Feline panleukopenia is a parvoviral infectious disease of kittens typically characterized by depression, anorexia, high fever, vomiting, diarrhea, and consequent severe dehydration. Adult cats are much less often affected. Diagnosis is usually based on clinical signs, severe neutropenia and lymphopenia, and fecal viral antigen or PCR testing. Treatment includes intensive fluid therapy, glucose and potassium supplementation, antimicrobial, anthelmintic, and antiemetic therapy, and sometimes immunotherapy.
Feline panleukopenia is a highly contagious, often fatal, viral disease of cats that is seen worldwide. Kittens are affected most severely. The causative parvovirus is very resistant; it can persist for 1 year at room temperature in the environment if protected in organic material. Feline panleukopenia is now diagnosed infrequently by veterinarians in many countries, presumably as a consequence of widespread vaccine use. However, infection rates remain high in some unvaccinated cat populations, and the disease occasionally is seen in vaccinated, pedigreed kittens that have been exposed to a high virus challenge. Feline panleukopenia has recently been recognized as a re-emergent disease in Australia. Large outbreaks have occurred in unvaccinated cats in shelters, and there has been spread among pet cats in the wider community.
Etiology, Transmission, and Pathogenesis of Feline Panleukopenia
Feline parvovirus (FPV; synonymous with feline panleukopenia virus) is closely related to mink enteritis virus and the type 2 canine parvoviruses (CPV) that cause canine parvoviral enteritis. All are now designated as members of the species Carnivore protoparvovirus 1. FPV can cause disease in all felids and in some members of related families (eg, raccoon, mink), but it does not harm canids. Conversely, some currently circulating CPV strains (CPV-2a, -2b, and -2c) have been shown to cause feline panleukopenia in domestic cats and larger felids. However, FPV dominates over CPV as the cause of feline panleukopenia worldwide. Vaccines that contain FPV protect cats against disease caused by CPV, although vaccines that contain FPV induce much lower antibody titers against CPV-2c than against FPV.
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 as long as 6 weeks after recovery. Being highly resistant to inactivation, parvoviruses can be transported long distances via fomites (eg, shoes, clothing). However, FPV can be destroyed by exposure to a 1:32 dilution of household bleach (6% aqueous sodium hypochlorite) for 10 minutes or more at room temperature. Peroxygen disinfectants (eg, potassium peroxymonosulfate) are also highly effective. It is important that contaminated surfaces are thoroughly cleaned of organic material before disinfectants are applied.
Cats are infected oronasally by exposure to infected animals, their feces, secretions, or contaminated fomites. Most free-roaming cats are thought to be 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.
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 early period of susceptibility.
Clinical Findings of Feline Panleukopenia
Most feline panleukopenia infections are subclinical, as evidenced by the high seroprevalence of anti-FPV antibodies among unvaccinated, healthy cats. Those cats that do become ill are usually < 1 year 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. Hypersalivation may be seen in some cases, associated with nausea or abdominal pain. Diarrhea may begin a little later than the vomiting but is not always present. In only 3%–15% of cases is the diarrhea hemorrhagic. 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 immediate 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 kittens < 5 months old.
Lesions
There are typically few gross lesions due to feline panleukopenia, although dehydration is usually marked. Bowel loops may be segmentally 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 seen only occasionally in formalin-fixed specimens; use of Bouin's or Zenker's fixative will increase the likelihood of seeing these. There may be a notable lack of lymphocytic or inflammatory cell infiltration in the bowel walls because of destruction of these leukocytes by the virus.
Diagnosis of Feline Panleukopenia
Typically based on clinical signs and leukopenia on a CBC
A presumptive diagnosis of feline panleukopenia is usually based on compatible clinical signs in an inadequately vaccinated cat and the presence of leukopenia (nadir 50–3,000 WBC/mcL). Neutropenia develops earlier than lymphopenia. Total WBC counts < 2,000 cells/mcL are associated with a poorer prognosis. During recovery from infection, there is typically a rebound neutrophilia with a marked left shift. Diagnosis can, in some cases, 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. The sensitivity of these tests has been reported to range from 50%–80%, but the specificity is much higher, 94%–100%.
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 feline panleukopenia in adult cats. FPV infections combined with various salmonellae or feline calicivirus cause much more severe disease than FPV alone.
Treatment, Prevention, and Prognosis of Feline Panleukopenia
Supportive care, prompt IV fluid treatment, and antibiotics are the primary treatments
Effective vaccines are available
Successful treatment of acute cases of feline panleukopenia 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 can 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. It also provides some anti-FPV antibodies. Whole blood is preferable for the occasional cat that is severely anemic.
Parenteral, broad-spectrum antibiotic therapy is indicated; however, nephrotoxic drugs (eg, aminoglycosides) must be avoided until dehydration has been fully corrected. For example, IV ampicillin (20 mg/kg, every 6–8 hours) could be given in combination with gentamicin (6–8 mg/kg, every 24 hours for 3–5 days), starting once rehydration has been achieved. Because of the nephrotoxic potential of the gentamicin, urinary protein dipstick findings, sequential urine sediments, and serum SDMA or creatinine should be monitored. There are single antibiotic agents, albeit more expensive, that are effective against the anaerobes and gram-negative aerobes that are the most important bacteria in feline panleukopenia. These include third-generation cephalosporins (eg, ceftiofur, cefotaxime) and extended penicillins (eg, piperacillin).
Intestinal parasitism commonly complicates feline panleukopenia, especially in shelter environments, so use of anthelmintics (eg, fenbendazole, 50 mg/kg, PO, every 24 hours for 2–5 days) is an important consideration and can be started once vomiting is controlled.
Antiemetic therapy (eg, maropitant, ondansetron or metoclopramide) usually provides some relief and allows earlier enteral feeding of soft, easily digested food. Maropitant is the first-choice anti-emetic. In severely affected cats it can be combined with ondansetron. Feeding (little and often) should be commenced as early as possible, even in the face of mild, intermittent, persistent vomiting. Feeding promotes healing of the GI mucosa and re-establishment of an effective mucosal barrier. Cats with severe vomiting should not be fed until the vomiting is better controlled. Parenteral nutrition is indicated only for the most severely affected cases, and its use should not delay vigorous attempts to start enteral feeding.
Recombinant feline interferon omega (rFeIFN; 1 MU/kg, SC, every 24 hours for 5 consecutive days, and three separate 5-day treatments must be performed at day 0, day 14, and day 60) should be considered for use in the treatment of feline panleukopenia. Although rFeIFN is not approved by the FDA for this purpose and has not been proven effective in feline panleukopenia, it is approved and effective in the treatment of canine parvoviral enteritis. Passive immunotherapy using immune serum from solidly immune cats, or using a commercial product raised in horses, is widely practiced in some countries. There is limited evidence of treatment efficacy, however.
Excellent inactivated and modified-live virus vaccines that provide solid, long-lasting immunity are available for prevention of feline panleukopenia. Live vaccines should not be given to cats that are pregnant, immunosuppressed, or sick or to kittens <4 weeks old. Most authorities recommend that kittens receive two or three modified-live vaccine doses SC, 3–4 weeks apart. The first vaccination is usually given at 6–9 weeks of age. The last dose of the initial vaccination series should not be administered before the kitten is 16 weeks old, to allow time for interfering maternal antibodies to wane so they do not inactivate the modified-live vaccine virus. A followup vaccine dose at 26–52 weeks is a new recommendation, because some kittens have residual interfering antibodies, even at 16 weeks, sufficient to prevent successful immunization. Exposure to virus should be avoided until 1 week after the initial vaccination series has been completed.
Adult cats should be revaccinated against FPV triennially or less frequently thereafter, although some manufacturers in some countries continue to recommend annual revaccination. Titer testing kits are commercially available to detect when individual cats are immune to feline panleukopenia. These can be used as an alternative to repeated, scheduled vaccinations, for clients who prefer that option.
Feline panleukopenia has a noticeably worse prognosis than CPV enteritis. Survival rates of 20%–51% have been reported in cats that received supportive treatment in-hospital for feline panleukopenia. By comparison, in one recent study, 90% of hospitalized puppies with CPV enteritis survived to discharge. It is not certain that the care routinely provided to cats with panleukopenia is equally as intense as that provided to dogs with CPV enteritis and that any difference would be reflected in these various reports. Studies have identified a variety of sometimes contradictory prognostic indicators in cats with feline panleukopenia. In one study, cats with hypothermia, lethargy, and low body weight at the time of admission fared worse.
Key Points
Feline panleukopenia is a highly contagious, often fatal, viral disease of cats.
A majority of infections are subclinical. In cats that do become ill, clinical signs include high fever, profound depression, and anorexia. Many affected cats vomit, and some develop diarrhea. Only a minority have hemorrhagic diarrhea.
Diagnosis is based on compatible clinical findings, including leukopenia, in an inadequately vaccinated kitten. Fecal antigen detection kits intended for diagnosis of CPV enteritis can also be used to diagnose feline panleukopenia. The sensitivity is moderate, and specificity is high.
Treatment includes fluid, electrolyte, and glucose supplementation; antiemetic therapy; antibiotics; and anthelmintics.
Excellent vaccines are available for prevention. They protect against both FPV and CPV.
For More Information
WSAVA Vaccination Guidelines (2016) Owner and breeder disease information handouts available on the same page.
Also see pet health content regarding feline panleukopenia.
