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| Feline panleukopenia virus | |
|---|---|
| Virus classification | |
| Group: | Group II (ssDNA) |
| Family: | Parvoviridae |
| Subfamily: | Parvovirinae |
| Genus: | Protoparvovirus |
| Species: | Feline panleukopenia virus |
Feline panleukopenia virus (FPV), also known as feline infectious enteritis, feline parvoviral enteritis,[1] feline distemper,[2] feline ataxia, or cat plague,[3] is a viral infection affecting cats, both domesticated and wild feline species. 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.[1] The name panleukopenia comes from the low white blood cell count (leucocytes) exhibited by affected animals.[3]
Panleukopenia is primarily spread through contact with an infected animal's bodily fluids, feces, or other fomites, as well as by fleas.[3] It may be spread to and by cats, minks and ferrets[3] 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 contractable by humans.[3] Like all parvoviruses, FPV is extremely resistant to inactivation and can survive for longer than one year in a suitable environment.[1]
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 complete 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 hours at their water bowl, although they may not drink much. Terminal cases are hypothermic and may develop septic shock and disseminated intravascular coagulation.[1] 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.[4]
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 panleukopaenia and canine parvovirus are extremely closely related, but viruses cannot be transmitted between dogs and cats.
A presumptive diagnosis is usually based on compatible clinical signs in an inadequately vaccinated cat and the presence of leukopenia (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 poorer prognosis. During recovery from infection, there is typically a rebound neutrophilia with a marked left shift. Diagnosis can sometimes be confirmed using an in-office immunochromatographic test kit intended for detection of fecal CPV antigen. However, fecal antigen is detectable only for a short time after infection. False-negative results are common.
Differential diagnoses include other causes of profound depression, leukopenia, and GI signs. Salmonellosis (see Salmonellosis) and infections with feline leukemia virus (FeLV, see Feline Leukemia Virus and Related Diseases) and feline immunodeficiency virus (see Feline Immunodeficiency Virus (FIV)) should be considered. Concurrent infection with FeLV and FPV can cause a panleukopenia-like syndrome in adult cats.
Protection is offered by commercial feline distemper vaccines (ATCvet codes: QI06AA02 (WHO) for the inactivated viral vaccine and QI06AD01 (WHO) for the live vaccine). A number of combination vaccines for several different diseases, including panleukopenia, are also available. Because of the serious disease and ubiquity of the virus vaccination is recommended for every cat. Even cats kept indoors can be infected since the virus is so stable that it can be transmitted on fomites.[5]
In a disease outbreak, unvaccinated kittens or adults can be given anti-FPV serum containing FPV antibodies subcutaneously or intraperitoneally, which may protect for 2–4 weeks.[6][7]
Feline panleukopenia requires aggressive treatment if the cat is to survive, as this disease can kill cats in less than 24 hours. Treatment involves whole blood transfusion to improve pancytopenia, intravenous fluids as most cats are dehydrated, injections of vitamins A, B, and C, IV antibiotics to prevent septicemia, which develops in most cats with feline panleukopenia if antibiotics are not used, and hospitalization.
A cat diagnosed with FPV should be first of all kept in isolation.[8]
Of affected kittens that are two months or less of age, 90–95% die regardless of treatment. Kittens that are more than two months old have a 60–70% mortality rate with treatment and a nearly 100% mortality rate if not treated. Adult cats have a 10–20% mortality rate if treated, and an 85% mortality rate if not treated. Elderly cats have a 20–30% mortality rate if treated and a 90% mortality rate if not treated.[citation needed]
Complications are quite common in feline panleukopenia [FPL]. The most prevalent one is dehydration, which develops in almost all FPL-infected cats that are clinically ill. Hyponatremia and other electrolyte disturbances are also quite common, as is hypotension, hyperpyrexia or, late in the disease, hypothermia. The patients' severe leukocytopenia predispose them to secondary infections, especially bacterial and fungal, though secondary viral infections also occur with some frequency. Disseminated intravascular coagulation may also occur, and is often fatal. Extreme thrombocytopenia may also occur, and can lead to severe hemorrhagic complications. Even if a cat survives acute FPL, late complications such as cardiomyopathy and myocarditis can occur, though there have never been any reported cases of hematologic or gastrointestinal sequalae, and it seems that late myocarditis or cardiomyopathy is extremely rare in feline panleukopenia-affected cats. Overall, any long-term sequalae in survivors of feline panleukopenia is extremely rare, with almost all cats who survive making a full recovery.
At the beginning of the 1950s, cats brought to Marion Island, one of the Prince Edward Islands, to deal with a mouse problem in the local meteorological station, went out of growth control. Starting from the first five domestic cats introduced on the island on 1949, there were about 3,400 cats in 1977, feeding on the burrowing petrels instead of the mice, threatening to drive the birds to extinction. A cat eradication program was set up and a few cats were intentionally infected with the panleukopenia virus, which reduced the number of cats to about 600 by 1982.[13]
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