Canine parvovirus 1 was first isolated from the feces of military dogs in 1967. It was named for its small size (18-26nm), from the Latin word parvus, meaning small. Initially, canine parvovirus 1 was thought to be nonpathogenic; however it can cause gastrointestinal disease, pneumonia, and myocarditis in young pups.
Canine parvovirus 1 was first isolated from the feces of military dogs in 1967. It was named for its small size (18-26nm), from the Latin word parvus, meaning small. Initially, canine parvovirus 1 was thought to be nonpathogenic; however it can cause gastrointestinal disease, pneumonia, and myocarditis in young pups. Canine parvovirus type 2 (CPV-2), was first seen in the U.S. in 1978, and it remains a leading cause of infectious diarrhea in dogs today. CPV-2 is a DNA-containing virus, but it mutates similar to RNA viruses, creating new variants. These mutations led to the emergence of CPV-2a in 1980, CVP-2b in 1984, and CVP-2c in 2000. When a mutation occurs, nucleotide substitutions lead to transformed amino acids in the capsid of the virus, which can allow for improved ability to infect cats, as well as easier transmission between hosts. The CVP-2b variant became very prevalent in the U.S. and worldwide, replacing earlier strains. CVP-2c has now also been found throughout the U.S.; however at this time the true prevalence of CVP-2c in the U.S. remains unclear.
Dogs at highest risk for parvoviral enteritis are puppies, ages 6 weeks to 6 months old, who do not have adequate antibody protection. Passive immunity, in the form of maternal antibodies, can be protective, but can also interfere with active immunity from vaccination. As maternal antibodies wane, vaccination is critical to protect puppies prior to exposure; unvaccinated dogs are 12x more likely to become ill from parvovirus than their vaccinated counterparts. Rottweilers, Doberman pinschers, American Staffordshire terriers, and German shepherds have all been reported to have an increased risk for parvovirus enteritis, suggesting that genetics plays a role in susceptibility. Another theory is that perhaps maternal antibodies persist longer in these breeds than in other breeds. Intact male dogs may have increased risk of infection. One study found dogs were at 3x more likely to become ill from parvovirus during July, August, and September. Although not all infected dogs will become ill, dogs with concurrent gastrointestinal bacterial infections, parasites, or viruses are at increased risk of developing illness.
Parvovirus is highly contagious, regardless of the variant. Transmission occurs mainly by direct contact via ingestion with contaminated diarrhea or vomitus. Transmission by fomites is also a concern, with parvoviruses known to survive on inanimate objects for up to 5 months. For this reason, all infected dogs should be quarantined for treatment in an isolation ward with established biosecurity protocols in place. Thorough cleaning protocols are important within isolation, as most common detergents and disinfectants (including quaternary ammonium disinfectants) will not kill CPVs. Diluted bleach (1 part bleach: 30 parts water) and potassium peroxymonosulfate are effective, and a 10-minute contact time with disinfectant is recommended.
After infection, CPV-2 infects rapidly dividing cells of the lymphoid system, intestinal tract, and bone marrow. Initially, replication occurs in the tonsils, retropharyngeal lymph nodes, thymus, and mesenteric nodes. Viremia is seen after 1-5 days. CPV-2 localizes in the epithelial lining extending from the tongue to the intestines. Infection of the intestinal crypt cells leads to villus blunting, decreased nutrient absorption, and increased permeability, as well as necrosis, hemorrhage, and associated gastrointestinal signs. Translocation of intestinal bacteria can lead to sepsis. CPV-2 infection of the bone marrow destroys white blood cell precursors, leading to classic leukopenia, and predisposes patients to secondary bacterial infections.
Dogs can have either subclinical infections or become quite ill from parvovirus. Development of illness depends on age, breed, immune status, stress, and presence of concurrent infections. Fever typically develops within several days. Gastrointestinal disease is characterized by severe vomiting, followed by hemorrhagic diarrhea, anorexia, dehydration, and lethargy. Intestinal intussusception is a potential complication. Secondary infections, including urinary tract infections and pneumonia, are common. Urinary tract infections may remain subclinical or silent, and are seen in up to 25% of parvovirus puppies; all attempts to keep these puppies clean should be made to minimize fecal contamination of their distal urethras. Infected dogs may develop neurologic signs from the virus itself, or more likely from electrolyte imbalances, hypoglycemia, or sepsis, or from disseminated intravascular coagulopathy causing hemorrhage into the central nervous system. Erythema multiforme has been reported in a dog with parvovirus, but cutaneous disease is considered rare. In puppies infected in utero or before 8 weeks of age, myocarditis may develop, causing "fading puppy syndrome" or acute death.
In-house fecal enzyme-linked immunosorbent assay (ELISA) antigen tests are the most commonly used diagnostic tests for parvovirus. All young dogs with consistent clinical signs and incomplete vaccine histories should be tested. Although sensitivity of fecal ELISAs has varied, specificity is consistently high. If testing is delayed 5 days after onset of clinical signs, false negative test results may occur due to decreased viral shedding. A false negative may rarely occur if a viral mutation prevents identification by the ELISA test. If a false negative is suspected, PCR or virus isolation from a fecal sample can be submitted for further analysis. PCR and DNA sequencing are available to distinguish between variants of CPV (2b and 2c); however this information may not be relevant for clinicians, as it would not alter treatment or prevention recommendations.
Dogs with confirmed parvovirus should be cared for in an isolation ward, completely separated from the general hospital population. The isolation ward should be cleaned thoroughly between patients and fully stocked with basic equipment (stethoscope, thermometer, fluid pump, IV catheter kit, etc.) to prevent cross-contamination between the wards. A limited number of personnel should be permitted to enter the isolation ward, to decrease exposure and risk of transmission via fomites to other patients. All personnel entering isolation should wash their hands and use a footbath prior to entry, and should wear a cap, gown, booties, and gloves throughout the visit. Intravenous catheters should be placed as sterilely as possible and well maintained, as bacterial colonization of IV catheters is a reported and potential complication for this population of dogs. Personnel should use the footbath again on exit, and wash hands thoroughly with soap and water or gel sanitizer. Staff should be reminded that dogs with parvovirus are extremely immunosuppressed, and there should be equal concern for what microbes we may bring into isolation as well as what we could bring out of isolation.
Therapy for dogs with parvovirus is supportive, with the goals of rehydration, correcting and maintaining electrolyte and glucose abnormalities, and providing antimicrobial and antiemetic support. Fluid dose should be calculated based on percent dehydration (8% dehydrated equates to 0.08xbody weight in kilograms to determine the number of liters of fluid to replace) plus maintenance needs (60ml/kg/day). A replacement isotonic fluid such as LRS or 0.9% saline would be appropriate. Most puppies require dextrose supplementation (2.5-5%) as well as potassium chloride. Baseline CBC, blood glucose, and electrolytes are recommended, and blood glucose and blood smear to assess neutrophil count should be monitored at least daily throughout hospitalization. Antimicrobial therapy is necessary due to immunosuppression and risk of gastrointestinal translocation and secondary bacterial infections. Either ampicillin-sulbactam (30mg/kg IV TID) or ampicillin (22mg/kg IV TID) is a good choice for broad-spectrum coverage. Antiemetic therapy can include metoclopramide (1-2mg/kg/day continuous rate infusion) or maropitant (1mg/kg SQ q 24hrs). Maropitant is not recommended for dogs under the age of 16 weeks due to potential for bone marrow suppression. Dogs should be encouraged to eat as soon as possible, as early enteral nutrition may result in further clinical improvement and improved outcome.
Vaccination is critical for the prevention of parvovirus. Developing a hospital protocol for vaccination and educating clients about the benefit of vaccination versus the severity of parvoviral enteritis is advised. Clients should be taught about the window of susceptibility for their puppy to develop parvovirus, and the importance of keeping them isolated from potential exposure during this vulnerable time. Although puppies are at highest risk, clients should be educated that unvaccinated adult dogs too can become infected and ill from parvovirus, and that vaccination is important in these dogs as well. The American Animal Hospital Association provides guidelines for vaccine protocols, and recommends that vaccinations in puppies are started at age 6-8 weeks, with boosters every 3-4 weeks until they are at least 16 weeks old. In predisposed breeds, continuing vaccination with additional boosters at 20 and 24 weeks may provide additional protection. For naïve adult dogs, initial vaccination should be followed by a booster 3-4 weeks later, a booster 1 year later, and then a booster every 3 years thereafter. Vaccination should be with a modified-live CPV vaccine. Currently available vaccines have been demonstrated in prospective studies by two independent research groups to offer cross-protection against both CPV-2b and CPV-2c variants. In order to provide full protection and to avoid perceived vaccine breaks, vaccines should be administered by veterinarians, so that proper schedules, storage, and administration can be strictly followed.
Hoelzer K, Parrish CR. The emergence of parvoviruses of carnivores. Vet Res 2010;41: 39.
Parrish CR. Emergence, natural history, and variation of canine, mink, and feline parvoviruses. Adv Virus Res 1990;38:403-50.
Hong C, Decaro N, Desario C, et al. Occurrence of canine parvovirus type 2c in the United States. J Vet Diagn Invest 2007;19:535-9.
Kapil S, Cooper E, Lamm C, et al. Canine parvovirus types 2c and 2b circulating in North American dogs in 2006 and 2007. J Clin Microbiol 2007;45:4044-7.
Houston DM, Ribble CS, and Head LL. Risk factors associated with parvovirus enteritis in dogs: 283 cases (1982-1991). J Am Vet Med Assoc 1996;208:542-6.
McCaw DL, Hoskins JD. Canine Viral Enteritis. 3rd ed. Infectious diseases of the dog and cat, ed. C. Greene. 2006, Atlanta: Saunders Elsevier. 63-70.
Hoskins JD, Mirza T, Taylor HW. Evaluation of a fecal antigen ELISA test for the diagnosis of canine parvovirus. J Vet Intern Med 1996;10:159.
Schmitz S, Coenen C, Konig M, et al. Comparison of three rapid commercial canine parvovirus antigen detection tests with electron microscopy and polymerase chain reaction. J Vet Diagn Invest 2009;21:344-5.
Desario C, Decaro N, Campolo M, et al. Canine parvovirus infection: which diagnostic test for virus? J Virol Methods 2005;126:179-185.
Burton JH, et al. Detection of canine parvovirus DNA from blood and feces collected from healthy puppies after administration of modified live vaccine. J Vet Intern Med 2008;22: 203.
Larson LJ, Schultz RD. Do two current canine parvovirus type 2 and 2b vaccines provide protection against the new type 2c variant? Vet Ther 2008;9:94-101.
Spibey, N., et al., Canine parvovirus type 2 vaccine protects against virulent challenge with type 2c virus. Vet Microbiol, 2008. 128(1-2): p. 48-55.
American Animal Hospital Association (AAHA) Canine Vaccine Task Force: AAHA canine vaccine guidelines, revised. J Am Animal Hosp Assoc 2006. 42: p. 80-89.
Stenske KA. Clinical Notes: Canine Parvovirus Update. NAVC Clinician's Brief. July 2010: p. 61-62.
Lobetti RG, Joubert KE, Picard J, et al. Bacterial colonization of intravenous catheters in young dogs suspected to have parvoviral enteritis. J Amer Vet Med Assoc 2002;220:1321-4.
Mohr AJ, Leisewitz AL, Jacobson LS, et al. Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis. J Vet Intern Med 2003;17:791-798.