What is feline panleukopenia?

    Panleukopenia is a highly contagious, sometimes fatal, viral disease of cats that is seen worldwide. Kittens are affected most severely. The causative parvovirus is very resistant; it can persist for months in the environment unless potent disinfectants are used to inactivate it. Panleukopenia is now seen infrequently by veterinarians, presumably as a consequence of the widespread vaccine use. However, infection rates remain high in unvaccinated cat populations, and the disease occasionally is seen in vaccinated, pedigreed kittens that have been exposed to a high virus challenge.

 

How is this disease produced?

     Feline panleukopenia virus (FPV) is closely related to mink enteritis virus and the type 2 canine parvoviruses (CPV-2, CPV-2a, CPV-2b). FPV can cause disease in all Felids and some members of related families (eg, raccoon, mink, and coatimundi), but it does not harm Canids. Conversely, CPV-2a and CPV-2b have recently been shown to cause a panleukopenia-like illness in domestic cats and large Felids. In a study of German and American cats with a clinical diagnosis of panleukopenia, CPV-2a or CPV-2b, rather than FPV, was isolated from ~10% of cases. In a Vietnamese study, 80% of parvoviruses isolated from healthy cats were canine rather than feline.

 

How is feline panleukopenia transmitted?

    Virus particles are abundant in all secretions and excretions during the acute phase of illness and can be shed in the feces of survivors for up to 6 wk after recovery. Parvoviruses are extremely resistant to inactivation; they can survive >1 yr in a suitable environment and can be transported long distances via fomites (eg, shoes, clothing). However, parvoviruses are destroyed by exposure to a 6% solution of household bleach (aqueous sodium hypochlorite) for 10 min at room temperature. Peroxygen disinfectants are also highly effective.

    

    Cats are infected oronasally by exposure to infected animals, their secretions, or fomites. Most free-roaming cats are exposed to the virus during their first year of life. Those that develop subclinical infection or survive acute illness mount a robust, long-lasting, protective immune response.

 

How this disease develops in the body?

    FPV infects and destroys actively dividing cells in bone marrow, lymphoid tissues, intestinal epithelium, and—in very young animals—cerebellum and retina. In pregnant queens, the virus may spread transplacentally to cause embryonic resorption, fetal mummification, abortion, or stillbirth. Alternatively, infection of kittens in the perinatal period may destroy the germinal epithelium of the cerebellum, leading to cerebellar hypoplasia, incoordination, and tremor. FPV-induced cerebellar ataxia has become a relatively rare diagnosis, because most queens passively transfer sufficient antibodies to their kittens to protect them during the period of susceptibility.

 

What are the clinical findings?

    Most infections are subclinical, as evidenced by the high seroprevalence of anti-FPV antibodies among unvaccinated, healthy cats. Those that become ill are usually <1 yr old. Peracute cases may die suddenly with little or no warning (fading kittens). Acute cases show fever (104-107°F [40-41.7°C]), depression, and anorexia after an incubation period of 2-7 days. Vomiting usually develops 1-2 days after the onset of fever; it is typically bilious and unrelated to eating. Diarrhea may begin a little later but is not always present. Extreme dehydration develops rapidly. Affected cats may sit for hours at their water bowl, although they may not drink much. Terminal cases are hypothermic and may develop septic shock and disseminated intravascular coagulation.

  

    Physical examination typically reveals profound depression, dehydration, and sometimes abdominal pain. Abdominal palpation—which can induce vomiting—may reveal thickened intestinal loops and enlarged mesenteric lymph nodes. In cases of cerebellar hypoplasia, ataxia and tremors with normal mentation are seen. Retinal lesions, if present, appear as discrete gray foci. The duration of this self-limiting illness is seldom >5-7 days. Mortality is highest in young kittens <5 mo of age.

Lesions:

    There are typically few gross lesions, although dehydration is usually marked. Bowel loops are usually dilated and may have thickened, hyperemic walls. There may be petechiae or ecchymoses on the intestinal serosal surfaces. Perinatally infected kittens may have a noticeably small cerebellum. Histologically, the intestinal crypts are usually dilated and contain debris consisting of sloughed necrotic epithelial cells. Blunting and fusion of villi may be present. Eosinophilic intranuclear inclusion bodies are only occasionally seen in formalin-fixed specimens.

 

Diagnosis:

    A presumptive diagnosis is usually based on compatible clinical signs and the presence of panleukopenia (nadir 50-3,000 WBC/µL). Neutropenia is a more consistent finding than lymphopenia. Total WBC counts <2,000 cells/µL are associated with a poor prognosis. During recovery from infection, there is typically a rebound neutrophilia with a marked left shift. Diagnosis can be confirmed by showing the presence of FPV antigen in feces. Some of the in-office immunochromatographic test kits for detection of fecal CPV antigen can also detect FPV antigen during the acute phase of infection.

Differential diagnoses include other causes of profound depression, leukopenia, and GI signs. Salmonellosis and infections with feline leukemia virus (FeLV) and feline immunodeficiency virus should be considered. Concurrent infection with FeLV and FPV can cause a panleukopenia-like syndrome in adult cats.

 

How is feline panleukopenia treated?

    Successful treatment of acute cases requires vigorous fluid therapy and supportive nursing care in the isolation unit. Electrolyte disturbances (eg, hypokalemia), hypoglycemia, hypoproteinemia, anemia, and opportunistic secondary infections often develop in severely affected cats. Anticipation of these possibilities, close monitoring, and prompt intervention are likely to improve outcome. IV fluid replacement and maintenance with a balanced isotonic crystalloid solution (eg, lactated Ringer’s solution with calculated potassium supplementation) is the foundation of therapy. B vitamins should be added to the infusion, together with 5% glucose if hypoglycemia is suspected or proved. In addition to crystalloid infusion, transfusion of fresh-frozen plasma helps support plasma oncotic pressure and provides clotting factors to severely ill, hypoproteinemic kittens. Whole blood is preferable for severely anemic patients. Parenteral, broad-spectrum antibiotic therapy is indicated; however, nephrotoxic drugs (eg, gentamicin, amikacin) should be avoided until dehydration has been corrected. Antiemetic therapy (eg, metoclopramide) may provide some relief and allow earlier enteral feeding of soft, easily digested food. Parenteral nutrition is indicated for severely affected cases.

 

How we prevent it?

    Excellent inactivated and modified live virus vaccines that provide solid, longlasting immunity are available for prevention of FPV infection. Live vaccines should not be given to cats that are pregnant, immunosuppressed, or sick, or to kittens <4 wk old. Most vaccine manufacturers recommend that kittens should receive 2 or 3 modified live vaccine doses, 3 wk apart. The first vaccination is usually given at 6-9 wk of age. The last dose of the initial vaccination series should not be administered before the kitten is 12-14 wk old, to ensure that interfering maternal antibodies do not inactivate the modified live virus. Exposure to virus should be avoided until 1 wk after the vaccination series has been completed. Most manufacturers recommend annual booster revaccination, although other authorities recommend triennial boosters.

 

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From The Merck Veterinary Manual

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