key: cord-022203-t2f0vr1w
authors: Dowers, Kristy L; Lappin, Michael R
title: The pyrexic cat
date: 2009-05-15
journal: Problem-Based Feline Medicine
DOI: 10.1016/b978-0-7020-2488-7.50024-7
sha: 
doc_id: 22203
cord_uid: t2f0vr1w

nan

• Temperature > 39.2˚C (102.5˚F).

• True fever results from a cascade of events, which starts with activation of leukocytes.

Pyrogenic factors released from the leukocytes increase the thermoregulatory set point in the hypothalamus. Signs that may be associated with fever include: • Elevated body temperature. • Reluctance to move. • Anorexia. • Depression. • Hyperpnea. • Muscle or joint stiffness/discomfort. • Shivering.

• Inflammation anywhere in the body can result in elevation of core body temperature above 39.2˚C (102.5˚F).

• The most common etiology for fever in the cat is percutaneous cellulitis or abscess. Viral diseases such as FIV, FeLV and FIP are important diseases to consider.

Conjunctivitis is the predominant sign and is often initially unilateral and becomes bilateral. Ocular discharge is serous initially then mucopurulent, but is usually mild. Fever, anorexia and lethargy may occur.

True fever must be differentiated from hyperthermia, which can be caused by increased muscle activity, increased environmental temperature and stress.

True fever results from activation of leukocytes that release factors (pyrogens) such as interleukin-1 and tumor necrosis factor. • These factors cross the blood-brain barrier and increase the thermoregulatory set point in the hypothalamus.

• Leukocytes are activated by a multitude of infectious agents, neoplasia, tissue necrosis and immune-mediated diseases.

Fever is defined as systemic elevation of core body temperature above 39.2˚C (102.5˚F).

The most accurate measurement of core body temperature is obtained rectally.

Aural temperature is approximately −17.2˚C (0.5˚F) lower than the rectal temperature.

Fever is a general clinical sign that can be associated with many different diseases.

The most common disease causing fever in the cat is percutaneous cellulites or abscess.

Many viral and bacterial diseases cause fever because leukocytes are recruited and activated as part of the general immune response.

Organ inflammation, such as pancreatitis, cholangiohepatitis and myocarditis, can be associated with an elevated temperature even when an infectious agent is not present.

Classical signs • Fever. • Anorexia (partial or complete). • Reluctance to move, lethargy and depression. • Pain, heat or swelling at site of abscess or cellulitis.

Cellulitis usually precedes an abscess, and if treated appropriately, the abscess may not even form.

Cellulitis may be the only evidence of a previous abscess.

An abscess may rupture spontaneously, and the owner may notice foul-smelling, purulent discharge on the fur.

• Some abscesses resolve on their own with or without rupture, if they have been present long enough.

Regional lymphadenopathy may occur near the affected site.

Cellulitis spreads rapidly with the development of multiple fistulae and a febrile response.

• Lameness from septic arthritis is a common sequelae to infection with L forms. Joints are affected by the hematogenous route and may be distant to the initial site. Lower limbs (tarsus and carpus) are most commonly affected. The joints often ulcerate with a grayish mucinous exudate. Infection remains confined to subcutaneous tissues and joints without systemic spread to internal organs.

History supports access to outdoors or conflict with other cats indoors.

Palpation reveals a tender area or fluctuant swelling, with or without evidence of puncture wounds.

Microscopic examination of a fine-needle aspirate of the abscess reveals a heterogeneous population of bacteria, numerous degenerate neutrophils and intracellular bacteria.

A complete blood count will generally show neutrophilia.

L forms are not visible in tissue samples even with special stains, nor do they grow on culture. On electromicroscopy, organisms are visible intracellularly within phagocytes. Diagnosis is often made by response to tetracyclines in a therapeutic trial (doxycycline 10 mg/kg PO, q 24 h). Response is rapid and evident within 48 h.

Non-healing abscesses should have histopathology and culture of tissue. Causes include nocardia, fungi, mycobacteria, and tumors. See page 1081, The Cat With Non-Healing Wounds.

In plague-endemic regions, Yersinia pestis (plague) must be considered, if the swelling is predominately in the neck region and the cat's fever is in the region of 40.5˚C (105˚F). Cautionary measures such as gloves, masks and isolation of the suspect cat should be taken until diagnosis established. (See below for discussion of Y. pestis infections).

Fracture.

Ligament/tendon injury.

Neoplasia.

Clip area looking for evidence of puncture wounds.

Drainage of the purulent material is the key to treatment. Surgical drainage can be done under sedation or general anesthesia with a #15 blade. Make a 1/4-1/2" incision over the dependent area, or the area most likely to allow for continued drainage.

Flush the wound thoroughly with sterile saline or a saline/betadine mixture.

Explore the wound with a sterile cotton swab or hemostats to assess the extent of dead-space and to look for a possible foreign body.

Leave the wound open to allow drainage of further purulent material. Do not suture incision closed, as this will only allow the abscess to reform. A Penrose drain may be placed for 2-3 days to allow maximum drainage for abscesses that close too early.

Antibiotic therapy for 7-10 days directed against anaerobes: penicillins, cephalosporins, clindamycin and metronidazole are reasonable choices. Most abscesses respond extremely well to drainage and amoxicillin at 10-20 mg/kg PO q 12 hours for 7 days or amoxicillin/clavulonic acid (12.5 mg/kg PO q 12 hours).

L-forms and Mycoplasma spp. respond to doxycycline or tetracycline within 48 hours, but not other antibiotics.

If the wound is not healing well, or the cat has had recurrent abscesses, FeLV/FIV testing is recommended to rule out an underlying immunodeficiency. Further considerations are inappropriate antibiotics (consider culture and sensitivity testing) or the presence of an undetected foreign body (consider surgical exploration of the area) or involvement of underlying bone (osteomyelitis).

Prognosis is good unless there is an underlying immunodeficiency.

Restrict the cat to an indoor environment only; although less effective, confine cat indoors at least from dusk to dawn.

Neuter male intact animals to decrease territorial behavior.

FeLV and FIV serology should be repeated 2-4 months following bite wounds.

Classical signs 

Acute onset of sneezing followed by oculonasal discharge.

Discharge progresses from serous to mucoid to mucopurulent.

Severe conjunctivitis with tearing, photophobia and chemosis.

Hypersalivation may occur as an initial sign before the classic signs of upper respiratory tract appear.

Punctate corneal ulcers that may coalesce to larger ulcers or perforation.

Fever of 1-2 days duration, anorexia and depression.

Retching or coughing may occur.

Cats with anterior uveitis have occasionally have herpesvirus 1 in the aqueous humor.

Presumptive diagnosis can be made on the basis of history and clinical signs because treatment for feline herpes virus-1 and calicivirus are similar.

Ocular ulcerations and chemosis are more suggestive of FHV-1.

Definitive diagnosis is by direct IFA of cells obtained from conjunctival or nasal scrapings, or by viral isolation or polymerase chain reaction assays from oropharyngeal or nasal swabs. 

Sudden onset of serous ocular discharge and mild conjunctivitis; these signs may begin unilaterally, but often progress bilaterally.

Initial signs are rapidly followed by sneezing, which are not paroxysmal and are less prominent than in herpesvirus.

Nasal discharge is primarily serous to mucoid and rarely progresses to purulent.

Oral ulcerations are common, especially on the tongue, and may be associated with drooling or hypersalivation. Ulcers may also occur at the mucocutaneous junction, hard palate and nose.

Fever generally spikes initially after infection prior to onset of signs, and returns with onset of clinical signs.

Viral pneumonia occurs occasionally with certain strains, and may produce significant mortality. Death is often sudden and preceded by laboured respiration.

A rare variant strain (FCV-Ari) reported from the United States, produces a high fever, facial and paw edema (50% of cats), ocular and nasal discharge, conjunctivitis and ulcerative stomatitis (50% of cats), hemorrhage from the nose, GIT, etc. (30-40% of cats), icterus (20% of cats) and rapid death. Mortality is high (30-50%).

Presumptive diagnosis can be made on basis of history and clinical signs because treatment for feline herpes virus-1 and calicivirus are similar.

Oral ulcerations or clinical signs of pneumonia are more suggestive of calicivirus.

Definitive diagnosis is by viral isolation or reverse transcriptase polymerase chain reaction assays from swabs taken from the oropharynx, ideally in the first week of illness.

Demonstration of increasing serum antibody titers to feline calicivirus in paired samples is also useful, whereas measurement of a single titer is not useful because many cats have titers from vaccination.

Identification of FCV-Ari is based on the clinical syndrome, pathology and culture of virus from blood, nasal or ocular discharge, spleen or lungs. 

Clinical signs are often non-specific and include fever, anorexia and weight loss.

Dyspnea and harsh lung sounds without coughing is common.

Peripheral and visceral lymphadenopathies are frequently present.

Pale mucous membranes, icterus, hepatomegaly or splenomegaly may be evident.

Ocular signs are uncommon, but can occur.

Gastrointestinal signs are uncommon in cats compared to dogs, and include chronic diarrhea, mesenteric lymphadenopathy and anorexia.

Osseous lesions produce soft tissue swelling and lameness.

Diagnosis is by demonstration of the organism in lymph nodes, draining tracts, bone lesions or vitreous humor.

The organism has a thin capsule and is intracellular within macrophages.

No reliable serologic test available. Genetic predisposition appears to play a role.

FIP is most common in catteries and multi-cat households.

There are two clinical forms of FIP, effusive or wet form and non-effusive or dry form. Both are characterized by a fluctuating fever unresponsive to antibiotics, anorexia, lethargy and weight loss.

Typical age of onset is 6 months to 2 years, but any age can be affected.

The effusive form may have any of the following signs:

• Abdominal effusion that is non-painful but progressive. The amount of effusion varies from volumes causing abdominal enlargement, to amounts only detectable by abdominocentesis. Fluid is straw-colored and highly viscous, like egg white. • Pleural effusion resulting in dyspnea occurs in 30% of cats with the effusive form. Pericardial fluid may be evident on ultrasound. Usually it not associated with clinical signs, but occasionally can produce cardiac tamponade. • Male cats may present with scrotal swelling.

The non-effusive form may have any of the following signs: • Ocular signs result from pyogranulomatous inflammation of the iris and ciliary body. They include bilateral uveitis, perivascular exudates (cuffing), retinal hemorrhage, retinal detachment. • Neurologic signs include cerebral and cerebellarvestibular signs such as seizures, personality changes, nystagmus, head tilt, circling, head tremor and hyperesthesia. • Dysfunction of any organ system may result from granuloma formation within the tissue of that organ, e.g., liver, kidney, spleen, intestines, lungs, etc., however, organ failure producing clinical signs only rarely occurs, and most dysfunction is only detected on biochemical tests. • Granulomatous masses may be palpable in abdominal viscera especially mesentery, mesenteric lymph nodes and omentum as tender, irregular masses. Occasionally vomiting or diarrhea results from extensive lesions on the bowel wall.

Jaundice may occur with either form of the disease.

Histopathology of affected tissues provides the only definitive antemortem diagnosis. The classic FIP lesion is pyogranulomatous infiltration around venules.

The following are typical abnormalities associated with FIP. All asterisked items must be present for a high likelihood of FIP; if any one parameter is not present, FIP is unlikely. A negative coronavirus ("FIP") titer suggests FIP is not the cause of the fever, although a few cats with the effusive form of the disease are titer negative.

Lymphopenia (< 1.5 × 10 3 cells/μl).* Occurs in many cats with FIP, and many cats without FIP. Except where the classical effusive fluid is present, definitive diagnosis of FIP requires organ biopsy and demonstration of classical histopathological lesions.

Various non-specific abnormalities may be evident on laboratory tests, including increased total white cell count, mild to moderate anemia, and increased concentrations of bilirubin, liver enzymes, BUN, creatinine, fibrinogen, globulin and mild proteinuria.

CSF typically has increased protein (> 2 g/L) and cell counts (>100 cells/ml) which are predominantly nonlytic neutrophils.

Ocular signs: toxoplasmosis, fungal agents.

Neurologic signs: toxoplasmosis, neoplasia (e.g., lymphoma), trauma, congenital abnormalities in young cats.

Other clinical signs: rule out other diseases associated with the apparent organ dysfunction.

Lymphocytic, plasmocytic cholangiohepatitis occasionally produces a high protein abdominal fluid similar to that of effusive FIP.

FIP is a fatal disease with no known treatments. The therapies listed below have been used in an attempt to slow progression and/or to improve quality of life.

Glucocorticoids at immunosuppressive doses (prednisolone 4 mg/kg/day).

Cyclophosphamide (200-300 mg/m 2 q 2-3 weeks or 2.2 mg/kg daily for 4 days each week) or chlorambucil (20 mg/m 2 q 2-3 weeks). +/− Broad-spectrum antibiotics to control secondary bacterial infections while the cat is immunosuppressed.

Prognosis is poor. The mortality is > 95%.

Fecal-oral transmission is most likely; transplacental transmission is rare.

Fomites, e.g., food bowls and litter trays, may be an important mode of transmission, as some strains of FCoV survive in dried secretions for several weeks.

A seronegative cat introduced into a household where coronavirus is endemic has a 1 in 6 chance of developing FIP; a seropositive cat under the same conditions has a 1 in 12 chance.

Both young and old animals seem to be most susceptible due to vulnerable immune systems.

Maternal antibodies that protect kittens wane at approximately 5-6 weeks of age.

Reduce fecal-oral contamination by providing one litterbox for every 1-2 cats, cleaning litterboxes daily, and placing litterboxes away from feeding areas.

Minimize stress, especially crowding in catteries.

Do not introduce FcoV-positive cats into a multi-cat household.

Wean kittens at 5 weeks and remove from the queen's environment if she is seropositive.

An intranasal vaccine is available for use in seronegative cats. However, efficacy has not yet been demonstrated against wild strains.

Classical signs

See main reference on page 540 for details (The Anemic Cat).

Onset of illnesses occurs over an extended period of time (months to years), although young kittens can become acutely ill.

Chronic, opportunistic infections occur that do not respond to appropriate antibiotic therapy and are primarily due to immunosuppression.

Fever may occur in any age cat but is primarily seen initially in the viremic stage or later in response to neoplastic, inflammatory or immunosuppressive effects. Chronic fever occurs in later stages of disease.

Weight-loss/cachexia.

Non-regenerative anemia.

Thrombocytopenia.

Lymphoma is associated with FeLV-positive cats, especially thymic and multicentric forms.

History and clinical signs may be suggestive.

Complete blood count showing anemia, thrombocytopenia, leukemias, increased MCV and leukopenia are supportive.

Bone marrow aspirate may show myeloproliferation and arrested erythroid differentiation.

A positive FeLV antigen test (viral core antigen p27) on whole blood using an IFA (can also be done on bone marrow sample) or an ELISA test (also on serum, plasma, saliva, tears). See page 543 for interpretation.

Polymerase chain reaction is available from some laboratories.

• Pale mucous membranes.

See main reference on page 530 for details (The Anemic Cat).

Classical signs are pale mucous membranes and/or icterus primarily from extravascular hemolysis due to complement binding of infected erythrocytes.

Severe, regenerative hemolytic anemia may ensue.

Anorexia and depression are typical.

Fever occurs in 50% of cats in the acute phase, and may occur intermittently in chronic infections.

History and clinical signs are suggestive, especially if an immunosuppressive disorder is present concurrently.

Diagnosis is via demonstration of the organism on the surface of erythrocytes. Use a marginated blood sample for diagnosis, e.g., ear vein. Multiple blood smears over a number of days may be required as most of the organisms are removed from circulation by the time clinical signs are apparent.

Infected cats may be Coomb's positive.

A polymerase chain reaction test is available in some laboratories for diagnosis.

Classical signs

Gastrointestinal signs, primarily abdominal discomfort and small bowel diarrhea, are due most likely to replication of the organism (tachyzoites) in enteroepithelial cells resulting in necrosis.

Clinical signs in the acute, fatal form of extraintestinal disease are caused primarily by tissue damage from the rapidly dividing tachyzoites.

Tachyzoites begin to disappear from tissues approximately 3 weeks after infection. The organism may persist in tissues as tissue cysts containing bradyzoites.

Chronic disease may be a result of delayed hypersensitivity reactions and tissue reaction to antibody-antigen complex deposition.

Concomitant illness, such as FeLV, FIV and immunosuppression with glucocorticoids, has been reported in some cases.

Gastrointestinal disease.

• Mild, self-limiting small bowel diarrhea may occur in the definitive host (cats), but only after ingestion of tissue cysts, oocysts or sporulated oocysts. • Young kittens are more likely to have gastrointestinal signs, although mild clinical disease has been reported in adult cats as well. All newborn kittens experimentally infected developed severe diarrhea 5-6 days later.

• Fatal extraintestinal disease is most likely to occur in transplacentally infected kittens. • Kittens may be stillborn or exhibit signs that are severe and rapidly progressive and reflect involvement of the lungs, liver and CNS tissues.

These signs may also be observed in postnatally infected kittens and include: -A distended abdomen from an enlarged liver and/or ascites. -Icterus from hepatitis or cholangiohepatitis.

-Dyspnea is present in most kittens and cats with signs of acute infection. -Neurologic deficits; continuous vocalization; excessive sleeping. -Fever, anorexia, depression often accompanies the tissue-specific signs.

• Cats may have a moderate fever, lethargy and depression that waxes and wanes. • Hyperesthesia and stiff painful joints or shifting lameness may be evident, presumably due to an immune-mediated process. • Unilateral or bilateral anterior or posterior uveitis may occur with possible sequelae of lens luxation, glaucoma or retinal detachment. • Seizures and ataxia may be present if CNS tissues are involved. • Rarely, a toxoplasma granuloma (tissue cyst) forms in the gastrointestinal tract or pancreas causing chronic vomiting.

Clinical signs consistent with toxoplasmosis are suggestive, especially when other causes of the signs have been ruled out.

IgM titers > 1:64 and a four-fold increase in IgG:IgM titers within 2 weeks correlate best with clinical toxoplasmosis. However, some cats do not develop detectable IgM titers, and in other cats, positive IgM titers can persist for months to years after infection.

Elevated ocular and CSF titers relative to serum titers in cats with ocular or neurologic signs, respectively, are very suggestive. Coefficient values > 1.0 are highly suspect and > 8.0 strongly suggest local production of T. gondii antibodies.

Response to therapy for toxoplasmosis is a useful indicator of infection.

Definitive diagnosis requires demonstration of the organism in inflamed tissues by histology, immunohistochemistry or polymerase chain reaction assay.

Rule out diseases associated with affected organs, e.g., FIP for neurologic and ocular signs.

Clindamycin at 10-12 mg/kg orally q 12 hours for 4 weeks is usually effective.

• Cats should respond within several days of treatment. • If no response is evident after 3 weeks of antibiotic therapy, reconsider the diagnosis. • The chronic form may recur even after successful treatment, as drugs tend to suppress replication rather than kill the parasite.

Other systemic drugs with potential efficacy include the trimethoprim sulfas combination, doxycycline, minocycline, azithromycin and clarythromycin.

Cats with ocular lesions should also be treated with corticosteroids, either topically (e.g. topical 0.5% Prednisolone acetate drops applied q 6-12 h) or systemically to control inflammation and its sequelae (glaucoma, lens luxation).

Gastrointestinal disease has a good prognosis, although it may lead to inflammatory bowel disease in rare cases.

Acute extraintestinal disease has a guarded to poor prognosis.

Chronic extraintestinal disease has a fair to good.

• The placenta or milk with tachyzoites.

• Ingestion of meat infected with tissue bradyzoites, e.g., rodents. • Ingestion of sporulated oocysts in food or water.

T. gondii has a zoonotic potential. Infection of humans can occur via: • Ingestion of undercooked meat containing tissue bradyzoites (most common mode of transmission). • Ingestion of sporulated oocysts from the environment.

• Transplacentally, if first-time exposure to the organism occurs during pregnancy.

Only cats host the sexual replication that results in oocysts in the feces.

• Oocysts are shed for 1-2 weeks.

• Most seropositive cats do not shed oocysts on repeat exposure.

Oocysts must sporulate to be infectious:

• Sporulation occurs 1-5 days after environmental exposure, thus handling individual cats rarely results in infection of humans.

Transplacental transmission occurs in cats and people after primary exposure.

Discourage cats from going outdoors and hunting behavior.

Do not feed cats undercooked meat.

• Cook meat at 80˚C (176˚F) for 15 minutes.

• Use gloves when gardening or changing the litterbox, and wash hands well. • Change litterboxes daily. Use litterbox liners or clean with scalding water.

• Lethargy and anorexia.

See main reference on page 272 for details (The Cat With Depression, Anorexia or Dehydration).

The classical signs are not as well-defined for cats as for dogs for the following reasons:

• Cats tend to have intermittent bouts of chronic pancreatitis. • Diagnostic tests for pancreatitis are not as reliable in cats. • There is poor correlation of biochemical parameters with pancreatitis in the cat.

Lethargy and anorexia is variable depending on chronicity.

Vomiting only occurred in 35% of cases in one study.

Dehydration occurred in 50% of cases in the same study.

Abdominal pain is quite variable.

Fever is variably present, and generally mild. In severe acute pancreatitis it may progress to hypothermia, which is a poor prognostic sign.

Diagnosis is unreliable based on a biochemistry panel. Lipase may be increased or normal in pancreatitis.

• Hyperbilirubinemia and elevated liver enzymes may be present. • Hypocalcemia occurs in 40% (total serum calcium) or 60% (plasma ionized calcium concentration) of cats due to soponification of fat. Cats with a plasma ionized calcium concentration < 1.00 mmol/L (< 4.00 mg/dl) have a grave prognosis (77% mortality) and aggressive medical treatment is indicated.

Pancreatic lipase immunoreactivity is probably a more sensitive diagnostic tool for confirming pancreatitis in cats than measurement of plasma lipase concentration or trypsin like immunoreactivity. A feline-specific assay must be used.

Abdominal ultrasound to visualize an enlarged pancreas or heterogeneous echogenicity in the area of the pancreas is considered by many to be most sensitive.

Demonstration of higher lipase levels in abdominal fluid compared to those of the serum is suggestive. Diagnostic peritoneal lavage may be necessary to obtain a fluid sample. 

Clinical signs may be acute, chronic or intermittent.

Typically, there is anorexia and depression together with icterus or increased bilirubin and liver enzymes on a biochemistry panel.

Vomiting and dehydration may be present.

Fever, especially in the suppurative form occurs in approximately 38% of the cases.

Chronic cholangiohepatitis may lead to end-stage liver disease and the cat may present with ascites and hepatic encephalopathy.

Multiple causes include bacterial, protozoal (T. gondii) and immune-mediated disease.

Complete blood count may show neutrophilia with a left shift, and mild non-regenerative anemia.

Biochemistry panel shows hyperbilirubinemia, elevated liver enzyme activities (ALP, ALT, GGT), +/− elevated serum bile acids.

• Signs of late-stage liver disease are occasionally present, such as decreased BUN, glucose and albumin concentrations.

Abdominal ultrasound should be performed to evaluate the gall bladder and bile duct for cholelithiasis, bile sludging and cholecystitis.

Liver aspirates/biopsy allows for differentiation of suppurative from non-suppurative forms of cholangiohepatitis. 

Clinical signs are primarily due to immunosuppression, i.e., chronic recurring infections that do not respond to appropriate therapy.

Gingivitis, stomatitis and peridontitis are more common findings in FIV infections than in FeLV, although one study suggests that these signs may be to an effect of age, rather than a consequence of FIV infection.

Fever is chronic and is related to production of tumor necrosis factor and/or IL-1 in infected cats.

Weight loss/cachexia are common in the late stages of FIV, as in human HIV infections.

Diarrhea resembles a panleukopenia-type syndrome that may be due to actual enterocyte infection by the virus or secondary to inflammation.

Cats are often thin and scruffy with an unkempt haircoat, and may have miliary dermatitis.

Diagnosis may be suspected based on history and clinical signs, but requires antibody or antigen tests for confirmation.

Virus isolation and polymerase chain reaction for virus detection is available at some research facilities.

Cats infected with FIV can be co-infected with FeLV. 

Chronic nasal discharge can be unilateral or bilateral and is generally serosanguineous. Sneezing and stertorous breathing is often present.

Facial deformity may occur due to invasion of the surrounding bone.

Chronic low-grade fever may be present.

Depression, anorexia and weight-loss are signs of disseminated disease.

Neurologic signs occur via hematogenous spread or invasion into the CNS through the cribiform plate but are uncommon. Signs include seizures, blindness, depression and ataxia.

The skin form typically produces nodules which often ulcerate.

Diagnosis is by demonstration of narrow-based budding yeast with a very thick capsule from affected tissue or by culture of affected tissue or CSF.

Demonstration of Cryptococcus antigen in serum, urine or CSF is also diagnostic. 

Occurs in cats of all ages, with and without outdoor access.

Progressive clinical signs occur over a period of 1-4 weeks. According to one study, non-supportive meningoencephalitis may be the most common cause of seizures in cats.

Systemic signs, which are not present in all cats, include fever, anorexia, lethargy, vomiting, diarrhea and lymphadenopathy.

The condition, however, does not appear to be contagious to other cats.

CSF tap can be very useful to rule out other causes of CNS signs, specifically toxoplasmosis and FIP; CSF analysis reveals a normal or mild protein elevation (typically < 1 g/L) and/or an increased white cell count (< 50 cells/μl).

Complete blood count findings are non-specific and may include leukopenia or leuko-cytosis, eosinophilia and anemia.

• Uniphasic or biphasic fever. • Depression. • Lethargy. • Mild generalized lymphadenopathy. • +/-Signs of cardiac failure.

• Viral, e.g., FIP has been shown to cause cardiac infection. • Trypanosoma cruzi, which causes Chagas' disease in humans. • Streptococcus and Borrelia (Lyme's disease) in certain geographic areas.

No single agent has been identified, and the disease may be multifactorial.

Fever is biphasic in 50% of the cats; if biphasic: • First fever occurs approximately 10 days after exposure, lasts 1-3 days and peaks at 39.3-40.7˚C (102.7-105.2˚F). • Second fever occurs 1-2 weeks after the first fever (at 3-4 weeks post-exposure), lasts 5 days and peaks at 39.9-40.9˚C (103.8-105.6˚F).

Appetite is mildly decreased in some cats, but most continue to eat and drink.

Some animals exhibit mild generalized lymphadenopathy.

Irritable disposition and hyperesthesia may occur, and are most likely due to fever and malaise.

In a few case reports, cats have died from peracute cardiac failure, but this outcome is not common.

Myocarditis/diaphragmitis is a diagnosis of exclusion.

Biochemistry and complete blood counts are unremarkable, except for a mild to moderate increase in CK in less than 50% of experimentally infected cats.

Definitive diagnosis can only be made at necropsy.

Histopathology shows a neutrophilic infiltrate with a foci of myonecrosis in myocardium and diaphragm.

Any other causes of fever should be ruled out including infectious, inflammatory, immune-mediated, drugs, neoplasia and metabolic.

Other causes of cardiac failure that should be ruled out include congenital deformities, hypertrophic cardiomyopathy, restrictive cardiomyopathy and dilatative cardiomyopathy.

Supportive therapy is indicated if dehydration or cardiac disease are present.

Broad-spectrum antibiotics are indicated if complete blood count supports an infectious cause.

Fever and depression resolve spontaneously in the majority of cats.

Prognosis is poor if peracute cardiac failure is present with systemic signs of fever and depression.

Although an infectious agent is suspected, no single etiologic agent has been identified, making recommendations for prevention difficult.

• Cardiovascular or respiratory compromise.

• External signs of injury. 

Cardiovascular compromise may result in tachycardia, hypovolemia or hypotension.

Respiratory compromise may produce dyspnea/ tachypnea due to pneumothorax, hemothorax or pyothorax.

Internal injuries may result in abdominal pain from organ rupture, bone/joint pain or focal swelling.

Diagnosis is based on clinical signs and history.

Radiographs of the chest, abdomen and/or limbs may be required to characterize the injury.

Complete blood count and biochemistry panel is indicated to rule out specific organ injury and primary infection.

• Alert, febrile cat being treated with antibiotics or antifungal agents.

History of treatment with antibiotics or antifungal agents.

Fever does not correspond to clinical appearance of animal. Cats are bright, alert and responsive, despite a temperature in the range of 39.4-40˚C (103-104˚F).

Onset of fever is idiosyncratic and variable, but the fever is generally present for the duration of the drug treatment.

Tetracycline is the most common antibiotic cause of drug-induced fever in cats.

Amphotericin B can cause fever by disrupting cell membranes and releasing pyrogens into circulation.

Be aware that other drugs (griseofulvin, chloramphenicol and chemotherapeutic drugs) can cause bone marrow suppression leading to a cat with fever, neutropenia and secondary bacterial infection. These cats are obviously sick, whereas the drug-induced fever animals are bright and alert in comparison.

• History is of treatment with fever-inducing drugs, especially tetracycline and amphotericin B. • Clinical signs are inappropriate, that is, the cat appears bright and alert although febrile.

Temperature normalizes after drug is discontinued.

Classical signs • Sneezing.

• Conjunctivitis and ocular discharge.

See main reference on page 13 for details (The Cat With Acute Sneezing or Nasal Discharge).

Marked conjunctivitis is the predominant sign, which often starts unilaterally, but usually progresses to both eyes.

Classic triad of upper respiratory infection signs including oculonasal discharge and sneezing.

Serous ocular discharge accompanied by blepharospasm, chemosis and conjunctival hyperemia are initial signs. Discharge becomes mucopurulent over the course of the disease.

Mild to moderate fever can be seen in the acute phase.

Pneumonia is rarely associated with this infection.

History and clinical signs are highly suggestive.

Cytology of conjunctival scrapings reveal dark blue inclusion bodies (Giemsa stain).

Immunofluorescent antibody staining or polymerase chain reaction assay to demonstrate the organism in conjunctival scrapings is available from some laboratories.

• Acute onset of depression.

• Acute onset of vomiting. 

Rapid onset of depression, anorexia, and vomiting especially in peracute and acute disease. Fetid diarrhea (may be hemorrhagic) typically follows 1-2 days after initial onset of signs.

Severe dehydration and electrolyte abnormalities.

Initial fever followed by hypothermia as the disease progresses.

High mortality rate when signs are severe.

The disease should be suspected in cats less than one year of age with no history of vaccination and a rapid clinical course.

Panleukopenia evident on hematology.

Parvoviral antigen can be detected in feces using the canine parvoviral antigen tests or electron microscopy.

Histopathologic changes include denuded intestinal crypts and blunted villi (often a post-mortem diagnosis).

Classical signs

Francisella tularensis is a Gram-negative coccobacillus. Clinical signs are associated with Gram-negative endotoxins and bacteremia.

There are two main strains of the organism, both of which have been isolated from cats.

• Associated with tick-rabbit cycle.

• Found only in North America.

• Highly virulent for laboratory rabbits.

• Associated with more severe disease in humans.

• Associated with a more complex cycle involving rodents, ticks, mosquitoes, mud and water. • Found throughout the northern hemisphere. • Avirulent for laboratory rabbits.

History of contact with rabbits, especially if the cat is a hunter.

Any age of cat can be infected, but younger cats are more susceptible to developing septicemia.

The spectrum of illness varies from severely affected to asymptomatic.

Fever is generally > 40˚C (104˚F).

Marked depression, anorexia and lethargy, with or without vomiting are typical.

On physical examination, peripheral lymphadenopathy, icterus and palpable splenomegaly and hepatomegaly are reported.

Oral, lingual or pharyngeal ulcers may be present.

Clinical signs together with a history of exposure to wild rabbits is highly suggestive.

Hematologic and serum biochemical abnormalities may include panleukopenia, with severe toxic changes in neutrophils, high band neutrophil count, thrombocyto-penia and hyperbilirubinemia.

Definitive diagnosis is via identification of the bacterial agent by IFA or bacterial culture, but should only be performed in a qualified laboratory. • Samples can be obtained from affected lymph nodes, bone marrow, urine or blood.

Serum antibody titers > 1:120 or a four-fold increase in serum antibodies in samples collected during acute and convalescent phases (10-14 days) are considered diagnostic.

FIP, FIV, panleukopenia.

Toxoplasmosis.

Multicentric lymphoma.

Antimicrobial efficacy studies have not been done in the cat, therefore therapy is derived from case reports and/or human therapy regimens.

Enrofloxacin (5 mg/kg q 12 hours IV or PO).

Tetracycline and chloramphenicol may be effective, but because they are bacteriostatic for F. tularensis, relapses can occur.

In humans, the drugs of choice are streptomycin and gentamycin.

Prognosis is poor to fair as mortality rate varies across case reports.

F. tularensis has a serious zoonotic potential if there is contact with infected animal tissue.

Bites from infected ticks, deer flies or mosquitoes are the most common method of transmission.

Infection can also occur via ingestion of infected meat.

• This is the most common method of transmission to humans in cat-associated cases. • The infected cat may have no obvious signs of illness, but have a history of hunting wild animals, especially rabbits.

Inhalation of aerosolized organisms may also transmit the disease. Care should be taken by veterinary and laboratory personnel handling suspected animals or samples being prepared for IFA or culture.

Discourage hunting behavior in cats.

Ectoparasite control, especially tick control. 

Onset of illness occurs 24-72 hours after exposure to the organism.

Transmission to cats is either via ingestion of infected rodents or a fleabite from infected fleas.

Rapid multiplication of organism causes tissue damage and necrosis. The host immune response contributes to pathology.

Three forms of the plague exist: bubonic (local infection), bacteremic/septicemic and pneumonic.

Bacteremia occurs in many cases, resulting in the septicemic or pneumonic form of plague.

Endemic regions of the world include the western USA, South America, Africa, Asia, eastern Europe.

History of hunting rodents, especially in known endemic areas.

Current flea infestation is evident.

Acute onset of fever, anorexia, depression over a period of 2-6 days. The clinical course may last 6-20 days.

Submandibular or cervical swelling associated with lymph nodes (can be unilateral or bilateral). The inflamed, swollen lymph node is referred to as a bubo.

Subcutaneous abscessation may occur and appear similar to a cat bite abscess.

In the pneumonic form (~10% of cases), upper and lower respiratory signs may be present, including sneezing, nasal discharge, coughing, dyspnea/tachypnea.

Initially, microscopic examination of a lymph node aspirate, especially a markedly swollen lymph node (bubo) should reveal a homogeneous population of bipolar-staining coccobacilli. • Blood should be examined in cats with the bacteremic/septicemic form.

Fluorescent antibody testing of sample provides a definitive diagnosis.

Culture of organism should be performed by a qualified laboratory only.

A four-fold rise in antibody titers (taken 10-14 days apart) is suggestive of plague. These results must be interpreted carefully, as high titers can persist for up to one year after infection.

Chest radiographs may reveal patchy, nodular lesions if the pneumonic form is present.

Be aware that the risk of exposing other staff members to the disease should be weighed against the benefit of the diagnostic test.

Reactive lymph nodes from a percutaneous abscess or tooth-root abscess.

• Aspirates of cat bite abscesses contain a mixed bacterial population compared to Y. pestis, which is homogeneous.

Neoplasia, although it is less common in the US for cats with lymphoma to have peripheral lymphadenopathy.

Respiratory signs may be due to other upper respiratory infections (calicivirus, herpesvirus, Chlamydophila) or lower respiratory disease (parenchymal lung disease, pleural disease).

Other diseases which cause high fever (tularemia, toxoplasmosis, FIP, etc.).

Absolute caution must be practiced in all suspect plague cases. Cautionary measures include gloves, mask, isolation of animal and limited exposure to other staff members.

Doxycycline/tetracycline: (1) Doxycycline at 5 mg/kg q 12 hours PO for 14-21 days or (2) tetracycline 25 mg/kg q 8 hours PO.

• Begin treatment immediately after samples for diagnosis have been collected. • Doxycycline is preferred as tetracycline has been associated with relapse.

Consider aminoglycosides or enrofloxacin (5 mg/kg IM q 8 hours) for the first 3 days to avoid placing hands into the cat's mouth (see Transmission section below).

Prognosis for bubonic plague is fair to good.

Prognosis for the pneumonic form is guarded to fair.

Prognosis for septicemic form is guarded.

Persistent fever > 40˚C (104˚F) despite treatment is associated with a poor prognosis.

Y. pestis has a serious zoonotic potential, and great care should be taken in suspect cats to prevent transmission to humans and other cats.

• Infected cats are no longer a zoonotic risk after 3 days of antibiotic therapy.

Infection can also occur via inhalation of aerosolized organism, either from aspirates of infected tissue or nasal discharge/sneezing of cats with pneumonic form.

Discourage hunting behavior especially during the peak flea season (April to October).

Provide effective flea control to prevent flea bites.

• Anorexia and weight loss.

See main reference on page 547 for details (The Anemic Cat).

This disease is uncommonly reported in cats and is difficult to diagnose because of its vague and variable clinical signs.

Age range of cats with documented disease was 2-10 years of age, with no breed or sex predilection reported.

Infection has a variable effect on appetite, from mild inappetence to anorexia and mild to moderate weight loss.

Chronic intermittent fever in the moderate range is common.

Lymphadenopathy was reported in three of 23 cats.

Hyperesthesia, joint pain or irritable disposition is common.

Complete blood counts may show a non-regenerative anemia with a leukopenia or a leukocytosis; thrombocytopenia is present in about 25% of the cats.

Biochemistry abnormalities are uncommon, except for hyperglobulinemia in about 33% of documented cases.

A complete blood count and biochemistry panel consistent with chronic Ehrlichia spp. infection is suggestive.

Diagnosis is by demonstrating E. canis and/or Anaplasma phagocytophilum serum antibody titers or a positive IFA test.

Demonstration of morulae in mononuclear cells, neutrophils or eosinophils (rare) is diagnostic.

PCR assays can be positive.

• Anorexia, lethargy, weight loss. • ± Fever. • Signs depend on tumor type and organ system involved.

Anorexia, lethargy and weight loss.

Poorly groomed coat.

Some cats have a fever associated with neoplasia, which is generally a secondary neoplastic syndrome. Tumors which destroy the bone marrow and result in neutro-penia are classically associated with fever. Fever may occur with other tumors via other mechanisms, including antibody stimulation from tumor antigens, and tissue necrosis which activates leukocytes to release pyrogenic factors.

Signs are specific to the organ system involved.

Lymphoma (mediastinal, GI, renal) , mammary adenocarcinoma, squamous cell carcinoma (nasal, oral) and mast cell tumor are the most common tumors in cats.

Hematology, biochemistry panel, radiology, ultrasound and/or bone marrow aspirates may be necessary to provide evidence that a tumor is present, especially if it involves the hematopoietic system (leukemia) or is located internally (splenic mast cell tumor).

Identification of the tumor type is via fine-needle aspirates and/or biopsies.

Organ dysfunction due to infectious or degenerative disease process.

FeLV/FIV or other immunosuppressive illness.

Benign masses (granulomas, abscesses, reactive lymph nodes, benign tumors).

Treatment involves surgical excision of identifiable masses +/− regional lymph nodes, especially for mammary adenocarcinoma, nasal squamous cell carcinoma, splenic mast cell tumor, etc.

Chemotherapy may be effective and needs to be based on tumor type, e.g., COP (cyclophosphamide, vincristine, prednisolone) protocol in lymphoma cases.

Radiation therapy is used for local disease only, and response to radiation therapy is tumor dependent (e.g., squamous cell carcinoma).

• Radiation therapy is most effective after surgical debulking of the primary mass. The effectiveness of radiation therapy may be enhanced with concurrent chemotherapy.

Classical signs 

Acute onset of fever and malaise are initial clinical signs.

Vomiting, diarrhea and abdominal pain may occur, however, approximately 50% do not have gastrointestinal signs.

Dehydration.

Shock may occur if septicemia/bacteremia develops.

Mortality rate approaches 10% and may be higher if the cat is concurrently immunosuppressed.

Typically, the cat is an outdoor cat with a history of hunting behavior, especially of birds.

Complete blood count and biochemistry panel supports infectious diarrhea or septicemia, e.g., neutropenia with a left shift, bacterial rods in blood leukocytes if overwhelming sepsis present, hypoglycemia, hypoproteinemia, pre-renal azotemia.

Blood cultures provide the best definitive diagnosis if positive. Three separate samples over a 4-6 hour period should be taken during febrile episodes using aseptic techniques.

Fecal cultures may isolate Salmonella organisms, but because many animals are subclinical carriers, positive culture does not prove that the organism is the cause of the clinical signs.

• Skin lesions.

• Respiratory signs.

• Ocular lesions.

• Fever, anorexia, depression.

The geographical distribution includes south-west USA, Central America and South America in areas that have sandy soil with low rainfall and high temperatures.

Soil is the reservoir for infection, and the highest frequency of cases occur when the soil is dry and dusty, and organisms are disseminated in the wind.

Most humans and animals in endemic areas become infected, but the majority of infections are subclinical or cause only mild, transient clinical signs.

Cats are more resistant to infection and signs are less common than in dogs.

Infection is contracted via inhalation, and only a few organisms are required to produce signs, which occur after 1-3 weeks.

Initial infection is confined to the respiratory tract, but dissemination may occur resulting in chronic disease over months or years with signs referable to bones, eyes, central nervous system and abdominal organs.

Localized infection following a penetrating skin wound appears to be rare.

Cats appear to be resistant to clinical disease.

Skin lesions are the most frequent types of infection in cats and were reported in 56% of cats in one study.

• Lesions begin as small bumps and progress to abscesses, ulcers or draining tracts. • In cats, underlying bone involvement is uncommon.

Systemic signs such as fever, anorexia and depression are commonly reported (44% of cats) and can be seen with skin lesions.

Respiratory signs such as coughing and wheezing are less common in cats and occur in approximately 25% of cases.

Musculoskeletal signs such as lameness, with or without painful bone swelling, were reported in 19% of cats.

Ocular lesions are seen infrequently and include chorioretinitis and anterior uveitis. Ocular or CNS signs were reported in 19% of cats.

Most cats have clinical signs for less than 4 weeks prior to diagnosis.

Hyperproteinemia is present in approximately 50% of cats.

Definitive diagnosis is by identification of the organism via biopsy of lesions.

Antibody detection is available using latex agglutination (IgM), AGID (IgM) or ELISA (IgM or IgG).

Tube precipitin (TP) for IgM and complement fixation (CP) for IgG were previously thought to be less reliable in cats, but have been subsequently demonstrated to detect feline infections.

Itraconazole (10 mg/kg PO if possible, q 24 h or 5 mg/kg q 12 h) is the treatment of choice. Treatment is required for 4-6 months and must be continued for at least 2 months after all signs have resolved. • Some cats develop anorexia, and less commonly vomiting or diarrhea. Stop the drug for a few days until the cat is eating, and then restart at 1/2 the dose for 7-10 days, before increasing back to the full dose, which is usually then tolerated.

Amphoteracin B is also effective (0.25 mg/kg in 30 ml dextrose 5% IV over 15 minutes q 48 h or given subcutaneously) -see page 26, for Cyptococcosis in The Cat With Signs of Chronic Nasal Disease. Continue amphotericin B therapy until a cumulative dose of 4 mg/kg is given or until BUN > 17.9 mmol/L (50 mg/dl). Amphotericin has the disadvantage of requiring frequent parenteral or subcutaneous administration and causes significant nephrotoxicity.

• Because of its quick onset of action, amphoteracin B in combination with itraconazole is useful in cats with severe pulmonary signs that are rapidly deteriorating. If the cat survives, after a few weeks treatment can be continued with itraconazole alone. • Lipid-complexed amphoteracin formulations allow higher dosages with less toxicity, and should be used in cats with severe pulmonary signs, although the cost is higher. Dose at 2-3 mg/kg IV 3 days per week for a total of 9-12 treatments (cumulative dose of 24-27 mg). Dilute to a concentration of 1 mg/ml in dextrose 5% and infuse over 1-2 hours.

If the titer has decreased four-fold and there is a similar improvement in physical and radiographic signs, treatment can be stopped after 4-6 months. Antibodies may persist for long periods and obtaining a zero titer is not a useful treatment goal.

Classical signs • Fever.

• Respiratory signs.

• Ocular signs.

• Lymphadenopathy.

The geographical distribution includes North America, Central America and Africa.

Soil is believed to be the reservoir for infection, and living near a lake or river increases the risk of infection in dogs.

Signs are more common in dogs than in the cats.

Disseminated disease is primarily contracted via inhalation.

Respiratory signs include coughing, dyspnea and harsh lung sounds.

Ocular disease, such as uveitis, glaucoma and retinal detachment, is a frequent finding.

Fever, anorexia, depression, weight loss and lymphadenopathy are systemic signs associated with disseminated disease.

Draining skin lesions may occur and are usually a manifestation of systemic disease rather than local disease.

Neurological signs are associated with CNS involvement of the brain or spine and include circling, disorientation, anisocoria, paresis, decreased conscious proprioception, or upper motor neuron signs, hyperesthesia and extensor rigidity.

Definitive diagnosis is by demonstration of an extracellular, broad-based budding yeast in aspirates or biopsies from lymph nodes, draining tracts, bone lesions or vitreous humor.

An antibody detection test is available, but may be negative.

Itraconazole (10 mg/kg PO if possible, q 24 h or 5 mg/kg q 12 h) is the treatment of choice. Treatment is required for 4-6 months and must be continued for at least 2 months after all signs have resolved.

• Some cats develop anorexia, and less commonly vomiting or diarrhea. Stop the drug for a few days until the cat is eating, and then restart at 1/2 the dose for 7-10 days, before increasing back to the full dose, which is usually then tolerated.

Amphoteracin B is also effective (0.25 mg/kg in 30 ml dextrose 5% IV over 15 minutes q 48 h or given subcutaneously) -see page 26, for Cyptococcosis in The Cat With Signs of Chronic Nasal Disease. Continue amphotericin B therapy until a cumulative dose of 4 mg/kg is given or until BUN > 17.9 mmol/L (50 mg/dl). Amphotericin has the disadvantages of requiring frequent parenteral or subcutaneous administration and causing significant nephrotoxicity. • Because of its quick onset of action, Amphoteracin B in combination with itraconazole is useful in cats with severe pulmonary signs that are rapidly deteriorating. If the cat survives, after a few weeks treatment can be continued with itraconazole alone. • Lipid-complexed amphoteracin formulations allow higher dosages with less toxicity, and should be used in cats with severe pulmonary signs, although the cost is higher. Dose at 2-3 mg/kg IV 3 days per week for a total of 9-12 treatments (cumulative dose of 24-27 mg). Dilute to a concentration of 1 mg/ml in dextrose 5% and infuse over 1-2 hours.

Classical signs

See main reference on page 534 for details (The Anemic Cat).

Primarily found in the south-central and southeast United States. The North American bobcat is the natural host.

There is usually a history of exposure to ticks in the previous 5-20 days (incubation period is 5-20 days).

The clinical course of disease is approximately 1 week and often ends in death.

Clinical signs are the result of an overwhelming hemolytic crisis.

Rapid onset of fever, dyspnea, anorexia, pale mucous membranes, icterus and dark-colored urine are typical.

Collapse and death occur 2-3 days after the fever peak. Hypothermia occurs in the terminal stages.

There appear to be non-pathogenic strains as well.

A complete blood count reveals regenerative anemia, hemoglobinemia and neutrophilia or neutropenia.

The biochemistry panel commonly has hyperbilirubinemia.

Urinalysis may show evidence of hemoglobin and bilirubin.

Demonstration of the organism in erythrocytes (merozoite stage) is possible only relatively late in the disease, approximately 1-3 days before death. Parasitemic cats usually have only 1-2% of RBCs affected, and up to 50% of cats have parasitemias that are very low or undetectable.

Demonstration of the organism in macrophages from bone marrow, spleen, liver or lymph node aspirates may be possible even when organisms are not evident in blood.

Serum antibody levels and direct FA test for detection of tissue phase are available through some labs. 

Weight loss in spite of normal to increased appetite.

Polyuria/polydipsia.

Behavioral changes which often include hyperactivity and aggression.

Unkempt, rough hair coat and sometimes overgrown nails.

Tachycardia accompanied by a "gallop" rhythm and/or a systolic murmur.

Mild fever which may be intermittent in nature and reflect the increased metabolic rate in this disease. These cats are easily stressed and may present dyspneic and tachycardic with a mildly elevated temperature, usually not greater than 39.4˚C (103.0˚F).

Enlarged thyroid glands are often evident on palpation of the neck.

Diagnosis is based on clinical signs and history and confirmed by demonstrating increased thyroid hormone concentrations (total T4, free T4).

Thyroid glands can be palpated in approximately 80% of cats with hyperthyroidism, and are unilaterally or bilaterally enlarged.

• Enlarged thyroid glands may not be palpable if the abnormal thyroid tissue is within the thoracic inlet.

Complete blood count and a biochemistry panel are required to rule out diseases such as diabetes mellitus, renal disease, etc.

A TRH stimulation test may be necessary when clinical signs are highly suggestive and total and free T4 are in the upper region of the reference range for normal cats.

Thyroid radionuclide uptake and imaging with pertechnetate ( 99m Tc) is also available at some institutions.

Response to therapy with anti-rickettsial drugs (tetracycline or doxycycline) is highly suggestive.

• Subclinical or mild fever and occasional ocular signs.

Bartonella henselae is an intracellular bacterium within erythrocytes.

Bacteremia is present in many healthy cats in the population, and cats are reservoirs for infection.

B. henselae is an important pathogen because of its zoonotic potential in immunocompromised humans.

• Humans may develop fever, malaise, lymphadenopathy and skin eruptions following cat scratches or bites. • B. henselae causes bacillary angiomatosis, bacillary peliosis and encephalitis in human AIDS patients.

Naturally infected cats usually only develop subclinical infection.

Mild, self-limiting fever lasting 48-72 hours has been documented in some experimentally infected cats.

Anterior uveitis and fever were documented in naturally exposed cats.

Lymphadenopathy.

Atypical seizures occur in some cats.

Antibody titers are prevalent in healthy cats, but there is a poor correlation with blood culture and PCR assay results.

Intermittent bacteremia may occur for longer than one year following infection, with 25-41% of healthy cats bacteremic for up to 22 months.

The organism is present within erythrocytes, therefore, hemolyzing red blood cells increases the sensitivity of the culture.

Other causes of mild transient fever need to be considered, such as mild cellulitis following a cat fight.

Other infectious causes of anterior uveitis need to be ruled out, such as toxoplasmosis, fungal diseases, FeLV, FIV, Cuterebra or dirofilaria.

Antimicrobial efficacy has not been clearly demonstrated.

Clinical signs of disease have resolved when the cats are administered doxycycline at 25-50 mg PO q 12 h for 28 days.

Azithromycin is used in humans and is a safe alternative in cats when administered at 10 mg/kg PO q 24 h for 28 days Fluoroquinolones also may be effective.

While clinical signs resolve, bacteremia is usually only temporarily suppressed.

B. henselae has very low pathogenicity in cats.

Once cleared of infection, cats are resistant to re-infection by innoculation, but are still susceptible if transmitted via blood transfusion.

Transmission is via arthropod vectors. In endemic areas, cats infested with fleas and/or ear mites are more likely to be seropositive.

The organism survives in flea feces for at least 9 days.

Because of the frequency of bacteremia in healthy cats, blood transfusions are a likely route of infection. 

Primary immune-mediated disease is extremely rare in cats.

Stimulation from primary infectious disease antigens is the most common cause of immune-mediated disease in cats, and is most often associated with hemobartonella (mycoplasma) and calicivirus.

Systemic lupus erythematosus is rare in cats. A multitude of signs may occur including fever, weight loss and cutaneous lesions.

Immune-mediated hemolytic anemia is most commonly associated with hemobartonellosis. Signs include anemia, icterus, fever and anorexia. Cats with immunosuppressive disorders such as FeLV may be more susceptible.

Immune-mediated thrombocytopenia is rarely reported in cats. FeLV-positive cats, however, may have thrombocytopenia that is thought to be the result of an immune-mediated response.

Immune-mediated polyarthritis is uncommon in cats, but has been documented in kittens and adult cats with post-calicivirus vaccination.

19 -THE PYREXIC CAT 391

A bacteriologic investigation of subcutaneous abscesses in cats

Clinical, clinicopathologic, and pathologic features of plague in cats: 119 cases (1977-1988)

Bacterial diseases; fungal diseases; and protozoal diseases

Feline toxoplasmosis: interpretation of diagnostic test results

Bartonella spp. antibodies and DNA in aqueous humor of cats

Feline toxoplasmosis and the importance of the Toxoplasma gondii oocyst

Feline infectious peritonitis. Part I. Etiology and diagnosis

Feline infectious peritonitis. Part II. Treatment and prevention

Consensus statement of ehrlichial disease of small animals from the infectious disease study group of the ACVIM

Feline infectious myocarditis/diaphragmitis

Diagnostic approach and medical treatment of seizure disorders

An appraisal of the value of laboratory tests in the diagnosis of feline infectious peritonitis

Tularemia in two cats