CANINE-Canine Parvovirus.part II.clinical Signs,Diagnosis and Treatment

V o l. 1 9 , No . 3 M a r c h 1 9 9 7

S m a l l An i m a l G a s t r o e n t e r o l o g y

Continuing Education Article Refereed Peer Review

FOCAL POINT 5Aggressive treatment can dramatically increase survival of patients with canine parvovirus enteritis.

Canine Parvovirus. Part II.Clinical Signs, Diagnosis, and Treatment*

KEY FACTS s

In-house ELISAs allow for rapid diagnosis, but false-positives can result when dogs have been recently vaccinated with attenuated virus vaccine, and false-negatives can result when antibodies from blood in the feces bind to antigen.

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If serum albumin drops below 1.5 g/dl or total protein decreases below 3.5 g/dl, an intravenous colloid should be given.

s

Intravenous bactericidal antibiotics are indicated for puppies with neutropenia and hemorrhagic diarrhea.

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Antiendotoxin should be given before antibiotics because endotoxins are released as bacteria are killed.

 Auburn University 

Douglass K. Macintire, DVM, MS Saralyn Smith-Carr, DVM, PhD

T

  wo clinical syndromes occur in dogs infected with canine parvovirus (CPV): enteritis and myocardial failure. Myocardial Myocardial failure can occur in in neonatal puppies infected in utero or shortly after birth as a result of  failure of passive transfer of colostral antibodies. In these puppies, CPV infects rapidly dividing cells of the myocardium, thus resulting resulting in delayed signs of cardiac failure, syncope, arrhythmia, or sudden death. Sometimes, the only evidence of myocardial disease is found at necropsy. necropsy. The myocardial form of CPV infection was seen primarily in the early 1980s. It is rare today because of the effectiveness of current vaccination protocols in promoting maternal antibody protection in young puppies. This article focuses on the enteric form of CPV infection.

DIAGNOSIS Clinical Findings The initial clinical signs of enteric CPV infection are nonspecific and include anorexia, depression, lethargy, and fever. Within 24 to 48 hours, most affected puppies begin vomiting. Intestinal disease is more severe in puppies with enteric parasites, environmental stresses, low maternal antibody titers, and delayed or impaired humoral immune response. 1,2   With severe dehydration, protein loss, concomitant infection, and inability to produce a rapid immune response, this syndrome can rapidly progress to systemic shock and death. *Part I of this two-part presentation appeared in the February 1997 (Vol. 19, No. 2) issue of Compendium. of Compendium.

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Small Animal

The Compendium  March 1997

Pathologic Findings Necrosis of mucosal and The gross intestinal lesions lymphoid tissue of the small of parvovirus are nonspecific intestine disrupts the gastroand variable.1,8 The lesions, if  intestinal mucosal barrier, present, are usually segmenthus permitting bacterial tally distributed, with the translocation. Gram-negative ileum and jejunum most ofand anaerobic bacteria can ten affected. These affected enter the general circulation, sections may be flaccid and producing septic shock and may exhibit serosal hemorthe systemic inflammatory  rhage or congestion. The response syndrome (SIRS). bowel lumen is usually empty  The outer cell wall of grambut may contain watery hemnegative bacteria contains endotoxins (lipopolysaccha- Figure 1— Photomicrograph of the duodenal mucosa from a orrhagic contents. The mesenrides [LPS]) that are also po- dog with parvovirus enteritis. There is severe villus collapse teric lymph nodes are usually  tent mediators of systemic and dilatation of the crypt glands secondary to viral-induced enlarged and swollen, with inflammation.3 necrosis of crypt epithelium. (Courtesy of Dr. J. Newton, petechial hemorrhages in the In humans, bacterial Department of Pathobiology, Auburn University, Auburn, AL) cortex. Cortical necrosis and atrophy of the thymus can be transloca translocation tion and gut-origi gut-origin n observed in puppies. sepsis are believed to be preThe microscopic lesions of CPV are seen in the prolifdisposing factors for adult respiratory distress syndrome 4 erating population of cells in the intestinal tract, bone (ARDS) and multiple-organ failure. In one study of 88 marrow, and lymphoid tissue. In the intestinal tract, the dogs that died of severe CPV infection, E. coli  was  was isolatearly lesions are necrosis of the crypt epithelium, resulted from the lung and/or liver of 90% of the dogs, and ing in dilated crypts that are filled with necrotic debris pulmonary lesions similar to those found in humans with 5 and/or intranuclear inclusions within crypt epithelial  ARDS were detected in 69% of the dogs. Secondary baccells. With the progression of disease, the villi become terial infection with clostridia, Campylobacter species, Campylobacter species, and blunted and malabsorption/maldigestion results (Figure salmonellae has also been reported to occur with par6,7 1). Complete collapse and destruction of the villi occurs vovirus infection. Septicemia and/or endotoxemia may  in severe cases. These lesions may be focal or may occur occur as a direct result of these bacterial pathogens. segmentally throughout the small intestine (and infreTransient lymphopenia is the most consistent hema2,8 quently in the large intestine). There is usually evidence tologic finding associated with parvovirus infection. of intestinal regeneration, even in severe cases. Panleukopenia, particularly neutropenia, occurs with The germinal centers of mesenteric and gut-associated severe disease. Blood-loss anemia, often associated with lymph nodes and the cortical area of the thymus are deconcurrent internal parasite infection, may be manifestpleted of lymphoid cells. Myeloid and erythroid hyed as anemia with panhypoproteinemia. Serum chempoplasia occur in the bone marrow during acute disistry analyses are nonspecific. Severe potassium loss secease. During recovery, recovery, there is hyperplasia of lymphoid, ondary to anorexia, vomiting, and diarrhea may  erythroid, and myeloid cells. contribute to the depression and weakness. Elevated blood urea nitrogen (BUN) and creatinine may occur Diagnostic Testing as a result of dehydration. Elevation in serum alkaline Many tests are available to practicing veterinarians phosphatase and alanine transaminase activities may  for detecting CPV in the feces of infected animals. Solidalso occur as a result of hepatic hypoxia caused by seriphase enzyme-linked immunosorbent assays (ELISAs) ous hypovolemia. Other electrolyte abnormalities may  have enabled in-house testing, which allows for rapid occur secondary to vomiting and severe diarrhea and identification, isolation, and treatment of animals with should be monitored. CPV infection while clinical signs are still vague. FalseNo specific radiographic findings are associated with negative results may occur because of binding of test parvovirus infection. Radiographic signs of gastroen-

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The Compendium  March 1997

Small Animal

TREATMENT though submission may deCanine parvovirus infeclay definitive diagnosis by 1 tion can produce severe dehyor 2 days. dration, endotoxic or septic Other tests that are availshock, and multiple-organ able through university and failure. Without treatment, it state diagnostic laboratories is often fatal. However, aginclude electron microscopy, gressive therapy and supporthemagglutination (HA), ive care (Figure 2) have virus isolation, latex agglutiachieved an 85% to 95% surnatio nation, n, and ELIS ELISA. A. These These vival rate at our hospital (see tests are performed on feces Treatment of Canine Parfrom animals in the acute vovirus Enteritis). The followphase of the disease. Coming recommendations should mercial laboratories can also Figure 2— 2—Canine parvovirus enteritis can be a debilitating diagnose parvovirus infec- disease, but most puppies can survive with intensive, aggres- be considered in the treatment of all dogs infected with tion in fresh-frozen and for- sive supportive care. CPV. malin-fixed tissue samples by immunocytochemistry, Initial Assessment immunofluorescence assay (IFA), radioimmunoassay   When an animal is presented to the hospital with a (RIA), or immunoperoxidase staining procedures. Spehistory suggestive of CPV enteritis, a fecal antigen test cialized ELISAs (e.g., indirect ELISA, competitive should be performed to confirm the diagnosis if possiELISA, and double-antibody sandwich ELISA [DASble. If the test is positive, the animal should be isolated ELISA]) that are currently being developed for detectfrom other hospitalized patients, and all contaminated ing CPV-specific antibodies in serum are reportedly  surfaces should be cleaned with a 1:30 dilution of housemore sensitive than hemagglutination inhibition (HI). hold bleach. Strict cleanliness should be observed to Various assays that use a polymerase chain reaction avoid spread of the disease to other animals. If the test is (PCR) for the detection of parvovirus in feces have negative, other causes of gastroenteritis (e.g., foreign been developed. The PCR test can detect fewer parti9–11 body, pancreatitis, intestinal parasitism, toxicity, or dicles of CPV than can conventional methods. This etary indiscretion) should be ruled out. Because of the sensitivity may reduce the number of false-negative repossibility of false-negative results with the fecal antigen sults that occur with fecal ELISAs. The PCR assays are test, animals with a compatible history should receive apalso highly specific and can differentiate wild-type virus propriate supportive care and be retested 48 hours later. from vaccine virus, thus eliminating false-positive re12 Disease severity should be assessed through evaluasults due to recent vaccination. tion of physical examination findings and blood drawn Serum IgM and IgG titers were used to detect parfor an initial minimum data base. Rapid screening tests vovirus infection when the disease first emerged. A high that aid in patient assessment and fluid choice include IgM titer with a low-to-negative IgG titer was used to hematocrit, total solids, serum electrolytes, blood gases, determine acute CPV infection in dogs with hemorand reagent sticks for blood glucose and BUN. A comrhagic diarrhea. Serologic testing was established before plete blood count or blood smear also aids in patient antigen tests were developed and could not be used to assessment because leukopenia is generally associated differentiate between previous subclinical infection, ac with more severe disease and a more guarded prognosis. tive infection, or vaccination. Dehydration should be estimated through physical exCurrently, serum antibody testing for parvovirus is amination findings. Animals with mild dehydration used to determine whether a dog has been immunized (5% to 7%) have dry, tacky mucous membranes; aniby vaccination or whether susceptible dogs have been mals with moderate dehydration (7% to 10%) have exposed to parvovirus. Diagnostic laboratories use HI, slow capillary refill time (>1.5 seconds), skin tenting, radial hemolysis, virus or serum neutralization (VN or and sunken eyeballs; and animals with severe dehydraSN), IFA, and RIA to detect CPV antibodies. The stan-

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Small Animal

The Compendium  March 1997

Treatment of Canine Parvovirus Enteritis Intravenous Fluids s Begin with balanced electrolyte solution s Replace deficit (dehydration [%] × body weight [kg]) s Immediately if the patient is in shock (90 ml/kg/hr) s Over 2 to 6 hours if the patient is only dehydrated s  Add to replacement volume s Maintenance needs (44 –66 ml/kg/day) s Continuing losses (estimate amount lost through vomiting and diarrhea)  Antibiotics (parenteral, bactericidal) s For severe cases (leukopenia, hemorrhagic diarrhea), choose one of the following: s Enrofloxacin (5 mg/kg every 12 hours intravenously) and ampicillin (22 mg/kg every 8 hours intravenously) s Gentamicina  (2.2 mg/kg every 8 hours or 6.6 mg/kg every 24 hours intravenously) or amikacin a  (10 mg/kg every 12 hours or 20 mg/kg every 24 hours intravenously) intravenously) and amoxicillin (15 mg/kg every 12 hours intravenously) intravenously) s Cefoxitin (25 mg/kg every 6 hours intravenously) intravenously) s For milder cases, choose one of the following: s  Ampicillin (22 mg/kg every 8 hours intravenously) s Cefazolin (20 mg/kg every 8 hours intravenously) Trimethoprim-sulfadiazine (30 mg/kg every 12 hours s Trimethoprim-sulfadiazine subcutaneously) Electrolyte Replacement s Monitor serum sodium and potassium s Expect hypokalemia after initial fluid replacement s Supplement fluids with potassium (14 –20 mEq/L) Increase Oncotic Pressure s Give plasma if total solids