Canine parvovirus type 2 is a virus affecting dogs. It is highly contagious and spread from dog to dog through direct or indirect contact with feces. It can be highly dangerous for puppies that don’t have maternal antibodies. It can present in cardiac or intestinal form. Vomiting and dysentery are common signs of the intestinal form while respiratory and cardiovascular failure are signs of the cardiac form. Vaccines can prevent infection but when not treated mortality can reach 91%. People bitten by an animal infected with parvovirus should seek medical attention due to possible bacterial infections of the bone called osteomyelitis.
CPV2 is a relatively new disease appearing in the late 1970s. First recognized in 1978 the disease spread worldwide in a year or two. It is 98% identical to feline panleukopenia. It is also highly similar to mink enteritis. At first it was thought that CPV2 was a mutant strain of feline panleukopenia although it could also be a mutated strain of unidentified parvovirus.
In 1979 and 1984 two more strains of canine parvovirus were identified. Most cases are believed to be caused by these two strains.
It is a non-enveloped single-stranded DNA virus with its name coming from the Latin parvus which means small. It can affect dogs, wolves, foxes, and other canids. It is also more common in larger cats than panleukopenia. Out of the two types of canine minute virus: CPV1 and CPV2, CPV2 causes the most serious disease.
Once ingested, the virus replicates in the lymphoid tissue in the throat and from there moves to the blood. From the blood the virus rapidly attacks cells especially those in the lymph nodes, intestinal crypts, and the bone marrow. The virus also depletes lymphocytes in lymph nodes and destroys the intestinal crypts. This allows anaerobic bacteria that normally reside in the intestines, to cross into the bloodstream and cause sepsis.
Clostridia, Campylobacter, and Salmonella are the most common bacteria involved in severe cases. These bacteria can lead to systemic inflammatory response syndrome which can cause hypercoagulability of the blood, endotoxaemia and acute respiratory distress syndrome. Dogs with CPV are susceptible to intussusception which is where part of the intestine prolapses into another part.
Rarely, the disease can lead to generalized infection in neonates and cause lesions and viral replication. The lining of the blood vessels are also severely affected which can cause the lesions to hemorrhage. The disease being active in a pregnant dog can lead to a fetus being infected and potentially having abnormalities.
Dogs that develop the disease usually show symptoms from 5 to 10 days which usually include lethargy, vomiting, fever, and diarrhea. Dehydration will eventually lead to the dog’s electrolytes being imbalanced. Blood and protein leaking into the intestines can lead to anemia and loss of protein.
Through detection of CPV2 in feces the virus can be diagnosed. Prevention is the only sure fire way to ensure that a dog remains healthy due to CPV2 becoming extremely virulent and contagious. The virus can live in feces for over a year through hot or cold temperatures. Puppies are generally vaccinated in a series of doses. Survival depends on the speed of diagnosis, the age of the animal, and treatment. If it is suspected testing for CPV should be undertaken quickly. If not caught early severe cases usually involve extensive hospitalization.
Treatment usually consists of crystalloid IV fluids, anti-nausea injections, and antibiotic injections. Fluids are typically a mix of sterile, balanced electrolyte solution with B-complex vitamins, dextrose, and potassium chloride. To provide immunity a blood plasma transfusion from a donor dog is administered to a sick dog.
There is no antiviral treatment for CPV although there are reports that oseltamivir has reduced the severity and hospitalization time of the disease.