key: cord-0044614-k2kys9dc
authors: Fox, James G.; Brayton, James B.
title: Zoonoses and Other Human Health Hazards
date: 2013-10-21
journal: Diseases
DOI: 10.1016/b978-0-12-262502-2.50029-8
sha: 20c6ef6f99ef5cdd70a64ad74892bbbb90a5e873
doc_id: 44614
cord_uid: k2kys9dc

This chapter discusses known or potential zoonotic agents and the disease manifestations produced in man by exposure to infected mice. It also discusses other health hazards that may be encountered when working with mice, such as bites and allergies. Selected transmission of human infectious agents to mice is also briefly described in the chapter. Of the many latent viruses present in the mouse, only the lymphocytic choriomeningitis virus (LCM) naturally infects man. A review of the literature attests to the ease with which the LCM can be transmitted from animals to man. Although its expression can vary greatly, the LCM virus infection appears most frequently as a mild influenza-like syndrome, with or without apparent involvement of the central nervous system. In one epidemic of the non-meningitic LCM virus infection caused by exposure to infected hamsters, an influenza-like illness was described with typical symptoms of retro-orbital headache, severe myalgia, malaise, anorexia, and aching pain in the chest. A variety of rodent hosts are included in the transmission cycle of the rickettsial disease in nature. The house mouse is the natural host of Rickettsia akari, which is the causative agent of rickettsialpox and a member of the spotted fever group of rickettsiae. Another rickettsial disease—murine typhus or endemic typhus—is transmitted to man by rat fleas; rats and mice are its natural reservoirs. Rickettsia mooseri—the causative agent—has not been isolated from natural infections in laboratory mice. Clinical signs, diagnosis, and control in man are similar to those described for rickettsialpox.

Derived from the Greek words zoon, meaning animals, and noses, meaning disease, zoonoses literally refers to diseases transmitted directly to man by animals. This chapter reviews known or potential zoonotic agents and the disease manifesta tions produced in man by exposure to infected mice. We dis cuss other health hazards that may be encountered when work ing with mice, such as bites and allergies. Selected transmis sion of human infectious agents to mice is also briefly men tioned.

Although the mouse, either feral, laboratory, or pet, is not commonly considered a reservoir for human pathogens, a re view of the literature contests that notion. It should also be noted that many of the zoonotic diseases affecting mice also occur in rats (Geller, 1979) . However, with the advent of modem laboratory animal production and management, zoono tic diseases are being curtailed and are nonexistent in many laboratories.

Of the many latent viruses present in the mouse, only LCM naturally infects man. A review of the literature attests to the ease with which LCM can be transmitted from animals to man (Lehmann-Grube, 1971 ; see also Chapter 12, this volume).

The natural association of LCM virus and the mouse pro vides for mutual survival in a symbiotic relationship. Neither the virus nor the host significantly suppresses the other, though each can do so. LCM exists in the wild mouse population throughout the United States, Europe, Asia, Africa, and prob ably the world (although it has not been isolated from mice in Australia). Wild mice are the ultimate reservoir of infection for laboratory mice and other susceptible hosts (Maurer, 1964) .

Mice, and hamsters to a lesser extent, are the only species in which a long-term, asymptomatic infection is known to exist (Hotchin, 1971; Parker et aL, 1976) . In an early study, 21.5% of mice surveyed in the Washington, D.C, area were infected (Armstrong etaL, 1940) . In a more recent survey (1967) (1968) (1969) (1970) in the United States, LCM infection was detected in only 2 of 22 production or research colonies (Poiley, 1970) . It was pre sent at a low-level incidence for at least 2 years in one colony.

However, this survey was conducted only in retired breeding stock, and the monitoring technique detected only nontolerant infections. LCM has also been reported in other mouse col onies used for research in the United States. (Soave and Van Allen, 1958) . Early investigations in the United Kingdom demonstrated infection in 1 of 18 mouse-breeding colonies (Findlay et aL, 1936) and in "many strains" surveyed at a later date (MacCallum, 1949) . LCM still existed in colonies in selected institutions in England in 1970 (Skinner and Knight, 1971 ) and undoubtedly persists in some colonies maintained in the United States. Infection has been eradicated in almost all colonies, however, by surgical derivation, routine serological monitoring, culling, and prevention of entry of wild mice into laboratory colonies.

Another source of infection for man is the presence of LCM virus in experimental tumors induced in mice. This source was first recognized in a much used, transplantable leukemia of C58 mice, line I, in which inoculation of the tumor produced mild clinical illness in mice. It had been assumed that the sickness was due to a toxic substance produced by the leukemia cells; it was discovered, however, that the etiologic agent was LCM virus (Lindorfer and Sy verton, 1953; Taylor and MacDowell, 1949) . Subsequently, LCM virus has been found in other commonly used tumor lines (Collins and Parker, 1972; Stewart and Haas, 1956) . LCM virus has also been found as a contaminant of mycoplasma and murine poliovirus (Findlay et aL, 1938; Wenner, 1948) .

Diagnosis and control of this infection in mouse colonies has been described in Chapter 12, Mice that are congenitally in fected are bom normal and appear normal for most of their life span, even though they are persistently viremic and vimric.

Virtually all cells can be infected with the virus. Most human laboratory infections have been associated with improper han dling of infected murine tissues (Baum et aL, 1966; Tobin, 1968) . Before manipulative procedures begin, all murine tumor lines should be screened for this virus. Man can also be infected with LCM virus either directly from feces or urine of mice or indirectly by inhaling the dried excreta carried on aerosolized dust originating from the animal cage or room. The wild house mouse plays an important role in the incidence of human disease from LCM vims (Dalldorf et aL, 1946; Mac Callum, 1949) . The original description of human infection with LCM was associated with a reservoir of the virus in the form of persistent latent infections in the wild house mice. Mus musculus (Armstrong and Lillie, 1934) . Although LCM infec tion can cause death in man, none of these cases was fatal, nor was there evidence of transmission by human contact. Several authors have emphasized that acutal handling of LCM-infected mice appeared to be important in causing the disease in humans (Havens, 1948; Smithard and Macrae, 1951) . The bite of an infected mouse can also cause human infection (Scheid et aL, 1964) .

In general terms, control of LCM is related directly to sani tary conditions in homes and laboratories; infestation of the premises with LCM-infected mice may increase the likelihood of LCM infection (Armstrong and Sweet, 1939 (Hotchin and Benson, 1973) . LCM virus can also occur spontaneously in cockroaches (Armstrong, 1963) .

Although its expression can vary greatly, LCM virus infec tion appears most frequently as a mild influenza-like syn drome, with or without apparent involvement of the central nervous system (Duncan et aL, 1951) .

In one epidemic of nonmeningitic LCM virus infection, caused by exposure to infected hamsters, an influenza-like ill ness was described with typical symptoms of retro-orbital headache, severe myalgia, malaise, anorexia, and aching pain in the chest (Baum et aL, 1966) . Fever was a consistent symp tom. The author compared this illness to the disease in two other meningitic human cases in his laboratory, caused by contact with infected mice. Sequelae to the initial infection can consist of arthritis, orchitis, parotitis, and a mild generalized alopecia of the scalp (Baum et aL, 1966; Lewis and Utz, 1961 ).

Rabies virus, a rhabdovirus, has been recognized since an cient times in Europe and Asia. This virus probably produces fatal disease, by inoculation, in all warm-blooded animals; mice must therefore be considered a potential source of rabies virus. In fact, laboratory diagnosis of rabies can be aided by intracerebral inoculation of mice with test suspensions.

Rabies occurs on all continents of the world except Australia;

islands such as New Zealand, Hawaii, and Great Britain are also free of the disease. It has been successfully excluded by rigid quarantine requirements. Rabies is uncommon in man, and its natural reservoirs are wild carnívora, bats, and rarely certain rodents, such as squirrels (Benenson, 1975) .

The incidence of rabies varies within select populations and geographic locations. No cases of human rabies in the United

States have been associated with the bite of rabid mice or rats.

However, in the Federal Republic of Germany, from 1961 to 1967, three mice, one rat (species unspecified), nine Norway rats, and eight muskrats were reportedly infected with rabies and had bitten humans (Scholz and Weinhold, 1969) .

Rabies is transmitted via virus-laden saliva and is inoculated by a bite of a rabid animal or contamination of a wound with sahva. Most rabid animals transmit virus 3-5 days before the appearance of clinical signs and during the course of clinical disease.

Rabies appears nearly the same in man and animals, with both furious and paralytic signs being presented. The incuba tion period can range from 12 days to 6 months or more.

In experimentally inoculated mice, paralysis of the hind limbs occurs as early as the seventh day or as late as the twenty-fifth day; death follows paralysis within 24 hr. Convul sions may be observed just before paralysis begins (Bruner and Gillespie, 1973) . Extreme caution should be used when work ing with experimentally infected mice, as with other infectious agents.

Other than in experimental settings involving rabies re search, routine antirabies prophylaxis is not practiced for indi viduals bitten by laboratory-reared mice. Though the likeli hood of rabid wild mice biting man is slim, the possibility does exist (Scholz and Weinhold, 1969) .

Three other viruses commonly associated with disease in mice have been implicated as being infective to man.

Complement-fixing and neutralizing antibody titers to mouse hepatitis virus, a Coronavirus, have been found in human sera (Hartley et aL, 1964) . The titer's presence is most likely due to cross-reactivity with antibody from infections with human coronaviruses, such as OC 38-OC 43 (Mcintosh et aL, 1967 (Mcintosh et aL, , 1969 and HCV 229B (Bradburne, 1970) , rather than to in dicators of zoonotic disease.

Another prevalent agent in mouse colonies, Sendai virus (parainfluenza virus), was originally isolated during an epidemic of fatal pneumonitis is Japanese children (Kuroya et aL, 1953a; Sano et aL, 1953) . Lung suspensions from fatal cases were inoculated intranasally into laboratory mice, and

Sendai virus was isolated from diseased lungs of the mice. A

year later, another investigator demonstrated the indigenous nature of the virus in mice (Fukumi et aL, 1954) . Rising antibody titers were demonstrated in patients, and the virus was supposedly capable of producing disease in human volun teers (see Parker and Richter, Chapter 8 , this volume, for a review). Others have also reported isolating the virus from cases of human respiratory illness (Gemgross, 1957; Kuroya et aL, 1953b; Zhdanoff et aL, 1957) . In a survey to detect the presence of antibody to murine viruses, antibody to Sendai virus was noted in personnel working with laboratory animals; significant titers were also present in personnel with no labora tory animal exposure (Tennant et aL, 1967) . Though a defini tive answer to the quesfion remains debatable, the antibody fiter is probably due to cross reactions with antigenically related parainfluenzea viruses ; see also Chapter 8, this volume).

Reovirus 3, a prevalent virus in mouse colonies, was first isolated in 1953 from the feces of a clinically ill child (Stanley et aL, 1953) . Since then, the presence of anfibody to reovirus 3 in human sera has been reported, although no human clinical syndrome has been well defined. The occurrence of reovirus 3 in mice and humans suggests possible natural transmission between these species and others that harbor these viruses.

Such transmission has yet to be demonstrated, but it may occur occasionally (Rosen, 1968 ).

A variety of rodent hosts are included in the transmission cycle of rickettsial disease in nature. The house mouse is the natural host of Rickettsia akari, the causative agent of ric kettsialpox and a member of the spotted fever group of ric kettsiae. The organism has also been isolated from rats {Rat tus) and voles (Microtus). Rickettsialpox in humans was first described by two physicians in New York City. The causative agent was isolated from the patient, the mite vector Liponyssoides {Allodermanyssus) sanguineus, and the wild house mouse (Huebner et aL, 1946a (Huebner et aL, ,b, 1947 which may infest rats (Flynn, 1973) . The tropical rat mite

bacoti, which also infests mice, has been infected experimentally but is not known to be in volved in the natural cycle of rickettsialpox.

Rickettsialpox is initially characterized by skin papules, chills, fever, and a rash; the clinical manifestafions range from mild to severe. Headache and general malaise, with muscular pain, are frequent. Clinical diagnosis is confirmed serologi cally by a positive complement fixation test between the sec ond and third week of the illness (Benenson, 1975) . Because many rickettsial infections mimic each other and occur in vary ing frequencies, rickettsialpox is difficult to diagnose either clinically or anatomically. Also, other bacterial and viral dis eases, such as typhoid fever, chickenpox, or measles, can pro duce similar febrile reacfions with an accompanying rash (Robbins, 1974) . Specific serologic tests (complement fixation and agglutination) are extremely important in making proper diagnoses. Skin biopsies may be helpful for early specific diagnosis (Dolgopol, 1948) . The blood of febrile patients can also be inoculated into mice and the organism recovered.

Laboratory mice are susceptible to R, akari; intranasal in oculation causes fatal pneumonia, and intraperitoneal injection of the organism produces severe illness and death in most animals. Anorexia, depression, and dypsnea are marked. Ne cropsy findings include peritonitis, splenomegaly, and lymph adenitis. Subcutaneous inoculation of R. akari causes active infection for 1 month, with organisms being recovered from the spleen but not from urine or feces. The nature of the natural infection in the mouse is not known (Bell, 1970) .

Control and eradication of the disease depend on preventing wild mice and the mite vector from entering animal research facilities and human dwellings.

Another rickettsial disease, murine typhus or endemic ty phus, is transmitted to man by rat fleas {Xenopsylla cheopis and Nasopsyllus fasciatus); rats and mice are its natural reser voirs. Rickettsia mooseri, the causative agent, has not been isolated from natural infections in laboratory mice. Clinical signs, diagnosis, and control in man are similar to those de scribed for rickettsialpox. A total of 18 laboratory workers were infected with R. mooseri while performing intranasal inoculations with this agent and while handling infected mice (Loffler and Mooser, 1942; Van den Ende et aL, 1943) .

Leptospira microorganisms were discovered in 1914, when isolated from jaundiced patients (Inada et aL, 1916) , and after further study were named in 1917 (Noguchi, 1918) .

Reservoir hosts of leptospirosis include rats, mice, field moles, hedgehogs, gerbils, squirrels, rabbits, hamsters, other mammals, and reptiles. A particular species of animal will usually act as the primary host of a particular serotype, but most serotypes can be carried by several hosts. Leptospira are well adapted to a variety of mammals, particularly wild ani mals and rodents; clinical manifestations in the chronic form are inconspicuous, with the organism being carried and shed in the urine for long periods of time. Rodents and perhaps hedgehogs are the only animal species that can shed leptospires throughout their life span without clinical manifestations (Babudieri, 1958; Faine, 1963 are found in the house mouse (Torten, 1979) . Leptospira baL lum has also been reported from mice and is most commonly associated with zoonotic outbreaks (Borst et aL, 1948; Fried mann et aL, 1973; Stoenner and Maclean, 1958) .

Rats and mice are common animal hosts for L. ballum, although it has been found in other wildlife, including skunks, rabbits, oppossums, and wild cats (Mailloux, 1975) . The infec tion in mice is inapparent and can persist for the animal's lifetime (Torten, 1979) . Although earlier reports indicated that several colonies of laboratory mice harbor the organism (Wolf et aL, 1949; Yager et aL, 1953) , no current estimates of the carrier rate among laboratory rodents in the United States are available. In several European laboratories, transmission of leptospires from laboratory rats to laboratory personnel has been reported (Geller, 1979) . In a study of leptospiral infec tions in feral rodents, 2673 rodents of 10 species were col lected in Georgia. Of the 933 tested for leptospires (by kidney culture), L. ballum was the only serotype cultured. It was isolated from 22% of the house mice and 0.8% of the old-field mice Peromyscus polionotus (Brown and Gorman, 1960) .

Since leptospirosis in humans is often difficult to diagnose, CDC, 1965 CDC, , 1966 Friedmann α/., 1973; Stoenner and Maclean, 1958) . Outbreaks in personnel working with laboratory mice in the United States have been documented (Barkin et aL, 1974; Boak et aL, 1960; Stoenner and Maclean, 1958 . In one study, 8 of 58 employees handUng the infected laboratory mice (80% of breeding females were excrefing L. ballum in their urine) experienced leptospirosis.

Humans have also contracted leptospiral infection by handling infected pet mice (Friedmann et aL, 1973) .

Infection with L. ballum most frequently results from han dling the infected mice (contaminafing the hands with urine) or from aerosol exposure during cage cleaning. Skin abrasions may serve as the portal of entry, since L. ballum presumably does not penetrate intact skin. In one instance, it was specu lated that a father was infected after his daughter, because of an argument, used his toothbrush to clean the contaminated pet mouse cage (Friedmann et aL, 1973) . Also, laboratory or wild mice that are to be used for primary kidney tissue cultures should be ascertained to be free of leptospires (Turner, 1970) .

Infected individuals experience a biphasic disease (Heath and Alexander, 1970) . They become suddenly ill with weak ness, headache, myalgia, malaise, chills, and fever. Leuko cytosis, usually associated with leptospirosis, is found incon sistently with L. ballum infection. During the second phase of the disease, a common finding is painful orchitis. Unlike the orchitis associated with mumps, leptospirosis caused en larged testes in only one patient (Friedmann et aL, 1973) .

Two infected personnel in a laboratory mice-associated out break required more than a month for recovery (Stoenner and Maclean, 1958) . Renal, liver, pulmonary, gastrointestinal, and conjunctival findings may be abnormal (Barkin et aL, 1974) .

Because of variability in the clinical symptoms and lack of pathognomonic pathological findings in man and animals, it is essential that serologic diagnosis or actual isolation of lepto spires be undertaken to establish a correct diagnosis (Torten, 1979) . As an aid to diagnosis, leptospires can somefimes be observed by examination or direct staining of body fluids or fresh dssue suspensions. A definitive diagnosis in man or mouse is made by culturing the organisms from üssue or fluid samples or by animal inoculation (particularly in 3-to 4-week-old hamsters) and subsequent culture and isolation.

rect hemagglutination, agglutination/analysis, complement fix ation, microscopic and macroscopic agglutination, and fluores cent antibody techniques (Stoenner, 1954; Torten, 1979) .

In a survey of trapped wild urban rats, diagnosis of lepto spirosis was more accurate by urine or kidney culture, rather than by either indirect fluorescent antibody or macroscopic slide agglutination (Sulzer et al., 1968) . Another survey of wild rats confirmed that culture techniques identified more positive rats than did macroscopic slide agglutination (Higa and Fujinaka, 1976) .

In mouse colonies infected with L. ballum, antibodies against L. ballum were detected in sera of mice of all ages, but leptospires could be recovered only from mature mice. Pro geny of seropositive females had detectable serum antibodies at 51 days of age, but not at 65 days. It was also reported that progeny of seropositive female mice, which possessed anti body at birth and acquired additional antibody from colostrum, remained free of leptospires if isolated from their mothers at 21 days of age, despite exposure durirj the nursing period (Stoenner, 1957) . cant. This led to the diagnostic approach, which specifies that both serologic and isolation methods must be utilized to deter mine the rate of leptospiral infection in rodents (Galton et al., 1962) .

Leptospira ballum is found frequently in the common house mouse (M. musculus) (Brown and Gorman, 1960; Yager et al., 1953) . Therefore, eradication of infected colonies, use of surgically derived and barrier-maintained mice or of conven tional laboratory mice free of leptospira infection, coupled with the prevention of ingress of wild rodents, should effec tively preclude introduction of the organism into research and commercial laboratories (Loosli, 1967) . Leptospira ballum has been elminated from a mouse colony by administration of feed containing 1000 gm chlorotetracycline hydrochloride per ton for 10 days. After 7 days of antibiotic therapy, mice were transferred to clean containers and administered clean water, both having been sterilized by steam. Mouse traps and DDT were used to destroy escaped mice and to prevent reintroduction of L. ballum by the common house mouse . 

Pasteurella pneumotropica, first identified and studied in 1948 (Jawetz, 1948 (Jawetz, , 1950 (and rarely P. multocida or Y.

pseudotuberculosis), usually occur as latent infections, though they can be a primary pathogen in laboratory mice (Brennan et al., 1965 (Brennan et al., , 1969 Hoag et al., 1962) . However, these or ganisms are rarely associated with human disease. Although direct transmission of P. pneumotropica from mice to man has not been reported, this organism has been transmitted via the bites of other animals (Miller, 1966; Olson and Meadows, 1969; Winton and Mair, 1969) . Because mice harbor this or ganism in the upper respiratory system and pharynx, exposure could result from mouse bites.

Reported cases in man are usually attributed to animal bites or exposure to ill animals. Also, P. pneumotropica was report edly introduced into a barrier-maintained, specific pathogenfree (SPF) rat and mouse colony by personnel working in the area, who carried this organism in their upper respiratory sys tem (Wheater, 1967) . Pasteurella pneumotropica with similar biochemical characteristics was isolated from sputum and sinus infections from humans (Henriksen and Jyssum, 1961; Henriksen, 1962 ). An organism closely related to P. pneumotropica was recovered from 1 % of sputum samples obtained during an 8-month period at a public health laboratory in England (Jones, 1962) . It is suspected, however, that transmission of pas teurella infection from man to mice is rare, and despite the lack of confirmatory literature, transmission of pasteurella or ganisms from mouse to man probably is also rare.

Pasteurellosis is seldom reported in man, possibly because Pasteurella is usually an opportunistic pathogen with low pathogenicity for man or because the organism may be con fused with Hemophilus influenzae or Acinetobacter sp. (e.g., (Freigang and Elliott, 1963; Schipper, 1947) . Deaths from P. pneumotropica infection have been recorded: One 51-year-old man died 48 hr after being bitten by a dog (Miller, 1966) . Local inflammation, purulent discharge, pyrexia, and pain have been caused by bite wounds from which P. pneumotropica has been isolated (Olson and Meadows, 1969) . Similarly, P. multocida was isolated from a wound after a bite from a laboratory rat, although the organism was not found in subsequent cultures from the rat (Bergogne- 1972) . Septicemia and meningitis due to pas teurella have also been reported (Cooper et aL, 1973; Rogers et aL, 1973) . Hubbert and Rosen (1970) listed 316 cases of P. multocida in man, usually associated with animal exposure.

Berezin et al,

in man is reported rarely, but man can develop severe systemic infections from it. Arkless (1970) and Gilbert et al. (1911) described infection caused by the bite of a laboratory mouse and a pet mouse, respectively. The disease is not commonly reported in man but has been reported in personnel engaged in research involving laboratory rodents, particularly rats (Cole et aL, 1969; Gilbert et al., 1971; Holden and MacKay, 1964) . Historically, how ever, wild rat bites and subsequent illness have been associated with social conditions of poor sanitation and overcrowding, and almost 50% of all cases have involved children under the age of 12 (Brown and Nunemaker, 1942; Raffin and Freemark, 1979; Richter, 1945; Roughgarden, 1965) .

Rat-bite fever is not a reportable disease; thus, its incidence, geographic location, racial data, or source of infection in hu mans is difficult to assess. Acute febrile diseases, especially if associated with animal bites, are routinely treated with penicil lin or other antibiotics without prior culturing of the bite wound. This therapeutic approach, though successful in abort ing cases of potential rat-bite fever, does not allow accurate recording of the disease in humans. One would suspect, there fore, because of the high number of rodent bites suffered by humans, that the incidence of rat-bite fever is low.

Rat-bite fever can be caused by either of two microor ganisms: Streptobacillus moniliformis (Actinomyces muris) or

synonym (sodoku).

These organisms are present in the oral cavity and upper respiratory passages of asymptomatic rodents. Reported inci dences of mice as asymptomatic carriers of S. moniliformis or Sp. minus were not found. Nearly 50% of the asymptomatic laboratory rats cultured in an early study harbored S.

as normal oral flora (Strangeways, 1933 (Holmgren and Tunevall, 1970; Rogosa, 1974) .

The bite of an infected rodent, usually a wild rat but occa sionally a laboratory rat or mouse, is the usual source of infec tion. In some reported cases, infection was attributed to dog, cat, or other animal bites and rarely to traumatic injuries unassociated with animal contact (Richter, 1945; Roughgarden, 1965 

Incubation varies from a few hours to 1 -3 days in infection with S. moniliformis and may range from 1 to 6 weeks with 

Although there are 1600 recognized serotypes. Salmonella typhimurium and S. enteritidis have been associated most commonly with infections in laboratory mouse colonies (Haberman and Williams, 1958; Hoag and Rogers, 1961) .

Other serotypes have also been reported in mice (Ganaway, Chapter 1, this volume). From 1974 to 1978, the most fre quently isolated serotype in the United States was S.

typhimurium (CDC, 1976; MMWR, 1980) . Other frequently isolated serotypes were S. newport, S. enteritidis, and S. heidelberg.

Salmonella infection in man and animals, including mice, occurs worldwide. The organism is an enteric bacterium in habiting the intestinal tract of many animals. Salmonella are routinely associated with food-borne disease outbreaks, are contaminants of sewage, and are found in many environmental water sources.

Although the reported incidence of salmonella in laboratory mice has decreased in the last several years because of man agement practices, environmental contamination with sal monella continues to be a potential source of infection for laboratory animals and, secondarily, for personnel handling these animals. Animal feed containing animal by-products con tinues to be a source of salmonella, especially if diets consist of raw meal and have not undergone a pelleting process (Hoag et al., 1964; Stott et al., 1975; Williams et aL, 1969) . Until rodent feeds in the United States and Europe are salmonellafree, laboratory rodent-associated cases of salmonellosis will remain a distinct possibility. and had infected food in the bakery (Brown and Parker, 1957) .

In another study, salmonella serotypes were isolated from 17% of 170 wild house mice. The authors concluded that house mice are a reservoir of infection and play an important role in human and animal salmonellosis (Shimi et aL, 1979) . Un doubtedly, rodent excreta is the source of other food-fome outbreaks.

Both man and animals are carriers and periodic shedders of salmonella; they may have mild, unrecognized cases or they may be completely asymptomatic. Asymptomatic animals that shed salmonella are particularly important in biomedical re search because they are a potential source of infection for other animals, animal technicians, and investigators (Fox and Beaucage, 1979) . The incidence of carrier mice in the colony may vary from 1% to 20% (Haberman and Williams, 1958) ;

indeed, one investigator suggested that clinically apparent sal monellosis is rare in infected mice (Margard etal., 1963) . In a survey of 19,137 nonhuman-origin salmonella isolations from pet-type animals, conducted in the United States from 1962 to 1965, a total of 227 isolates were recovered from rodents (Kaufman, 1966) . The incidence of salmonellosis in man ac quired from mice or vice versa is unknown; however, a treatise on diseases of laboratory mice (Hoag and Meier, 1966) states, "Occasional paratyphoid carriers are found among mouse handlers, but are not important sources of animal infection" (p. 594). No further expansion of this statement was provided.

The most common clinical sign of salmonellosis in man is acute gastroenteritis with sudden onset, abdominal pain, diarrhea, nausea, and fever. Loose bowels and anorexia may persist for several days. When organisms invade the bowel wall, some cases can lead to febrile septicemia without severe intestinal involvement; in these cases, most clinical signs are attributed to hematogenous spread of the organisms (Robbins, 1974 

Erysipelas, caused by Erysipelothrix rhusiopathiae, which affects a variety of fishes and mammals, including man, was first recognized when Koch discovered an organism he called

The disease in man, called erysipeloid (not human erysipelas), was recognized by Rosenbach in 1887. The first report of natural infection in wild mammals appears to be an epizootic among migrating meadow mice and house mice in California (Wayson, 1927) . Although the laboratory mouse is susceptible to experimental infection, neither natural disease nor human infection from handling dis eased mice has been reported. (Dvorak and Otechenasek, 1964; Krempl Lamprecht and Bosse, 1964; Maφles, 1967; Refai and Ali, 1970) . In almost all mouse-associated ringworm infections in man, T. mentagrophytes has been isolated as the etiological agent (Table I) .

A.

Dermatophytes are distributed throughout the world, with some species being reported more commonly in certain geo graphic locations. For example, in a study of small mammals in their natural habitat, T. mentagrophytes was isolated from 57 of 1288 animals representing 15 different species. The der matophyte was isolated most commonly from the bank vole (Clethrionomys glariolus), followed by the common shrew (Sorex araneus) and the common house mouse (M. musculus) (Chmel et al., 1975) . In this survey, agricultural workers, exposed to these mammals in granaries and bams, risked con tracting T. mentagrophytes infection. Trichophyton menta grophytes was isolated from 77% of the 137 agricultural work ers infected with ringworm, whereas T. verrucosum was iso lated from only 23% of the cases. In the same study, of 445 ringworm-infected personnel working with farm animals, 75%

were infected with T. verrucosum and 28% with T. menta

Human infection with T. mentagrophytes has also followed handling of bags of grain in which mice had been living (Alteras, 1965; Blank, 1957) . Thus, specific exposure to Davies and Shewell (1964) White mice 1 laboratory worker % ND, loss of hair, increased scaling on head and back, 10 mice Booth (1952) White mice 1 bacteriologist 60 of400, crusted or crustless plaques, circular with prominent periphery; general alopecia; mortality in some mice Cetin etal. (1965) reservoir hosts harboring different dermatophytes determines the type and incidence of infection in man.

tic and is not recognized until personnel become infected. A prevalence of Γ. mentagrophytes among laboratory mouse stocks as high as 80-90% has been recorded (Davies and Shewell, 1964 

The disease, dermatomycosis or ringworm in man, is non fatal, often self-limiting, sometimes asymptomatic, and thus often ignored by the affected person. In general, the der matophytes cause scaling, erythema, and occasionally vesicles and fissures. The fungi cause thickening and discoloration of the nails. On the skin of the tmnk and extremities, the lesion may consist of one or more circular lesions with a central clearing, forming a ring (Fig. 1 ) (Mescon and Grots, 1974) . T h e author concluded that h u m a n -r o d e n t contact is not respon sible for the introduction of Entamoeba s p . (most likely E. muris) in S P F barrier-maintained rodent colonies. There is n o evidence in the literature that h u m a n s are E. muris carriers.

T h e m o u s e can be infected experimentally with E. his tolytica, but natural infections with this parasite have not been reported (Flynn, 1973) .

Entamoeba coli, SL nonpathogenic protozoan in m a n , is m o φ h o l o g i c a l l y similar to E. muris seen in mice and rats. It is not definitely k n o w n whether transmission between h u m a n s and rodents is possible. A n early report described the estab lishment of E. coli infection in rats; however, little attempt was m a d e to reduce the possibility of cross-infection with E.

muris (Kessel, 1923) . In a later thorough study, E. coli w a s not transmitted to or established in either mice or rats (Neal, 1950 Larval development in Tribolium s p . at 30°C requires 8 days.

Therefore, man becomes infected only by ingestion of infected insects, such as flour beetles, which may contaminate rodent food or cereal marketed for human consumption.

The infection in man is usually asympto matic, but in moderate to heavy infections it may cause head aches, dizziness, and abdominal discomfort.

The dwarf tapeworm is a common parasite of both the wild house mouse and the labora tory mouse. As indicated earher in the text, in most wellmanaged mouse colonies, H. nana incidence is low compared to earlier reports of its high incidence in rodent colonies (Wes cott, Chapter 20, this volume).

North America and 20 million in the world. Surveys conducted in Central Europe report that this tapeworm in man is more prevalent in warm than in temperate regions. An incidence of 10% has been noted in some South American countries (Jelliffe and Stanfield, 1978 (Jelliffe and Stanfield, 1978) . The diagnosis was based on idenfificafion of the characteristic eggs or proglotfids in the stool.

Syphacia obvelata is a ubiquitous parasite in both wild and laboratory mice. Although parasitology texts report that Syphacia is infectious to man, this citation originates from a publicafion in 1919, in which two S. obvelata aduh worms and eggs reportedly were found in the formalin-preserved feces of a Filipino child whose enfire family of five was infected with H.

nana (Riley, 1919) . No menfion is made of the method of collecfion of the feces, whether the feces could have been contaminated with murine feces or with the parasite and/or eggs. The only other report is an unpublished finding of S. muris eggs in the feces of two children and two rhesus monkeys, cited in a personal letter from Dr. E. C. Faust of Tulane University, dated January 6, 1965 (Stone and Manwell, 1966 

Contamination of food or utensils, or accidental ingestion of Syphacia ova (e.g., via contaminated hands) could result in infection of man. People working with infected mice probably ingest ova occasionally, but there is no evidence that acfive infection results from this exposure.

Because Syphacia infection in man has not been described, clinical signs have not been noted.

There are striking differences in size between specimens of female. S. obvelata and those of Enterobius vermicularis, the pinworm, in man (Markell and Voge, 1965 

Though many species of mites are found on laboratory mice, only Ornithonyssus bacoti, the tropical rat mite, and Liponyssoides sanguineus, the house mouse mite, are vectors of human disease. Ornithonyssus bacoti is seen in laboratory "For more information regarding life cycles, pathogenicity, and host range, see Flynn (1973) .

mice ( F o x , 1982) ; L. sanguineus has been identified only on wild m i c e (Table II) 

During a 2-year surveillance period (1971-1972), 196,684 animal bite cases were reported from the 15 reporting areas in the United States (Moore et aL, 1977) . The type of biting animal was reported for 196,117 persons bitten; 4% were ro dents, type unspecified. By tradition, and public emotion, rabies has been the primary reason for investigating animal bite cases. Rodent bites (especially from wild rats), however, pre sent other serious public health hazards, particularly in im poverished areas, where feral rodents are plentiful. Important effects of animal bites that must be considered are pain, anx iety, disfigurement, and infections caused by bacteria such as Pasteurella spp., Clostridium tetani, S. moniliformis, and Sp.

minus. Reported incidences and severity of laboratory rodentassociated bites are few, except for published cases of rat-bite fever and Pasteurella infections (Hubbert and Rosen, 1970) .

Depending on the nature of the wound and the health status of the animal inflicting the bite, medical attention may be re quired. Minimally, for minor mice bites, the wound should be cleaned thoroughly and treated topically as necessary. Current tetanus immunizations should be maintained for personnel working with animals (ILAR, 1978).

Allergic skin and respiratory reactions are quite common in laboratory workers working with mice. Hypersensitivity reac tions to mouse dander and urine are serious occupational health problems. Because of the large number of mice used in biomedical fields, numerous people are constantly exposed to laboratory mouse allergens. Historically, it was believed that only rabbit and cat danders produced laboratory animal-related asthma. This notion has been disproven and the mouse has been incriminated in producing asthma (Rajka, 1961; Newman-Taylor et al., 1977) . A biologist developed a typical mild anaphylactic reaction with hypotension, asthma, and giant urticaria after a mouse bite (Lincoln et al., 1974) . Hyper sensitivity reactions include nasal congestion, rhinorrhea.

sneezing, itching of the eyes, angioedema, and asthma. These would also include various skin manifestations such as localized urticaria and eczema (atopic dermatitis). Skin wheal and flare reactions were demonstrated in eight subjects sensi tive to mice when tested with mouse pelt extracts (Ohman et al., 1975) . Maximal allergenic activity was demonstrated when the skin testing was done using the extract fraction which had the electrophoretic mobility of albumin. Figs. 3 and 4 illustrate a typical wheal and flare reaction on the skin of a patient who is hypersensitive to mouse urine. The patient de veloped hypersensitivity after working with mice for several years. A mouse whose feet were contaminated with urine walked across the patient's arm and produced these lesions.

Often the complaint is manifested by intense itching when the mouse urine or serum has touched the skin (Ohman, 1978) .

Delayed reactions are also seen. Asthma may develop during the night after an exposure during the working day.

Some allergic disorders exhibit a familial prevalence. This familial predisposition to respond to allergies is called atopy and suggests that inheritance plays a role in the pathogenesis of atopic diseases (Gupta and Good, 1979) . Members of the same family may manifest their atopy in different ways, with some having asthma and others eczema. These clinical manifesta tions of atopy are determined by the location of the shock organ, i.e., the skin, mucous membranes, respiratory or gas trointestinal tracts (Criep, 1976 ).

It appears that the major sources of antigen for personnel working with mice would be mouse dander (Sorrell and Gottesman, 1957; Lincoln et al., 1974) and mouse urine (Newman-Taylor et al., 1977) . Newman-Taylor evaluated five patients, all of whom had a history of hay fever or asthma.

Four of these patients handled mice. Levy (1974) studied and quantitated allergic activity of pro- (Schumacher, 1980) .

Other antigens in laboratory animal quarters m a y cause al lergic reactions; these include mold spores and proteins in food that might be aerosolized (Patterson, 1964) . responses, including smooth muscle contraction, vascular dila tation, and increased vascular permeability. T h e allergic reac tion described above is often classified as type I.

T y p e II reactions occur when an IgG or I g M antibody reacts

with an antigen on target cells. This reaction activates com plement which causes cell lysis (Lutsky and Toshner, 1978) . This type of reaction is most often seen w h e n drugs act as the antigen and therefore is relatively unimportant in people work ing with laboratory mice. sure often helps to narrow the n u m b e r of allergens considered in the differential diagnosis. Nonoccupational exposure to po tential allergens must also be considered. T h e family history of allergy is also important, since atopy predisposes a person to type I allergic reactions.

T h e physical examination must be thorough and well documented; often a repeat physical examination is helpful if performed when the patient is not having an acute allergic attack. Repeated pulmonary function tests, especially when the lungs are the target organ, are often helpful; radiological exam inations are occasionally used. Bronchial challenge tests with suspected allergens, though rarely indicated and difficult to evaluate, together with pulmonary function tests may detect the efiologic allergen. Skin testing with suspected antigens often identifies the hypersensitivity. Skin tests are almost al ways positive when properly done on a pafient who has type I sensifivity to animal dander. Useful laboratory tests include a complete blood count; immunoglobulins and IgE anfibody spe cific to one allergen, as measured by the radio-allergosorbent test (RAST); nasal smears for eosinophilia; and serum precipitants to specific allergens. The in vitro RAST, however, is less sensitive and no more specific than the skin test. The direct eosinophil count is another useful laboratory test; it is often elevated in the presence of nasal allergy and is almost always elevated in patients with asthma.

caps on animal cages, using exhaust hoods when working with mice, and using protective clothing, masks, or respirators when working with mice.

With the adoption of modem laboratory animal manage ment, which includes routine disease surveillance, proper sani tary regimens, acceptable personal hygiene, and personnel health monitoring, laboratory mice usually do not present a zoonotic or health hazard. Well-designed animal facilities to prevent ingress of wild rodents and other vermin help preclude the introduction of animal and human pathogens. Careful atten tion to design of caging and air-flow dynamics within animal rooms is necessary to minimize exposure to allergens.

After an allergic disorder associated with exposure to mice has been diagnosed definitely, pharmacological agents are often used to relieve the acute attack. Useful agents include antihistamines, sympathomimetic agents, corticosteroid, and bronchodilators. Some pharmacological agents are somewhat useful on a long-term basis; these include antihistamines for allergic rhinitis, allergic conjunctivitis, and allergic skin reac tions. /3-Adrenergic agonists, cromolyn sulfate, and xanthines are sometimes useful in asthmatic patients.

Immunotherapy has been employed to reduce symp tomatology of a laboratory worker sensitive to mice (Sorrell and Gottesman, 1957) . Allergen immunotherapy is the sys temic administration of etiological antigens in increasing dos ages to produce hyposensitivity to animal proteins in the patient. This type of therapy may not be recommended because in highly sensitive individuals, it can be accompanied by uncom fortable local and systemic reactions. There is also a serious risk of inducing anaphylaxis in the patient (Gupta and Good, 1979) . The risk of treatment of patients with animal dander extract, however, is probably no greater than that of treatment with pollen extracts. Newer forms of immunotherapy are still experimental, but some may prove clinically useful. Complete avoidance of the offending antigen is the method of choice for preventing an allergic reaction to mice. However, when com plete avoidance of the allergen is unfeasible for socioeconomic reasons such as eaming a living, other avenues of treatment and control must be considered (Lutsky and Toshner, 1978) .

Reduction of the contact intensity of the offending allergen is frequently used. Methods include reduction of direct animal contact time, increasing the room ventilation, employing filter

The relationship of Trichophy ton quinckeanum to Trichophyton mentagrophytes

Human infection from laboratory animals

Rat-bite fever at Albert Einstein Medical Center

Lymphocytic choriomenigitis

Experimental lymphocytic chorio meningitis of monkeys and mice produced by a virus encountered in studies of the 1933 St. Louis encephalitis epidemic

Lymphocytic choriomeningitis; report of 2 cases, with recovery of the virus from gray mice {Mus musculus) trapped in 2 infected households

Lymphocytic chorio meningitis: gray mice, Mus musculus, a reservoir for the infection

Animal reservoirs of leptospires

Infection by Leptospira ballum: a laboratory-associated case

Epidemic nonmeningitic lymphocytic-choriomeningitis-virus infectionan outbreak in a population of laboratory personnel

Tick-borne (pasture) fever and rickettsial pox

Control of Communicable Diseases in Man

Human Pasteurella infections from bites: epidemiologic survey in a laboratory environment

The influence of maternal antibodies on the epidemiology of leptospiral carrier state in mice

The apparent transmission of staphylococci of human origin to laboratory animals

Favus of mice

A case of Lepto spirosis ballum in California

Mouse ringworm

Eeen Geval van Leptospirosis Ballum

Antigenic relationships amongst Coronavirus

Pasteurella pneumo tropica: cultural and biochemical characteristics and its association with disease in laboratory animals

Murine pneumonia: a review of the etiologic agents

Salmonella infection in rodents in Manchester

The occurrence of leptospirosis in feral rodents in southwestern Georgia

Rat-bite fever: review of Ameri can cases with re-evaluation of its etiology and report of cases

Hägen's Infectious Diseases of Domestic Animals

Favus heφeticus, or mouse favus: possibility of production of favus in man from Australian wheat

Epizootic of Trichophy ton mentagrophytes {interdigitale) in white mice

Spread of Trichophyton mentagrophytes Var. Gran, infection to man

Rat-bite fever

Murine virus contaminants of leukemia viruses and transplantable tumors

Zoonoses Surveillance: Lep tospirosis

Zoonoses Surveillance: Lep tospirosis Annual Summary

Salmonella Surveillance: An nual Summary 1975

Pasteurella meningitis

Fungal diseases of rats and mice

Allergy and Clinical Immunology

Multiple cases of choriomeningitis in an apartment harboring infected mice

The use of pathogen free animals

Control of mouse ringworm

Streptococci. In "Microbiology

Ringworm epizootics in laboratory mice and rats; experimental and accidental transmission of infection

Histologic changes in rickettsial pox

Lymphocytic choriomeningitis. Review of ten cases

Geophites zoophilic and anthropohilic dermatophytes: a review

Bacterial interference and staphylococcal coloniza tion in infants and adults

Antibody in the renal tubules and urine of mice

Craig and Faust's Clinical Parasitol ogy

The virus aetiology of one form of lymphocytic meningitis

Rolling disease-new syndrome in mice associated with a pleuropneumonia like organism

Mites. In "Parasites of Laboratory Animals

The incidence of salmonella in random-source cats purchased for use in research

Ulcerative dermatitis in the rat

Outbreak of tropical rat mite dermatitis in laboratory personnel

Pasteurella séptica infections in humans

Leptospirosis ballum contracted from pet mice

A pneumotropic virus from mice causing hemagglutination

Leptospirosis

Health hazards for man

Peculiarities of the 1956 influenza outbreak in Vla divostok due to D. virus

Rat-bite fever

Cellular, Molecular and Clinical Aspects of Allergic Disorders

Salmonellosis in laboratory animals

Antibodies to mouse hepatitis viruses in human sera

LCM: Report of a case occurring in a granary harboring infected mice

Joseph Brenneman's Practice of Pediatrics

Serological studies with Sendai virus

Some pasteurella strains from the human respiratory tract

A study of some pasteurella strains from the human respiratory tract

Prevalence of rodent and mongoose leptospirosis on the island of Oahu

Infectious diseases

Techniques for the isolation of Sal monella typhimurium from laboratory mice

A study of latent pasteurella infection in a mouse colony

Isolation of Salmonella spp. from laboratory mice and from diet supplements

Rat-bite fever-an occupational hazard

Case report: rat-bite fever. Scand

The contamination of laboratory animals with lymphocytic choriomeningitis virus

Infectious Diseases of Wild Mammals

Pasteurella multocida infection due to animal bite

Serum antibody response in a population of Microtus californicus and associated species during and after Pasteurella pestis epizootics in the San Francisco Bay area

Rickettsialpox-a newly recognized rickettsial disease. I. Isolation of the etiological agent

Rickettsialpoxa newly recognized rickettsial disease. IV. Isolation of a rickettsia apparendy identical with the causative agent of rickettsialpox from Allodermanyssus sanguineus, a rodent mite

Rickettsialpox-a newly recognized rickettsial disease. V. Recovery of Rickettsia akari from a house mouse {Mus musculus)

The etiology, mode of infection and specific therapy of Weil's disease

A latent pneumotropic pasteurella of laboratory animals

A pneumotropic pasteurella of laboratory animals. I. Bac teriological and serological characteristics of the organism

Diseases of Children in the Subtropics and Tropics

A pasteurella-like organism from the human respiratory tract

Pets and salmonella infection

Experimental infection of rats and mice with the common intestional amoebae of man

Epidermophyton floccosum (Harz) Langeron und Milochevitsch als spontanin fektion bei Mausen

Newborn virus pneumonitis (type Sendai) II. Report: the isolation of a new virus pos sessing hemagglutinating activity

Newbom virus pneumonitis (type Sendai). II. The isolation of a new virus

Lymphocytic choriomeningitis virus

Allergic activity of proteins from mice

Orchitis, parotitis, and meningoen cephalitis due to lymphocytic-chorio-meningitis virus. Λ^, Engl

Occupational allergy to animal dander and sera

The characterization of an unidentified virus found in association with Line 1 Leukemia

Mode of transmission of typhus fever. Study based on infection of group of laboratory workers

Zoonoses in common laboratory animals

A review of allergic respiratory disease in laboratory animal workers

The virus of lymphocytic choriomeningitis (LCM) as a cause of benign aseptic meningitis. Laboratory diagnosis of five cases

Ratbite fever due to Streptobacillus moniliformis

Growth in suckling-mouse brain of "IBV-like" viruses from patients with upper respiratory tract disease

Antigenic relationships among the corona viruses of man and between human and animal coronaviruses

Trichophyton mentagrophytes in mice: infec tions of humans and incidence amongst laboratory animals

Leptospiroses-Zoonoses

Salmonellosis in mice-diagnostic procedures

Nondomestic animals in New Zealand and in Rarotonza as a reservoir of the agents of ringworm

Lymphocytic choriomeningitis

The skin

Human pasteurellosis in New York State

Surveillance of animal-bite cases in the United States

Human Salmonella isolates-United States, 1978, surveillance summary

An experimental study of Entamoeba muris (Grassi 1879); its moφhology affinities and host parasite relationship

Respiratory allergy to urine proteins of rats and mice

Relationship of habits of house mouse and mouse mite {Allodermanyssus sanguineus) to spread of rickettsialpox

Moφhological characteristics and nomenclature of Lep tospira (Spirochaeta) icterohemorrhagiae (Inada and Ido)

Allergy in man caused by exposure to mammals

Allergens of mamma lian origin

Pasteurella pneumotropica infec tion resulting from a cat bite

Attempted transmission of Entamoeba coli to specifiedpathogen-free rodents

Microbial flora of the larynx, trachea, and large intestine of the rat after long-term inhalation of 100 percent oxygen

Lymphocytic choriomeningitis virus infection in fetal, new born, and young adult Syrian hamsters

The problem of allergy to laboratory animals

Erythema Arthriticum Epidemicum (Haverhill Fever)

A survey of indigenous murine viruses in a variety of production and research animal facilities

Streptobacillary rat-bite fever: a pediatric problem

Ten cases of occupational hypersensitivity to laboratory animals

Laboratory acquired infection with Keratinomyces ajelloi

Staphylococcal pneumonia in a labora tory rabbit: an epidemiologic follow-up study

Incidence of ratbites and ratbite fever in Baltimore

A mouse oxyurid, Syphacia obvelata, as a parasite of man

Pathologic Basis of Disease

Septicaemia due to Pasteurella pneumotropica

Streptobacillus moniliformis and Spirillum minor

Reoviruses

Antimicrobial therapy of rat-bite fever

Nasal carriers of Staphylococcus aureus by various domestic and laboratory animals

Newbom virus pneumonitis (type Sendai). I. Report: Clinical observation of a new virus pneumonitis of the newborn

Distri bution of the virus of LCM in Western Germany

Unusual pathogenicity of Pasteurella multocida isola tion from the throats of common wild rats

Epidemiology of rabies in rats and mice

Characterization of allergens from urine and pelts of laboratory mice

Studies on salmonellosis in the house mouse Mus musculus

Staphylococcal botryomycosis in a specific-pathogen-free mouse col ony

Monitoring mouse stocks for lymphocytic choriomeningitis virus-a human pathogen

LCM: Associated human and mouse infections

LCM in a mouse breeding colony

Mouse allergy: case report

Studies on the pathogenesis of a hitherto undescribed virus (Hepatoencephalomyelitis) producing unusual symptoms in suckling mice

Lymphocytic choriomeningitis in mouse neoplasms

Application of the capillary tube test and a newly developed plate test to the serodiagnosis of bovine leptospirosis

The laboratory diagnosis of leptospirosis

Leptospirosis (ballum) contracted from Swiss albino mice

Elimination of Leptospira ballum from a colony of Swiss albino mice by use of Chlortetracycline hydrochloride

This wormy world

Potential helminth infections in humans from pet or laboratory mice and hamsters

Incidence of Salmonel lae in animal feed and the effect of pelleting on content of enterobacteriaceae

Rats as carriers of Streptobacillus moniliformis

Compaison of diagnostic technics for the detection of leptospirosis in rats

Mouse leukemia, XIV. Freeing Line I from a contaminating virus

Incidence of murine virus antibody in humans in contact with experimental animals

Viruses transmissable from laboratory animals to man

Leptospirosis. In "CRC Handbook Series in Zoonoses

Leptospirosis III

Laboratory infection with murine typhus

An outbreak of Pseudomonas aeruginosa infection in a colony pre viously free of this infection

Development of Hymenolepis nana and Hymenolepis diminuta (Cestoda: Hymenolepididae) in the intermediate host Tribolium confusum

The Zoology of Tapeworms

An epizootic among meadow mice in California, caused by the bacillus of mouse septicemia or of swine erysipelas

Isolation of LCM virus in an effort to adapt poliomyelitis virus to rodents

The bacterial flora of an SPF colony of mice, rats and guinea-pigs

A tenmonth study of Salmonella contamination in animal protein meals

Pasteurella pneumotropica isolated from a dog-bite wound

Researches on Lepto spirosis ballum-The detection of urinary carriers in laboratory mice

Natural occurrence of Leptospira ballum in rural house mice and in an opossum

Infections of laboratory animals potentially dangerous to man: ectoparisites and other arthropods, with emphasis on mites

Influenza D in early infancy