. 983, 1887 ; also G@. Sticker, ibid.,
p. 768.
#9 HF, Salkowski, Zeitschr. fiir physiol. Chemie, v. 285, 1882.
499 Volhard, Annalen der Chemie, exc. 24, 1877.—See Leube and Salkowski, l.c.,
p- 168.
491 Bouylants, Maly’s Jahresbericht, xviii. 134 (ref.), 1890.
42 See £. Salkowski, Virchow’s Archiv, lviii. 472, 1873; Pfliiger’s Archiv, xxxix.
201, 1887; Berliner klin. Wochenschr., No. 36, 25, 1888. ‘
493 Hefiter, Archiv fiir die ges. Physiologie, xxxviii. 476, 1886.
494 Zennmalm, Lakare forenings Forhandlingen, xxv. No. 34, 1890.
495 J, Teissier, Lyon médicale, xix. 307, 1875; Maly’s Jahresber, v. 311 (ref.),
1876.
496 Stokvis, Centralbl. fiir d. medic. Wissensch., xiii. $01, 1875; see also Z. A.
Ewald, Berliner klin. Wochenschr., xx. 484, 502, 1883 ; Ziilzer, Virchow’s Archiv,
Ixvi. 223, 1876; Luiyi Vanni and Lnrico Pons, Maly’s Jahresber.,"xvii. 446 (ref.)
1888 ; Mosse and Banal, Centralbl. f. klin. Med., xi. 303 (ref.), 1890.
497 V, Jaksch, Fortschrift zu Henoch, p. 11.
498 Lennmalm in 1.c. (494) gives full references to the literature.
499 See Peycr, Volkmann’s klinische Vortrage, No. 336, 1880.
500 Neubauer, Archiv fiir wissenschaftl. Heilk., iv. 288, 1859, v. 319, 1860; and
Huppert, 1.c., p. 450.
501 See Huppert, l.c., p. 520.
471
472
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432 BIBLIOGRAPHY.
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503 Schinbein, Journal fiir prakt Chemie, xcii. 150, 1864.
04 Rihmann, Zeitschr. fiir physiol. Chemie, iv. 248, 1880.
505 Striimpell, Archiv fiir Heilk., xvii. 390, 1876.
506 Salkowski, 1.c., p. 393.-—Presch, Virchow’s Archiv, cxix. 148, 1890.—See also
Virchow’s Archiv, cxxv. 102, 1891.
507 Pfeiffer, Verhandl. d. Congresses f. in. Med., ix. 408, 1890.
508 Sertoli, Gazett. med. ital. lomb., ii. Serie vi. 197, 1869.—Munk, Virchow’s
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509 Betz, Memorabilien, xxvi., 1874; see LZ. Thomas, Neubauer, and Vogel, l.c.,
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510 Fr, Miller, Berliner klin. Wochenscbhr., xxiv. 405 and 436, 1887.— Rosenheim,
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‘ll Emil Fischer, Ber. der deutschen chem. Gesellsch., xvi. 2234, 1883.
‘2 Schénbein, Journal fiir prakt. Chemie, xcii. 168, 1860.
‘3 See Huppert, Neubauer, and Vogel, l.c., p. 25.—Leube and Salkowski, 1.c.,
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4 See Wurster and Schmidt, Centralbl. fiir Physiol., i. 421, 1887.—Miiller, Ber-
liner klin. Wochenschr., xxvi. 889, 1889.
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16 1). G. Goldschmidt, Miinchener medic. Wochenschr., xxxiii. 35, 1886.
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519 Khrlich, Charité-Annalen, xi. 139, 1886.
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> V. Jaksch, Prager med. Wochenschr., xvi. 94, 1891.
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524 Glaser, ibid., xvii. 1193, 1891.
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57 Fischl, Zeitschr. fiir Heilkunde, vii. 279, 1886.
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*29 Compare also Arogius, Maly’s Jahresbericht, xx. 469 (ref.), 1891.
530 Gwyon, Wiener med. Presse, Xxx. II, 55, 95, 1889.
531 Boekhart, Monatshefte fiir prakt. Dermatologie, No. 4, 134, 1886.
582 Neisser, Centralbl. fiir die med. Wissensch., xvii. 497, 1879.—Bumm, Der
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533 V7, Zeissl, Wiener Klinik., Pts. xi. and xii. Wien, 1886.—Hartdegen, Centralbl.
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534 Wertheim, Zur Lehre von der Gonorrhoe, Vortrag gehalten in Bonn,
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CHAPTER VII.—THE URINE. 433.
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588 C. Schiitz, Miinchener med. Wochenschr., xxxvi. 235, 1889.
87 See also Finger, Die Blennorrhoe der Sexualorgane, p. 14. Wien-Leipzig,
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588 Fiirbringer, Archiv fiir klin. Med., xxxiii. 79, 1881.
5389 Schultzen and Riess, Charité-Annalen, xv. 1869.
540 Frerichs, Leberkrankheiten, i. 216, 1861.
54 Schultzen and Riess, Chemisches Centralbl., xiv. (2), 681, 1869.—Rohmann,.
Berliner klin. Wochenschr., xxv. Nos. 43 and 44, 1888.
52 V7. Jaksch, Zeitschr, fiir physiol, Chemie, x. 536, 1886.
* Kraus and Ludwig, see (234).
°4 Compare Fawitzky, Deutsches Archiv f. klin. Med., xlv. 429, 1889.
54° Stokvis, Verhandl. des Congresses fiir innere Med., v. 125, 1886.
546 R. v. Engel, Prager med. Wochenschr., xvi. 323, leon
547 Minkowski, Archiv fiir exper. Pathol. und Pharmak., xviii. 35 and 147,
1884.—Kiilz, Zeitschr. f. Biologie, xx. 165, 1884; and Archiv f, exper. Pathol, und
Pharmak., xviii. 291, 1884.
58 V. Jaksch, Zeitschr. fiir klin, Med., xi. 307, 1886.
549 Kiilz, Zeitschr. fiir Biologie, xxiii, 329, 1886.
550 Leo, Deutsche med. Wochenschr., xii. 869, 1887.
551 Kiilz, Vernhandl. des Congresses f. in, Med., x. 345, 1891.
52 Hunter, Lancet, vol. ii., 1888, p. 654.
5538 Halliburton, l.c., p. 174.
554 Flcischer and Penzoldt, Deutsches Archiv fiir klin. Med., xxvi. 368, 1880.—
Jacubasch, Virchow’s Archiv, xliii, 196, 212, 1868.
555 Prus, see (108).
556 Salkowski, ibid., lii. 58, 1871.—Nencki and Sieber, Journal f. prakt Chemie,
cxxxiv. 241, 1882; compare also Bohlund and Schwarz, Pfliiger’s Archiv, xlvii.,
Pts. ix. and x., 1890.
557 Miiller, see (223).—Obermayer, see (224).
558 VY, Jaksch, Zeitschr. f, physiol. Chemie, xvi. 243, 1892.
559 Colasanti and Moscatelli, Maly’s Jahresber., xvii. 212 (ref.), 1888—Moscatelli,
Archiv f. experiment. Pathol., xxvii. 158, 1891.
560 Heuss, ibid., xxvi. 147, 1890.
561 Keller, Archiv fiir Gyniikologie, xxvi. 107, 1885.
562 Piirbringer, Berliner klin. Wochenschr., xv. 332, 1873.
563 Tudwig, Wiener med. Jahrbiicher, 143, 1877, and 493, 1880.
564 Schneider, see Chap. v. (151).
565 Wolf and Nega, Deutsche med. Wochenschr., xii. 15, 16, 1886; see also F,
Welander, Ann. de Dermat. et de Syphil.; vii. 7-8, 1886 ; Schmidt’s Jahrb., ccxii.
270 (ref.), 1886.
566 Alt, Deutsche med. Wochenschr., xii. 732, 1886.
587 Winternitz, Archiv f. experiment. Pathol., xxv. 225, 1889.
568 Almén, Maly’s Jahresber. fiir Thierchemie, xvi. 221 (ref.), 1887.—See also-
Brugnatelli, ibid., xix. 217 (ref.), 1890.
569 #. Schultz, see (401).
570 Donath, Archiv fiir die gesammte Physiologie, xxxviii. 528, 1886.
57l De Ruitter and Donders, see v. Beck, Ziemssen’s Handbuch, lxxv. 368, 1876,
' 572-4, Paltauf, Wiener klin. Wochenschr., i. 113, 1888.
573 Glaser, see (524).
574 Tieben, Annal. der Chemie und Pharmacie, vii. (sup. vol.), 236, 1870.
575 Kast and Mester, Zeitschr. f. klin. Med., xviii. 469, 1891.
25
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434 BIBLIOGRAPHY.
76 Compare C. Thiem and C. Fischer, Maly’s Jahresbericht, xx. 58 (ref.), 1891.
77 Maréchal, Zeitschr. fiir analyt. Chemie, viii. 99 (ref.), 1869; see also 0. Neu-
bauer, ibid., vii..394, 1868.
578 Baumann and Preusse, see (9) and (364).
579 (. A, Ewald, Berliner klin. Wochenschr., xii. 3, 1875.— V. Mering, Centralbl,
fiir d. med. Wissensch., xiii. 945, 1875.
380 Grandhomme, Vierteljabrsschr. fiir gerichtl. Med., xxxii. 1880 ; see Lewin’s
Toxikologie. :
381 Fr, Miller, Deutsche med. Wochenschr., xii. 27, 1887.
582 See v. Jaksch, Prager med. Wochenschr., vii. 161, 1882; and Zeitschr. f.
klin. Med., xi. 20, 1886.
83 FE. Harnack, Berliner klin. Wochenschr., xxii. 98, 1885.
58 Compare Quaedvlieg, Maly’s Jahresbericht, xvii. 218 (ref.), 1888.
°85 Compare Chopin, Maly’s Jahresbericht, xix. 192 (ref.), 1890.
386 Kerner, Pfliiger’s Archiv, ii. 230, 1869.
87 V. Mering, Zeitschr. fiir klin. Med., vii. 148, 1884.
588 -V, Jaksch, Zeitschr. fiir klin. Med., viii. 551, 1884.
89 Fr, Miiller, see (581).
° Yvon, Journal de Pharmac. et de Chimie, No. 1, 1887; Therapeutische
Monatshefte, i. 80 (ref.), 1887.
*l Mérner, Zeitschr. fiir physiol. Chemie, xiii, 12, 1889; cf. Jaffé and Hilbert,
ibid., xii. 295, 1888.
2 Miiller, Therapeutische Monatshefte, ii. 355, 1888.
°8 Ubaldi, Centralbl. f. klin. Med., xi. 329 (ref.), 1891.
°%4 Munk, Virchow’s Archiv, xxii. 136, 1879.
G. Hoppe-Seyler, Berl. medic. Wochenschr., xxiii. 436, 1886.
Penzoldt, Archiv fiir experim. Pathol. und Pharmakol., xxi. 34, 1886.
Edlefsen, Congress fiir innere Med., vii. 435, 1888.
595
596
597
CHAPTER VIII.
EXUDATIONS, ETC.
1 Boettcher, Virchow’s Archiv, xxxix. 512, 1867.
2 Bizzozero, l.c., p. 108.
* Klemperer, Zeitschr. fiir klin. Med., x. 158, 1886; see further Baumgarten’s
Jahresber., i. 23, 1886 ; ii. 13, 1887 ; iii. 11, 1888.—A. Zuckermann, Centralbl. fiir
‘ Bacteriol. und Parasitenk., i. 497, 1887.
+ Grawitz and W. de Bary, Virchow’s Archiv, cviii. 67, 1887.—Scheuerlen, Archiv
fiir klin. Chirurgie, xxxvi. 925, 1888.—Kreibom and Rosenbach, ibid., xxxvii. 737,
1888.—Grawitz, Virchow’s Archiv, cx. 1, 1887.
° Ogston, Archiv fiir klin. Chirurgie, xxv. 588, 1880.—Rosenbach, Ueber die
Wundinfectionskrankh. des Menschen. Wiesbaden, 1884.
5 Passet, Fortschr. der Med., iii. 33, 68, 1885; and Untersuchungen iiber die
Aetiologie der eiterigen Phlegmone des Menschen. Berlin, 1885.
7 Brieger, Charité-Annalen, xiii, 198, 1888.—A. Fréinkel, ibid., p. 147.
* Levy, Archiv f. experiment. Pathol. u, Therapie, xxvii. 379, 1890; xxix.
135, 18901.
* Bujwid, Centralbl. f. Bacteriol. und Parasitenk., iv. 577, 1888.
0 Tnicke, Archiv fiir klin. Chirurgie, iii. 135, 1862.—Girard, Chirurg. Centralbl.,
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CHAPTER VIII.—EXUDATIONS, ETC. 435
li. 50, 1875.—Lrnst, Zeitschr. fiir Hygiene, ii. 369, 1887.—Ledderhose, Centralbl, fiir
Bacteriol. u. Parasitenk., iii. 581 (ref.), 1888.
1 Habermann, Prager med. Wochenschr., x. 50, 1885.—B. Meyer, Centralbl. f,
klin. Med., xi. 72, 1891.
12 Metschnikoff, Virchow’s Archiv, xcvi. 177, 1884.
13 Lustgarten, Med. Jahrbiicher (Vienna), 89 and 193, 1885.
4 Alvarez and Tavel, Archives de Physiologie norm. et pathol., vi. 303, 1885.
Kamen, Internationale klinische Rundschau, iii. 66, 114, 1889.
De Giacomi, Baumgarten’s Jahresber., i. 96 (ref.), 1886.—Doutrelepont and
Schiitz, Deutsche med. Wochenschr., xi. 320, 812, 1885.—Markuse, Vierteljahrsschr.
fiir Dermatol. und Syphilis, xv. 343, 1888.—Bawmgarten, Jahresber., ii. 263, 1887 ;
lil. 75, 232, 1888 ; iv. 223, 1889; v. 237, 1890; vi. 238, 1891.—Bender, Centralbl.
fiir Bacteriol. und Parasitenk., i. 327, 357, 1887.
7 Bollinger, Centralbl. fur die med. Wissensch., xv. 481, 1877.
18 Ponfick, Die Actinomycose. Berlin, 1882.
19 J. Israel, Virchow’s Archiv, lxxiv. 15, 1878; lxxviii. 421, 1879.
*” Roser, Deutsche med. Wochenschr, xii. 369, 1886. See also Bostrém, Verhandl.
des Congresses fur interne Med. in Wiesbaden, iv. 94, 1885.—Zemann, Wiener
medic. Jahrb., 477, 1883.—J. Israel, Klin. Beitrige zur Diagnostik und Casuistik
der Actinomycose. Berlin, 1885.—0. Zsracl, Virchow’s Archiv, xcv. 140, 1884;
and ibid., xevi. 175, 1884.— Virchow, ibid., xev. 534, 1884.—R. Paltauf, Sitzungsber.
ider k.k. Gesellsch. der Aerzte in Vienna, Jan, 29, 1886.—Bawmgarten, Jahresber.,
1. 137, 1886; ii. 311, 1887; iii. 309, 1888; iv. 288, 1889; v. 395, 1890.—Fliigge, l.c.,
p. 116.—C. Frankel, Grundriss der Bacterienkunde, 361. Berlin, 1887.—Partsch
yv. Volkmann's Sammlung klin. Vortriige, Nos. 306-307, 1888.
“1 Trans. Path. Soc., 1885 ; Trans. Med. Chir. Soc., 1886 and 1889.
~ Lindt, Centralbl. fur klin, Med., 48.
*3 Lancet, May 17, 1890.
Orlow, Deutsch. med. Wochenschr., 16, 1890.
* Anderson, Trans. Med. Chir. Soc., Nov. 10, 1891.
*6 Bostrim, Verhandl. des Congresses fiir interne Med. in Wiesbaden, iv. 94, 1885.
—R., Paltauf, Sitzungsber. der k.k. Gesellsch. der Aerzte in Vienna, Jan. 29, 1886.
7 Crookshank, Brit. Med. Journ., Nov. 14, 1891.
3 Dr. W. Hill; ibid.
* Weigert, Virchow’s Archiv, 1xxxiv. 285, 1881.
30 Wedl, ibid., lxxiv. 142, 1878.
3 Baranski, Deutsche med. Wochenschr., xiii. 1065, 1887.
Bujwid, Centralbl. f. Bacteriol. u. Parasitenkunde, vi. 630, 1889.
Buchner, ibid., iv. 149, 1888.
Lifler, Arbeiten aus dem kaiser]. Gesundheitsamte, i. 171, 1886.
Kranzfeld, Centralbl. fur Bacteriol. und Parasitenk., i. 273, 1887.
Raskin, Petersburger med. Wochenschr., xii. 357, 1887.
Baumgarten, Centralb]. fur Bacteriol. und Parasitenk., ili, 397, 1888. See
further, Bawmgarten, Jahresber., ii, 181, 1887; iii. 156, 1888; iv. 154, 1889; v
226, 1890.
38 See Baumgarten’s Jahresber., ii. 118, 1887 ; and iii. 100, 1888.
39 4, Hansen, Virchow’s Archiv, lxxix. 31, 1880, and xc. 542, 1882.—WNeisser,
ibid., Ixxxiv. 514, 1881.
40 Of, Wesencr, Centralbl. fiir Bacteriol. u. Parasitenk., i. 450, 1887 ; ii. 131, 1887;
and Baumgarten, ibid., i. 573, 1887, and ii. 291, 1887.— Baumgarten’ edabresberiy ht;
ii, 243, 1887; iii. 217, "1888 ; iv. 167, 216, 1889; v. 240, 1890.
41 Melcher and Ortmann, Berliner klin. Wochenschr., xxii. 193, 1885.
42 Bordoni- Uffreduze, Zeitschr. fur Hygiene, iii. 1079, 1887.
48 Manson, Patrick, Jour. Lepr. Investig. Com., i. 40. c Bsmt}
15
16
4
32
33
34
35
36
37
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436 BIBLIOGRAPHY.
44 Campana, Riforma med., xiv. 1891.
4 Kanthack and Barclay, Brit. Med. Journ., 1891 ; Virchow’s Archiv, cxxv. 398,
1801, :
4% Beavanm Rake and Buckmaster, Indian Lepr. Com. Report.
47 Stallaro, Occid. Med. Times, 1890.
4% Byron, New York Dermatol. Soc., 1892.
49 Cf, Baumgarten’s Jahresber., ii. 270, 1887; iii. 236, 1888; iv. 230, 1889; v.
201, 1890.
50 Kitasato, Zeitschr. f. Hygiene, vii. 225, 1889.—Baumgarten’s Jahresbericht,.
iv. 230, 1889; Vv. 201, 1890.
51 R. Pfeiffer, Deutsche med. Wochenschr., xviii. 28, 1892.
52 Kitasato, ibid., xviii. 28, 1892.
53 Canon, ibid., xix. 28, 48, 1892.
54 R. Paltauf, Centralbl. f. Bacteriol., xi. 93, 1892. Compare Baumgarten’s
Jahresbericht, vi. 82, 1891.
55 Eppinger, Wiener klin. Wochenschr., iii. 321, 1890.
56 Kiinstler and Pitres, Compt. rend. Soc. Biolog., 523, 1884. See Leuckart, l.c.,
p. 964. .
57 Titten, Verhandlungen des Congresses fur interne Medicin, v. 417, 1886.
Nasse, Deutsche med. Wochenschr., xvii. 881, 1891.
See M. Leo, Heller’s Archiv fur Chemie und Mikroskopie, i. 236, 1848.
Babesiu, see Grassi (61).
Grassi, Centralbl. fur Bacteriol. und Parasitenk., i. 617, 1887.
Sarcani, Wiener med. Presse, xix. 222, 1888.
Leyden, Deutsche med. Wochenschr., xv. 46, 1889.
Hofmeister, Zeitschr. fur physiol. Chemie, iv. 253, 1880.
Miescher, Hoppe-Seyler, Med.-chem. Untersuchungen, iv, 441, 1871.—Naunyn,
Reichert’s and Du Bois-Reymond’s Archiv fur Anat. und Physiol., 166, 1865.
6 Guttmann, Deutsche med. Wochenschr., xiii. 1097, 1887.
8 VY. Jaksch, Zeitschr. f. Heilkunde, xi. 440, 1890.
8 Qwincke, Deutsches Archiv fur klin. Med., xxx. 569, 580, 1882.
9 Bizzozero, l.c., p. 94.
” Fichhorst, Zeitschr. fur klinische Medicin, iii. 537, 1881.—V. Jaksch, ibid.,
xi. 20, 1886; and (67).
71 A. Reuss, Deutsches Archiv f. klin. Med., xxiv. 601, 1879, and xxviii. 317, 1881.
? F, A, Hoffmann, Virchow’s Archiv, lxxviii. 250, 1878.
73 Boulengier, Schmidt’s Jahrbuch, ccxxvi. 28 (1890).
™ Hasebrock, Zeitschr. f. physiol. Chemie, xii. 289, 1888. Compare also A.
Hirschler and Buday, Maly’s Jahresbericht, xix. .468 (ref.), 1890.
Frdnkel, Charité-Annalen, xiii. 147, 1888.—Levy, Archiv f. experiment. Pathol.
u. Pharmakol., xxvii, 369, 1890; xxix. 135, 1891; he cites Levy, and gives exhaus-
tive references.
76 Méhu, Archiv gén. de Med., i. and ii., 1872 and 1875.—A. Reuss, Deutsches
Archiv f. klin, Med., l.c., (71).—Hoffmann, ibid., xliv. 313, 1889.—Neuenkirchen,
Petersburger med. Wochenschr., xiv. 13, 1889.—Citron, Deutsches Archiv f, klin.
Med., xlvi. 129, 1890.
65
7 Mya and Viglezio, Rivista clinica, xxvii. 712, 1888.—Moritz, Inaug. Dissert.,
Leipzig, 1886.—Fichtner, Deutsches Archiv f. klin. Med., xliv. 323, 1889.
% Runeberg, ibid., xxxiv. 1, 1884, and xxxv. 266, 1884.—Ranke, Mittheilungen aus
der med. Klinik zu Wiirzburg, ii. 189, 1886.—A. Reuss, see (71).
See Hofmann, Neuenkirchen, and Citron (76).
8° Bock, Du Bois-Reymond’s Archiv fiir Anat. und Physiol., Pt. v., 1873.—
O. Rosenbach, Breslauer irztl. Zeitung, No. 5 (sep. sheet), 1882.—Hichhorst, see
(70).— V. Jaksch, see (70).—Ranson, Centralbl. f, klin, Med., xi. 339 (ref.), 1891.
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CHAPTER IX.—SECRETIONS OF GENITAL ORGANS. 437
81 See Senator, Virchow’s Archiv, cxi. 210, 1888.
& Moscatelli, Zeitschr. fiir physiol. Chemie, xiii. 202, 1889.—V. Jaksch, see (70).
8 J. Munk, Virchow’s Archiv, lxiii. 255, 1875.
84 Schatz, Archiv fiir Gyniikologie, ix. 15, 1$76.—Gusserow, ibid., ix. 478, 1876.
— Westphalen, ibid., viii. 72, 1875.
% Hammarsten, Zeitschr. fiir physiol. Chemie, vi. 194, 1882.
86 Huppert, Prager med. Wochenschr., i. 321, 1876.
8 VY. Jaksch, Zeitschr. fiir physiol. Chemie, xii. 116, 1887.
88 P. Wagner, Deutsche Zeitschr. fiir Chirurgie, xxiv. 505, 1886.
89 Karewski, Deutsche med. Wochenschr., xvi. 1035, 1069, 1890 (full references
are given).
% Hofmeister, see Gassenbaucr, Prager med. Wochenschr., xvi. 365, 377, 1891.
2 V. Jaksch, see Wolfler, Zeitschr. f. Heilkunde, ix. 126, 1888.
Boas, Deutsche med. Wochenschr., xvi. 1095, 1890.
% Wolfler, Zeitschr. f. Heilkunde, ix. 127, 1888.
% See A. v, Rosthorn, Wiener klin. Wochenschr.,, ii. 125, 1889.
CHAPTER IX.
SECRETIONS OF GENITAL ORGANS.
1 Fiirbringer, Zeitschr. f. klin. Med., iii. 310, 1881.
2 Kehrer, Beitr. z. klin. u. experiment. Gyniikologie, ii. 1879. Giessen. See
also Ultzmann, Wiener Klinik, p. 36, 1879.
3 Fiirbringer, see (1).
4 Posner, see Chap. vii. (200).
5 Cerny, Festschrift f. Henoch. p. 194. Berlin, 1890.
6 Lscherich, Fortschritte der Medicin, iii. 231, 1885.
7 Karlinski, Wien. med. Wochenschr., xxxviii. No. 28, 1888.
8 Neelsen, Cohn’s Beitrage zur Biologie der Pflanzen, iii. 187, 1880.
9 M. Kohn and H. Neumann, Archiv f. pathol. Anatomie, cxxvi. 391, 1891.
See also a forthcoming contribution from V. Jaksch’s clinic by Dr. Ernest Otl.
10 Neelsen, see (8).—Hueppe, Mittheil. aus dem kaiserl. Gesundheitsamte, ii.
309, 1884.
1 V, Jaksch, Prager med. Wochenschr., v. 83, 1880.
12 Hausmann, Deutsche med, Wochenschr, i. 206, 1877.
13 Winter, Zeitschr. fiir Geburtskunde und Gynikologie, xiv. 443, 1888.
14 Déderlein, Archiv fiir Gyniikologie, xxxi. 412, 1887.—Samschin, Deutsche
med. Wochenschr., xxi. 332, 1890.
16 Zweifel, ibid., xviii. 359, 1881.
16 Gf, F. Winckel, Lehrbuch der Geburtshilfe, p. 188. Leipzig, 1889.
7 Déderlein, Archiv fiir Gynikologie, xxxi. 412, 1887.
18 Thomen, Centralbl. f. d. med. Wissensch., xxviii. 537, 1890. See also
Artemjew, Prager med, Wochenschr., xiv. 574 (ref.), 1889.
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438 BIBLIOGRAPHY.
CHAPTER X.
BACTERIOLOGICAL RESEARCH.
1 The following list includes the most important works on Bacteriology, with
special reference to those which describe the methods of examination and the
morphology of Bacteria. .We direct attention, as a basis of study, above all, to
the already-mentioned works of.&. Koch and his school.—Crookshank, Chap. iv.
(40).—Fliigge, Chap. i. (140).—Cornil and Babes, Les Bactéries. Paris, 1885.—C.
Frankel, Grundriss der Bacterienkunde. Berlin, 1887.—4. Johne, Ueber die
Koch’schen Reinculturen und die Cholerabacillen. Leipzig, 1885.—W. Zopf, Die
Spaltpilze, 3rd edit. Berlin, 1885.—C. Friedliinder and Lberth, Mikroskopische
Technik, 4th edit., 1890.—Stebenmann, Die Fadenpilze. Wiesbaden, 1883.—A. de
Bary, Vergleichende Morphologie und Biologie der Pilze, Leipzig, 1884; and A.
de Bary, Vorlesungen iiber Bacterien, Leipzig, 1885.—H. Huber and A. Becker,
Die pathologisch-histologischen und bacteriologischen Untersuchungsmethoden.
Leipzig, 1886. — H. Mittenzweig, Die Bacterien-Aetiologie der Infectionskrank-
heiten. Berlin, 1886.—Duclauxz, Le Microbe et la Maladie. Paris, 1886.—
Gottstein, Die Verwerthung der Bacteriologie in der klinischen Diagnostik.
Berlin, 1887.—Bawmgarten, Lehrbuch der pathol. Mykologie. Brunswick, 1886
to 1888.—Léfier, Vorlesungen iiber die geschichtliche Entwicklung der Lehre
von den Bacterien. Leipzig, 1887.—Hueppe, Die Methoden der Bacterienfor-
schung, 5th edit. Wiesbaden, 1891.—Giinther, Hinfiihrung in das Studium der
Bacteriologie, 2nd edit. Leipzig, 1891.—Azel Holst, Uebersicht iiber die Bak-
teriologie fiir Aerzte und Studirende, German translation by Rayher. Basel,
1891.—Zisenbery, Bakteriologische Diagnostik. Hamburg and Leipzig, 1891.—
For exhaustive literary notices see Fliigge, Zopf, and de Bary. Woodhead and
Hare, Pathological Mycology, 1885.
2 R, Koch, Untersuchungen iiber Wundinfectionskrankheiten. Leipzig, 1878.
3 Giinther, Deutsche med. Wochenschr., xiii. 471, 1887.
4 Unna, Centralbl, fiir Bacteriol. und Parasitenk., iii. 22, 61, 93, 120, 153, 189,
218, 254, 285, 312, 345, 1888.
5 Kiihne, Zeitschr. fiir Hygiene, i. 552, 1886 ; and Kiihne, Praktische Anleitungen
zum mikroskopischen Nachweise der Bacterien. Leipzig, 1888.
6 Kithne, l.c., p. 28.
? Kiihne, |.c., p. 34.
8 Hueppe, l.c., 1st edit., p. 59.
® For other methods see Lisenberg, Bakteriologische Diagnostik, App., p. 23.
0 Léfier, Centralbl. f. Bacteriologie und Parasitenkunde, v. 209, 1889; vii. 625,
1890.—Fisenberg, l.c., p. 24.
1 Unna, Deutsche med. Wochenschr., xii. 742, 1886; and Monatshefte fiir
praktische Dermatologie, v., No. 9, 1886.
2 Pasteur, Annal. de Chim. et Phys., lviii. (3), 388, 1860.
183 C. v. Négeli, Untersuchung iiber niedere Pilze. Munich, 1882.
44 Buchner, see v. Néigeli, l.c., p. 11.
A. Schultz, Mayer’s Gihrungschemie, p. 214.
16 V, Jaksch, Zeitschr. fiir physiol. Chemie, v.398, 1881.
WV H. Hueppe, Mittheilungen aus dem kaiserlichen Gesundheitsamte, ii. 337,
1884. ‘
18 Cf. Meade-Polton, Zeitschr. fiir Hygiene, i. 104, 1886.
19 Schottelius, Centralbl. f. Bacteriol. u. Parasitenk., ii. 47, 1888.
20 Richter, Berl. klin. Wochenschr., xxiv. 600, 1837.
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*1 A. Pfeiffer, see Eisenberg, l.c.
2 Birch-Hirschfeld, Archiv fiir Hygiene, vi. 314, 1888.
23 See Neisser and Jacobi, Centralbl. fiir Bacteriol. und Parasitenk., iii. 506 and
586, 1888; further Noegerath, Fortschritte der Med., vi. 1, 1888.
4 Marpmann, Centralbl. fiir allg. Gesundheitspflege, Supplement ii. Pt. ii.,
1886.—Cahen, Zeitschr. fiir Hygiene, ii, 386, 1887.
25 Klebs, Archiv fiir experiment. Pathol. u. Pharmak., i. 31, 1873.
6 Brefeld, Methode zur Untersuchung der Pilze, med.-phys. Gesellschaft.
Wiirzburg, 1874.
7 £, Esmarch, Zeitschr, fiir Hygiene, i. 293, 1886.
*8 See H. Rohrbeck, Chemisches Centralbl., xvii. (3), 705, 1886 ; and Deutsche
med. Wochenschr., xiii. 1089, 1887.
*® R, Fischl, Fortschr, der Med., v. 663, 1887.
* Neisser, see (23).
31 Buchner, Centralbl. f. Bacteriol. u. Parasitenkunde, iv. 149, 1888.
2 Nikiforoff, Zeitschr. f. Hygiene, viii. 489, 1890.
33 Bliicher, ibid., viii. 499, 1890.—Hesse, Zeitschr. f. Hygiene, xi, 237, 1891.
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INDEX.
ABBE’S condenser, 372, 375
Abbe-Zeiss, counting cell,-9
Abscess, pulmonary, 113, 121
pus from, 348
Absorption bands, 60, 292, 293
Absorption, rate of, in stomach, 142
Accidental albuminuria, 255
Acetic acid, 139, 201, 305
—— acid in feces, 201
— acid in gastric juice, 139
— acid in sputum, 113
acid in urine, 305
— acid reaction in gastric juice, 127
—— acid tests for, 305 }
acid and ferrocyanide of potas-
sium test for albumin, 256
Acetonzmia, 77
Acetone, auto-intoxication with, 303
in blood, 77
— estimation of, 303
— in pus, 358
in urine, 303
— tests for, 303
Acetonuria, 303
Acetphenetidin, 345
Acetylparaamidophenol, 345
Acholic stools, 210
Acid, acetic, 113. 139, 201, 305
a-crotonic, 337
— ether-sulphuric, 297
— albumin, 256
— b-oxybutyric, 75
—- benzoic, 275
—— butyric, 129, 201
— capric, 202
—— caproic, 113, 202
carbolic, tests for, 161
carbolic, estimation of, 299
chrysophanic, 345
diacetic, 305
diazobenzol-sulphonic, 328
— formic, 201, 305
—— hippuric, 243
— homogentisic, 300
—— hydrochloric, 139
—- hydrocyanic, 162
—— hydroparacumaric, 300
-—— hyposulphurous, 327
— indoxyl-sulphuric, 297
— isobutyric, 202
Acid, lactic, 75, 139, 337
metaphosphoric, 257
— metatungstic, 160
nitric, 151
oleic, 202
—— oxalic, 151, 307
— oxyamygdalic, 335
—— palmitic, 202
—— paraamido-phenol-sulphuric, 342
—— parakresol-zther-sulphuric, 300
—— paroxy-phenyl-acetic, 300
paroxy-phenyl-propionic, 300
—— phenol-ether-sulphuric, 300
— phosphates, 323
—— phosphomolybdic, 160 _
— phosphotungstic, 160, 266
— phosphoric, 324
propionic, 202
salicylic, 275, 343
salicyl-sulphonic, 258
sarcolactic, 75, 338
skatoxyl-sulphuric, 298
stearic, 202
succinic, 362
sulphanilic, 328
sulphuric, 150, 297, 323
uric, 70, 240
uroleucic, 300
valerianic, 202
Acid-forming fungi, 384
Acidity of gastric juice, 127 ; action on
fungi, 389
— of urine, 217
Acids in feces, 201
organic, in blood, 74
—— organic, in feces, 201
organic, in gastric juice, 139
——— organic, in sputum, 113
— organic, in urine, 305, 337
— poisoning with, 150, 338
— volatile fatty, 74, 112, 139, 203,
305, 358
aera
Actinomyces, 351
| —— in buccal secretion, 86
| ——in pus, 351
| ——in sputum, 109
44z
Digitized by Microsoft®
442
Actinomyces in urine, 237
Acute bronchitis, 114
—— enteritis, 207
—— gastritis, 146
—— nephritis, 329
—— yellow atrophy, 335
Addison’s disease, urine in, 291, 293
Aither-sulphuric acids, 297
— tests for, 299
—— estimation of, 297
Aithylinimin, 366
Agar-agar, cultivations in, 354
—— nutrient, 383
Ague, parasites of, 49
Albumin, estimation of, in urine, 259
in cysts, 363
in feces, 199
in gastric juice, 144
in pus, 358
in sputum, 113
—— in transudations, 361
—— in urine, 252
—— tests for, 255; Fiirbringer’s, 258 ;
Hindenlang’s, 257; Heller's, 257;
Heynsius’, 257; Johnson's, 258
Albuminate, 256
Albuminimeter, 263
Albuminous putrefaction, 297
Albuminuria, 251
-— accidental, 255
— Bright on, 252
—— causation of, 253
— cyclical, 252
—— experimental, 252
—— febrile, 254
—— hematogenic, 254
in boys, 252
—— intermittent, 252, 25
-— of anemia, 254
—— paroxysmal, 252
—- pathological, 253
—— physiological, 251
—— remittent, 252
—— renal, 253
—— Stewart on, 251
Albumose in semen, 367
Albumosuria, 268
Alcohol, detection of, 161
Alcoholic poisoning, 161, 341
Alimentary canal, diseases of, feeces in,
207
— canal, diseases of, urine in, 335
—— canal, diseases of, vomit in, 146
Alkalies, poisoning with, 152, 338
Alkaline stools, 164
urine, 247
Alkalinity ‘of the blood, 2, 4
of the blood, changes of, in dis-
ease, 4
— of the blood, estimation of, 2
— of the blood, Hayeraft and William-
son’s test for, 3)
— of the plood, Kraus’ test for, 5
—— of the blood, Liebreich’s test for, 2
LIT
ue
INDEX.
Alkalinity of the blood, Zuntz’ test for, 2
— of the urine, 216
Alkaloids, animal, 158, 261
— poisoning with, 156, 340
—- Stas-Otto tests for, 156
Alkapton, 301
Alkaptonuria, 301
Allantoin, 361
Almén’s fluid, 277
—— test, 271, 339
Alt’s test for mercury, 339
Alum-carmine, 89
Alveolar epithelium, 94
Amido-acids, 311
Ammonia, urate of, in sediment, 249 ©
—— in gastric juice, 141
in vomit, 152
Ammoniacal fermentation, 217, 233
—— silver solution, 30S
Ammoniemia, 77
Ammonia-salts, in gastiic juice, 141
—— estimation of, 141
—— in urine, 249
—— in vomit, 152
—— poisoning with, 152
Ammonio-magnesic phosphate, see
Triple phosphate
Ameba coli, 180
Ameebee in urine, 237
Amorphous hemateidin, 61, 241
sediment of urine, 239
Amphoteric urine, 217
Amyloid concretions, 366
—— kidney, 331
Anemia, albuminuria in, 254
blood in, 38
—-— infantum pseudoleukemica, 33
—— pernicious, blood in, 38
—-— secondary, 39
-— urine in, 337
a-naphthol, 280
Anchylostoma duodenale, 190
Anchylostomiasis, 191
Angina, croupous, 88
— diphtheritic, 88
—— follicularis, 89
Ludovici, 351
Anguillula intestinalis, 194
—— stercoralis, 194
Aniline, 104, 162
brown, 40
—— dyes, 48, 378
—— oil, 104
—— poisoning with, 162, 342
—— poisoning, urine in, 342
—— tests for, 162
——- tests for hydrochloric acid, 129
—— -water gentian-violet, 104
Animal alkaloids, 158, 341
alkaloids, tests for, 159, 341
—— gun, 287
—— parasites of blood, 49
Annelides, 188
Anthelmintics, 190
Digitized by Microsoft®
INDEX.
Anthomyia canicularis, 195
Anthomyiz in feces, 195
Anthracosis of lung, 123
Anthrax, bacillus of, 42, 354
—— bacillus of, detection of, 42, 354
— bacillus of, in blood, 42
— bacillus of, in pus, 354
Antifebrin in urine, 344
test for, 345
Antipyrin in urine, 215, 344
Antisepsis of urine, 218
Anuria, 212
Apochromatic lens, 377
Areolar tissue in stools, 167
tissue in vomit, 145
Aromatic oxy-acids, 300
Arsenic, detection of, 154
poisoning with, 154, 340
Arterio-sclerosis, 341
Arthritis, 71, 311
Ascarides in feces, 188
-—— in nose, 91
in sputum, 110
in urine, 238
Ascaris lumbricoides, 188
—— mystax, 189
Ascites, chylous, 360
Asiatic cholera, bacillus of, 173
—— —— feces in, 209
Aspergillus fumigatus, 102
Asphyxia, 63
Asthma, 115
bronchial, 98
Atrophic cirrhosis, urine in, 335
Atrophy, gastric, 147
Atropin, detection of, 157
in urine, 341
poisoning with, 157, 341
Aurantia, 32
Auto-intoxication with acetone, 303
—— with diacetic aeid, 305
— with sulphuretted hydrogen, 327
Automatic pipette, 3
Autotoxicosis, 319
Azoospermia, 366
Azoturia, 311
BACILLI in blood, 39
in buccal secretion, 80
—— in exudations, 348
—— in feces, 170
in gastric juice and vomit, 145
—— in milk, 368
—— in nasal secretion, 91
— in sputum, 103
—— in urine, 233
—— in vagina, 369
Bacilluria, see Bacteriuria
Bacillus, crassus sputigenus, 81
cyanogenus, 369
— Lustgarten’s, 349
— of anthrax, 42, 354
— of Asiatic cholera, 173
— of cholera infantum, 165
443
Bacillus of cholera nostras, 177
of decaying teeth, 81
of diphtheria, 88
of Finkler and Prior, 177
of glanders, 46, 353
of hay, 179
of hen-cholera, 378
of hydrophobia, 48
of influenza, 356
of lactic-acid, 206
of leprosy, 355
of septicemia of the mouse, 171,
356
of smegma, 349
of syphilis, 349
of tetanus, 48, 355
of tubercle, 45, 103, 179, 349
of typhoid, 46, 81, 177
of whooping-cough, 109
pyocyanogenus, 349
salivarius septicus, 81
septicus sputigenus, 81
subtilis, 171
Bacteria, see Fission-fungi
Bacterial colonies or casts, 227
—— decomposition of urine, 234
Bacteriological methods, 371
Bacteriology, 372
Bacterium termo, 171
Bacteriuria, idiopathic, 235
Balantidium coli, 171, 182
Bamberger’s hematogenic albuminuria,
254
Barium salts, 134
Basic aniline dyes, 40, 378
—— phosphate of magnesia, 242
— phosphatic earths, 249
Basidiomycetes, 352
Basophil granules, 33
Baumann and Udransky’s method, 160
Bence Jones on alkaline urine, 217
Benzoic acid in urine, 273
zethers, 280
Benzo-purpurin, 131
test for HCl, 131
test-papers, 132
Eee de test for sugar, 74, 76,
280
—— for diamines, 318
for carbo-hydrates, 280
Beri-beri, 192
Berlin-blue reaction, 302
Betain, 315
Betol, 343
Bettelheim’s granules, 36
Bidder and Schmidt's method for esti-
mating HCl, 133
Biedert’s boiling method, 107
Bilberries,amylic alcoholextract of, 132
Bile acids in blood, 75
— acids in feces, 200
—— acids in pus, 358
-—— acids in urine, 287
—— acids, tests for, 75, 288
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Bile pigment in blood, 76
—— pigment in cysts, 363
—— pigment in feces, 164, 204
— in pus, 358
— in semen, 367
pigment in urine, 288
— pigment, tests for, 288
Bilifuscin, 288
Biliprasin, 288
Bilirubin, 62, 76, 118, 241, 288, 363, 367
formula of, 62
Biliverdin in blood, 77
in feces, 165
—— in meconium, 206
— in sputum, 118
in urine, 288
-—— in vomit, 150
Biology of micro-organisms, 390
Bismarck-brown, 105
Biuret, 69
Biuret-test, 69, 257
Bizzozero’s chromo-cytometer, 14
Bladder, calculus of, 333
Bladder, catarrh of, 332
—-— epithelium of, 221
—— foreign bodies in, 250
tumours of, 233, 333
Blennorrhea, 220
Blood, the, 1
acetone in, 77
—— alkalinity of, 2, 5
—— animal parasites of, 49
—— bile substances in, 75
—- cellulose in, 74
— chemical changes in, 59
— colour of, 1
— colouring matter of, 59
-— crystals in, 30
estimation of sugar in, 72
—— fatty acids in, 74
—— fibrin of, 67
——. formed elements of, 6
— fungi of, 39
——— glycogen in, 74
—— hemoglobin of, 320
in anemia, 38
in carcinoma, 70
in chlorosis, 37
in dyspnea, 63
in feces, 168, 208
in fever, 78
in melanzmia, 35
—— in poisoning, 63
—— in pus, 348
—- in sputum, 122
—— in urine, 219
—— in vomit, 148
—— lactic acid i in, 74
——- organic acids of, 74
—— parasites of, 39
—- peptone of, 67
proteids of, 67
— protozoa in, 49
—— reaction of, 2
aan
INDEX.
Blood, sarcolactic acid in, 74
—— specific gravity of, 5
—— urea in, 68
uric acid in, 70
Blood-colouring matter, relation of, to
bile-pigment, 61
Blood-cells, see Blood-corpuscles and
Leucocytes
Blood-corpuscles, red, apparatus for
counting, 8
— changes in, 6
— counting of, 9
—— in buccal secretion, 79
—— in cysts, 362
—— in feces, 168
in pus, 348
in sputum, 94, 122
—— in transudations. 361
in urine, 219, 270
tests for, 271
Blood-pigment, 59
—— detection of changes in, 60
in faeces, 168, 205
—— in gastric juice, 148
Blood-platelets, 6
Blood-serum, lutein in, 59
— spectrum of, 59
—— sterilised, 380
Blue milk, 369
Bodo urinarius, 237
Bothriocephalus cordatus, 186
latus, 186
liguloides, 186
Bittger’s test, 277
B-oxy-butyric acid, 75, 336
tests for, 337
Brandberg’s method, 260
Braun's method for estimation of HCl,
136
maa in the nutrition of fungi, 383
Brieger’s method for separation of
ptomaines, 158
Bright on albuminuria, 252
Brilliant-green tests for HCl, 130
Bromide of potassium, detection of, in
urine, 243
of potassium, detection of, in
saliva, 83
Bromine salts in urine, 343
Bronchial asthma, 98
catarrh, 114
Bronchiectasis, 115
— sputum of, 112
Bronchitis, acute, 114
—— chronic, 115
—— plastic, 115
putrid, 115
Broth, nutrient, 333
Browning’s spectroscope, 59, 66
Buccal secretion, 79
secretion, chemical constitution
of, 81
—— secretion, ferment of, 80
— secretion, fungi of, 80, 85
Digitized by Microsoft®
INDEX.
Buccal secretion in disease, 82
— secretion, nitrites of, 82
— secretion, physical characters of,
— secretion, sulphocyanide of, 83
urea in, 83
Bujwid’s staining process, 176
Bumsen’s tables, 314
Butyric acid, detection of, 201
— acid in feces, 201
— acid in gastric juice, 129
— acid in sputum, 113
acid in urine, 305.
acids
See also Fatty
CADAVERIN, 160, 318
Calcium carbonate, crystals of, 197
— phosphate in fzeces, 197
— phosphate, crystals of, 197, 242
sulphate, crystals of, 197, 247
— sulphate in feces, 197
sulphate in urine, 242, 247
Calculus, 333
Calliphora erythrocephala, 195
Calomel, 212
Canada balsam, 105
Cancer, blood in, 74
of alimentary canal, 215
— of stomach, 148
—— urine of, 215
Capric acid, 202
Caproic acid in faces, 202
acid in sputum, 113
Carbohydrates in blood, 72
Carbol-fuchsin, 106
-gelatine, 179
Carbolic acid, estimation of, 299
— acid in feces, 202
—— acid in urine, 299, 341
—— acid in vomit, 161
—— acid poisoning, 161, 341
—— acid, tests for, 161, 342
— acid in feces, 200
acid in gastric juice, 142
— acid, tests for, 200
Carbolo-chloride of iron test for lactic
acid, 139
Carbonate of lime in faces, 197
of lime in sputum, 113
— of lime in urine, 253, 326
of magnesia in sputum, 113
Carbonates of the alkaline earths, 250
in sputum, 113
— of urine, 326
test for, 326
Carbonic oxide, detection of, 63
oxide hemoglobin, 63
— oxide hemoglobin, spectrum of,
63
oxide poisoning, 63, 273, 342
Carburetted hydrogen in feces, 205
Caries of teeth, 81
Casein in feces, 168
— in milk, 368
445
Casts, cellular, 225
— chemistry of, 232
—— classification of, 224
— “detritus,” 224
— examination of, 232
— fatty, 229
— granular, 227
—— hyaline, 230
— metamorphosed, 224
— of micrococci, 226
organised, 224
staining of, 232
unorganised, 224
urinary, 224
waxy, 228
Cat, round worm of, 189
Catarrh, bronchial, 114
—— gastric, 146
—— nasal, 91
vesical, 332
Catarrhal urethritis, 334
Caustic potash, poisoning with, see
Poisoning with alkalies
— soda, poisoning with, sce Poisoning
with alkalies
Cellulose in blood, 74
Cercomonads in feces, 181
—— in pus, 357
— in sputum, 109
in urine, 237
Cercomonas intestinalis, 181
Cerebral hemorrhage, urine in, 291
Cerebro-spinal fluid, 91
meningitis, 273
Certoneura stabulans, 195
Cestodes, 182
Charcot-Leyden crystals, 30, 99, 110,
195
Cheese-maggot, 195
—-— spirillum of, 177
Chemical examination of blood, 59
—— examination of buccal secretion,
81
—— examination of cystic fluids, 363
—— examination of feces, 198
— examination of gastric juice, 143
examination of milk, 369
examination of pus, 358
examination of semen, 367
examination of sputum, 113
examination of transudations, 362
examination of urine, 255
examination of vomit, 150
Chinanisol, 344
Chloral in urine, 273
Chlorate of potash in blood, 65
—— of potash, poisoning with, 65, 152
—— of potash, spectrum of, 65
Chloride of ammonium in urine, 320
—— of barium, 134
—— of gold test, 160
—— of magnesium in sputum, 114
—— of magnesium in urine, 320
—— of platinum test, 160
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|
LTT TTI
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446
Chloride of potassium in urine, 320
— of sodium in blood, 78
— of sodium in feces, 204
—— of sodium in urine, 320
—— of zinc solution, 316
Chlorides, estimation of, 320
—— in feces, 204
—— in sputum, 114
in urine, 320
tests for, 320
‘Chloroform, poisoning with, 161, 341
— tests for, 161
Chlorophyll, 167
Chlorosis, blood changes in, 37
urine in, 217
Cholzemia, 75
Cholecyanin test, 289
Choleglobin, 62
Cholera, Asiatic, 209
—— Asiatic, bacillus of, 173
—— infantum, bacillus of, 165
—— nostras, bacillus of, 177
-red, 176
Cholesterin crystals, detection of, 111
—- crystals in feces, 203
—— crystals in pus, 357
—— crystals in sputum, III
—— crystals in urine, 249
-—— tests for, 203
Chololithiasis, 166
Choluria, 287
Chromocytometer, 14
Chromogens of urine, 214
Chromogens of urobilin, 214
Chromometer, 14
Chronic bronchitis, 115
—— enteritis, 207
—— gastritis, 146
— inflammation (non-tubercular) of
lung, 117
nephritis, 330
Chrysophanic acid, 345
Chyliform exudation, 360
Chyluria, 306
Ciliated epithelium in cysts, 363
—-~— epithelium in sputum, 93
Cladothrix, 352 g
Claret, colouring matter of, 132
Claude Bernard’s method, 73
Clostridium butyricum, 171
Coagulated albumin, 168
Coating of the tongue, 87
Coccidia in pus, 357
Coccidium perforans, 181
—— oviforme, 89
Coccus salivarius septicus, 81
Cochin-China diarrheea, 194
Coffin-lid crystals, see Triple phosphate
Colloid cysts, 362
Colour of blood, 1
— of exudations, 347
—— of feces, 164
—— of sputum, 93
—— of transudations, 361
INDEX.
Colour of urine, 214
— scale for urine, 214
—— tests for albumin, 257
Colouring matter of bile, 61, 204
—— matter of blood, 61
—— matter of faeces, 164
—— matter of urine, 214
Colostrum, 368
Comma-bacillus, 173
Compensation eye-piece, 373
Compound sulphuric acids, 297
Concretions of feeces, 166
—— of nasal secretion, 91
—— of urine, 247, 250
Condenser, Abbe’s, 372
Congo-red test for HCl, 131
— staining micro-organisms with,
384
Connective tissue in sputum, 100
tissue in stools, 167
-—— tissue in vomit, 145
Contracted kidney, 331
Copaiba balsam, 346
Copper, poisoning with salts of, 154,
339
Cornil’s marrow cells, 32
Corpora amylacea in sputum, IOI
Correction collars, 373
Cover-glasses, preparation of, 40, 105
Croton oil, 348
Croup, gastric, 150
Crystals, calcium carbonate, 197
—— calcium phosphate, 197, 242
— calcium sulphate, 197
— Charcot-Leyden, 30, 99, 110, 195
— cholesterin, 111, 195, 249, 357
— cystin, 243
-—— fatty, 111, 196, 357
— hippuric acid, 243
— hemin, 61 ;
—— hematoidin, 61, 110, 195, 241, 357
— hemoglobin, 38
—— in blood, 38
—— indigo, 248
—— in blood, 30
—— in feces, 195
—— in pus, 357
—— in sputum, 110
in urine, 240
— leucin and tyrosin, 112, 244
—— magnesium phosphate, 242, 249
—— margarine, 112
—— oxalate of lime, 113, 197
-—— phenyl-glucosazon, 276
—— Roussin’s, 157
—— spermatic, 367
—— sulphide of bismuth, 198
— Teichmann’s, 63
— triple phosphate, 113, 197, 242,
247, 358.
—— tyrosin, 112, 244
—— urate of ammonia, 249
—— uric acid, 240
—— xanthin, 244
Digitized by Microsoft®
INDEX.
Crystalline sediment of urine, 239
Cultivation, cylinder-, 387
by exclusion of air, 388
—— drop-, 388
in depth of nutrient substances,
387 :
on glass slides, 388
—— on surface of nutrient substances,
386
plate-, 385
Curschmamn’s spirals, 98
spirals, Zroup on, 98
Cupric oxide, reduction of, 274
Cutaneous inoculation, 389
Cyanotic induration of kidneys, 228
Cylinder-cultivations, 387
Cylindroids, 232
Cystic kidney, 363
Cystin, 243
Cystinuria, 308
Cystitis, 332
Cysts, colloid, 362
— contents of, 361
-—-- dermoid, 362
— hydatid, 362
—— of broad ligament, 363
ovarian, 362
Cytometer, 13
DAHLIA, acid solution of, 33
Dammar varnish, 41
D’ Arsonval's incubator, 387
Deneke’s spirillaum, 177
Deposit on teeth, 86
Dermatitis, urine in, 269
Dermoid cysts, 362
“Detritus ” casts, 244
Detritus in feeces, 169
Deutero-albumose, 268
Dextrin in faeces, 200
in urine, 287
Dextrose, see Grape-sugar
Diabetes, blood in, 74
—— insipidus, 337
-—— mellitus, 336
Diabetic acetonuria, 303
Diacetic acid, tests for, 305
Diaceturia, 304
Diamines in sputum, 115
in urine, 318
—— tests for, 318
Diaphragms, 372
Diastase, 205
in urine, 320
Diastatic ferment of cysts, 363, 364
—— ferment of faeces, 205
—— ferment of saliva, 82
ferment of urine, 320
Diathesis, uric acid, 308
Diazobenzol, 160
Diazobenzol-sulphonic acid, 328
Diazo reaction, Lhilich’s, 328
Dickinson on coating of tongue, 87
Differentiation of proteids in urine, 259
447
Digestion, stages of, 140
Digitalis, 212
Dilatation of stomach, 149
Dioxyquinin, 344
Diphtheria, bacillus of, 88
—— gastric, 150
Diplococci in ozzna, 91
in pneumonia, 120
—— in pus, 348
Dipteral larvee, 91, 195
Disseminated sarcoma, 265
Distoma eggs in blood, 58
eggs in urine, 237
—— hematobium, 57
— hematobium in blood, 57
— hematobium in sputum, 110
-—-— hematobium in urine, 237
—- hepaticum, 187
— lanceolatum, 187
— Rathonisi, 188
Dochmius duodenalis, 190
Double sulphate of iron and ammonia
solution, 321
Dragendorf’s test for bile-pigment, 289
Dreschfeld’s test for HCl, 133
Drop-cultivations, 388
of cholera-bacillus, 175
Drosophila melanogastra, 195
Drugs, effect of, on the stools, 164
Dry measurement, 38
Duodenal ulcer, 148
Dysentery, 208
Dyspepsia, acid in, 127
urine in, 335
Dyspneea, blood changes in, 63
EARTHY phosphates, 323
Echinococcus in sputum, 109
—— in urine, 238
— cysts in feces, 187
—— cysts in sputum, 109
— cysts in urine, 238
— hooklets from cysts, 362
—— hooklets in feces, 187
—— hooklets in gastric juice, 150
hooklets in urine, 238
Ehrlich’s granules, 31
staining method, 41
—— test for bilirubin, 290
test for typhoid urine, 328
Lhrlich-Weigert fluid, 41, 105
Eggs of helminthz in blood, 58
—-- of helminthe in feces, 192
—— of helminthe in sputum, 120
of helminth in urine, 237
Elastic fibres in feces, 163
fibres in gastric juice and vomit,
145
—— fibres in sputum, 94
Embolic lipzemia, 75
—— nephritis, 227
Emerald-green test for HC], 130
Emulsifying ferment, 144
Emphysema, urine in, 215
Digitized by Microsoft® -
448
Endocarditis, 47, 236
Enteritis, acute, 207
—— chronic, 207
—— membranacea, 165
—— mucosa, 165
Entero-colitis, monadines in, 180
Enterogenic peptonuria, 205
Entozoa in nose, 91
Eosin, 31
Eosinophil granules, 31
Epileptic urine, casts in, 231
urine, spermatozoa in, 233
Epithelium, alveolar, 95
—— ciliated, 95
—— in buccal secretion, 79
in exudations, 348
— in feces, 169
in gastric juice, 124
in nasal secretion, 91
in sputum, 95
in transudations, 361
in urine, 221
in vaginal secretion, 369
obsolete in feeces, 169
of male urethra, 222
renal, 223
vesical, 22
Eristalis arbustorum, 195
Erysipelas, streptococcus of, 47, 235
Erythro-dextrin, test for, 142
Esbach’s albuminimeter, 263
Esmarch’s cylinder-cultivations, 386
Eustrongylus gigas, 238
Ewald’s test for HCl, 129
Exogenic toxicosis, 319
Experimental albuminuria, 252
Exsiccator, 40
Exudations, 347
—— chylous, 349
—— hemorrhagic, 348
—— purulent, 347
—— putrid, 359
—— sero-purulent, 359
—— serous, 347
—— see also Pus
Eye-piece, 374
—— periscopic, 375
eee
FRCES, the, 164
— albumen in, 198
—— blood in, 168, 209
— chemistry of, 198
—— colour of, 164
colouring matters of, 204
— crystals of, 195
-—— detritus of, 169
—— fats in, 167
—- ferments in, 205
—— foreign bodies in, 167
— formed elements of, 168
—— fungi of, 170
—- hydatids in, 186
—— indiseases of the alimentary canal,
207
INDEX.
Feces, insects in, 195
microscopical characters of, 166
mucin in, 166, 198
naked-eye, characters of, 164
non-pathogenic fungi of, 169
parasites of, 169
pathogenic fungi of, 173
proteids of, 168, 198
—— ptomaines in, 205
—— quantity of, 164
— reaction of, 164
—— worms in, 182
Fat crystals, 112, 196
—— crystals in feces, 196
—— crystals in pus, 357
— crystals in sputum, 112
— crystals in vaginal secretion, 369
—- crystals in urine, 249
— crystals in vomit, 145
—— crystals, separation of, 112
Fat in blood, 75
—— in feces, 196, 203
—— in sputum, 112
— in urine, 247
Fatty acids in pus, 358
acids in urine, 305
— acids, non-volatile, of faeces, 203
——- acids of sputum, 113
— acids, tests for, 305
—— acids, volatile, of blood, 74
—— acids, volatile, of feces, 200
—— casts, 229
—— needles, sce Fat crystals
Favus of stomach, 150
Febrile acetonuria, 303
— albuminuria, 254
states, urine of, 328
urobilin, 290
Fehling’s fluid, 281
titration method, 280
Ferment, diastatic, 82, 144
emulsifying, 144
— of feces, 205
—— inverting, 144
—— milk-curdling, 126
LITT
of saliva, 82
of sputum, 114
of urine, 319
Fermentation test for sugar, 275
Ferments of feces, 205
— of gastric juice, 126
— of urine, 319
pancreatic, 144
Ferric salts in sputum, 114
Ferrocyanide solution, 325
Fibres, elastic, in feces, 167
elastic, in gastric juice and vomit,
145
—— elastic, in sputum, 97
Fibrin, estimation of, in blood, 68
—— estimation of, in exudations, 358
estimation of, in urine, 270
of blood, 68
Fibrinous coagula in sputum, 100
Digitized by Microsoft®
INDEX.
Fibrinous coagula in urine, 270
Fibrinuria, 270
Filaria inermis, 357
—— sanguinis hominis, 58, 238
Filarie in blood, 58
—— in pus, 356
—— in urine, 238
Finkler-Prior bacillus, 177
Fission-fungi of blood, 39
— of feces, 170
— of sputum, Io1
— of urine, 233
—— of vaginal secretion, 369
of vomit, 146
Fistula, secretions from, 365
Flagella, staining of, 379
Fluke, 57
Foreign bodies in faeces, 251
—— bodies in sputum, 95
bodies in urine, 251
Formic acid, detection of, 201
—— acid in blood, 74
-—— acid in feces, 201
—— acid in gastric juice, 132
—— acid in urine, 305
—— acid reaction in gastric juice, 132
Frinke’s pneumonia-coccus, 107
Fresenius and Babo’s test for lead, 152
Friedlinder’s method for staining fungi,
107
pheumonia-coccus, 108
Frohde’s reagent, 157
Fruit-sugar, 287
Fuchsin for staining micro-organisms,
40
test for HCl, 130
Fungi, in ozeena, 92
of blood, 39
—— of buccal secretion, 80
—— of faeces, 170
—— of nasal secretion, 91
—— of pus, 348
—— of serous exudation, 360
—— of sputum, Io1
—— of urine, 233
of vaginal secretion, 369
— of vomit, 146
spores of, 45, 354, 379-
Micro-organisms
Fungoid plugs, 103
Fiirbringer’s test, 258
Furfurol, 74, 76, 200, 280
test for bile acids, 200, 288
—— test for carbohydrates, 74, 280
— test for urea, 69
Fusiform degeneration, 169
See also
GABBETT’S staining method, 107
Gangrene of lung, 121
Gangrenous stools, 209
Gases in blood, 63
—— intestinal, 205
—— of urine, 328
Gastric croup, 150
449
Gastric diphtheria, 150
Gastric juice, acetic acid in, 139
—— juice, acidity of, 127
—— juice, acids of, 127
—— juice, ammonia salts in, 141
—— juice and vomit, 124
—— juice, butyric acid in, 139
—— juice, carbohydrates in, 142
juice, chemical examination of,
143
—— juice, chemistry of, 125
juice, excessive secretion of, 127
-—— juice, formed elements of, 124
juice, hyperacidity of, 127
—— juice, lactic acid in, 139
juice, method of obtaining, 124
—— juice, milk-curdling ferment of,
126
— juice, naked-eye characters of,
124
—— juice, organic acids of, 139
——- juice, pepsin of, 126
—— juice, proteids of, 140
—— juice, urea in, 141
juice, zymogen of, 127
Gastric sound, 124
ulcer, 147
Gastritis, acute, 146
atrophic, 147
—— chronic, 146
Gelatine, nutrient, 383
Genital organs, secretions of, 366
Gentian-violet, 104
aniline-water solution, 105
Giacomi’s method for staining micro-
organisms, 350
Giant-corpuscles, 348
Gibbes’ staining method, 107
Glanders, bacillus of, 46
bacillus of, in blood, 46
bacillus of, in pus, 353
bacillus of, in urine, 236
Globulin in pus, 358
in semen, 367
—— in urine, 270
—— test for, 270
Globulinuria, 270
Glycerine in urine, 274
Glycogen in blood, 74
in exudations, 367
—— in sputum, 114
— in pus, 358
Glycogenic reaction, 221
Glycosuria, 273
— pathological, 273
—— persistent, 273
—— physiological, 273
—— transitory, 273
Glycuronic acid phenomenon, 344
Gmelin’s test, 289
Goblet-cells in feeces, 169
Gonococci, 334
Gonorrheeal urethritis, 334
Gout, blood in, 70
2p
Digitized by Microsoft®
450
Gout, urine in, 311
Gowers’ hemacytometer, 13
Griiber’s solution, 8
Gram and Grdber’s theory of micro-
cytes, 35
Gram’s staining method, 41
Granular casts, 227
Granules in colourless blood-corpuscles,
I
Goape sugar. tests for, see Sugar
Grass-green sputum, 118
Green stools, 164
Guanidin carbonate, 202
Guanimin of isobutyric acid, 202
Guanin in pus, 358
Giinther’s staining method, 45
Gunzburg’s reagent, 131
HMACYTOMETER, 13
Hemameceba malaric, 49
Hematemesis, 148
Hematin, formula of, 62
—— in vomit, 148
—— reduced, 60
spectrum of, 60
Hematogenic albuminuria, 254
—— jaundice, 288
—— peptonuria, 265
Hematoidin, amorphous, 61, 241
—— crystals, 61, 110, 195, 241, 357
Hematomonas malarie stellata, 51
Hematophyllum malariz, 49
Heemato-porphyrin, 61, 293
Hemato-porphyrinuria, 293
Hematoscope, 21
Hematospectroscope, 23
Hematoxylin solution, 232
Heematozoa, 49
Hematuria, 270
-—— intermittent, 220
Heemin-crystals, 61.
crystals
Hemoglobin, amount of, 20
—— changes in, I
proteid of, 60
— reduced, 60
rhombic crystals of, 38
-—— spectrum of, 60
Heemoglobinzemia, 65
Hemoglobinuria, 65, 271
—— paroxysmal, 271
Hemometer, 19
Hemoptysis, 122
Hemorrhagic exudation, 359
— infarction of lung, 123
—— sputum, 122
—- stools, 209
Hairs in urine, 251
Halliburton’s test for globulin, 270
Hay-bacillus, 179
Haycraft’s method of estimating urea, 69
Haycraft and Williamson’s test for alka-
linity of blood, 3
Hayem’s solution, 6
See Teichmann’s
INDEX.
Heat-apoplexy, 209
Hedge-hog crystals, 249
Hedin’s heematocrite, 25
Heller's test, 257, 271
Helminthiasis, 182
Hemialbumose, 269
Hen-cholera, bacillus of, 378
Hénocque’s double spectroscope, 23
formula, 24
—— hematoscope, 21
—— hemato-spectroscope, 23
Hepatic diseases, faeces in, 210
diseases, urine in, 335
Hepatogenic jaundice, 283
Hering’s lensless spectroscope, 66
Hexahydro-hematoporphyrin, 61
Heynsius’ test, 257
Hindenlany’s test, 257
Hippuric acid, 243
Hofmann’s method for estimating HCl,
136
Hofmeister’s test for peptone, 266
Homogeneous immersion lens, 373
Homogentisic acid, 300
Homolomyia, 195
Hufner's apparatus, 312
Hunter on pernicious anemia, 290
Huppert’s test for bile-pigments, 76,
289
Hyaline casts, 230
Hydatid cysts, 362
Hydatids in feces, 186
— in sputum, 109
—— in urine, 238
Hydremia, 67
Hydriodic acid, 123
Hydrobilirubin in feces, 165
Hydrochinon, 300
Hydrochloride of phenyl-hydrazin, 72,
274
Hydrochloric acid, benzo-purpurin test
for, 131
acid, bilberries, test for, 132
—— acid, Congo-red test for, 131
— acid, detection of, 129
— acid, Dreschfeld’s test for, 133
—— acid, emerald-green test for, 130
— acid, estimation of, 133
— acid, Mwald’s test for, 129
— acid, fuchsin test for, 129
— acid, in cancer of stomach, 148
—— acid, in gastric juice, 129
— acid, methy]-aniline-violet test for,
129
— acid, Mohr’s test for, 129
— acid, oo-tropzolin test for, 130
acid, phloro-glucin and vanillin
test for, 131
—— acid, Uffelmann’s tests for, 132
— acid, ultramarine and zinc sul-
phide test for, 133
Hydrocyanic acid poisoning, 64, 162
Hydronephrosis, 363
Hydroparacumaric acid, 300
Digitized by Microsoft®
INDEX.
Hydrophobia, micro-organism of, 48
Hydrothza meteorica, 195
Hydrothionzemia, 64 :
Hydrothionuria, 327
Hyperacidity of gastric juice, 127
Hypersecretion of gastric juice, 127
Hypoazoturia, 311
Hypopyon, 348
Hyposulphites of urine, 323
Hyposulphurous acid in urine, 327
Hypoxanthin, 315, 317
Hysteria, 255
IDIOPATHIC bacteriuria, 235
oxaluria, 307
Incubator, 388
Indican, 294
estimation of, 295
—— tests for, 295
Indicanuria, 293
Indigo, 248, 293
— -blue, 293
-carmine test-paper, 278
crystals of, 248
Indigotin, 293
Indirubin, 296
Indol in feces, 202
in urine, 302
Indoxyl-sulphate, 248
-sulphuric acid, 293
Indulin, 40
Infarction, heemorrhagic, of lung, 123
Infectious diseases, blood in, 39
diseases, urine in, 328
Inflammation, non-tubercular, of Jung,
117
Influenza, bacillus of, 356
Infusoria in fieces, 181
——- in pus, 357
in sputum, 109
in urine, 237
in vaginal secretion, 370
Inoculation with micro-organisms, 3&9
Inorganic substances in blood, 78
—— substances in feces, 205
substances in semen, 367
substances in sputum, 114
substances in urine, 320
Inosite in cysts, 362
test for, 301
Inosituria, 301
Insects in feeces, 195
Intermittent albuminuria, 252, 255
hematuria, 220
Intestinal catarrh, 207
gases, 205
juice, 143
—— putrefaction, 293
ulcer, 269
Intestines, the, diseases of, 207
tuberculosis of, 208
Invertin, 205
Todates, 343
Iodide of bismuth and potash test, 160
451
Iodine in urine, 343
-— test for, 343
Todo-ammonic-iodide, 151
Todoform in urine, 343
— test for, 343
Iodo-potassic-iodide test for micro-
organisms, 171
Iris diaphragm, 377
Tron, salts of, in sputum, 114
Iso-butyric acid, 202
Iso-cyan-phenyl test, 162
JACQUEMIN’S test for nitrobenzol, 162
Jaffe’s test for indican, 295
for kreatin, 316
Jaundice, 77, 210
— casts in, 224
hematogenic, 288
Jaundice, hepatogenic, 288
inogenic, 288
urine of, 214, 231, 335
urobilin, 291
Johnson’s picric acid test for sugar, 278
KAIRIN in urine, 215, 344
—— potassium sulphate, 344
Kidney, amyloid, 331
—— caseation of, 237
—— contracted, 331
— cyanotic induration of, 228
—— cystic, 363
— epithelium of, 223
—— large white, 230
small red, 331
Klebs and Vommasi-Crudeli’s bacillus of
malaria, 49
Klemperer on thrush fungus, 86
Knife-rest crystals, see Triple phosphate
Koch and Lhrlich’s staining methods,
104
Koch’s pure cultivations, 384
Kreatin, 315
Kreatinin, 315
Kreatinin-zine chloride, 316
Kiihne’s staining methods, 378
Lactic acid bacillus, 206
acid, detection of, 337
— acid fermentation, 146
— acid in blood, 75
— acid in gastric juice, 139
— acid reaction in gastric juice, 139
— acid, tests for, 337
Lactosuria, 287
Levulosuria, 287
Landois’ test for reaction of blood, 2
Larve, dipteral, 91, 195
Lassar’s test for reaction of blood, 2
Latent disseminated sarcoma, 265
Laverania malarie, 49
Lead colic, 338
Lead, poisoning with salts of, 152, 338
Lecithin corpuscles, 366
Legal’s test for acetone, 304
Digitized by Microsoft®
452
Lensless spectroscope, 66
Leo’s method for estimation of HCl, 134
Leprosy, bacillus of, 355
Leptothrix buccalis, 80, 103
buccalis in sputum, 103
Leube and Salkowski's titration process,
280
Leucin in sputum, 113
—— in urine, 244
tests for, 245
Leucocytes in blood, 28
-—— in exudations, 348
—— in feces, 169
—— in semen, 366
in sputum, 94
—— in urine, 220
in uterine secretion, 370
in vomit, 144
Leucocytosis, 28
Leucohypobilin, 210
Leucomaines, sce Ptomaines
Leucourobilin, 210
Leukemia, 29
crystals, 30
—— lymphatico-splenic, 30
—— myelogenic, 29
—- splenic, 30
Lichtheim’s plate, 385
Lieben’s test for acetone, 303
Lipacidzemia, 74
Lipaciduria, 305
Lipemia, 75
Lippich’s polarimeter, 284
Lipuria, 306
Litmus, extract of, 353
Liver, acute yellow atrophy of, 241
—— diseases of, feeces in, 210
diseases of, urine in, 385
Lochia, the, 370
Lifler’s staining process, 41
Lowenberg’s diplococcus, 91
Lucilia cesar, 195
—— regina, 195
Inudwig’s filter, 309
process, 308
Lumniczer’s bacillus, 115
Lung, sce Pulmonary
Lustgarten’s bacillus, 349
Lutein, spectrum of, 66
Lymphatico-splenic leukemia, 30
Macxay’s test for bile-acids, 76, 288
Macwilliam’s test for peptone, 268
Magenta solution, 107
Magnesia mixture, 308
soaps of, in feces, 196
Magnesium phosphate, 242
Maguire on globulin in urine, 270
Malaria, micro-organisms in, 49
Maltose in urine, 287
Maly’s test for HCl, 130
Mammary secretion, 368
Margarine needles in sputum, 112
Martin, 8., on peptonuria, 268
INDEX.
Marrow-cells, 32
Mason’s lung, 123
“ Mastzellen,” 33
Measles, urine test for, 328
Measurement of urine, 211
Meconic acid, 82
Meconium, 206
Megaloblasts, 35
Megastoma entericum, 181
Melanemia, 35
Melanin, 301
—— tests for, 302
Melanogen, 302
Melanuria, 301
Melithemia, 72
Menstruation, 370
Mercury, poisoning with salts of, 153,
9
3 tests for, 154, 339
Metadiamidobenzol, 327
Metalbumin in cysts, 363
—— test for, 363
Metallic poisons, 152
Metamorphosed casts, 224
Metaphosphoric acid test for albumin,
257
Metatungstic acid, 160
Methemoglobin in blood, 62
—— in urine, 272
spectrum of, 62
Methan, 251
Methyl-aniline-violet test for HCl, 129
-— for staining fungi, 41
Methylene blue, 41
Methyl-violet, 104
Microbes in pneumonic sputum, 119
Micrococci in buccal secretion, 80
—— in nasal secretion, 91
-— in pus, 348
—~— in urine, 233
see also Fungi
Micrococcus chlorinus, 119
— de la rage, 80
—— erysipelatos, 47
— gonorrhoicus, 334
— of sputum-septicemia, 80
-—— prodigiosus, 369
—— tetragenus, 81
—— uree, 234
Microcytes, 35
Microcythemia, 3
Micro-organisms, cultivation of, 379
detection of, 372
—— examination of blood for, 40
— in hydrophobia,. 48
-— in malaria, 49
—— in scarlatina, 47
—— in small-pox, 48
—— methods of staining, 40, 103
— of feces, 170
of milk, 369
of mouth, 80
of nasal secretion, 91
of pus, 348
Digitized by Microsoft®
INDEX.
Micro-organisms of urine, 233
— of vaginal secretion, 369
—— of vomit, 146
—— spores of, 45, 354, 355
—— transmission of, to animals, 389
see also Fungi
Microscope, the, 372
Microscopical examination of the blood,
examination of cystic fluids, 361
examination of exudations, 348
examination of the buccal fluids, 79
examination of the feces, 166
examination of the gastric con-
tents, 124
—— examination of the nasal secretion,
LT |
— examination of the semen, 366
—- examination of the sputum, 94
— examination of the urine, 217
— examination of the vomit, 144
—— examination of transudations, 361
— examination of vaginal secretion,
369
Miliary tuberculosis of lung, 116
tuberculosis of urinary organs, 333
Milk, the, 368
—— -curdling ferment in gastric juice,
126
—— -curdling ferment in urine, 320
-sugar, 287
Millon’s reagent, 202, 258
Mohr’s estimation of chlorides, 320
tests for HCl, 129
Milisch’s sugar reactions, 279
Molybdate of soda, 156
Monadines in feces, 180
in sputum, 109
Monads in feces, 181
in sputum, 109
Monilia candida, 86
Monohydroxyl-benzol derivatives, 258
Moore’s test for sugar, 274
Mordants in staining micro-organisms,
33, 379. .
Morphia in urine, 340
poisoning, 156, 340
tests for, 156
Mott on pernicious anzemia, 290
Mould fungi of blood, 39
fungi of feces, 170
— fungi of gastric juice ani vomit,
146
— fungi of mouth, 80
fungi of nose, 90
—— fungi of sputum, 102
fungi of urine, 233
—— fungi of vaginal secretion, 370
fungi of vomit, 146
Mucin in feces, 198
in nasal secretion, go
—— in saliva, 81
— in sputum, 118
— in urine, 272
453
; Mucin, tests for, 272
Mucinuria, 272
Mulder’s test, 278 S
Murexide test, 71
Muscle fibres in feces, 167
—— fibres in vomit, 145
Myelin droplets, 94, 110
Myelogenic leukemia, 29
NAPHTHALINE in urine, 346
Naphthalol, 343
Naphthol-poisoning, 271
Nasal catarrh, 91
—— secretion, 90
— secretion, cerebro-spinal fluidin, 91
—— secretion, characters of, 90
—— secretion, Charcot- -Leyden guide
in, 91
—— secretion, concretions in, 91
—— secretion in disease, go
—— secretion, micro-organisms of, oe
— secretion, pus in, 91 :
Nematodes, 188
Nephritis, 329
—— acute, 329
— chronic, 330
—— embolic, 227
gravidarum, 241
—— sp. gr. of urine in, 213
—- toxic, 338
Nephrolithiasis, 250
Neubauer’s method, 307, 316
Neuralgia, saliva in, 80
Neutral phosphate of lime in feces,
197
—- phosphate of lime in urine, 242
——- phosphates, 323
Neutrophil granules, 33
Nitrate of silver solution, 321
Nitrates in urine, 326
Nicotin, poisoning with, 157, 341
Nitric acid, poisoning with, 151
acid test for albumin, 255
Nitrites in the blood, 65
in the saliva, 82
——- in the urine, 326
-—— tests for, 326
Nitrobenzol, poisoning with, 65, 162,
342
—— tests for, 162, 342
Nitrogen, estimation of, in urine, 315
Nitro-prusside test, 162
of sodium as a test for acetone,
393
— of sodium as a test for melanuria,
302
Normal acid solution, 3
salt solution, 10
— soda solution, 13
—- urobilin, 290
Non-pathogenic fungi of blood, 39
—— fungi of feces, 170
—— fungi of gastric juice and vomit,
145
Digitized by Microsoft®
454 INDEX.
Non-pathogenic fungi of pus, 348
—- fungi of sputum, 103
— fungi of urine, 233
—— fungi of vaginal secretion, 370
Nose, secretion from, 90
Nose-piece of microscope, 377 -
Nosotoxicosis, 319
Nuclein, 358
—— in milk, 368
—— in pus, 358
— in semen, 367
—— in sputum, 113
Nucleo-albumin. See Mucin
Nutrient agar-agar, 383
— blood serum, 383
fluids, 382
— fluids, sterilisation of, 380
gelatine, 383
— gluten, 384
— milk peptone, 354
— potato, 384
— starch, 384
— substances, 381
substances, stained, 384
substances, sterilisation of, 380
Nylander’s test for sugar, 277
OBERMAYER’S test for indican, 295
Objectives, 373
—— apochromatic, 374
Gidema, pulmonary, 122
Oidium albicans, 84
Oil-immersion lens, 373
Oil of cloves, 41
Oleic acid, 202
Oligochromzmia, 8
Oligocythzemia, 7
Oliguria, 212
Omichol, 317
Optimum temperature, 387
‘Orchitis, 367
Organic acids of blood, 74
— acids of freces, 202
-—— acids of gastric juice, 139
— acids of sputum, 113
—— acids of urine, 305
salts of lime in faces, 198
Organised sediment of urine, 219
casts in, 224
Osteomalacia, 78
Ovarian cysts, 362
Oxalate of lime, amorphous, 247
crystals of, 113, 197, 240
Oxalic acid diathesis, 306
acid, estimation of, 307
— acid in urine, 241, 306
— acid, poisoning with, 151
Oxaluria, 306
—- idiopathic, 307
— vicarious, 307
Oxyacids, aromatic, 300
Oxyamygdalic acid, 300
Oxyhemoglobin, spectrum of, 60
reduction of, 25
Oxyuris vermicularis, 190
Ozena, 91
Ozone, 328
P-AMIDO-dimethyl-aniline, 327
Pacini’s solution, 9
Palmitic acid, 202
Pancreatic cysts, 364
Paraamido-phenol-sulphuric acid, 342
Parakresol, 297
Parakresol-eether-sulphuric acid, 297
Paralbumin, 363
Paramcecium coli, 182
Parasites of blood, 39
— of buccal secretion, 80
— of feces, 169
—— of gastric juice and vomit, 146
— of malaria, 49
—— of milk, 369
—— of nasal secretion, 91
-—— of pus, 343
—- of sputum, 101
—— of urine, 233
-—— of vaginal secretion, 369
Parasite affections of stomach, 150
Paroxyphenyl-acetic acid, 300
— -propionic acid, 300
Paroxysmal albuminuria, 252
hemoglobinuria, 272
Pathogenic fungi of blood, 39 a
fungi of buccal secretion, 80, 84 -
—— fungi of feces. 173
—— fungi of gastric contents, 146
—— fungi of milk, 369
—- fungi of nose, 91
—— fungi of pus, 349
—— fungi of sputum, Io1
—— fungi of urine, 234
—— fungi of uterine secretion, 370
Pathological albuminuria, 253
acetonuria, 303
—— glycosuria, 273
——- urobilin, 290
Pavy’s fluid, 275
Pavy’s method for estimating sugar, 73
Pentamethylene-diamine, 115, 160, 318
Penzoldt’s test, 279
Pepsin, detection of, 126 ar
estimation of, 126
—— in gastric juice, 126
— in urine, 319
—— in vomit, 149
Peptone in blood, 67
—— in feces, 199
—— in gastric juice, 140
—— in pus, 358
-—— in sputum, 113
— in urine, 264
tests for, 266
Peptonuria, 264
——- enterogenic, 265
— hematogenic, 265
—— puerperal, 265
—— pyogenic, 264
Digitized by Microsoft®
INDEX.
Peptonuria, syphilitic, 266
Periscopic eye-piece, 375
Peritonitis, 200
Pernicious anemia, 38
urine in, 215
Peroxide of hydrogen in urine, 32%
Persistent glycosuria, 274
Pettenkofer’s test, 76
Phantom corpuscles, 219
Pharyngomycosis leptothricia, 89
Phenacetin, 345
Phenol in feces, 202
—— in urine, 297
tests for, 202
—— -ether-sulphuric acid, 297
Phenols, estimation of, 299
Phenyl-glucosazon, 72, 276
—— -hydrazin chloride, 72, 276
-lactosazon, 287
Phlegmon, 347
Phloro-glucin, 131
Phloxin-red, 178
Phosphates, estimation of, 324
in feces, 197
in sputum, 114
in urine, 242, 249, 323
tests for, 324
Phosphatic sediment, 239, 249
Phosphomolybdic acid test, 160
Phosphoric acid, estimation of, 324
Phosphorus poisoning, 155, 340
Phospho-tungstic acid, preparation of,
159
acid test, 160
Phthisis, urine of, 215, 329
Physiological acetonuria, 303
albuminuria, 329
glycosuria, 273
Picrate of indol, 302
Picric acid test for albumin, 258
acid test for sugar, 277
Picro-carmine, 232
Pilimictio, 251
Pilocarpin, 83
Pimaric acid, 256
Pinic acid, 256
Piophila casei, 195
Plasma of blood, 1
Plasmodium malariz, 49
Plastic bronchitis, 115
Plate cultivations, 385
Platinum chloride test, 160
Platodes, 182
Plehn’s solution, 57
Pneumaturia, 251
Pneumoconiosis, 123
Pneumonia, 118
—— fibrinous coagula in, 100
--— micro-organisms of. 107, 118
sputum of, 107, 118
Pneumonia-coccus, detection of, 108
—— of Friinkel, 108, 120
~— of Friedldnder, 107, 120
Poikilocytes, 31, 36
455
Poikilocytosis, 31, 36
Poison elaborated by cholera bacillus,
176
Poisoning with acids, 150, 338
with alkalies, 152, 338
— with alkaloids, 156, 340
— with aniline, 342
with carbolic acid, 161, 341
—— with carbonic oxide, 63, 273, 342
— with chlorate of potash, 65, 152
— with chloroform, 161, 341
-—- with ethylic alcohol, 161, 341
— with hydrocyanic acid, 64, 162
—— with metals and metalloids, 152,
a
33
with nitro-benzol, 65, 342
—-— with nitrous oxide, 65
—— with ptomaines, 158
— with sulphuretted hydrogen, 64
Polarimeter, 284
Polarisation, 284
Pollenia rudis, 195
Polymitus malarie, 50
Polyuria, 212
Potato, sterilised, 380, 384
Prava? syringe, 389
Preparation of cover-glasses, 40, 105
Propeptone in gastric juice, 141
—— in semen, 269
—— in urine, 269
tests for, 269
Propionic acid, 202
Prostatic fluid, 366
Proteids formed in gastric digestion,
141
—— of blood, 67
— of buccal secretion, 83
—— of cystic fluids, 363
-— of feces, 168, 198
— of gastric juice, 140
—— of pus, 358
—— of sputum, 113
—— of transudations, 361
—— of urine, 251
—— tests for, 141
Proto-albumose, 268
Protozoa of blood in small-pox, 57
—— in malaria, 49
— of feces, 180
—— of pus, 357
of sputum, 109
Prune-juice sputum, 118
Prussic acid poisoning, 64, 162
acid, tests for, 162
Pseudo-diphtheria bacillus, 89
Psorospermia, 181
Ptomaines, detection of, 159
—— in blood, 77
—— in feces, 205
—— in gastric juice, 158
—— in urine, 317, 341
—— poisoning with, 158, 341.
-— tests for, 159
Ptomato-atropin, 160
Digitized by Microsoft®
456
Ptyalism, 81
Puerperal fever, 47
peptonuria, 265
Pulmonary affections, sputum in, 114
—— abscess, 121
—— gangrene, 121
—- edema, 122
Pure cultivations, preparation of, 384
Purulent exudations, chemical exami-
nation of, 358
—— exudations, crystals in, 358
exudations, fungi of, 348
exudations, naked-eye characters
347
characters of, 347
chemistry of, 358
crystals of, 358
fungi of, 348
in feces, 169
in nasal secretion, 91
in sputum, 94
in stomach, 150
in urine, 221
Vitali’s test for, 221
Putrefaction bases, 317
Putrescin, 160, 318
Putrid bronchitis, 115
-— exudation, 359
Pycnometer, 212
Pyelitis calculosa, 332
Pyelo-nephritis, casts in, 22
Pyogenic peptonuria, 264
Pyrocatechin, 299
separation of, 300
—— tests for, 300
Pyuria, 221
0
us,
Las)
Fb
eae!
QUARTAN ague, parasite of, 53
Quincke’s inogenic jaundice, 288
Quinine in urine, 215, 344
Quinone-tyrosin reaction, 245
REACTION of blood, 2
of feces, 164
of gastric juice, 127
of pus, 347
of sputum, 93
of urine, 216
blood-corpuscles, see Blood-cor-
puscles
Reduced hematin, 60
— hemoglobin, 60
— hemoglobin, spectrum of, 60
Reducin, 317
Reichert’s lenses, 373
Relapsing fever, spirillum of, 44
Renal albuminuria, 253
—- casts, 224
—— colic, 247
—— epithelium, 223
Resorcin in urine, 214
Retention-toxicosis, 318
Reynolds’ test for acetone, 304
Rhabditis genitalis, 238
ELE
Red
INDEX.
Rhabdonema strongyloides, 194
Rheumatic arthritis, urine in, 311
Rhinoliths, 91
Rhizopoda, 180
Rhubarb in urine, 214
Ribbert’s small red kidney, 331
Rice-water stools, 209
Richet’s method for estimation of HCl,
133
Rickets, 78
Roberts’ fermentation process, 282
method of estimating albumen,
260
—— test for serum-globulin, 270
Rochelle salts, 281
Rosanilin hydrochloride, 107
Rosenbach’s test for bile pigments, 289
Round worms, 188
Roussin’s crystals, 157
Rubner’s test for sugar, 278
SACCHAROMYCES cerevisie, 145
—— ellipsoideus, 170
Saccharomycetes, 170
Safranin, 232
Sago-grain forms in feces, 166
Sahli’s test for pepsin, 319
Salicylates in urine, 343
Salicyl-sulphonic acid test, 258
Saliva, chemistry of, 81
fungi of, 80, 85
in disease, 82
microscopical appearances of, 80
naked-eye characters of, 79
sec also Buccal secretion
Salivary corpuscles, 79
Salkowski’s colorimetric process, 296
Salol, 343
Salts of the blood, 77
Santonin, 346
Sarcina of urine, 234
—— pulmonis, 103
—- variegata, 103
—— ventriculi, 146
Sarcolactic acid in blood, 75
acid in urine, 338
Sarcophaga hematodes, 195
——- hemorrhoidalis, 195
Sarkin, 315
Scarlatina, nephritis in, 223
—— streptococcus of, 45
Skatol, 202
Scheme of a bacteriological investiga-
tion, 390
Scherer’s test for phosphorus, 155
Schottelius’ method of cultivation, 175
Schreiner’s base, 366
Scolices, 362
Scurvy, urine in, 217, 290
Searchers, 377
Sediment, urinary, 219
Sedimentator, 218
Seegen’s method for estimating grape-
sugar, 73
Digitized by Microsoft®
INDEX.
Semen, chemistry of, 367
—— physical characters of, 366
Senna in urine, 215
Sepsis occulta, 264
Septicemia of mouse, bacillus of, 171,
356
—— milk in, 368
—— urine in, 236
Seropurulent exudation, 358
Serous exudation, 359
Serum-albumin in pus, 358
-albuminuria, 253
— -globulin in urine, 270
—— -globulin, Roberts’ test for, 271
—- in semen, 367
in sputum, 113
in urine, 253
tests for, 255
Siderosis pulmonum, 123
Silicates in sputum, 114
Simple sulphuric acid, 323
estimation of, 323
Sjoqvist’s method for
HCl, 134
Skatoxyl, 296
sulphuric acid, 296
Small-pox, protozoa in, 57
Smegma bacillus, 334
Soaps of lime and magnesia, 246
Soda solution, normal, 13
Sodium pyrophosphate, 325
Spasmotoxin, 48
Spectra, 59
Specific gravity of the blood, 5
gravity of the blood, estimation
of,
Saeedeape: Browning's, 59, 66
— double, 23, note.
lensless, 66
Spermatic crystals, 367
Spermatozoa, 233, 366
Spirals, 98
Spirillum of cheese, 177
of relapsing fever, 44, 236
of relapsing fever, spores of, 45
Spirochete buccalis, 80
— dentium, 80
Spores, preparation of, 354, 355
staining of, 45, 379
Sporozoa in feces, 181
Sputum, the, 93
— alveolar epithelium in, 94
— bacteria in, 102
— blood in, 94, 122
—— chemical examination of, 113
— colour of, due to micro-organisms,
II
ene rrcctive tissue in, 100
erystals in, 112
diamines in, 115
—— elastic fibres in, 97
— fatty acids in, 113
—— ferment in, 114
—— fibrinous coagula in, 100
estimation of
457
Sputum, glycogen in, 114
in disease, 114
inorganic constituents of, 114
microscopical examination of, 94
naked-eye characters of, 93
parasites of, 1or
—— proteids of, 113
quantity of, 93
reaction of, 93
specific gravity of, 93
spirals in, 98
stratification of, 93
Staining fluids, preparation of, 105
of micro-organisms, Biedert’s me-
thod, 107
— Ehrlich’s method, 105
—- Gabbet’?s method, 107
Giacomi’s method, 350
—— Gibbes’ method, 107
— Gram’s method, 41
——— Giinther’s method, 45
—— Friedldnder’s method, 107
— Koch's method, 104
— Liffler’s method, 41
— Lustgarten’s method, 349
| —— Toison’s method, 12
— Wedl’s method, 352
—— Weigert’s method, 352
with aniline dyes, 41, 104
Staphylococcus pyogenes albus, 81
| —— pyogenes aureus, 81, 348
| —— pyogenes citreus, 81
pyogenes in milk, 368
Starch as a nutrient substance, 384
digestion of, 142
granules in feces, 167
——- in feces, 167
—— in gastric juice, 142
-— in urine, 250
Starvation, indican in, 293
Stas-Olto method, 156
Stearic acid, 202
Stenbeck’s sedimentator, 218
Stercobilin, 165
Sterilisation, methods of, 379
Sterilised blood-serum, 380
blotting-paper, 386
— nutrient substances, 380
— test-tubes, 380
Steriliser, 380
steam, 381
Stewart, Grainger, on albuminuria, 251
Stomach, atrophy of, 147
— cancer of, 148
contractile activity of, 142
dilatation of, 149
mucous catarrh of, 147
rate of absorption in, 142
Stomatitis, 84
Stratified sputum, 93
Streptococci, 47, 235
Streptococcus erysipelatos, 47, 235
— of scarlatina, 48
— pyogenes, 47, 235, 349
Digitized by Microsoft®
458
Strongylides, 190
Strongylus duodenalis, 1go0
Stutz capsules, 258
Succinic acid, 362
Sugar, fruit, see Levulose
grape, estimation of, 230
grape, estimation of, by fermenta-
tion, 282
grape, estimation of, by polarisa-
tion, 283
grape, estimation of, by titration,
280
grape, estimation of, Claude Ber-
nard’s method, 73
grape, estimation of,
method, 73
grape, in blood, 72
grape, in exudations, 358
-—— grape, in urine, 273
—— grape, tests for, 274
—— milk, 287
Sulphanilic acid test, 328
Sulphates of sputum, 114
of urine, 323 :
Sulphide of bismuth crystals, 198
of sodium solution, 309
Sulphocyanide of ammonium solution,
321
— of saliva, 83
of urine, 322
Sulphur in urine, 323
Sulphuretted hydrogen in blood, 64
— hydrogen in feces, 205
—— hydrogen in urine, 327
—— hydrogen poisoning, 64
hydrogen, tests for, 327
Sulphuric acid, compound, 297
— acid, poisoning with, 150
— acid, simple, 323
Syntonin in gastric juice, 141
Syphilis, bacillus of, 349
— hemoglobinuria in, 271
—— of liver, 334
peptonuria in, 266
Seegen’s
TANIA cucumerina, 185
— elliptica, 185
-—— flavopunctata, 185
—— leptocephala, 185
——- madagascariensis, 185
—- mediocanellata, 182
—— nana, 184
saginata, 182
— solium, 183
Tannin in urine, 346
test for ptomaines, 160
Tanret’s reagent, 257
Tartrate of potassium and sodium, 281
Taurocholate of soda, 84
Teat-worm, 190
Teeth, deposit on, 86
Teichmann’s crystals, 61
test, 61 :
Tertian ague, parasites of, 51
INDEX. mm
Testicle-cells, 366
Test-meal, 140
Test-tube cultivation, 387
Test-tubes, sterilised, 380
Tetanin, 48
Tetanotoxin, 48
Tetanus, bacillus of, 355
Tetramethylene-diamine, 160, 318
Tetramethyl-paraphenyl-diamine, 134
Tetra-paper, 134
Thallin in urine, 344
Thermostat, 387
Thiosulphates, 323
Thomas’ cylindroids, 232
Thoma-Zeiss’ apparatus, 9
Thoracic-duct, obstruction of, 349
Thread-worms, 190
Thrush fungus, 85
in feeces, 170
—— —— in mouth, 85
—— —— in nose, 91
in stomach, 150
in vagina, 369
Thymol test for chloroform, 161
—— test for sugar, 279
to preserve urine, 218
Titration method for estimating sugar,,
280
Yoison’s staining fluid, 12
Toluol, 300
Tongue, coating of, 87
Tonsillitis, 87
Tonsils, coating of, 87
Toxalbumins, 158
Toxic nephritis, 338
states, urine of, 338
Transitory glycosuria, 273
Transudations, 361
Traube on elastic fibres, 97
Traube’s corpuscles, 219
Trematodes, 187
Tribromophenol, 299
Trichina spiralis, 193
Trichinosis, 194
Trichocephalus dispar, 192
Trichomonas intestinalis, 182
—— vaginalis, 370
Trichotrachelides, 192
Trigeminal neuralgia, 82
Trimethylamin, 370
Triple phosphate crystals, 242
phosphate crystals in feces, 197
—— phosphate crystals in pus, 358
—— phosphate crystals in sputum, 113,
—— phosphate crystals in urine, 242,
247
Trommer’s test, 274
Tropzolin (00) test for HCl, 130
Troup on alveolar epithelium, 96
on spirals, 98
Trypsin, 319
Tubercle, bacillus of, 45, 103
bacillus of, detection of, 103
bacillus of, in blood, 45
Digitized by Microsoft®
INDEX.
Tubercle, bacillus of, in fecés, 179, 208
—— bacillus of, in milk, 369
—— bacillus of, in pus, 350
bacillus of, in semen, 366
—— bacillus of, in sputum, 103
bacillus of, in urine, 236
— bacillus of, spores of, 116
Tubercular infiltration of lung, 116
—— infiltration of lung, pneumonic
type of, 116
infiltration of lung, typhoid type
of, 116
Tuberculin, 46
Tuberculosis, chronic, 116
—— miliary, 116
— of lung, 116
— of urinary organs, 237, 333
urine in, 328
Tumours, fragments of, in feces, 167
in urine, 233
Tunnel-borer’s anemia, 191
Turpentine, oil of, 346
Typhoid fever, 208
fever, bacillus of, 46, 81, 177
—— fever, blood in, 46
fever, Lirlich’s urinary test for, 328
—— fever, feces in, 177
fever, urine in, 328
Tyrosin crystals, 244
crystals in faeces, 196
erystals in sputum, 112
— crystals in urine, 244
crystals, tests for, 244
Tyrotoxin, 160
UFFELMANN’S tests for HCl, 132
Ulcer, chronic gastric, 147
— duodenal, 148
—— tubercular, 91
Ulceration, tubercular, of urinary or-
gans, 333
Ulcerative endocarditis, 236
enteritis, 207
rhinitis, 91
Ultramarine and zinc sulphide test, 133
Ultzmann’s test, 289
Unna’s blood-serum plates, 381
Unorganised casts, 224
sediment, 239
Uremia, 77, 331
casts in, 225
Uranium solution, 325
Urates, casts of, 224
in urinary sediment, 239 246
Urea, estimation of, 311
excretion of, 311
—— in blood, 68
—— in feces, 200
in gastric juice, 141
in saliva, 83
in urine, 311
— tests for, 68
Ureteritis membranacea, 332
Urethra, epithelium of, 222
459
Urethritis, 334
Uric acid crystals, 240
— acid diathesis, 308
— acid, estimation of, 308
—-- acid in blood, 70
—-— acid in exudations, 360
— acid in urine, 240
— acid, tests for, 70
Urina spastica, 215
Urinary concretions, 247, 250
—— organs, tuberculosis of, 236
—— sand, 250
sediment, 219, 240
Urine, the, 211
actinomyces in, 237
— ether-sulphuric acids in, 297
— albumin in, 251
— amorphous deposit of, 219
—— bile acids in, 287 ,
bile pigments in, 241, 288
— blood in, 219
— carbohydrates in, 273 |
— casts in, 224 ;
--— chemical examination of, 255
—— chlorides in, 320
— chromogens of, 214
—— colour of, 214
—— crystalline deposit of, 239
—— detection of drugs in, 343
-——- diacetic acid in, 305
— diamines of, 318
—— epithelium in, 221
— fat in, 247, 306
— fatty acids in, 305
faecal substances in, 255
—— ferments of, 319
— foreign bodies in, 250
-— fragments of tumours in, 233
—— gases of, 328
—— in anemia, 337
— in congestion, 329
in diabetes, 336
in diseases of alimentary canal,
335
inzfebrile states, 328
infusoria of, 237
in hepatic affections, 335
—— in measles, 328
—— in nephritis, 329
—— inorganic constituents of, 320
--— in, septicemia, 236
—— in tuberculosis, 236
—— in typhoid, 328
—— leucocytes in, 220
-—— microscopical examination of, 217
—— organic acids of, 305
—— naked-eye inspection of, 211
—— organised sediment of, 219
—— oxalic acid in, 307
—— parasites of, 233
—— phosphates in, 323
—— pigments of, 214
proteids of, 251
—— ptomaines in, 317
Digitized by Microsoft®
460 INDEX.
Urine, pus in, 221
quantity of, 211
—— reaction of, 216
— specific gravity of, 212
—— spermatozoa in, 233
sugar in, 273
urea in, 311
—— urobilin in, 290
vermes in, 237
Urinometer, 213
Urobilin, febrile, 290
blood derived from, 76
—— in feces, 164, 204
—— in urine, 214, 290
—— normal, 214
—— of transudations, 361
separation of, 204
spectrum of, 292
—— tests for, 291
Urobilin-jaundice, 291
Urobilinuria, 250
Urochrome, 214, 317
Uroerythrin, 214, 240
Urohzmatoporphyrin, 293
Uroleucic acid, 300
Urotheobromin, 317
Uterine secretion, 370
VAGINAL secretion, 369
Valerianic acid, 202
Vanillin, 131
Vapour-sterilisation apparatus, 380
Vermes in blood, 57
in feeces, 182
—— in pus, 357
in sputum, 110
in urine, 257
Vesical calculus, 333
-— epithelium, 221
—— tumours, 333
Vesuvin, 105
Vibrio buccalis, 80
Vicarious oxaluria, 307
Victoria blue, 377
Vierordt’s spectrophotometer, 297
Vitali’s guaiacum test, 221
Vogel’s colour scale, 215
Volatile fatty acids in blood, 74
——. fatty acids in feces, 200
——— fatty acids in gastric juice, 139
—— fatty acids in sputum, 113
fatty acids in urine, 305
Volhard’s method, 320
Vomit, the, 144
—— acids in, 150
— alcohol in, 161
—— alkalies in, 152
—— alkaloids in, 156
-—— blood in, 144
— carbolic acid in, 161
Vomit, chloroform in, 161
— contents of, 144
— diamines in, 159
fecal substances in, 150
——- fungi of, 145
— hydrocyanic acid in, 162
— in acute gastritis, 146
-— in cancer of stomach, 148
in chronic gastritis, 146
in gastric ulcer, 147
—— in parasitic affections of stomach,
150
—— in poisoning, 150
— nitric acid in, 151
—— oxalic acid in, 151
—— ptomaines in, 158
—— pus in, 150
—— sulphuric acid in, 151
yeasts in, 145
Vomitus matutinus, 146
Von Fleischl’s hemometer, 19
Von Meringand Cahn’s method for esti-
mation of HCl, 133
Vortmann’stest for hydrocyanicacid, 163
WASTING diseases, indican in, 294
Waxy casts, 228
Weber's test for indican, 295
Wedl’s litmus solution, 352
Weigert’s staining process, 352
Weyl’s test for kreatinin, 316
Whetstone crystals, see Triple phos-
phate
Whipworm, 192
White blood-corpuscles, see Leucocytes
Whooping-cough, bacillus of, 109
—— protozoa in, 109
Wool-sorters’ disease, 42
Working eye-piece, 377
Worm-Miiller’s test for sugar, 275
Worms, see Vermes
Wiirster’s test for tyrosin, 244
XANTHIN, 315
bases, 71
Xantho-kreatinin, 315
Xantho-proteic test, 258
Xylol, 45
YEAST-FUNGI of buccal secretion, 80
— of feces, 170
— of sputum, 103
— of urine, 233
—— of vaginal secretion, 369
— of vomit, 145
ZUISS’S lenses, 377
Zichl-Neelsen fluid, 106
Zinc sulphide and ultramarine test, 133
Zuntz test for reaction of blood, 2
Zymogen of gastric juice, 127
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