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Feline Panleukopenia

(Feline Parvoviral Enteritis, Feline Infectious Enteritis)

ByLena DeTar, DVM, MA, DACVPM, DABVP-SMP, Maddie's Shelter Medicine Program
Reviewed/Revised Feb 2025
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Feline panleukopenia is a highly contagious, often fatal parvoviral disease of cats worldwide. It is characterized by depression, anorexia, high fever, vomiting, diarrhea, and consequent severe dehydration. Kittens are most commonly and severely affected; sudden death is common. Diagnosis is usually based on a patient's history and clinical signs, patient-side ELISA, and characteristic severe neutropenia and lymphopenia. Supportive treatment, which includes intensive fluid therapy and antimicrobial, antiemetic, and anthelmintic therapy, is frequently unsuccessful. Without proper disinfection, the virus remains viable in the environment and can persist for up to 1 year under favorable conditions. Vaccination, when not confounded by maternal antibodies, provides long-lasting immunity.

Feline panleukopenia is uncommonly encountered by general practice veterinarians in many countries, likely as a consequence of widespread vaccination. However, infection rates remain high in feral, free-roaming, and pet cat populations with limited access to preventive care, especially in areas with large numbers of kittens. Outbreaks are relatively common worldwide in animal shelters that house cats, especially when kittens are housed in groups and vaccination is not provided at intake (1, 2).

Feline panleukopenia is often referred to as feline distemper; however, the virus that causes disease in cats is unrelated to canine distemper virus that affects dogs and other carnivores.

Etiology, Transmission, and Pathogenesis of Feline Panleukopenia

Feline parvovirus (FPV; also known as feline panleukopenia virus or feline viral enteritis) is a single-stranded, nonenveloped DNA virus closely related to the canine parvovirus group type 2 (CPV-2) that causes canine parvoviral enteritis. FPV, CPV, and mink enteritis virus are members of the viral species Carnivore protoparvovirus 1.

FPV can cause disease in all felids and in some members of related families (eg, raccoon, mink); however, FPV does not harm canids. Currently circulating CPV strains (CPV-2a, -2b, and -2c) can also cause clinically significant disease in domestic cats and larger felids; worldwide, however, FPV causes substantially more feline viral enteritis than CPV does.

Vaccines that contain FPV cross-protect cats against disease caused by CPV, although they induce lower antibody titers against CPV than against FPV.

In parvovirus-infected animals, infectious viral particles are abundant during the acute phase of illness in all secretions and excretions, including vomitus, saliva, urine and feces, and can be detected in the feces of survivors for up to 6 weeks after recovery, although most patients stop shedding after 2 weeks.

Because they are highly resistant to inactivation, parvoviruses can be transported long distances via fomites (eg, clothing, mechanical vectors, medical equipment) or persist in unsanitary environments. However, FPV can be destroyed by exposure to a number of strongly oxidizing disinfectants including a 1:32 dilution of household bleach (6% aqueous sodium hypochlorite) for 10 minutes, potassium peroxymonosulfate at 1:100 dilution for 10 minutes, or accelerated hydrogen peroxide at 1:16 dilution for 5 minutes. Contaminated surfaces and equipment must be thoroughly cleaned of organic material before applying disinfectants, and adequate contact time must be allowed for disinfectants to work

Quaternary ammonium products may display label claims against parvoviruses; however, they have been found ineffective in multiple field studies (3, 4, 5).

Pearls & Pitfalls

  • Quaternary ammonium products may display label claims against parvoviruses; however, they have been found ineffective in multiple field studies.

Cats are infected oronasally by exposure to infected animals, their feces and secretions, and contaminated fomites and environments. The incubation period is usually 2–7 days but in some cases may be up to 14 days.

Parvoviruses require host cellular machinery for reproduction, infecting and destroying actively dividing cells in bone marrow, lymphoid tissues, and intestinal epithelium. In pregnant queens, FPV not only affects the queen's health, but also spreads transplacentally to cause embryonic resorption, fetal mummification, abortion, stillbirth, and dystocia. Infection in the perinatal period may destroy kittens' rapidly dividing cerebellar or retinal cells, leading to cerebellar hypoplasia, incoordination, and tremors that persist throughout life.

FPV is not shed after the immediate clinical period; cats that survive subclinical infection or acute illness, or that respond to vaccination, mount robust, potentially lifelong, protective immune responses.

Clinical Findings of Feline Panleukopenia

Unvaccinated adult cats with competent immune systems often survive low-level or subclinical feline panleukopenia infections (6), although mortality and morbidity rates for this group are not well-documented. Cats that develop clinical signs of viral enteritis are usually between 4 weeks and 2 years old (2).

Peracute cases are common in kittens found outside or living in shelters and catteries, where sudden death may be the first clinical sign noted.

Acute cases show high fever (40–41.7°C [104–107°F]), depression, severe dehydration leading to shock, and complete anorexia. Vomiting, which usually develops 1–2 days after the onset of fever, is typically bilious and unrelated to eating. Hypersalivation, associated with nausea and abdominal pain, can occur in some cases. Unlike in cases of canine parvoviral enteritis, with feline panleukopenia infections, diarrhea is not always present and usually does not contain blood when it occurs. Hypothermia and hypoglycemia develop alongside septic shock and disseminated intravascular coagulation.

Physical examination typically reveals profound depression, dehydration, and sometimes abdominal discomfort. Abdominal palpation—which can induce immediate vomiting—may reveal thickened intestinal loops and enlarged mesenteric lymph nodes.

The duration of acute FPV is seldom > 5–7 days; median survival time after hospital admission is around 3 days (7). Frequently, one kitten after another in an affected litter will develop severe clinical signs over a period of several days.

Lesions

Typically, few gross lesions are seen with feline panleukopenia, although dehydration and anorexia are usually marked.

On necropsy, bowel loops may be segmentally dilated and have thickened, hyperemic walls. Petechiae or ecchymoses may be present on the intestinal serosal surfaces.

Histologically, intestinal crypts are usually dilated and contain debris consisting of sloughed necrotic epithelial cells. Blunting and fusion of intestinal villi may be present. Eosinophilic intranuclear inclusion bodies are evident only occasionally in formalin-fixed specimens. Viral destruction of leukocytes may result in a notable lack of lymphocytic or inflammatory cell infiltration in bowel walls (8).

Perinatally infected kittens may have noticeably small cerebella.

Diagnosis of Feline Panleukopenia

  • Clinical signs

  • Parvovirus antigen ELISA

  • CBC or blood smear

A presumptive diagnosis of feline panleukopenia can be made based on compatible clinical signs in a juvenile or unvaccinated adult cat with a history of plausible exposure.

Positive results of parvovirus ELISA (which detects FPV antigen in vomitus, feces, or rectal swab) strongly support a panleukopenia diagnosis and can be performed after death. Sensitivity of patient-side tests for FPV is 50–80%, depending on viral shedding load, which can be intermittent. Vomitus, if available, may be a more reliable medium for detecting FPV antigen than rectal swab. Both strong and weak color changes should be considered positive results (9, 10).

Negative test results in kittens with typical clinical signs should be confirmed with subsequent testing. Although vaccination within 14 days may cause false positive results, the specificity of ELISA is generally very high (94–100%) (9, 10).

Confirmation of ELISA results or presumptive diagnosis can be made by a visually decreased WBC fraction in a blood smear or by the presence of leukopenia in a CBC. Neutropenia develops before lymphopenia, and total WBC counts < 2,000 cells/mcL are associated with a poorer prognosis.

Thrombocytopenia may occur in cats progressing toward DIC. In cats recovering from infection, rebound neutrophilia with a marked left shift can occur.

Differential diagnoses include other causes of profound depression, leukopenia, and GI signs. Salmonellosis, feline infectious peritonitis, toxoplasmosis, sepsis, and severe GI parasitism should be considered.

For vaccinated adult cats with clinically apparent FPV infection, coinfection with feline leukemia virus (FeLV) should be investigated. FPV infections are more severe in cats with other concurrent viral or parasitic diseases. Because of FPV's high mortality rate, community cat outbreaks can be mistaken for mass poisoning.

Treatment, Prevention, and Prognosis of Feline Panleukopenia

  • Supportive care, IV fluids, antiemetics, and antimicrobials

  • Vaccination

Successful treatment of acute cases of feline panleukopenia is challenging. When disease is severe, resources are limited, or risk of spread to vulnerable populations is high, poor prognosis for survival and concern over patient welfare should prompt strong consideration of humane euthanasia.

When treatment is elected, vigorous fluid therapy and supportive nursing care provide the best chance of survival.

Electrolyte disturbances (especially hypokalemia), hypoglycemia, hypoproteinemia, anemia, and opportunistic secondary bacterial infections often develop in severely affected cats. Anticipation of these possibilities, close monitoring, and prompt intervention may improve outcome.

In appropriately selected mild cases, outpatient therapy with subcutaneous fluids, antimicrobials, and antiemetics can be successful. Whenever treatment is elected, close attention to biosecurity in the clinic and home is essential.

Administration of IV balanced isotonic crystalloid solutions (eg, lactated Ringer’s solution [LRS] with calculated potassium supplementation) for fluid deficit replacement and maintenance is the foundation of treatment for cats and kittens in shock.

B vitamins may be added to the fluid infusion.

If hypoglycemia is present, 2.5–5% dextrose can be administered in IV fluids (eg, add 2–4 mL of concentrated stock 50% dextrose solution [500 mg/mL] to 20 mL of LRS for fluid pump infusion) until normoglycemia is achieved.

In addition to crystalloid infusion, transfusion of fresh-frozen plasma can help support plasma oncotic pressure, provides clotting factors, and may provide some anti-FPV antibodies. Whole blood is preferred for severely anemic cats.

Antiemetic therapy provides patient relief and allows earlier enteral feeding of soft, easily digested food. Maropitant (1 mg/kg, SC or IV, every 24 hours) is the first-choice antiemetic due to its safety, efficacy, and potential analgesic effects. In severely affected cats, maropitant can be combined with ondansetron (0.5 mg/kg, IV, intermittently, or followed by 0.5 mg/kg/hour as a constant-rate infusion).

Parenteral, broad-spectrum antimicrobial therapy is indicated for all cats with clinical signs to counteract GI bacterial translocation. When selecting antimicrobials, anaerobes and gram-negative aerobes are the most important bacteria to target in feline panleukopenia–related sepsis. Nephrotoxic drugs, such as aminoglycosides, should be avoided until dehydration has been fully corrected.

Potentiated penicillins, combined with fluoroquinolones or third-generation cephalosporins, are commonly used. For example, ampicillin sulbactam (10–20 mg/kg, IV, every 6–8 hours) could be given in combination with marbofloxacin (2.75–5.5 mg/kg, PO, every 24 hours). Alternatively, cefovecin (8 mg/kg, SC, once) could be administered to an outpatient.

Intestinal parasitism commonly complicates feline panleukopenia, especially in shelter environments, so broad-spectrum anthelmintics should be started once vomiting is controlled.

Feeding (small amounts frequently) should be started as early as possible, even in the face of mild, intermittent, persistent vomiting. Feeding promotes healing of the GI mucosa and reestablishment of an effective mucosal barrier.

Several expensive immune-targeted therapies have been advertised with currently limited evidence of treatment efficacy. These include recombinant feline interferon omega, which has not proved effective in field trials (7, 11), and filigrastin (neupogen), for which only one uncontrolled case study and no peer-reviewed studies exist.

Passive immunotherapy using immune serum from vaccinated cats or a commercial product raised in horses is widely practiced in some countries; evidence of efficacy is not well-documented. A proprietary canine parvovirus monoclonal antibody has shown promise for treatment of parvoviral disease in dogs but has not been formally tested in cats (12).

Excellent subcutaneous modified live virus (MLV) vaccines that provide complete long-lasting immunity are widely available for the prevention of feline panleukopenia. Appropriately boosted killed virus vaccines are preferred for pregnant queens in low-risk homes and likely contribute to robust passive transfer of immunity to kittens. In high-risk shelter, rescue, or community scenarios, the benefits of MLV vaccination often outweigh potential risks associated with vaccination during pregnancy, illness, or immunosupression (1).

In low-risk homes and for kittens of vaccinated queens, routine vaccination is recommended by the World Small Animal Veterinary Association (WSAVA), American Animal Hospital Association (AAHA), and the Feline Veterinary Medical Association (FVMA, formerly American Association of Feline Practitioners). The 2020 AAHA/AAFP Feline Vaccination Guidelines recommend starting vaccination at 6 weeks, with revaccination every 3–4 weeks until 16–20 weeks of age. This practice allows time for maternal antibodies to wane and increases the chance of successful immunization.

Revaccination should be considered at 6 months to 1 year of age. Following that, cats should be revaccinated against FPV every 3 years.

In high-risk, community cat, or shelter settings, AAHA/FVMA, WSAVA, and the Association of Shelter Veterinarians (ASV) recommend MLV vaccination for all cats immediately upon intake and ideally again 2 weeks later. Starting at 4 weeks of age, kittens should be vaccinated every 2 weeks while in the shelter until they are 20 weeks old.

In outbreak scenarios, prompt MLV (re)vaccination of the entire cat population is a key part of any response. Even an incomplete immune response before exposure may improve chances of survival (13).

Titer testing kits are commercially available to detect circulating antibodies against FPV. These tests can be used as an alternative to repeated scheduled vaccinations in adult cats and can be useful in population risk assessment during an outbreak.

The prognosis for cats with acute panleukopenia is poor; for cats with feline panleukopenia hospitalized for supportive treatment, survival rates of 20–51% have been reported (6, 7). These rates do not include cases that died peracutely. By comparison, reported survival rates for puppies hospitalized for treatment of CPV enteritis are as high as 90% (or 80% for those treated on an outpatient basis) (14).

Poor prognostic indicators for cats with panleukopenia include hypothermia, low body weight, severe leukopenia, thrombocytopenia, hypoproteinemia, and hypokalemia. Positive prognostic indicators include WBC rebound and return of appetite.

Key Points

  • Feline panleukopenia is a highly contagious, often fatal, viral disease of young cats.

  • Clinical signs of FPV include fever, profound depression, shock, emesis, and anorexia. Some cats die acutely, while others are mildly or subclinically affected.

  • Diagnosis is supported by compatible signalment (young, unvaccinated, group-housed), clinical findings, positive results of ELISA testing, and presence of leukopenia.

  • Supportive treatment includes fluid therapy and administration of antiemetics, antimicrobials, and anthelmintics.

  • Effective vaccines are widely available for almost complete prevention.

For More Information

References

  1. DeTar L, Doyle E, O'Quin J, et al. Association of Shelter Veterinarians guidelines for standards of care in animal shelters. J Shelter Med Community Anim Health. 2022;1(S1):29-37. doi:10.56771/ASVguidelines.2022

  2. Rehme T, Hartmann K, Truyen U, Zablotski Y, Bergmann M. Feline panleukopenia outbreaks and risk factors in cats in animal shelters. Viruses. 2022;14(6):1248. doi:10.3390/v14061248

  3. Eleraky NZ, Potgieter LND, Kennedy MA. Virucidal efficacy of four new disinfectants. J Am Anim Hosp Assoc. 2002;38(3):231-234. doi:10.5326/0380231

  4. Omidbakhsh N, Sattar SA, Broad-spectrum microbicidal activity, toxicologic assessment, and materials compatibility of a new generation of accelerated hydrogen peroxide-based environmental surface disinfectant. Am J Infect Control. 2006;34(5):251-257. doi:10.1016/j.ajic.2005.06.002

  5. Kennedy, MA, Mellon VS, Caldwell G, Potgieter LN. Virucidal efficacy of the newer quaternary ammonium compounds. J Am Anim Hosp Assoc. 1995;31(3):254-28. doi:10.5326/15473317-31-3-254

  6. Kruse BD, Unterer S, Horlacher K, Sauter-Louis C, Hartmann K. Prognostic factors in cats with feline panleukopenia. J Vet Intern Med. 2010;24(6):1271-1276. doi:10.1111/j.1939-1676.2010.0604.x

  7. Porporato F, Horzinek MC, Hofmann-Lehmann R, et al. Survival estimates and outcome predictors for shelter cats with feline panleukopenia virus infection. J Am Vet Med Assoc. 2018;253(2):188-195. doi:10.2460/javma.253.2.188

  8. Barrs VR. Feline panleukopenia: a re-emergent disease. Vet Clin North Am Small Anim Pract. 2019;49(4):651-670. doi:10.1016/j.cvsm.2019.02.006

  9. Neuerer FF, Horlacher K, Truyen U, Hartmann K. Comparison of different in-house test systems to detect parvovirus in faeces of cats. J Feline Med Surgery. 2008;10(3):247-251. doi:10.1016/j.jfms.2007.12.001

  10. Jacobson LS, Janke KJ, Giacinti J, Weese JS. Diagnostic testing for feline panleukopenia in a shelter setting: a prospective, observational study. J Feline Med Surgery. 2021;23(12):1192-1199. doi:10.1177/1098612X211005301

  11. Paltrinieri S, Crippa A, Comerio T, Angioletti A, Roccabianca P. Evaluation of inflammation and immunity in cats with spontaneous parvovirus infection: Consequences of recombinant feline interferon-omega administration. Vet Immunol Immunopathol. 2007;118(1-2):68-74. doi:10.1016/j.vetimm.2007.04.007

  12. Larson L, Miller L, Margiasso M, et al. Early administration of canine parvovirus monoclonal antibody prevented mortality after experimental challenge. J Am Vet Med Assoc. 2024;262(4):506-512. doi:10.2460/javma.23.09.0541

  13. Larson LJ, Schultz RD. Effect of vaccination with recombinant canine distemper virus vaccine immediately before exposure under shelter-like conditions. Vet Ther. 2006;7(2):113-118.

  14. Venn EC, Preisner K, Boscan PL, Twedt DC, Sullivan LA. Evaluation of an outpatient protocol in the treatment of canine parvoviral enteritis. J Vet Emerg Crit Care (San Antonio). 2017;27(1):52-65. doi:10.1111/vec.12561

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