starlitekennels
UKC Forum Member
Registered: Jun 2003
Location: Madison, Georgia
Posts: 274 |
saw this at www.merckvetmanual.com
thought it was interesting
Canine Parvovirus
Etiology and Pathophysiology
Clinical Findings
Diagnosis
Treatment
Prevention and Control
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Etiology and Pathophysiology:
The origin of the canine parvovirus has not been established. The virus is very stable in the environment, able to withstand wide pH ranges and high temperatures. It is resistant to a number of common disinfectants and may survive for several months in contaminated areas. Rottweilers, American Pit Bull Terriers, Doberman Pinschers, and German Shepherds are at increased risk of disease. Toy Poodles and Cocker Spaniels appear at decreased risk for developing the enteric disease. Mortality associated with canine parvovirus infection is variably reported to be 16-48%.
The virus is transmitted by direct contact with infected dogs. Indirect transmission, eg, from fecal-contaminated fomites, is also an important source of infection. The virus is shed in the feces of infected dogs for up to 3 wk after infection. Recovered dogs may serve as carriers and shed the virus periodically.
After ingestion, the virus replicates in lymphoid tissue of the oropharynx; from there, it spreads to the bloodstream. It attacks rapidly dividing cells throughout the body, especially those in the bone marrow, lymphopoietic tissue, and the crypt epithelium of the jejunum and ileum. Early lymphatic infection is accompanied by lymphopenia and precedes intestinal infection and GI signs. Replication in the bone marrow and lymphopoietic tissue causes neutropenia and lymphopenia, respectively. By 3 days after infection, rapidly dividing intestinal crypt cells are infected. Viral shedding in the feces begins 3-4 days after infection and peaks when clinical signs appear. Viral shedding decreases rapidly and may no longer be detected 10-14 days after initial infection. Replication of the virus in the crypt epithelium of the gut causes collapse of intestinal villi, epithelial necrosis, and hemorrhagic diarrhea. Normal enteric bacteria, eg, Clostridium perfringens and Escherichia coli enter the denuded mucosa and may gain entry to the bloodstream, resulting in bacteremia.
Clinical Findings:
Infected dogs are often asymptomatic. Clinical disease may be triggered by stress (eg, boarding), and clinical signs may be exacerbated by concurrent infection with opportunistic enteric pathogens (eg, Salmonella , C perfringens , E coli , Campylobacter , coronavirus, and various parasites). The dose of virus required to cause clinical disease may also be a factor. Prolonged contact with a dog shedding high levels of virus increases the likelihood of disease. The incubation period is 3-8 days. Viral shedding may begin on day 3, before the onset of clinical signs.
Initially, 2 common clinical forms of the disease were recognized—myocarditis and gastroenteritis. Myocarditis was seen in young pups, especially in the early neonatal period. Infection led to myocardial necrosis with either acute cardiopulmonary failure (causing pulmonary edema, cyanosis, and collapse) or scarring of the myocardium and progressive cardiac insufficiency. However, myocarditis is no longer seen because effective immunization of bitches protects pups during this early period of life.
Gastroenteritis is most common in pups 6-20 wk old, ie, the period when maternal antibody protection falls and vaccination has not yet adequately protected the pup against infection. Most affected dogs (~85%) are <1 yr old. In dogs >6 mo old, intact males are more likely to develop enteritis than intact females, reflecting the tendency of male dogs to roam. Dogs with the enteric form suffer from an acute onset of lethargy, anorexia, fever, vomiting, and diarrhea. The feces are loose and may contain mucus or blood. The severity of clinical signs varies. Most dogs recover within a few days with appropriate supportive care; others can die within hours of the onset of clinical signs. A common complication is pulmonary edema or alveolitis.
Other clinical problems that have been associated with canine parvovirus include birth defects and infertility; however, supportive evidence is lacking.
Diagnosis:
Diagnosis is based on an appropriate history and clinical signs and confirmed by a positive fecal ELISA or hemagglutination test. The ELISA may be positive on the first day of clinical signs and for 3-4 more days. The ELISA may be false negative if run too early in the disease course; it should be repeated if the history and clinical signs support the likely presence of the virus. Leukopenia or lymphopenia is seen in most infected dogs during the course of illness. Neutropenia is suggestive of the disease. Hypoalbuminemia, hyponatremia, hypokalemia, and hypochloremia may be seen. Serum ALT levels are increased in some dogs. Diagnosis may also be confirmed by a 4-fold increase in serum IgG titer over 7-14 days, detection of serum IgM antibody to parvovirus in dogs that have not been vaccinated within the last 3-4 wk, or the detection of parvovirus particles in the feces using immunofluorescence, immunoperoxidase staining, or electron microscopy.
Treatment:
There is no specific therapy to eliminate the virus. Most dogs recover with appropriate supportive care directed to restoration of fluid balance. Oral electrolyte solutions may be used in mildly dehydrated dogs without a history of vomiting. More severely affected dogs should receive IV fluid therapy (lactated Ringer’s and 5% dextrose with additional potassium chloride [10-20 mEq/L]) to counter dehydration and maintain fluid balance. Monitoring of electrolyte changes is advisable. Most dogs that survive the first 2-3 days of disease recover. Persistent vomiting can be controlled with metoclopramide, 0.2-0.5 mg/kg, PO or SC, qid, or 1-2 mg/kg/day, slow IV).
Routine use of antibiotics is discouraged. More severe cases (eg, dogs with severe blood loss, fever, or loss of intestinal integrity) are predisposed to bacteremia and septicemia. In these cases, a combination of either ampicillin or a first- or second-generation cephalosporin, plus an aminoglycoside or enrofloxacin, provide broad-spectrum coverage.
Food and water should be withheld until vomiting has subsided. After this, small amounts of a bland diet (eg, cottage cheese and rice or a commercially available prescription diet) should be offered frequently. A small volume of warm, salted meat broth should be given concurrently. If GI signs recur after feeding, the dog should be fasted for an additional 12-24 hr before feeding again. If food can be tolerated, the bland diet is continued for 7-14 days, after which the dog’s regular diet can be gradually reintroduced.
Prevention and Control:
Contaminated areas should be thoroughly cleaned. Household bleach (1:30 dilution) or commercial products labeled for use against parvovirus are potent inactivators of the virus. The same solutions may be used as footbaths to disinfect footwear. Disinfection of hands, clothing, and food and water bowls is recommended. Pups should be kept isolated from adult dogs returning from shows or field trials.
Vaccination is critical in the control of the disease. Variants of the virus have appeared since the disease was first recognized, but current vaccines protect dogs against all strains of the virus. Vaccines containing live attenuated canine parvovirus generally induce more effective immunity than inactivated virus vaccines. The high-titer canine parvovirus vaccines now available effectively protect puppies against viral challenge, even during the period when maternal antibody titers remain high enough to interfere with active immunization but have declined enough to predispose pups to infection. Vaccination of pups should begin at 5-8 wk of age, preferably with a high antigen-density vaccine. The last vaccination should be given at 16-20 wk of age, and annual vaccination thereafter is recommended.
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01-31-2008 02:46 AM
