Canine Parvovirus Infection

Chapter 112 Canine Parvovirus Infection



Karen R. Humm, MA, VetMB, CertVA, MRCVS, Dez Hughes, BVSc, MRCVS, DACVECC



KEY POINTS



• Canine parvovirus (CPV) is a common pathogen in young dogs and usually is seen between the ages of 6 and 20 weeks.

• Parvoviridae are very stable, surviving a pH range of 3 to 9 and temperatures of 60°C for 60 minutes. They can survive for 5 to 7 months in the environment.

• Parvovirus is a highly pathogenic virus that can cause severe vomiting and diarrhea and may be fatal.

• Vaccination against parvovirus is widely practiced, but maternal antibodies can prevent a normal response to vaccination.

• A fecal enzyme-linked immunosorbent assay with high sensitivity and specificity allows for a rapid in-house diagnosis.

• Treatment is mainly supportive with fluid therapy, nutritional support, antiemetics, and antibiotics.

• Reported survival rates for treated dogs with CPV vary widely (64% to 92%), but prompt and aggressive treatment often results in a live animal, the first few days being crucial.


EVOLUTION OF CANINE PARVOVIRUS 2


Canine parvovirus (CPV)-1 was discovered in 1967 and causes mild diarrhea.1 A completely new form of CPV that was recognized in 1978 and causes a much more severe disease resembling panleukopenia in cats. A sudden death syndrome due to myocarditis and congestive heart failure was also seen. A parvovirus was isolated in both syndromes and has also been named CPV-2.2 CPV-2 is genetically distinct from CPV-1 but is closely related to feline and mink parvoviruses, differing by only a few deoxyribonucleic acid (DNA) bases.3 It is therefore presumed to have evolved from another parvovirus by mutation. It infects feline cells in culture but does not infect cats. It is suspected to have evolved in Europe, with DNA analysis suggesting that this occurred approximately 10 years prior to discovery.2 It spread around the world rapidly because of the immunologically naïve population of both domesticated and wild members of the family Canidae. Subtypes of CPV-2 were recognized in 1979 and 1984 and named CPV-2a and CPV -2b, respectively. CPV-2b is thought to be more pathogenic in some dogs and a study in 1991 showed that it had replaced CPV-2a as the cause of parvovirosis in many regions of the United States.4 CPV is undergoing continual genetic evolution, and large phenotypic variations can result from single nucleotide substitutions.5 Recent mutations have been noted and a CPV-2c has been found in Europe and Asia, which appears to cause a relatively mild disease.6,7



SIGNALMENT


CPV is seen most commonly in dogs less than 6 months of age, generally between the ages of 6 and 20 weeks.8 Infection occurs from either failure of passive transfer, early waning of maternal antibodies, or passive maternal immunity preventing an efficacious response to vaccination. This latter mechanism means that CPV can infect and cause symptoms in vaccinated animals, although this is uncommon.9 In dogs under 6 months of age there is no gender predilection, but in those over 6 months, male intact dogs are over-represented.9 Doberman Pinschers, Rottweilers, American Pit Bull Terriers, and German Shepherd Dogs are all thought to be more susceptible than other breeds; however, Rottweilers and Doberman Pinschers have not been shown to have a more severe form of the disease.9,10 An inherited immunodeficiency in Rottweilers has been postulated as a cause for the increased susceptibility, and von Willebrand disease has been suggested as a potential explanation for the increased likelihood of developing enteritis once infected.10 A seasonal occurrence has been shown in the United States, with 3 times as many cases seen from July to September than from November to June.9



PATHOGENESIS


CPV is a small, nonenveloped, single-stranded DNA virus that replicates in the nucleus of dividing cells in late the S phase or early G2 phase of the cell cycle. This leads to the preferential infection of rapidly dividing cells, hence the effects of the virus on the bone marrow and the GI tract. CPV is spread by ingestion of virus-containing material from the environment. One gram of feces from an acutely infected dog is thought to contain enough viral material to infect over 10 million susceptible dogs by oral exposure.8 The virus replicates initially in oropharyngeal lymphoid tissue and is then thought to spread via plasma. Intestinal crypt epithelium is usually infected by day 4 after infection. Antibodies start to appear approximately 5 days after infection and increase to maximal levels by days 7 to 10.8 Clinical signs appear 4 to 10 days after infection.


When CPV first appeared, myocarditis was common, because passively acquired maternal antibodies were not present. However, these antibodies are now nearly universal and they cover the period of rapid myocardial cell division (completed within the first 2 weeks of life), so myocarditis is now an extremely rare manifestation of CPV infection.



CLINICAL SIGNS


The leukopenia and enteritis syndrome is by far the most common clinical presentation of CPV infection. Sudden onset of vomiting, depression, abdominal pain, anorexia, and pyrexia are followed 12 to 48 hours later by diarrhea. Antibody titer measurement in unvaccinated dogs suggests that many dogs experience an asymptomatic parvoviral infection or have only mild signs. Diarrhea may not be seen in mild cases, especially in adult dogs.11 This later appearance or absence of diarrhea should be remembered when considering the differential diagnosis for a vomiting dog. Vomiting can be profuse and can lead to a secondary esophagitis.


The viral destruction of the intestinal crypts leads to intestinal bleeding, and hematochezia is common. The intestinal damage coupled with the neutropenia makes these puppies vulnerable to translocation of bacteria and endotoxin into the bloodstream. Systemic inflammatory response syndrome (SIRS), sepsis, septic shock, and multiple organ dysfunction syndrome may occur in severe cases. Hypoperfusion is usually present to varying degrees and can result in clinical evidence of shock, including tachycardia, poor pulse quality, prolonged capillary refill time, cold extremities, and depression. Mucous membranes are usually pale but may be injected in a dog with concurrent SIRS. When myocarditis does occur, puppies usually die suddenly from pulmonary edema due to congestive heart failure. Retching and dyspnea may precede death. If death does not occur, the focal myocardial necrosis that results can progress to fibrosis or dilated cardiomyopathy.



DIAGNOSIS


In-house enzyme-linked immunosorbent assay test kits are available that detect fecal antigen via an immunochromatographic assay, allowing for a rapid and inexpensive diagnosis. False-positive results can occur with some fecal viral tests if the dog has received a live parvoviral vaccine during the preceding 5 to 15 days. False-negative results can occur if the sample is taken very early in the disease, so the test should be repeated 36 to 48 hours later if clinical signs are suggestive of parvovirosis. False-negative results can also occur if fecal antigen levels are low or if large numbers of antibodies are present, binding the antigen.12 Other external laboratory tests are available, including electron microscopy (although CPV-1 is morphologically identical), virus isolation, hemagglutination, and polymerase chain reaction (PCR). PCR is the most sensitive of these and is the test of choice for a dog with suspicious clinical signs that has negative results on in-house testing. A new real-time PCR test has been developed that has improved sensitivity.6,12 In the past, serology (immunoglobulins G and M) was used to diagnose parvovirosis, but this has, now been surpassed by the aforementioned methods because it is not possible to differentiate between previous subclinical infection, active infection, or the result of vaccination.


A lymphopenia is seen initially as a result of direct lymphocytolysis, followed by a neutropenia due to peripheral consumption and destruction of white blood cell precursors in the bone marrow. This leukopenia can aid in diagnosis but has been reported in less than 50% of infected dogs.9 Biochemical changes may include hypoproteinemia, hyperbilirubinemia, elevated liver enzymes, hypokalemia, hypoglycemia, and a prerenal azotemia.13 Thrombocytopenia, prolonged activated clotting time, prothrombin time, activated partial thromboplastin time, and increased D-dimer levels can be seen in severe cases suggesting disseminated intravascular coagulation (DIC). Hypercoagulability has also been noted in dogs suffering from CPV enteritis without DIC.14 This has been postulated to be due to hyperfibrinogenemia and a reduction in antithrombin activity.14


Diagnostic imaging can be useful to rule out other causes of vomiting and diarrhea such as intestinal obstruction; however, radiography often reveals a dilated small bowel ileus that is sometimes difficult to differentiate from surgical ileus. Intussusception is both an important differential diagnosis for parvovirus and also a potential sequela. Thoracic radiographs may be required if aspiration pneumonia is suspected.

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  4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Canine Parvovirus Infection

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