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Intestinal form

Dogs become infected through oral contact with CPV2 in feces, infected soil, or fomites that carry the virus. Following ingestion, the virus replicates in the lymphoid tissue in the throat, and then spreads to the bloodstream. From there, the virus attacks rapidly dividing cells, notably those in the lymph nodes, intestinal crypts, and the bone marrow. There is depletion of lymphocytes in lymph nodes and necrosis and destruction of the intestinal crypts. Anaerobic bacteria that normally reside in the intestines can then cross into the bloodstream, a process known as translocation, with bacteremia leading to sepsis. The most common bacteria involved in severe cases are Clostridium, Campylobacter and Salmonella species. This can lead to a syndrome known as systemic inflammatory response syndrome (SIRS). SIRS leads to a range of complications such as hypercoagulability of the blood, endotoxaemia and acute respiratory distress syndrome (ARDS). Bacterial myocarditis has also been reported secondarily to sepsis. Dogs with CPV are at risk of intussusception, a condition where part of the intestine prolapses into another part. Three to four days following infection, the virus is shed in the feces for up to three weeks, and the dog may remain an asymptomatic carrier and shed the virus periodically. The virus is usually more deadly if the host is concurrently infested with worms or other intestinal parasites.