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Feline Parvovirus
Margaret C. Barr, DVM, PhD

College of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, USA

Feline parvovirus (FPV) is the causative agent of feline Epidemiology
panleukopenia, a disease that has also been called feline
infectious enteritis, feline plague or feline distemper. Domestic and wild felids are susceptible to FPV infection,
along with some nonfelid species like mink, raccoons, and
foxes. Although canids are resistant to FPV infection, only
Etiology/Pathophysiology a few mutations in the VP2 capsid protein gene led to the
emergence of CPV‐2. Feline parvovirus‐associated disease
Feline parvovirus is so closely related to canine parvovi- is most often seen in multicat housing situations like animal
rus type 2 (CPV‐2), mink enteritis virus, and raccoon shelters and breeding catteries, especially if rigorous sanita-
parvovirus that all these viruses are now classified as a tion, isolation, and vaccination protocols are not followed.
single species, feline panleukopenia virus. The genome of Parvoviruses are shed at high titer in the feces of infected
this small single‐stranded DNA virus is packaged tightly animals for several days after infection. Transmission is
in an icosohedral, nonenveloped capsid that is very through the fecal–oral route, either directly or indirectly on
resistant to environmental conditions. The feline trans- fomites such as shoes, clothing, or feeding dishes.
ferrin receptor allows FPV access to a broad range of Extensive prevalence data are lacking. The prevalence
host cells, where it replicates in actively dividing cells of anti‐FPV antibodies in cats entering a Florida animal
including lymphocytes, enteric crypt epithelial cells, and shelter, indicating either past exposure or vaccination,
bone marrow myeloid progenitor cells. Similar to the was just under 40%. If other cat populations in the US are
pathology seen with CPV‐2 infection in dogs, intestinal similar, about 60% of cats are at risk for FPV infection.
villi are severely blunted, absorptive capacity is impaired, Anecdotal reports also suggest a recent resurgence of
and gastrointestinal integrity is compromised in FPV‐ feline panleukopenia outbreaks, possibly associated with
infected cats. The interruption of myeloid cell prolifera- antigenic variation in FPV variants and the associated
tion along with lymphocytolysis and redistribution of decreased efficacy of commercial vaccines.
circulating white blood cells to inflamed tissues results
in the characteristic and severe panleukopenia seen with Signalment
this disease.
Perinatal infection (approximately three weeks before Susceptible cats of all ages can be infected, but young kit-
birth to three weeks after birth) of kittens results in tens experience a higher mortality rate (up to 90%) than
infection of the central nervous system and impacts older animals if not treated. There are no breed or sex
development of the cerebellum. The virus replicates in predispositions reported for FPV.
the dividing neuroblasts of the external granule cell
layer, causing cerebellar hypoplasia in kittens that sur-
vive the infection. There is also evidence of FPV replica- History and Clinical Signs
tion in Purkinje cells of the cerebellum but it is unclear
how the virus replicates in these presumably postmi- The typical FPV patient will have a history of exposure to
totic cells. other cats in a high‐density multicat environment and

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical