The parvoviruses are small nonenveloped single stranded DNA virus. 3 known to infect dogs:
1) CPV-1 (minute virus of canines) - uncertain pathogenicity - has been associated with "fading pups" – lethargy, loose stools, respiratory distress, sudden death.
2) Canine adeno-associated virus - apparently non-pathogenic.
3) CPV-2 replicates in dividing cells especially intestinal, lymphoid, bone marrow and fetal tissues and is severely pathogenic. This virus is known simply as canine parvovirus or CPV, and is closely related to feline panleukopenia virus and mink enteritis virus. CPV-2 is a new canine virus appearing about 1977. Current isolates (CPV-2a,b first observed in 1980, 2c reported in Italy in 2000, and widespread in USA and world by 2007) have different antigenic structures, increased pathogenicity, and a shorter incubation period (4-5 days vs 5-8) than CPV-2. These variants also replicate efficiently in cats. MLV vaccines of 2 and 2b protect against 2c.
Of clinical importance are a few features of the virus:-
Host Range and Predisposing Factors
• Parvoviruses- resistant to inactivation; can remain infectious outside the host > 5 months.
• Most common detergents and disinfectants fail to inactivate these viruses.
• CPV-2 hemagglutinates RBCs from a number of species so hemagglutination assays are useful for diagnosis.
• Probably all Canidae are susceptible. Within domestic dog populations, Dobermans pinschers, Rottweilers, English Springer Spaniels, and in some studies, American Pit bull terriers and German Shepherds are at higher risk of severe illness.
• Intact male dogs seem more predisposed to infection than intact females.
• Unvaccinated dogs - about 13 X more likely to become infected than vaccinated dogs.
• Concurrent infection with other gastrointestinal pathogens (Giardia, hookworms and roundworms, coronavirus) may exacerbate the severity of CPV infection. Stress of overcrowding, poor nutrition, and age at infection can dictate the outcome of infection.
• Fecal-oral route. A vast amount of virus is shed in the feces of clinically infected dogs. However, the persistence of virus in the environment is thought to be more important than chronic carriers in perpetuating disease – not clear if carrier state exists?
• Active shedding of virus occurs up to the first 2 weeks post inoculation. Generally, dogs that recover from infection do not transmit disease to susceptible kennel mates.
• After oronasal exposure - primary replication occurs in regional lymph nodes of the pharynx/tonsils followed by plasma-associated viremia (develops even as early as the 1st or 2nd day post-infection (PI) although becomes high 3 to 4 days PI); other lymphoid tissue (thymus, mesenteric nodes, bone marrow) becomes infected by the 3rd day PI; virus can be detected in intestinal epithelial cells by day 4 PI (it is suspected that the virus initially arrives in the GIT by way of plasma or in infected lymphocytes).
• Active excretion of virus in the feces occurs as early as day 3 PI before clinical signs occur.
• Viral fecal shedding increases rapidly to peak at day 4 to 7 PI - coincides with the onset of clinical signs; virus can rarely be found in the feces by 12 to 14 days PI.
• CPV-2 depends on dividing cells for replication and cells that become infected die. Thus, cell loss is present in tissues of high multiplication rates – small intestinal crypt cells, lymphatic tissue and bone marrow, and myocardial cells in very young pups.
• Age and immunity determine whether CPV infection results in myocardial disease or enteritis.
• Cardiac myocyte replication is sufficient enough only to support virus until 2 weeks of age. Although myocarditis is seen in pups at 6 to 8 weeks of age, it is the result of infection several weeks earlier.
• Myocardial disease is exceptionally rare in the US these days because most bitches (greater than 85% in one census in 1991 in the USA) are immune and the pups are protected by passive immunity in-utero or during the first weeks of life.