Intestinal Viruses

Chapter 14 Intestinal Viruses



Robert G. Sherding


Parvoviruses, coronaviruses, and rotaviruses are established causes of viral enteritis and diarrhea in dogs and cats and are discussed in this chapter. In addition, numerous other viruses of uncertain significance and enteropathogenicity have been found in the feces or intestines of dogs and cats.


• In dogs these include herpesvirus, enteroviruses, calicivirus, parainfluenza virus, adenovirus, and picornavirus.

• In cats these include astrovirus, calicivirus, reoviruses (types 1, 2, and 3), torovirus, and togavirus.

• In addition, the intestine may be involved as part of generalized viral infections in disorders such as canine distemper in dogs (see Chapter 13), and feline leukemia virus (see Chapter 8), feline immunodeficiency virus (see Chapter 9), and feline infectious peritonitis (see Chapter 10) in cats.


CANINE PARVOVIRUS



Etiology and Epidemiology


Canine parvovirus type 2 (CPV-2), a non-enveloped, single-stranded DNA virus, causes an acute, highly contagious enteritis of dogs that has been prevalent worldwide since the late 1970s. CPV is believed to have evolved from the feline panleukopenia virus or a closely related virus. Since 1980, variants designated CPV-2a and CPV-2b have evolved, the latter now being the predominant strain in North America. Both of these variants and a newer CPV-2c variant can also infect and replicate in cats.



Transmission


CPV infection occurs by the fecal-oral route. During acute illness, and for about 1 to 2 weeks after recovery, massive amounts of parvovirus (over 1 billion virions per gram of feces) are shed in the feces of infected dogs. Because the virus can survive and remain infectious for 5 to 7 months in the environment, fomites and environmental contamination play a major role in transmission. A peak seasonal incidence in the months of July, August, and September was found in a Canadian study, but this may vary by climatologic region.



Incubation


Signs of enteric disease usually begin 4 to 7 days after exposure, coincident with localization of virus in the mitotically active zones of intestinal crypt epithelia.



Age Incidence


Dogs of any age can be infected, but the incidence of clinical disease is highest in puppies between weaning and 6 months of age. Puppies younger than 6 weeks of age generally are protected by passive maternal antibody, whereas most mature animals have been immunized or have seroconverted from natural exposure.



Breed Incidence


All dogs are susceptible to infection; however, certain breeds have a higher risk for parvovirus infection and appear to be more susceptible to a severe form of the disease. These include rottweilers, Doberman pinschers, American pit bull terriers, German shepherds, and possibly Labrador retrievers. The biologic basis for these breed susceptibilities is unclear.



Pathogenesis




Key Point


CPV has an affinity for the rapidly dividing cells of the intestines, bone marrow, and lymphoid tissues and thus causes intestinal crypt necrosis, severe diarrhea, leukopenia, and lymphoid depletion.



• Intestinal epithelial damage from CPV causes breakdown of the intestinal mucosal barrier. This allows translocation of bacteria (especially Escherichia coli) and absorption of endotoxin, predisposing to bacteremia, endotoxemia, and the development of fatal systemic inflammatory response syndrome (SIRS).


Clinical Signs



• CPV causes sudden onset of anorexia, depression, fever, vomiting, diarrhea, and severe dehydration. The diarrhea can be profuse, foul smelling, and hemorrhagic. Abdominal palpation may reveal intestinal loops that are painful and distended with fluid and gas.

• Hypothermia, hypovolemic shock, icterus, hemorrhagic diathesis (disseminated intravascular coagulation), and pulmonary edema because of acute respiratory distress syndrome may develop terminally in cases complicated by bacterial septicemia, endotoxemia, and SIRS.

• Death may occur in severe cases, particularly in very young puppies and in the highly susceptible breeds, and is usually attributable to dehydration, electrolyte depletion, endotoxic shock, or overwhelming bacterial sepsis associated with severe leukopenia. Septic puppies often develop hypoglycemia.

• The severity of clinical illness may be increased by factors such as stress, overcrowded or unsanitary kennel conditions, secondary bacterial infection, and concurrent diseases such as canine distemper, coronavirus, salmonellosis, campylobacteriosis, and intestinal parasitism (e.g., nematodes or giardia).

• In susceptible mature dogs, mild or inapparent infection that results in seroconversion without obvious clinical signs is common.

• In utero or postnatal infection can cause acute neonatal myocarditis in neonatal puppies that did not receive maternal antibodies. However, this form of perinatal parvoviral infection is rare because most nursing puppies receive abundant maternal antibodies from colostrum. Signs of parvoviral myocarditis include dyspnea caused by acute heart failure, sudden death caused by arrhythmias, and sometimes delayed-onset chronic congestive heart failure caused by chronic myocardial fibrosis.


Diagnosis


Suspect parvovirus infection in young dogs that have an abrupt onset of vomiting and foul-smelling bloody diarrhea, especially if associated with severe depression, fever, or leukopenia or if these signs follow potential exposure to infected dogs or fomites.




Key Point


Because of the difficulty in breaking through maternal antibody interference with vaccination in young puppies, prior vaccination does not necessarily exclude parvoviral infection, especially in puppies 6 to 20 weeks of age.



Hematology



• A complete blood count is particularly useful because approximately 50% of dogs with parvoviral enteritis develop severe leukopenia caused by lymphopenia and granulocytopenia, often with a total of only 500 to 2000 leukocytes/μl and sometimes less. Depletion of circulating mature neutrophils is caused by extensive loss of neutrophils through the damaged intestinal mucosa coupled with impaired myelopoiesis caused by bone marrow disruption from the virus. The severity of the leukopenia is generally proportional to the severity of the clinical illness. A rebound neutrophilia is a positive indicator of impending recovery.

• The hematocrit is variable. The PCV is often normal but can be moderately decreased (especially after rehydration with fluids) in some dogs because of intestinal hemorrhage. In some dogs, the PCV can be elevated initially because of hemoconcentration from dehydration.


Serum Chemistries


Serum chemistry abnormalities are variable and non-specific. Findings may include electrolyte abnormalities (most frequently hypokalemia), prerenal azotemia, hypoglycemia, hypoalbuminemia, increased bilirubin, and increased liver enzymes (alanine transaminase and alkaline phosphatase).



Abdominal Radiography


Gas and fluid distention of the gastrointestinal (GI) tract due to generalized ileus is frequent in parvoviral enteritis and must be differentiated from small intestinal obstruction (e.g., foreign body or intussusception). Carefully palpate the abdomen to help rule out mechanical obstruction, including complicating intussusception. Barium contrast radiography often reveals mucosal irregularity (corrugation or scalloping) and prolonged transit time.



Serology



• Determination of an anti-CPV antibody titer in serum is not sufficient for diagnosis because up to 95% of dogs in the population have seroconverted from prior vaccination or natural exposure.

• Detection of early-appearing immunoglobulin (Ig) M antibodies by an indirect fluorescent antibody (IFA) test or 2-mercaptoethanol procedure provides presumptive evidence of recent infection because IgM antibodies are only found during or a few weeks after infection.


Virology




Key Point


Definitive diagnosis of parvoviral enteritis requires demonstration of active excretion of virus or viral antigen in the feces.



• Massive quantities of virus are shed in the feces during the acute illness, and shedding is over within 1 to 2 weeks after recovery. The most practical methods for detecting parvovirus in the feces are the commercially available, rapid in-office tests; including the enzyme-linked immunosorbent assays (ELISAs), such as the SNAP-Parvo Test (IDEXX Laboratories) and ASSURE-Parvo Test (Synbiotics), or the rapid immunomigration assay, such as Witness CPV (Synbiotics). These tests are sensitive and accurate.

• Consider that false-positive results are occasionally seen on these CPV immunoassays 5 to 12 days following vaccination with modified live virus (MLV) vaccines. False-negative results occur rarely when fecal antigen is bound to neutralizing antibodies or viral shedding stops early.

• Other methods for detecting fecal excretion of parvovirus, such as hemagglutination, latex agglutination, electron microscopy (EM), virus isolation, and polymerase chain reaction (PCR) assay, are less convenient for routine clinical use because they require a commercial or research laboratory.


Necropsy


Necropsy diagnosis of parvovirus is based on identification of the characteristic intestinal lesions of necrosis of the intestinal crypt cells with secondary villous collapse and dilatation of the crypts with necrotic debris. Myeloid degeneration and widespread lymphoid depletion also are seen. Parvovirus can be demonstrated in frozen tissue samples by immunofluorescence and in fixed specimens by PCR.



Treatment


The treatment of parvovirus is mainly supportive and similar in most ways to the treatments used for other types of severe gastroenteritis. The intensity of the treatment depends on the severity of the signs. In dogs with fully developed clinical signs, withhold food and water for 12 to 24 hours to rest the GI tract, administer IV crystalloids to replace fluid and electrolytes, and give parenteral antibiotics to control bacterial complications. Initiate therapy whether or not definitive tests are done or while awaiting the return of results.



Fluid Therapy




Key Point


The cornerstone of treatment for CPV infection is IV fluid and electrolyte therapy.


See Chapter 5 for specific guidelines and procedures for fluid and electrolyte therapy.


• Use the intravenous route for fluid and electrolyte replacement using a balanced crystalloid solution (e.g., lactated Ringer’s solution, Plasma-Lyte 148, or Normosol-R). For animals presented in hypovolemic shock, administer up to 90 ml/kg IV in the first 1 to 2 hours to restore hemodynamic stability (see Chapter 156), then switch to a maintenance rate. For most other animals, correct dehydration over the first 24 hours, then use a maintenance rate for fluids plus replacement of ongoing losses. Two to three times normal maintenance levels are often required. Continue fluid therapy until vomiting ceases and oral intake resumes.

• Add potassium (20–30 mEq/L) to IV fluids to control hypokalemia.

• Add dextrose to IV fluids at a 2.5% solution to control complicating hypoglycemia of sepsis. Monitor serum glucose and increase to 5% if needed to maintain serum glucose from 120 to 160 mg/dl.

• Consider supplementing magnesium according to guidelines in Chapter 5, as magnesium is often deficient in severe cases of parvoviral enteritis.

• Infuse colloid solution (e.g., hetastarch) at 20 ml/kg, IV, if infusion of balanced crystalloid solution does not restore hemodynamic stability or if serum albumin drops below 2 g/dl.

• Avoid administration of fluids by the subcutaneous route, especially in dogs with severe leukopenia, because this has been associated with secondary infection, cellulitis, and skin necrosis at administration sites.

• Monitor fluid therapy by tracking body weight, physical parameters, urine output, estimates of ongoing fluid losses (vomitus, diarrhea), and hematocrit and total plasma protein. Also evaluate serum potassium concentration daily and adjust potassium level added to IV fluids accordingly.


Antibiotics



• Administer bactericidal, broad-spectrum antibiotics to control bacterial complications. Initially, administer antibiotics parenterally.

• Use cefazolin or ampicillin in mild cases.

• Use cefazolin, ampicillin, or penicillin combined with an aminoglycoside (e.g., gentamicin or amikacin) or a fluoroquinolone (e.g., enrofloxacin) in severe and leukopenic cases. Fluoroquinolones may damage joint cartilage in young, growing pups. If an aminoglycoside is used, maintain hydration to prevent nephrotoxicity and monitor the urine daily for casts and proteinuria as early indicators of nephrotoxicosis.

• Consider a third-generation cephalosporin (e.g., ceftiofur; Naxel) combined with clindamycin in dogs with severe life-threatening bacterial sepsis.


Dietary Restriction



• Give nothing per os (fluid needs are met by IV infusion) for the first 12 to 24 hours. Prolonged food restriction may be detrimental to intestinal recovery. One study showed improved outcome in dogs treated with early enteral nutrition (using a nasoesophageal tube feeding starting at 12 hours) compared with dogs treated by prolonged dietary restriction.

• Persistent vomiting can sometimes take 3 to 5 days to abate in severe cases, sometimes requiring partial parenteral nutrition.

• When feeding is resumed, give small, frequent feedings of a bland and digestible diet, such as a commercial GI diet or cooked skinless chicken and rice, until GI function appears to have recovered. The transition back to regular feeding should be gradual.


Antiemetics



• For frequent or persistent vomiting associated with delayed gastric emptying that sometimes occurs in parvoviral infection, administer metoclopramide, a dopaminergic antagonist, at 0.5 mg/kg every 8 hours SC or most effectively as a constant rate infusion of 1 to 2 mg/kg every 24 hours diluted in IV fluids.

• For gastritis, control gastric acid secretion with an H2 receptor blocker, for example, ranitidine (Zantac; 2 mg/kg IV, q8–12h), or famotidine (Pepcid; 0.5 mg/kg IV, q12–24h).

• If these are unsuccessful for controlling vomiting, consider the broad-spectrum phenothiazine antiemetic, chlorpromazine (0.5 mg/kg SC or IM, q6–12h), but not until dehydration has been corrected because phenothiazines have a hypotensive effect. Avoid the use of metoclopramide and chlorpromazine together because they can produce central nervous system excitation and, rarely, seizures.

• For persistent vomiting that is refractory to other treatments, give ondansetron (Zofran; 0.1–0.2 mg/kg slow IV, q6–12h), a serotonin-antagonist antiemetic.

• Avoid the use of anticholinergics in parvoviral enteritis because they can worsen GI hypomotility.


Antidiarrheals



• Parvoviral diarrhea is usually self-limiting, and treatment to control diarrhea is rarely needed as long as fluid needs are met; however, when diarrhea is profuse and persistent, administer loperamide (Imodium; 0.2 mg/kg PO, q8h).


Infusion of Whole Blood or Plasma



• Consider whole blood transfusion (5–10 ml/kg IV) for treatment of severe blood loss anemia and hypoproteinemia.

• Consider plasma infusion (5–10 ml/kg IV) for cases that develop disseminated intravascular coagulopathy. Plasma may also help correct hypoproteinemia, but hetastarch is a preferred source of colloid for raising colloid osmotic pressure. Plasma may also provide anti-CPV antibodies, but the benefit of this is questionable.


Treatment for Septic Shock



• Use the recommendations in Chapter 156 for fluid therapy in shock.

• Dexamethasone (2–4 mg/kg IV) can be used as a single dose to treat septic shock.

• Flunixin meglumine (Banamine), a nonsteroidal anti-inflammatory drug, is an alternative to corticosteroids as a single injection to treat septic shock. Beware of gastric ulceration; do not give repeated doses or combine with corticosteroids.

You may also need

Tags:
Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Intestinal Viruses

Full access? Get Clinical Tree
Get Clinical Tree app for offline access