Introduction...Pathogenesis...Clinical Signs...Diagnosis...Treatment...Prevention


Parvovirus is a single-stranded DNA-containing virus that only replicates in cells actively synthesizing cellular DNA that also have cell surface receptors for parvovirus. Therefore, growth and propagation of the virus in animals requires the presence of newly emergent, actively multiplying cells with appropriate viral receptor sites, such as are found in the GI tract...the stomach and intestine (small and large intestine). Other sites of infection in dogs include the myocardium (muscle of the heart), where growth and cellular proliferation of heart tissue occurs for a short while after parturition, the bone marrow and lymphoid tissue. [The myocardium has fewer receptors than the other tissues and is more readily protected by maternal antibodies; thus myocardial damage is much less common than intestinal and lymphoid destruction. Most clinical cases of parvo- myocarditis result from infection in utero and subsequent problems after whelping or infection of puppies younger than 8 weeks of age.] Viruses invade susceptible cells and redirect cellular synthetic machinery such that more virus particles are produced. The host cells themselves then die while new virus particles are released to infect more cells. In cats, viruses may also invade the cerebellum portion of the central nervous system. In both species, infection can be transmitted during pregnancy; infected pups and kittens either die in utero, are aborted, die after birth or, if they survive, experience the effects of birth defects (most likely myocarditis and/or central nervous system defects) caused by the infection.

The canine parvovirus was first identified in the United States 1978. It was believed to be closely related, if not a mutation of the feline parvovirus (aka feline panleukopenia or feline distemper). Since then, more virulent strains have evolved. All strains are highly resistant to most disinfectants and to environmental extremes. Thus, contaminated environments remain a significant risk factor for infection of susceptible animals. Other risk factor are overcrowding, lack of maternal antibody protection, poor sanitation, malnutrition, parasites and stress. Certain breeds are purported to be more susceptible: Rottweilers, Doberman Pinchers and Labrador Retrievers. However, various studies have claimed alternative breed susceptibilities, depending upon the region of the world in which a given study was conducted. For the sake of practicality, all breeds are considered susceptible and at risk. However, most animals, after vaccination, exposure or recovery from disease are protected for an extended period (some think for many years) from subsequent infections. Thus, while disease is possible in unvaccinated, unexposed adult animals, it is primarily a disease of puppies and kittens.


Infection is usually via the fecal-oral-nasal route. However, given that the virus persists in the environment, transmission via humans or by contact with contaminated fomites is also likely. Initially, viruses invade the lymphoid tissue of the oral-pharyngeal cavity from which infection spreads to local lymphoid tissue then to lymph of the thymus and intestinal mesentery. Virus enters the bloodstream and is passed to susceptible (rapidly-dividing, viral-receptor-positive) tissues, within about 1-5 days.  In puppies, the severity of the disease appears to relate to the rate of turnover/proliferation of the infected lymphoid and intestinal tissues (primarily the crypts...see below); there are few if any viral receptor in the canine cerebellum. Kittens, on the other hand, may also develop infection of the cerebellum portion of the brain. On occasion, virus is found in lungs, spleen, kidney,

The targeted portions of the small and large intestinal epithelium are the crypts. As described previously, crypt cells are the germinal tissue...the source of replacement cells for the tips of villi (which are shed often). Destruction of crypts is thus tantamount to the death of associated villi. Absorptive (and digestive) capacity of the intestine is lost with the collapse of the intestinal epithelium. There is destruction of white cells in marrow and lymphoid tissue in severe infections. Additionally, the integrity of the intestine-blood barrier can become compromised in severe disease, allowing the translocation of bacteria or bacterial toxins from the intestine into the blood, where these may be distributed system-wide, causing secondary sepsis, endotoxemia with multi-system damage or collapse, including DIC (Disseminated Intravascular Coagulopathy...a major topic for discussion itself, but not here) and septic shock. Profuse, watery bloody diarrhea and frequent vomiting are common and contribute to dehydration and electrolyte imbalances leading to worsening tissue perfusion, thus exacerbating the systemic failure. Virus is shed in the feces 3-4 days after exposure, usually before overt signs of infection are apparent. Shedding persists for about 7 days at which time, in animals who recover, there is development of localized anti-parvo antibodies which quell further shedding.

Clinical Signs

Clinical signs are not apparent for 5-7 days following exposure (though virus may be shed sooner, at 3-4 days following exposure). Vomiting followed by diarrhea and the rapid development of dehydration are cardinal signs (that, unfortunately are not in themselves specific for this disease). Many victims are extremely painful on abdominal palpation. Animals are extremely depressed, hyperthermic or hypothermic, dehydrated, nauseaus with sometimes altered mentation or other signs of central nervous system involvement. Neurologic signs in dogs (seizures, twitches, altered mentation), if present, are not the result of virus infection of the central nervous system itself but the results of hypoglycemia (low blood sugar due to sepsis) or hemorrhage into the central nervous system due to DIC, or from blood acid-base or electrolyte imbalances. Feces color varies from yellow-gray to black and may impart the often-recognized foul smell of blood. When sepsis or DIC are manifest, the prognosis is grave, with death sometimes within two days of the appearance of the initial clinical signs. Poor prognosticators are young age, absence of vomiting and the absence of monocytes (a type of white blood cell) in the blood.


Fecal Eliza Test:

Detection of Virus in Tissues or by Electron Microscopy of Feces

Hemagglutination -Inhibition Antibody Assay


The goals of treatment are symptomatic and supportive. Since the GI tract is non-functional, all treatments are parenteral (non-GI)); the preferred routes are intravenous and intramuscular.

Supportive care means restoring fluids and correcting electrolytes derangements, adding glucose to control hypoglycemia if present, providing antimicrobials to treat sepsis, plasma + heparin for controlling DIC, anti-nausea medications to control vomiting, analgesics for pain and warmth if the patient is hypothermic. Food is withheld for 24-48 hours or as long as the patient is still vomiting. Water may be offered in small amounts if it does not result in vomiting. When food is offered, it should be highly digestible (e.g. cooked white rice, boiled, skinned chicken, low-fat cottage cheese) and provided in small amounts over three to six feedings daily. Initially, the amount fed is about 1/3 the caloric needs for maintenance. Later, as symptoms abate, some advocate providing a diet containing moderate quantities of stimulate mild peristalsis, thus passing the nutrients to the more distant portions of the intestinal tracts.

Extreme measures are sometimes employed. These include marrow stimulants (G-CSF) to increase production of white blood cells, administration of anti-endotoxin serum. The efficacy of these treatments is not clear; some believe that the outcome is significantly improved by these adjunct treatments.

In general, animals who survive the first 3-4 days of severe illness are likely to recover. Severely ill patients may take several weeks IF they recover, to return to normal.

There is anecdotal evidence that some animals in the early phases of disease may actually benefit from oral Tamiflu® twice daily for 4-5 days.


Newborns receive protection from disease via maternal antibodies present in the colostrum (first milk) that persist for approximately 5-18 weeks, and gradually decline. These antibodies, while helpful in protecting puppies and kittens early in life, actually interfere with the stimulation of protection provided by the commercial parvovirus vaccinations. In fact, there is a period during which the maternal antibody levels, while present, are too low to protect, yet their presence still prevents the provision of protection via vaccination! For this reason, vaccinating pups or kittens younger than 6 weeks of age with traditional low-titer vaccines is fairly pointless, given the beneficial effects of the vaccine are neutralized by maternal antibodies. In some animals, maternal antibodies persist longer so vaccination may likewise be ineffective for several weeks or even months, yet the pup may still be susceptible to infection (because maternal antibody levels are too low). The level and persistence of maternal antibodies that interfere with commercial vaccination varies from bitch to bitch, and pup to pup. As a rule of thumb, the following are guidelines: With low titer vaccines, about 25% of pups will be successfully vaccinated at 6 weeks of age, 40% by 9 weeks of age, 60% by 13 weeks, 80% by 16 weeks and > 95% by 18 weeks. Therefore, some recommend modifying the traditional vaccination protocol by offering additional boosters with low-titer vaccines at 20 and at 22 weeks of age. High titer vaccines (see below) have more recently been created to address the problem of maternal antibody interference.

In general, the most beneficial parvovirus vaccines are the modified live vaccines (MLV); these consist of attenuated, live parvovirus constructed with limited ability to invade and proliferate in the host. Animals receiving MLVs are transiently ill and low quantities of attenuated virus are shed in the feces for a brief period. With appropriate immunization, especially after age 20 weeks of age, adequate protection from infection is achieved that lasts at least two years. MLVs come in (the traditional) low-titer and more recently a high-titer version. There are killed versions that do not cause illness in vaccinated animals, but these vaccinations are much less protective that the MLVs.

The commercial vaccines called High-Titer Attenuated are designed to circumvent the problem of maternal antibody interference. These products contain large numbers of highly immunogenic attenuated viruses. Data show that pups with low to moderate levels of maternal antibody who are vaccinated at 6, 9, 12 and at 15-16 weeks develop protective levels of anti-parvovirus antibodies.


Smith-Carr, Saralyn etal., Canine Parvovirus. Part I. Pathogenesis and Vaccination, Compendium February 1997 pp126
Macintire, Douglass K. & Saralyn Smith-Carr, Canine Parvovirus. Part II, Clinical Signs, Diagnosis and Treatment, Compendium March 1997 pp291
Greene, Craig, Infectious Diseases of the Dog and Cat 2nd ed. pp42, WB Saunders, Philadelphia 2001

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