Canine parvovirus (CPV) is a highly contagious and relatively common cause of acute, infectious GI illness in young dogs. Although its exact origin is unknown, it is believed to have arisen from feline panleukopenia virus or a related parvovirus of nondomestic animals.

It is a nonenveloped, single-stranded DNA virus, resistant to many common detergents and disinfectants, as well as to changes in temperature and pH. Infectious CPV can persist indoors at room temperature for at least 2 months. Infectious CPV outdoors, if protected from sunlight and desiccation, can persist for many months and possibly years.

Young, unvaccinated or incompletely vaccinated dogs are most susceptible. Assuming sufficient colostrum ingestion, puppies born to a dam with CPV antibodies are protected from infection for the first few weeks of life. However, susceptibility to infection increases as maternally acquired antibody wanes. Stress (eg, from weaning, overcrowding, malnutrition, etc), concurrent intestinal parasitism, or enteric pathogen infection have been associated with more severe clinical illness.

CPV is shed in the feces of infected dogs within 4–5 days of exposure (often before clinical signs develop), throughout the period of illness, and for ~10 days after clinical recovery. Infection is acquired through direct oral or nasal contact with virus-containing feces or indirectly through contact with virus-contaminated fomites (eg, environment, personnel, equipment). Viral replication occurs initially in the lymphoid tissue of the oropharynx, with systemic illness resulting for subsequent hematogenous dissemination. CPV preferentially infects and destroys rapidly dividing cells of the small-intestinal crypt epithelium, lymphopoietic tissue, and bone marrow. Destruction of the intestinal crypt epithelium results in epithelial necrosis, villous atrophy, impaired absorptive capacity, and disrupted gut barrier function, with the potential for bacterial translocation and bacteremia.

Lymphopenia and neutropenia develop secondary to destruction of hematopoietic progenitor cells in the bone marrow and lymphopoietic tissues (eg, thymus, lymph nodes, etc) and are further exacerbated by an increased systemic demand for leukocytes. Infection in utero or in pups <8 wk old or born to unvaccinated dams without naturally occurring antibodies can result in myocardial infection, necrosis, and myocarditis. Myocarditis, presenting as acute cardiopulmonary failure or delayed, progressive cardiac failure, can be seen with or without signs of enteritis.

To limit environmental contamination and spread to other susceptible animals, dogs with confirmed or suspected CPV enteritis must be handled with strict isolation procedures (eg, isolation housing, gowning and gloving of personnel, frequent and thorough cleaning, footbaths, etc). All surfaces should be cleaned of gross organic matter and then disinfected.

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