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Prior to 1977-78, parvovirus did not exist in the dog. The virus is a close relative of feline panleukopenia (feline distemper) and in fact, may have mutated from the cat and infected the dog in the late 1970s. The virus is extremely hardy and survives for long periods outside its host.  The virus will live in the environment up to 6 months and survives winter nicely under a blanket of snow where the temperature is usually around 25-28 degrees F. Extremely  cold temperatures prior to snow fall will kill the virus. Sodium hypochlorite (bleach) is an effective disinfecting agent.

The virus is transmitted by oral ingestion of viral contaminated faeces. Upon ingestion by the new host it infects local lymph nodes, quickly multiplies and then via the blood moves to the small intestine where signs of the disease begin in approximately 12-36 hours. The virus is extremely deleterious to the lining (mucosa) of the small intestine. The surface of the mucosa is stripped away upsetting crucial barriers and interfering with normal balance of digestive enzyme secretion and nutrient absorption. Additionally, the normal bacterial flora of the small intestine which aid in digestion are now exposed to ulcerated mucosa,  providing a direct route into the blood stream. Fluid loss from both vomiting and diarrhoea is dramatic and dehydration ensues. The onslaught of bacteria and toxins into the blood will ultimately cause death. Precipitous drops in white blood cell (WBC) counts are common and relate directly to the prognosis and outcome of the infection. Ominous drops in white blood cells are attributed to overwhelming degradation of WBCs and the direct depressive viral effect on WBC production in the bone marrow.

The incidence of the disease is highest in young dogs and tends to start some time after the puppy has lost its maternal protection passed on at birth with the first milk (colostrum). Any age can be infected but, most dogs are infected between the ages of 2-6 months  when maternal antibody decreases below a protective level in the puppy. Signs of the disease usually are mild to nonexistent. However, a full blown case of parvovirus can easily be fatal.

Generally, a diagnosis is made on the signs of the disease and falling white blood cell counts. Good rapid diagnostic tests are also available at veterinary clinics. Additionally, the virus can be found in the faeces by commercial labs using electron microscopy.

Treatment for the disease is primarily supportive although recently immunotherapy has become important. Historically, dogs were supported by aggressive intravenous fluid therapy to combat hydration and antibiotics given to reduce secondary bacterial infection. Food is withheld until vomiting has ceased. Many veterinarians employ antiemetics to lessen the signs and aid in the control of dehydration. Blood transfusions have been employed to increase the level of globulins, red blood cells and serum protein being lost via the bowels bloody diarrhoea. Most recently, antitoxins and anti-parvo serum are showing results. With hospitalisation and vigorous support some young pups may survive severe cases of parvo virus.  Early detection and aggressive therapy are the key to success.

Prevention of parvo virus is by vaccination.  Producing an effective level of protection requires vaccination starting as early as 6 weeks of age but not before the pups have weaned from their dam for at least 2 weeks. 

Recently, it has been suggested that repeated annual vaccination may also produce persistent antibody interference to the vaccination.