Most viral enteritides of dogs and cats, especially the parvovirus infections, cause an acute and usually self-limiting diarrhea, although severe cases in young or immunocompromised patients may be fatal. Canine parvovirus infection is described here as the index case for viral enteritides.
Canine parvovirus type 2 (CPV-2) is a highly contagious cause of acute enteritis. It emerged as a pathogen in the late 1970s, perhaps from a mutation of a feline vaccine as it is related to feline panleukopenia and mink enteritis viruses. CPV-2b has emerged as the most prevalent antigenic variant. There have been reports of cats being infected with canine parvovirus type 2, but the severity of signs is much reduced.
Infected dogs shed massive quantities of virus particles in feces during the acute illness and then for about 8 to 10 days afterward. Parvovirus is extremely stable and can remain infectious in the environment for many months. Infection is acquired via the fecal-oral route and is more common in the summer months. The virus has an affinity for rapidly dividing cells and localizes to the intestine (crypt cells), bone marrow, and lymphoid tissues. It causes apoptotic cell death, leading to intestinal crypt necrosis and severe diarrhea, leukopenia, and lymphoid depletion.
Clinical signs of diarrhea typically occur 4 to 7 days after infection. Anorexia, depression, fever, vomiting, diarrhea (often profuse and hemorrhagic), and dehydration are common. Hypothermia and disseminated intravascular coagulation (DIC) are associated with terminal bacterial sepsis or endotoxemia. Dogs of any age can be affected, but the incidence of clinical disease is highest in puppies between weaning and 6 months. Puppies younger than 6 weeks usually are protected by maternal antibody. In dogs older than 6 months, males are more likely to become infected than females. Overcrowding, intestinal parasitism, concurrent infection with distemper virus, coronavirus, Giardia, Salmonella, or Campylobacter spp. can increase the severity of illness.
Puppies infected in utero or shortly after birth may develop myocarditis and either die suddenly or develop cardiomyopathy if maternal antibody is absent. This situation rarely arises nowadays because widespread vaccination and infection have left few seronegative dams. Yet death still occurs, especially in young puppies, and particularly in susceptible breeds such as rottweilers, Dobermans, English springer spaniels, and American pit bull terriers. Death is usually attributed to dehydration, electrolyte imbalances, hypercoagulability, endotoxic shock, or overwhelming bacterial sepsis related to mucosal barrier disruption and leukopenia. Infected dogs are immunosuppressed and susceptible to catheter infections. Endotoxemia, TNF activity, coliform septicemia, and proliferation of enteric C. perfringens determine morbidity and mortality.
Parvovirus should be suspected in young dogs with sudden onset of vomiting and diarrhea, especially if they are also depressed, febrile, or leukopenic or if they have been in contact with infected dogs. Leukopenia (often 500 to 2000 white blood cells per microliter) may be detected in up to 85% of field cases and is very suggestive of parvovirus infection. It reflects neutropenia and lymphopenia. Neutropenia results from impaired bone marrow production with concurrent r. eutrophil loss through the damaged gastrointestinal tract, and severe neutropenia crudely correlates with a poor prognosis.
In the absence of leukopenia, clinical signs are indistinguishable from those of other bacterial or viral enteritides, gastrointestinal foreign bodies with peritonitis, or intussusception. Abdominal radiographs may reveal non-specific gas and fluid accumulation, and ileus. Biochemical abnormalities often include hypokalemia, hypoglycemia, prerenal azotemia, and increased bilirubin or liver enzymes.
Definitive diagnosis requires demonstration of canine parvovirus type 2 virus (orviral antigens) in the feces. Fecal enzyme-linked immunosorbent assay is regarded as an accurate and specific diagnostic test but is most sensitive in the first 7 to 10 days when virus excretion is greatest. Single anti-CPV antibody determination in serum (by hemagglutination inhibition) is not useful for diagnosis except in the presence of typical clinical signs in an unvaccinated animal. A rising IgG titer by paired serology provides only a retrospective diagnosis. Serum IgM analysis may provide evidence of recent infection.
Treatment is supportive and is similar to regimens used in most animals with severe gastroenteritis. Intravenous fluid therapy usually is indicated and is continued until vomiting stops and oral intake resumes. A balanced electrolyte solution (e. g., lactated Ringer’s solution) supplemented with potassium and 2.5% glucose is often used. Plasma or whole blood infusions are given to treat severe hypoproteinemia or anemia. Antibiotics are used to control potentially fatal sepsis (see above).
Traditionally, oral intake is withheld until vomiting has stopped for at least 24 hours; this may take 3 to 5 days in severe cases. Rather than avoid the oral route completely, it may be better to trickle feed small amounts of glutamine-containing solutions to reduce bacterial translocation. Once vomiting has been controlled, small amounts of a bland diet are fed initially. Frequent or persistent vomiting can be managed with intermittent injections or constant-rate infusion of metoclopramide, once intestinal obstruction has been ruled out. Phenothiazines (e. g., chlorpromazine) can be used if metoclopramide is ineffective and the animal has been rehydrated.
Administration of corticosteroids is of unproven benefit and is probably best limited to dogs with severe endotoxic shock. Flunixin meglumine is best avoided because of its adverse effects on the gastrointestinal tract and kidneys. Antiendotoxin therapy has been useful in some patients, but the timing of antiendotoxins in relation to antibiotic therapy may be important. Because antibiotics may increase endotoxin liberation, it may be preferable to administer antiendotoxin serum before antibiotics. However, one study showed that the use of the antiendotoxin rBPI21 had no beneficial effect on survival, and in another study, use of antiendotoxin was correlated with decreased suvival. Administration of recombinant human granulocyte colony-stimulating factor (G-CSF) to neutropenic parvoviral enteritis patients may raise neutrophil counts but is of no clinical benefit, because the endogenous granulocyte colony-stimulating factor concentration is already elevated. In contrast, administration of feline interferon-omega was found to improve clinical signs and reduce mortality.
Severe infection and leukopenia are associated with a high mortality rate, but most dogs with parvovirus recover if dehydration and sepsis are treated appropriately. Complications include hypoglycemia, hypoproteinemia, anemia, intussusception, and secondary bacterial or viral infections.
Prevention is achieved by limiting exposure to the virus, adequate disinfection (1:32 dilution of sodium hypochlorite bleach), and vaccination. Vaccination is an effective means of preventing and controlling canine parvovirus type 2, but maternal antibody interference is a problem. Maternally derived antibodies (MDAs) can persist for up to 18 weeks and can interfere with vaccination, although most modern vaccines can overcome maternally derived antibodies by 10 to 12 weeks of age. Modified live canine parvovirus type 2 vaccines are most commonly used; killed vaccines provide less duration of immunity but may be recommended in pregnant dogs and puppies younger than 5 weeks. Vaccines may differ in efficacy; low-passage, high-titer vaccines are considered most effective, and only one injection at or after 12 weeks may be needed. In susceptible breeds and dogs in high-risk areas, vaccination may begin at 6 to 8 weeks of age and be repeated every 3 to 4 weeks until 18 weeks of age. There is good correlation between the antibody titer and resistance to infection with canine parvovirus. Annual revaccination is currendy recommended.
Feline Parvovirus (Feline Panleukopenia)
Feline panleukopenia is a highly contagious infection of cats that causes severe acute diarrhea and death, similar to canine parvovirus. Mortality in young kittens is high (50% to 90%), therefore the prognosis is guarded until the vomiting and diarrhea stop and the leukopenia resolves.
Canine coronavirus (CCV) can cause diarrhea of variable severity in dogs. Transmission is by the fecal-oral route. The incubation period is 1 to 4 days, and infected dogs may shed virus intermittently for months after clinical recovery. However, the significance of coronavirus as a primary pathogen is unclear. Experimental inoculation is associated with only mild disease and canine coronavirus infection, and antibodies against canine coronavirus are present in many healthy and diarrheic dogs. Infection is very prevalent, particularly in animal shelter and laboratory dogs. Most canine coronavirus infections are probably subclinical, although severe enteritis may occur in dense populations or with concurrent infections. In such situations, vaccination may be helpful.
Feline enteric coronavirus (FECV) is ubiquitous in the cat population. Mild to moderately severe diarrhea, which may be associated with weight loss, is seen in kittens infected with feline enteric coronavirus. Inapparent infection is common in normal cats, many of which shed FECV in feces and are seropositive. Feline enteric coronavirus infection is important, because enteric coronaviruses may mutate to feline infectious peritonitis virus (FIPV).
Intestinal Feline Infectious Peritonitis
An unusual manifestation of feline infectious peritonitis (FIP) of isolated mural intestinal lesions has been reported. Predominant clinical signs were diarrhea and vomiting, and all cats had a palpable mass in the colon or ileocecocolic junction. Affected intestine was markedly thickened and nodular, with multifocal pyogranulomas extending through the intestinal wall.
Feline Immunodeficiency Virus
Infection with feline immunodeficiency virus (FIV) is associated with a 10% to 20% incidence of chronic enteritis. Although secondary and opportunistic infections may be responsible for signs, sometimes no other etiologic agent can be identified. Anorexia, chronic diarrhea, and emaciation are typical. Palpably thickened bowel loops reflect chronic enteritis with transmural granulomatous inflammation.
Feline Leukemia Virus
Among its many manifestations, feline leukemia virus (FeLV) infection can be associated with fatal peracute enterocolitis and lymphocytic ileitis.
A torovirus-like agent has been isolated from the feces of cats afflicted with a characteristic syndrome of chronic diarrhea and protruding nictitating membrane. However, a clear association with clinical signs was not demonstrated.