Parvovirus is a virulent infection that most commonly afflicts dogs less than one year of age. The infection is characterized by vomiting, bloody diarrhea, and leukopenia. More recently a new variant of canine parvovirus (CPV2c) has been recognized. This new form of the disease affects a wider range of ages, since vaccination against the typical form (CPV2b) does not generate sufficient protection. In addition, the diarrhea associated with CPV2c tends to be more mucoid than hemorrhagic. Puppies with parvovirus frequently demonstrate dull mentation, fever, tachycardia, tachypnea, and weak pulses, all signs of shock. If left untreated the majority of dogs will die. Treatment, consisting of aggressive supportive care and extended hospitalization, can improve survival rates from approximately 10% to 75-90%.

In order to improve treatment strategies and reduce the severity of disease in affected puppies, it is important to understand the pathophysiology of parvovirus. While the initial insult is the result of viral infection, the destruction of the intestinal crypt cells results in a breakdown in the normal protective intestinal barrier. The viremic phase occurs at 3-4 days after exposure; however clinical signs do not occur until 6-10 days after exposure. It has been shown in several studies that the clinical disease associated with parvovirus infection is the result of bacteremia. The most likely source of bacteremia is bacterial translocation from the injured intestine. In germ-free dogs, the clinical signs of parvovirus infection are negligible. Dogs with parvovirus are actually suffering from gram negative sepsis. In addition, these dogs are severely immunocompromised as a result of viral destruction of white blood cells.

Several specific treatment strategies have been investigated for the treatment of parvovirus. These can be divided into three categories: first, anti-viral approaches; second, strategies directed at bacteremia and endotoxemia; and third, strategies at improving immune function. In order to evaluate the efficacy of a new drug or treatment strategy, double-blinded, placebo controlled clinical trials represent the gold standard. There are few such trials available in veterinary medicine.

The best anti-viral approach is prevention, through the use of vaccination. This is an extremely effective means to prevent parvovirus; it is however, not helpful in the treatment of clinical disease.

Anti-viral drugs historically are expensive and have not been systematically investigated in the treatment of parvovirus. The one drug that has attracted a lot of attention is Tamiflu, (oseltamivir). This drug is a neuramidase inhibitor for the use in treatment of influenza. Influenza virus depends upon neuramidase for cellular invasion and budding. In theory this is an attractive anti-viral, however parvovirus does not rely on this mechanism for its pathogenesis. It has been theorized that neuramidase may be beneficial in combating bacterial adhesion, because cholera vibrio uses this enzyme to unmask its receptor on cells. The one clinical trial evaluating the efficacy of this treatment in parvovirus failed to show a benefit in survival or duration of hospitalization, however dogs treated with oseltamivir did gain more weight than the controls.

Passive immunity may act through an anti-viral mechanism, however the potentially beneficial effects of plasma in the treatment of parvovirus have never been subjected to controlled clinical trials. In addition, there are many factors in plasma that may be responsible for a treatment effect.