ACVIM – Journal of Veterinary Internal Medicine

Canine parvovirus (CPV-2) was recognized in 1978 as the cause of 2 diseases in dogs, myocarditis, and enteritis.1,2CPV has particulartropism for tissues containing rapidly dividing cells. Viral replicationoccurs initially in the oropharynx and local lymphoid tissue, followedby viremia, 1-5 days after infection. The virus localizes predominantlyin the epithelial lining of the gastrointestinal tract, bone marrow, andlymphoid tissues, 3 resulting in intestinal crypt epithelium destructionand necrosis, villous atrophy, impaired absorptive capacity, anddisrupted gut barrier function, allowing for bacterial translocation andbacteremia.

CPV-2 spreads rapidly among dogs by direct transmission (dog todog) via the fecal-oral route or indirectly from the environmentthrough oronasal exposure.4The virus is shed in the feces typically forseveral days, although shedding has been detected up to 6 weeks.4Weaned puppies are at increased risk for infection because ofdecreased serum concentration of maternal antibodies and changes inthe gastrointestinal bacterial flora.

Preliminary diagnosis is made based on the vaccination history,signalment, clinical signs, and leukopenia, while confirmation rests onlaboratory tests such as antibody or antigen detection and moleculartests (eg, PCR, ELISA).6,7Electron microscopy and virus isolation areadditional diagnostic methods6; however, these are not available inthe clinical setting. Accurate diagnosis is important as positive dogsneed to be hospitalized in isolation and are at high risk of becominginfected in the isolation ward if they are incorrectly diagnosed. Diag-nostic methods have varying degrees of sensitivity and specificity.8Molecular methods based on various types of PCR protocols are con-sidered 1 of the most precise and sensitive methods for CPVdetection.