Canine parvovirus

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Electron microscopy of canine parvovirus
Classic bloody watery diarrhoea associated with canine parvovirus infection[1]

Canine parvovirus (CPV) is one of the most prevalent and morbid viral diseases resulting in myocarditis or fatal gastroenteritis in young dogs (usually under 6 months of age) worldwide[2].

Parvoviruses are single-stranded DNA viruses which are ubiquitous in nature and infect most animals among the order Carnivora[3]. CPV particles measure 26 nm in diameter and consist of an icosahedral capsid that packages the ∼5-kb single-stranded DNA genome[4]. CPV exploits the transferrin receptor type-1 genes[5] that project from the 3-fold axes of capsid symmetry[6], and cells internalize the receptor-bound capsids by clathrin-dependent endocytosis[7]. Capsids then penetrate endosomal compartments and deliver the viral genome to the nucleus to initiate replication[8].

After its re-emergence in the late 1970s (likely resulted from the re-adaptation of a parvovirus to the resistant receptor of multiple wild carnivore hosts[9][10]), CPV-2 underwent a rapid re-evolution (mutation) which was clearly a variant of feline panleukopenia virus.

Within few years, new antigenic types termed CPV-2a and CPV-2b, completely replaced the original CPV-2[11]. In 2001, an antigenic variant was reported in Italy[12]. That variant has an amino acid substitution, Asp-426 → Glu, which occurs in a residue of the capsid protein that is considered important for the antigenic properties of CPV-2.

This variant (CPV-2/Glu-426 mutant), currently named as CPV-2c, has resulted in epizootic outbreaks across Italy[13], Spain[14], United Kingdom[15], and recently in Portugal[16], India[17], Brazil[18], France and Belgium[19].

The virus, which is very stable in the environment, is able to withstand wide pH ranges and high temperatures, has an incubation period of 3 - 8 days.

Transmission is by direct contact with infected dogs or contaminated feces (up to 3 weeks). Carrier dogs (and cats) which have recovered from acute parvoviral infections may also transmit infection periodically[20].

A breed predisposition has been reported in the Rottweiler, American Pit Bull Terrier, Doberman Pinscher and German Shepherd, with greater mortalities noted in non-vaccinated pure-bred dogs during summer months[21][22][23].

After ingestion, the virus replicates in lymphoid tissue of the oropharynx; from there, it spreads to the bloodstream. It attacks rapidly dividing cells throughout the body, especially those in the bone marrow, lymphopoietic tissue, and the crypt epithelium of the jejunum and ileum. Early lymphatic infection is accompanied by lymphopenia and precedes intestinal infection and GI signs. Replication in the bone marrow and lymphopoietic tissue causes neutropenia and lymphopenia, respectively. By 3 days after infection, rapidly dividing intestinal crypt cells are infected. Leucoencephalopathy has been reported rarely in dogs following parvovirus infection[24].

Viral shedding in the feces begins 3 - 4 days after infection and peaks when clinical signs appear. Viral shedding decreases rapidly and may no longer be detected 10 - 14 days after initial infection. Replication of the virus in the crypt epithelium of the gut causes collapse of intestinal villi, epithelial necrosis, and hemorrhagic diarrhea. Normal enteric bacteria, eg, Clostridium perfringens and Escherichia coli enter the denuded mucosa and may gain entry to the bloodstream, resulting in bacteremia.

Clinical signs

Clinically affected dogs present with signs of gastroenteritis, including vomiting and a characteristic malodorous diarrhea, often 3 - 4 days after initiation of viral shedding in the feces.

Symptoms can be exacerbated by concurrent infections with Salmonella spp, Clostridium perfringens, Escherichia coli, Campylobacter spp, canine distemper virus and enteric parasites. Clinical disease is exacerbated by secondary infections, underlying stressors and environmental factors such as overcrowding.

The occurrence of myocarditis, once prevalent in puppies is now considered rare following the introduction of aggressive vaccination protocols of pregnant bitches.

Most dogs recover within a few days with appropriate supportive care; others can die within hours of the onset of clinical signs. A common complication is pulmonary edema or alveolitis.

Blood tests may reveal leucopenia, lymphopenia[25] and thrombocytopenia[26], which in recovering dogs, usually begins to rise 24 - 48 hours post-treatment[27] and in non-recovering dogs is usually depressed due to development of systemic inflammatory response syndrome[28].

Hypoalbuminemia, hyponatremia, hypokalemia, and hypochloremia due to vomiting and diarrhea may also be evident.

Elevated blood levels of cardiac troponin-1, cortisol, creatine kinase, lactate dehydrogenase, AST[29], C-reactive protein, ceruloplasmin and haptoglobinare[30] are associated with a poorer prognosis. A non-responsive lymphopenia and reduced thyroxine[31] and cholesterol[32] are also associated with a poorer prognosis.


Diagnosis is based on presenting clinical signs and ELISA based in-house tests. PCR assays are available, but are not usually required for clinical management of individual cases[33].

A differential diagnosis would include anticoagulant rodenticides, canine bocavirus, intestinal parasites (particularly Blastocystis spp, Giardia intestinalis, Toxocara canis, Isospora spp, Trichuris vulpis) and hemorrhagic gastroenteritis due to Clostridium spp.


Treatment is usually palliative and supportive with intravenous fluids, antiemetics such as metoclopramide (0.2 - 0.5 mg/kg parenterally ad lib) and broad-spectrum antimicrobials (e.g. cephalexins or enrofloxacin) if indicated.

The use of NSAIDs is not normally recommended due to promoting further gastrointestinal bleeding.

Adjunct therapies such as chicken egg yolk[34], immunostimulatory glucans[35], the antiviral drug oseltamivir (tamiflu)[36] and the recombinant human granulocyte-colony stimulating factor[37] show promise as possible alternative therapies.

Hyperimmune serum has been utilized with valuable or at-risk patients[38], but the evidence of benefit in both clinical response and reducing viremia is lacking[39].

Severe cases with hemorrhagic diarrhea may require blood transfusions.

Food and water should be withheld until vomiting has subsided, followed by a cooked chicken, egg and rice diet for 3 - 4 days. Contaminated areas should be thoroughly cleaned.

Vaccination is critical in the control of the disease and current vaccines protect dogs against all strains of the virus, which are numerous and vary geographically worldwide[40][41]. Avoiding socializing puppies untill fully vaccinated is critical to minimize exposure to the virus.

Vaccines, both parenteral and intranasal[42], containing live attenuated canine parvovirus generally induce more effective immunity than inactivated virus vaccines, although not without risk due to constant CPV mutations[43] and possible contamination of vaccine batches with feline retroviruses (most produced with Crandell-Rees feline kidney cell cultures[44][45]). Newer DNA based vaccines appear less problematic[46].

Vaccination of pups should begin at 5 - 8 wk of age[47], then at 12 weeks and 16 - 20 weeks of age. Duration of immunity in adults dogs extends beyond 18 months and up to 9 years[48].

Booster vaccinations do not give a significant increase in CPV-2 antibody titers[49].


  1. Animal Pet Doctor
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