Feline panleukopenia: A diagnostic laboratory's perspective


Feline panleukopenia: A diagnostic laboratory's perspective

Despite the development of highly effective vaccines, this ancient feline disease continues to be the bane of cats housed in close contact. Find out what you need to watch for in at-risk populations and how to approach diagnosis and disease prevention.

FELINE PANLEUKOPENIA (FPL) is a highly contagious disease with a worldwide distribution in wild and domestic felids. It has been officially recorded in cat populations since the early 20th century but has likely existed for hundreds of years.1 Settings such as farms, animal shelters, pet shops, kennels, and research colonies are ideal for the spread and transmission of FPL. Practitioners working with sick cats from these populations and with stray cats that have unknown contact and vaccination histories should have a good working knowledge of the pathogenesis of FPL and how to diagnose it. They must also be diligent in using procedures and precautions that will minimize the risk of infecting their facilities and spreading the disease among its inhabitants. Diagnostic laboratories frequently perform necropsies on and receive samples from cats suspected of having FPL. In this article, we review the necropsy findings and histopathologic lesions of FPL and discuss which diagnostic tools are available as well as preventive measures.


FPL virus is a member of the family Parvoviridae, a group of small, nonenveloped, single-stranded DNA viruses. Other members of this family include mink enteritis virus and canine parvovirus. Canine parvovirus is thought to have emerged from FPL virus in the late 1970s,2,3 and while this original strain of canine parvovirus (canine parvovirus type 2 [CPV2]) could not infect cats, more recently emerged isolates of canine parvovirus, CPV2a and CPV2b, can.3,4 All of these viruses infect rapidly dividing cells in the intestinal tract and cause marked enteritis. Parvoviruses do not make their own DNA polymerase, so replication occurs in the nucleus, and the initial step of DNA replication depends on the DNA polymerase expressed in infected cells during mitosis. Intranuclear inclusion bodies, observable by light microscopy, provide visible evidence of viral replication.


During the acute phase of the infection, FPL virus particles may be shed in saliva, vomit, feces, or urine.1,5 Virus particles can be transmitted to a susceptible host, usually by an oronasal route, either through direct contact with an infected cat or by fomites. The virus initially infects and replicates in oropharyngeal lymphoid tissue.6 It then disseminates to other tissues between two and seven days7 and is present in Peyer's patches in the intestine by three or four days after infection.8 Cell replication is required for parvoviral DNA synthesis, so rapidly dividing cells are the preferred sites of replication. Thus, in cats with FPL, intestinal crypt epithelium, bone marrow progenitor cells, and lymphoid organs are most severely affected. Mitotic rates are lower in the colon than they are in the small intestine, and lesions are also milder in the large intestine.7 Mitotic rates in the cerebella and retinas of neonates are increased, making these organs primary sites affected in neonatal kittens.7