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3 March 1997
Small Animal Gastroenterology
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*
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. s 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. s Antiendotoxin should be given before antibiotics because endotoxins are released as bacteria are killed.
Douglass K. Macintire, DVM, MS Saralyn Smith-Carr, DVM, PhD
wo clinical syndromes occur in dogs infected with canine parvovirus (CPV): enteritis and myocardial failure. Myocardial failure can occur 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 in delayed signs of cardiac failure, syncope, arrhythmia, or sudden death. Sometimes, the only evidence of myocardial disease is found at 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.
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 translocation and gut-origin observed in puppies. sepsis are believed to be preThe microscopic lesions of CPV are seen in the prolifdisposing factors for adult respiratory distress syndrome erating population of cells in the intestinal tract, bone (ARDS) and multiple-organ failure.4 In one study of 88 marrow, and lymphoid tissue. In the intestinal tract, the dogs that died of severe CPV infection, E. coli 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 and/or intranuclear inclusions within crypt epithelial ARDS were detected in 69% of the dogs.5 Secondary baccells. With the progression of disease, the villi become terial infection with clostridia, Campylobacter species, and blunted and malabsorption/maldigestion results (Figure salmonellae has also been reported to occur with par1). Complete collapse and destruction of the villi occurs vovirus infection.6,7 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 hemaquently in the large intestine). There is usually evidence tologic finding associated with parvovirus infection.2,8 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, 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 gastroenantigen with serum-neutralizing antibodies in bloody teritis are fluid- and gas-filled bowel loops. Radiogradiarrhea. False-positive results may occur shortly after phy or abdominal ultrasonography may be used to invaccination with attenuated virus vaccines because of vestigate the possibility that a foreign body is causing fecal shedding of vaccine virus. Samples may also be the clinical signs or to identify intussusception as a submitted to commercial laboratories for diagnosis, alcomplication of severe parvovirus disease.
CLINICAL FINDINGS s DESCRIPTION OF LESIONS s IN-HOUSE ELISAs
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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% surnation, and ELISA. 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. Commercial laboratories can also Figure 2—Canine parvovirus enteritis can be a debilitating ing recommendations should 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 partibody, pancreatitis, intestinal parasitism, toxicity, or dicles of CPV than can conventional methods.9–11 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 reDisease severity should be assessed through evaluasults due to recent vaccination.12 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, acwith 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 stantion (10% to 12%) are usually moribund and in a state dard for demonstration of protective antibody titer has of circulatory collapse. long been the HI test, which measures both IgM and IgG antibodies in serum. More recently, many laboratoInitial Fluid Therapy ries have used the IFA and SN titers to determine the Fluid replacement for losses incurred through vomitlevel of protective immunity.
OUTSIDE TESTING s FECAL ANTIGEN TEST s RAPID SCREENING TESTS
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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 amikacina (10 mg/kg every 12 hours or 20 mg/kg every 24 hours intravenously) and amoxicillin (15 mg/kg every 12 hours intravenously) s Cefoxitin (25 mg/kg every 6 hours 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) s Trimethoprim-sulfadiazine (30 mg/kg every 12 hours 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 <3.5 g/dl (10–20 ml/kg) s Give whole blood if patient is anemic s Give synthetic colloids (hetastarch) if patient is septic and edematous (10–20 ml/kg over 24 hours)
Glucose Replacement s If patient is hypoglycemic, give 0.5 g/kg 10% dextrose slowly intravenously s After rehydration, add 50–100 ml of 50% dextrose/L of replacement fluids to make 2.5% to 5% solution s Consider partial parenteral nutrition for puppies that have been anorectic for more than 3 days Consider Anthelmintic s Check stool for Giardia organisms, coccidia, or nematodes s Consider injectable ivermectin (250 µg/kg) for nonvomiting dogs—except for collies and related breeds Control Vomiting s No oral intake until 24 hours after vomiting has ceased s Choose one or more antiemetics: s Metoclopramide (1–2 mg/kg over 24 hours in fluids) s Chlorpromazine (0.1 mg/kg every 4 to 6 hours intravenously) s Ondansetron (0.1–0.15 mg/kg every 6 to 12 hours intravenously ) Immunotherapy s Antiendotoxin (4.4 mg/kg diluted 1:1 with fluids, administered over 30 to 60 minutes) s Hyperimmune serum (1.1–2.2 ml/kg intravenously or subcutaneously) s Recombinant granulocyte colony-stimulating factor (5–10 µg/kg/day subcutaneously) Nutrition s Partial parenteral nutrition (3% amino acids, 5% dextrose in balanced electrolyte solution) s Early enteral diet s Liquid diet (small amounts frequently) s Glutamine (0.5 g/kg/day in two divided doses in drinking water) s Easily digestible recovery diet
not be used in dehydrated animals.
ing and diarrhea is the cornerstone of treatment for dogs with CPV enteritis and should be continued until oral intake is resumed. The initial fluid of choice is a balanced electrolyte solution (e.g., lactated Ringer’s solution). These solutions mimic plasma electrolyte concentrations, are isotonic, and can be given rapidly, if necessary, to replace acute fluid losses. The route and rate of initial fluid therapy varies with the patient. If CPV infection has resulted in hypovolemic shock, a rapid intravenous fluid bolus of up to 90
ml/kg/hr may be necessary to restore perfusion. Animals in shock will have pale or muddy mucous membranes and a slow capillary refill time. Fluid therapy should be administered at a fairly rapid rate until mucous membrane color becomes pinker and capillary refill time is restored to 1 to 1.5 seconds. If circulatory collapse prevents venous access, fluids can be administered initially via a 20-gauge, 3.8-cm (1.5-inch) spinal needle placed into the intraosseous space in the shaft of the femur. Once circulation has improved with intraosseous fluids, an intra-
FLUID REPLACEMENT s SHOCK s CIRCULATORY COLLAPSE
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aise. 13 Serum potassium should be monitored daily in these patients. If it is low, potassium chloride should be added to the fluids (Table I). If potassium is in the normal range, potassium chloride (14 to 20 mEq/L) should be added to prevent the levels from dropping. Puppies with CPV enteritis often experience severe protein-losing enteropathy because of destruction of the intestinal villi. If the albumin decreases below 1.5 supplementation. g/dl, the total protein deDehydration (%) × Body creases below 3.5 g/dl, or weight (kg) = Deficit (L) the animal develops evidence of pitting edema, administration of a colloidal fluid is indicated to maintain inMaintenance requirements (2 to 3 ml/kg/hr) as well as travascular oncotic pressure.14 continuing losses from vomiting and diarrhea must also If the puppy is anemic because of parasitism or gasbe taken into consideration during initial fluid therapy. trointestinal blood loss, a transfusion of whole blood (preferably from a recovered animal with a high CPV Maintenance Fluid Therapy antibody titer) is indicated. A dose of 10 to 20 ml/kg Once perfusion has been restored, the fluid rate can can safely be administered to most puppies over a 4be decreased to 4 to 6 ml/kg/hr for most patients. Hyhour period. If the puppy is not anemic but is hydration should be monitored by evaluating mucous poproteinemic, a plasma transfusion (10 to 20 ml/kg membrane color, capillary refill time, pulse quality, intravenously) should be administered through an inpacked cell volume and total solids, urine output line filter over 2 to 4 hours. In addition to providing (which should be approximately 1 to 2 ml/kg/hr), and oncotic components, whole blood and plasma contain urine specific gravity (which should range from 1.015 antibodies and serum protease inhibitors that may help to 1.020). Fluid therapy must be adjusted to replace neutralize circulating virus and control the systemic incontinuing losses through vomiting and diarrhea. As flammatory response associated with the disease. Plasfluid losses subside, the fluid rate is gradually tapered. ma and blood products are Many puppies, particularTABLE I available though commerly toy breeds or those with Potassium Replacement cial blood banks. sepsis, are prone to hypoIf natural colloids are unglycemia as a result of CPV Potassium available, puppies with deenteritis (Figure 3). After reChloride creased total protein and hydration, 2.5% to 5% dexSerum Added edema should receive a syna trose can be added to the Potassium to Fluid Maximum Infusion Rate thetic colloid, such as hetabalanced electrolyte solution (mEq/L) (mEq/L) ml/lb/hr ml/kg/hr starch or dextran 70. To (100 ml of 50% dextrose avoid potential volume added to 1 L will make a 3.6–5.0 20 11 25 overload, the dosage of 20 5% solution). 3.1–3.5 30 8 17 ml/kg/day should not be exPuppies with anorexia, 2.6–3.0 40 5.5 12 ceeded; however, colloid invomiting, and diarrhea are fusions can be repeated after also prone to hypokalemia, 2.1–2.5 60 4 8 24 hours if needed.15 Colwhich can result in muscle <2.0 80 3 6 loids can be given rapidly to weakness, gastrointestinal patients in shock or as a ileus, polyuria, cardiac ar- aSo as not to exceed 0.5 mEq/kg/hr. continuous infusion over 24 rhythmia, and general malvenous catheter can be placed for continued fluid therapy. Animals that are severely dehydrated or in a state of circulatory collapse cannot absorb subcutaneous fluid because of peripheral vasoconstriction. Also, hypertonic solutions should be avoided in dehydrated patients. Animals that are dehydrated but not in shock should be rehydrated over 4 hours. The amount of fluid Figure 3— Toy-breed puppies, such as this 9-week-old given is estimated by the fol- pomeranian, are prone to hypoglycemia secondary to gaslowing formula: trointestinal disease and often require intravenous glucose
HYDRATION MAINTENANCE s COLLOIDS s TRANSFUSIONS
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hours to more stable patients. General guidelines are to supply one third of fluid needs as a colloid and two thirds as a crystalloid solution.
Systemic Antibiotics Hemorrhagic diarrhea and mucosal sloughing are commonly seen in dogs with CPV enteritis and indicate breakdown of the gastrointestinal mucosal barrier, which can lead to bacterial translocation, endotoxemia, and sepsis.5,16 Severe neutropenia often coincides with the severe enteritis and contributes to the risk of systemic sepsis. For these reasons, intravenous broad-spectrum, bactericidal antibiotics are indicated for severely affected puppies.1 A combination of an aminoglycoside (gentamicin [2.2 mg/kg] or amikacin [10 mg/kg] every 8 hours) with a β-lactam antibiotic (ampicillin [2 mg/kg] or cefazolin [22 mg/kg] every 8 hours) provides excellent coverage against gram-negative and anaerobic bacteria that may originate from the gut.17 Aminoglycosides can cause acute renal failure and should only be administered after rehydration has been accomplished.18 Once-a-day dosing of aminoglycosides may minimize renal damage while maximizing bacterial kill because of high peak and low trough antibiotic concentrations.19 The high dose, however, should never be given to dehydrated patients. Urine sediment should be monitored for proteinuria or renal tubule casts, which would warrant discontinuation of aminoglycoside therapy. Enrofloxacin (5 mg/kg every 12 hours) is an alternative to the aminoglycosides. It has an excellent gramnegative spectrum but is not approved for intravenous use and may cause cartilage abnormalities in young, growing animals.20 We have not encountered any problems with enrofloxacin when it is diluted 1:1 with saline and administered slowly (intravenously) for a relatively short term (usually 3 to 5 days) in puppies with CPV enteritis. Rapid administration may cause vomiting. Mildly affected dogs with adequate white blood cell counts generally do not require combination antibiotic therapy. Appropriate antibiotic choices include ampicillin, first-generation cephalosporins, or trimethoprim–sulfonamide in these patients. Antiemetics Vomiting often decreases when oral intake of food and fluid is discontinued; but in some patients, the problem persists and must be treated to reduce fluid losses and increase patient comfort. The two antiemetics most commonly used in dogs with CPV enteritis are metoclopramide and chlorpromazine. Metoclopramide is a gastric promotility drug
that can reduce vomiting by stimulating gastric emptying and inhibiting the chemoreceptor trigger zone.21 The promotility effect may prevent gastric atony and ileus from occurring in dogs with CPV infection. Metoclopramide can be added to the intravenous fluids or administered as a constant-rate infusion of 1.0 to 2.0 mg/kg over 24 hours. If metoclopramide is ineffective in controlling vomiting, a more effective antiemetic is chlorpromazine.22 This drug is a phenothiazine derivative and acts on the emetic center, the chemoreceptor trigger zone, and peripheral receptors to reduce the vomiting reflex. The recommended dosage is 0.1 mg/kg intravenously every 4 to 6 hours or 0.2 to 0.5 mg/kg intramuscularly every 6 to 8 hours, as needed. Phenothiazine derivatives can cause hypotension and systemic vasodilatation through their α-adrenergic blocking effect and should only be given after the patient is well hydrated.22 In dogs with intractable vomiting, metoclopramide and chlorpromazine may be used together, but only with caution because the potential for side effects may increase. Dogs should be monitored for restlessness, hyperactivity, bizarre behavior, or extreme drowsiness. If any of these signs occur, antiemetic therapy should be discontinued. Intractable vomiting may respond to treatment with the new serotonin antagonist ondansetron HCl (Zofran®, Glaxo Wellcome Inc) at dose of 0.1 to 0.15 mg/kg intravenously every 6 to 12 hours.23 Although the drug is highly effective and safe, it is also very expensive. Anticholinergic drugs should not be given to dogs with CPV enteritis because these drugs increase the potential for gastric atony, ileus, and intussusception of an irritated bowel segment.22 Dogs with intractable vomiting should always be evaluated for foreign body obstruction or intussusception. Other causes of continued vomiting include reflux esophagitis and acute pancreatitis. Reflux esophagitis may be manifested by signs of drooling, nausea, and exaggerated swallowing motions. Treatment involves administration of a systemic antacid (famotidine [0.5 mg/kg] or ranitidine [5 mg/kg] intravenously every 12 hours) and an oral suspension of sucralfate (1 g dissolved in 10 ml warm water, every 8 hours). Ideally, the antacid should be administered 1 to 2 hours after the sucralfate.
Immunotherapy Bacterial endotoxemia is believed to be an important factor in the terminal acute shock that occurs in dogs with severe CPV enteritis. A polyvalent equineorigin antiserum against LPS endotoxin is available for use in small animals (SEPTI-serum®—IMMVAC
BACTERICIDAL ANTIBIOTICS s ANTIEMETICS s ONDANSETRON
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Inc). In one study, the mortality rate for dogs with CPV enteritis treated conventionally was 48% (10 of 21 dogs) compared with 17% (5 of 30 dogs) for dogs that received antiendotoxin plus conventional treatment.24 It is recommended that the product be administered over 30 to 60 minutes at the dosage of 4.4 ml/kg and diluted 1:1 with intravenous crystalloid fluids.25 Antiendotoxin should be most effective if it is administered before antibiotic therapy because circulating plasma LPS concentrations can increase dramatically after an antibiotic kills off gram-negative bacteria.26 Patients receiving equine-origin antiserum must be observed closely during administration for signs of anaphylaxis. If a second administration of antiserum is deemed necessary, it should be given within 5 to 7 days after the initial treatment. After that time, a severe immunologic reaction is more likely to occur.27 Anecdotal reports describe the use of convalescent serum (1.1 to 2.2 ml/kg intravenously or subcutaneously) collected from dogs that have recovered from CPV infection in an effort to provide passive immunity to exposed or infected dogs.2,28 Research is needed to determine the efficacy and safety of this practice.
Recombinant Granulocyte Colony-Stimulating Factor Recently, the use of recombinant granulocyte colonystimulating factor (rG-CSF) in dogs with leukopenia secondary to CPV enteritis has been described.31 The recommended dose is 5 to 10 µg/kg per day subcutaneously. Animals that respond generally show an increase in white blood cell count within 24 hours. Unfortunately, preliminary findings do not show an increased survivability associated with use of this product,32 and it is very expensive (approximately $130 to $150 to treat a puppy). Eradication of Intestinal Parasites Intestinal parasites can exacerbate CPV enteritis by enhancing intestinal cell turnover and subsequent viral replication.2 Fecal samples should be evaluated to identify coccidia, Giardia species, hookworms, roundworms, or whipworms. Appropriate oral therapy can be initiated as soon as vomiting ceases, or ivermectin (250 µg/kg subcutaneously) can be given–except to collies and related breeds. Nutrition Dogs with severe CPV enteritis may have a prolonged course of hospitalization and may require nutritional support to prevent catabolism and immune dysfunction associated with negative nitrogen balance. Partial parenteral nutrition (PPN) does not supply all of the patient’s nutrient needs but can provide shortterm support for animals that are expected to recover soon. PPN solutions can be delivered through a peripheral vein rather than through a large central vein.33 These solutions are usually given at a maintenance dose (60 ml/kg/day); additional fluid needs are met with crystalloid solutions. A commercial product that contains 3% amino acids, 3% glycerol, and electrolytes can be used. A PPN solution can be made by adding 300 ml of 8.5% amino acid solution to 700 ml of lactated Ringer’s solution with 5% dextrose. The addition of lipid emulsions is controversial. Although lipids are rich in calories, they have been associated with immunosuppression through impairment of reticuloendothelial function and white blood cell phagocytosis.34 Partial parenteral nutrition solutions are hypertonic and therefore often cause phlebitis near the catheter site. Catheters must be placed aseptically and the site monitored carefully for redness, swelling, or pain.35 Dextrose solutions should be tapered off gradually to prevent rebound hypoglycemia. Most practitioners offer water after vomiting has ceased for 12 to 24 hours. Early enteral nutrition is important to promote intestinal regeneration. A liquid
Aggressive Adjunctive Treatments Steroids and Flunixin Meglumine Corticosteroids and flunixin meglumine have shown beneficial effects in animal models of septic and endotoxic shock if administered early in the shock state.29 Potential beneficial effects of corticosteroids include improved tissue perfusion, decreased leukocyte margination, enhanced membrane stabilization, and reduced absorption of endotoxins. Flunixin meglumine is a potent nonsteroidal antiinflammatory analgesic that has antidiarrheal and antipyretic effects and that may reduce the severity of the intestinal inflammation associated with CPV infection. Corticosteroids and flunixin meglumine can cause severe gastrointestinal ulceration.30 Because of this possibility, we reserve use of these agents for animals exhibiting early signs of sepsis or endotoxemia: fever, tachycardia, injected or muddy mucous membranes, and evidence of breakdown of the gastrointestinal mucosal barrier. These agents should not be administered until after the initial fluid bolus has been given. In select cases, we use either dexamethasone sodium phosphate (2 to 4 mg/kg intravenously) or flunixin meglumine (1 mg/kg intravenously). Repeated doses are not recommended because they increase the likelihood of side effects.
ANTIENDOTOXIN s STEROIDS s FLUNIXIN MEGLUMINE s PPN
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diet can be offered initially, or a gruel can be made with an easily digestible, high-carbohydrate, low-fat diet. The addition of glutamine powder (0.5 g/kg/day in two divided doses) to drinking water has been recommended to promote gastrointestinal healing in dogs recovering from CPV enteritis.36 Various commercial diets are formulated for animals that are recovering from gastrointestinal illness. Intestinal malabsorption and protein-losing enteropathy may persist until the intestinal villi are repaired. Initial feeding should consist of small amounts of an easily digestible diet fed frequently. The normal diet is gradually reintroduced after appetite and stool have returned to normal. After recovery, immunity to parvovirus infection lasts at least 2 years and may even be lifelong.
14. 15. 16. 17. 18. 19.
About the Authors
Drs. Macintire and Smith-Carr are affiliated with the Department of Small Animal Surgery and Medicine, College of Veterinary Medicine, Auburn University, Alabama. Dr. Macintire is a Diplomate of the American College of Veterinary Internal Medicine and the American College of Veterinary Emergency and Critical Care.
1. Pollack RVH, Coyne MJ: Canine parvovirus. Vet Clin North Am Small Anim Pract 23:555–568, 1993. 2. Brunner CJ, Swango LJ: Canine parvovirus infection: Effects on the immune system and factors that predispose to severe disease. Compend Contin Educ Pract Vet 7(12):979–989, 1985. 3. Wessels BC, Gaffin SL: Anti-endotoxin immunotherapy for canine parvovirus endotoxaemia. J Small Anim Pract 27: 609–615, 1986. 4. Fein AM, Lippmann M, Holtzman H, et al. The risk factors, incidence, and prognosis of ARDS following septicemia. Chest 83:40–42, 1983. 5. Turk J, Miller M, Brown T, et al: Coliform septicemia and pulmonary disease associated with canine parvoviral enteritis: 88 cases (1987–1988). JAVMA 196:771–773, 1990. 6. Turk J, Fales W, Miller M, et al: Enteric Clostridium perfringens infection associated with parvoviral enteritis in dogs: 74 cases (1987–1990). JAVMA 200:991–994, 1992. 7. Sandstedt K, Wienup M: Concomitant occurrence of Campylobacter and parvoviruses in dogs with gastroenteritis. Vet Res Comm 4:271–273, 1981. 8. Macartney L, McCandlish IAP, Thompson H, Cornwell HJC: Canine parvovirus enteritis 1: Clinical, hematological and pathological features of experimental infection. Vet Rec 115:201–210, 1984. 9. Mochizuki M, San Gabriel MC, Nakatani H, et al: Comparison of polymerase chain reaction with virus isolation and hemagglutination assays for the detection of canine parvoviruses in faecal specimens. Res Vet Sci 55:60–63, 1993. 10. Hirasawa T, Kaneshige T, Mikazuki K: Sensitive detection
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