Feline panleukopenia virus (FPV), also known as Feline infectious enteritis, Feline distemper, Feline ataxia, or cat plague, is a viral infection affecting cats, both domesticated and wild feline species. While often mistaken for feline distemper, the two conditions are not synonymous. It is caused by feline parvovirus, a close relative of both type 2 canine parvovirus and mink enteritis. Once contracted, it is highly contagious and can be fatal to the affected cat. The name, panleukopenia, comes from the low white blood cell count (leucocytes) exhibited by affected animals.
Panleukopenia is primarily spread through contact with an infected animal’s bodily fluids, feces, or other fomites, as well as by fleas. It may be spread to and by cats, minks and ferrets and can be spread long distances through contact with bedding, food dishes, or even by clothing and shoes of handlers of infected animals. It is not, however, contagious or contractible by humans. Like all parvoviruses, FPV is extremely resistant to inactivation and can survive for longer than one year in a suitable environment.
The virus primarily attacks the lining of the gastrointestinal tract, causing internal ulceration and, ultimately, total sloughing of the intestinal epithelium. This results in profuse and usually bloody diarrhea, severe dehydration, malnutrition, anemia, and often death. It causes a decrease in the cat's white blood cells, thus compromising its immune system. Typically, it also causes a decrease in hematocrit and platelet counts on a completer blood count. This is often key in diagnosing panleukopenia. Other symptoms include depression, lethargy, loss of appetite, fever, vomiting, loss of skin elasticity due to dehydration, and self-biting in the tail, lower back and back legs. Affected cats may sit for yours at their water bowl, although they may not drink much. Terminal cases are hypothermic and may develop septic shock and disseminated intravascular coagulation. Most panleukopenia deaths are due to secondary infections or dehydration resulting from diarrhea. This is because the virus affects the infected cat’s immune system, leaving it vulnerable to secondary infection.
If a cat is exposed during pregnancy, the virus can cause cerebellar hypoplasia in her offspring. This is why administering modified live feline panleukopenia vaccine during pregnancy is discouraged. Feline panleukopenia and canine parvovirus are extremely closely related, but viruses cannot be transmitted between dogs and cats.
Generally, a clinical diagnosis of feline panleukopenia can be made based on characteristic gastroenteric illness and severe pancytopenia in a susceptible cat, but fecal analysis and blood culture is typically performed as well to rule out other illnesses. Differential diagnosis for FPV include salmonellosis, enteric toxosis, FIV, feline leukemia, cryptosporidiosis, pancreatitis, septicaemia with acute endotoxemia, toxoplasmosis, peritonitis, and lymphoma. In an unvaccinated cat, the presence of antibodies against FPV indicate that the cat either has the disease or has had the disease in the past. Elevated IgM titers (1:10 or greater) indicate active infection and if clinical signs are obvious (diarrhea, panleukopenia) the prognosis is poor. Elevated IgG titers (1:100 or greater) in a cat with clinical signs indicates a better prognosis. Protection is offered by commercial feline distemper vaccines (ATCvet codes: QI06AA02 for the inactivated viral vaccine and QI06AD01 for the live vaccine). A number of combination vaccines for several different diseases, including panleukopenia, are also available. After vaccination IFA titers of 1:10 or greater are considered protective.
Our test for feline panleukopenia is an indirect fluorescent antibody (IFA) procedure that is carried out on Teflon matted glass slides with parvo virus (CPV2A Black Isolate/CRFK) infected cells fixed to their surface. This method requires the use of diluted patient serum being placed on the slide and incubated for 30-minutes at which time the slide is washed and a fluorescein conjugated anti-cat globulin is placed on the slide. If any antibodies to FPV are present in the patient serum they will combine with the FPV antigen fixed to the slide surface. The fluorescent antibody conjugate will then be bound to the FPV antibodies and the resulting antibody-conjugate complex viewed with an ultraviolet microscope are seen as bright areas of fluorescence in the infected cells. The total number of infected cells on our slides does not exceed 40% which leaves the negative cells to enhance contrast.
