Canine Parvoviral Enteritis – Important Features

  1. Canine parvovirus was first identified in dogs in the late 1970s and was named CPV-2 (CPV type-2)
  2. It was quickly recognized world-wide but was replaced in the early 1980s by an antigenically and genetically distinct strain, CPV type 2a (CPV-2a).
  3. Since then, novel antigenic and genetic strains have continued to evolve and have been named CPV-2b and CPV-2c. CPV-2c was recognized in 2001.
  4. Results of some studies indicate that CPV-2c causes more severe disease, infects properly dogs, may not be detected by in-clinic diagnostic tests and frequently results in poor patient outcomes.
  5. Results of other studies indicate that dogs vaccinated with available CPV-2 are protected when challenged with CPV-2c.
  6. CPV-2 infection is an acute systemic illness characterized by hemorrhagic enteritis (bloody diarrhea and vomiting).
  7. It is often fatal in pups – can see collapse in a “shock-like” state and die suddenly without intestinal signs. Highly dangerous in pups less than 4 months of age.
  8. Parvovirus requires actively dividing cells for growth such as the rapidly dividing crypt cells of the small intestine.
  9. After ingestion of the virus there is a 2-4 day period of viremia with growth in the lymphatic tissues throughout the body.
  10. By the third day the intestine is infected with viral shedding occurring in the feces. Virus shedding ceases by days 8-12 post-infection.
  11. A major component of the disease process is the absorption of bacterial toxins from the gut through the damaged intestinal lining as well as translocation of bacteria from the lumen of the gut into the body.
  12. Severity of the illness appears to be related to the viral dose, the viral strain, the age of the dog and the presence of protective antibodies/immunocompetence in the dog (maternal antibodies or vaccine antibodies).
  13. Clinical signs – bloody diarrhea, loss of appetite, vomiting, rapid weight loss, dehydration, abdominal pain, bloating, enlarged lymph nodes +/- fever. In rare cases the heart can be involved leading to myocarditis and heart failure.
  14. Crowding and poor sanitation increases the risk of infection especially in kennels and shelters.
  15. Lab findings – decreased lymphocytes (days 4-6 post-infection), severe decreases in white blood cells, decreased serum protein levels and decreased blood sugar.
  16. Virus may be detected in the stool for a few days after the onset of the disease. Blood tests may not be diagnostic due to the presence of vaccine/maternal antibodies.
  17. Treatment is symptomatic – intravenous fluid therapy, antibiotics, pain medication, anti-vomiting drugs and early return to feeding -highly digestible, low fat diets.
  18. This virus is highly contagious – strict sanitation is critical. Use of a 1:30 dilution of bleach will destroy the virus. If possible, isolate pups until 3 months of age. The virus is shed for less than 2 weeks after infection – no carrier state has been substantiated.
  19. Controversial therapies include treating affected pups with hyperimmune serum from vaccinated dogs or from recovered dogs and the use of Tamiflu® (oseltamivir)an antiviral drug ( a neuraminidase inhibitor) used on the human side for influenza treatment.

©Jeff Vidt, DVM (7/4/12)

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