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THE VIRUS
The original canine parvovirus (CPV), discovered in 1967 was called "CPV-1". A new variant, "CPV-2", emerged worldwide in 1978 and caused severe gastrointestinal signs. In the mid-1980s, the original CPV-2 evolved into 2 variants, CPV-2a and CPV-2b. In 2000, a new variant, CPV-2c, was detected in Italy and is currently likely widespread in the United States. 3
Parvoviruses are small and consist of a protein coat (a capsid) and a single strand of DNA. They are very hardy in the environment because they are not enveloped in fat. They are able to overwinter in the ground despite freezing temperatures. Indoors, many household disinfectants are not capable of killing parvoviruses. Thus they are readily carried on shoes or clothing to new areas which accounts for their rapid spread around the world within a short period of time.
PATHOGENESIS
Dogs become infected through oral contact with the virus in feces, infected soil, or fomites that carry the virus. The incubation period is 3-7 days. Whether an individual dog gets infected or not depends on the number of viral particles the dog is exposed to, what kind of immune experience the dog has had with the virus before (vaccinated? previously infected? how much past exposure?), and how strong the individual dog is (stress factors, diet etc.)
The initial replication occurs in the oropharyngeal lymphoid tissue. Once the virus enters blood stream, it localizes to areas that have rapidly dividing cells: intestinal crypts, lymphoid tissue and bone marrow.
Within the bone marrow, the virus destroys young precursor white blood cells resulting in a decrease in circulating white blood cells. A relative immunodeficiency develops due to the low numbers of neutrophils and lymphocytes. Leukopenia may make it easier for the viral particles to invade the dividing cells of the gastrointestinal (GI) tract. Breakdown of the cellular barrier in the gut enables enteric pathogens to invade the intestines.
Infected dogs shed huge amounts of virus in their feces, saliva and vomitus; thus the need to isolate infected dogs from other dogs. In surviving dogs, the virus may be shed for 2-3 weeks postinfection.
MYOCARDITIS
In the neonate, the virus attacks myocardial cells causing a lymphocytic, end stage myocarditis with myofiber loss and replacement with extensive fibrosis. Early in the disease viral inclusions are found in the myofibers without inflammation; later stages include myofiber necrosis and mild inflammatory infiltrates.4
CLINICAL SIGNS
Hemorrhagic diarrhea and mucosal sloughing are commonly seen in dogs with CPV enteritis, and indicate breakdown of the GI mucosal barrier which can lead to bacterial translocation, endotoxemia, and sepsis. Severe neutropenia often coincides with the severe enteritis contributing to the risk of systemic sepsis.
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 drooling, nausea, and exaggerated swallowing motions.
DIAGNOSIS
Clinical signs: The diagnosis is most often based on appropriate clinical signs in conjunction with a positive fecal ELISA test.
Fecal ELISA test: If the test is negative, other causes of gastroenteritis such as foreign body, pancreatitis, intestinal parasitism, toxicity, or dietary indiscretion should be ruled out. Because of the possibility of false negative results, animals with a compatible history should receive appropriate supportive care and be retested 48 hours later. False positive tests may be seen with recent (within previous 15 days) vaccination for CPV.
Hemogram results may show leukopenia and neutropenia. Leukocytosis may be seen in the recovery phase.
Chemistry profile results may show elevated liver enzymes, hypoglycemia, panhypoproteinemia, azotemia, and electrolyte changes.
Less commonly used tests include real time PCR, virus isolation, serology (hemagglutination inhibition), tissue culture, and electron microscopy.
Post mortem diagnosis of CPV-2 may be hampered by the severity of enteric lesions, secondary bacterial overgrowth, and rapid onset of autolysis. The virus has been shown to reside in the tongue of infected dogs. Since tongue epithelium is less sensitive to postmortem changes than the gut, it is an excellent complementary sample to submit, especially if there has been autolysis. 6
SUPPORTIVE
1) Fluid replacement, for losses incurred through vomiting and diarrhea, is the cornerstone of treatment for dogs with CPV enteritis and should be continued until oral intake is resumed.
2) The initial fluid of choice is a balanced electrolyte solution. Note that subcutaneous fluids will not be absorbed by animals with severe dehydration or circulatory collapse because of peripheral vasoconstriction. In addition, hypertonic solutions should be avoided in dehydrated patients. The route and rate of initial fluid therapy will vary with the patient, but IV route is usually required. If CPV-2 infection has resulted in hypovolemic shock (pale or muddy mucous membranes and a slow capillary refill time), a rapid intravenous fluid bolus of up to 90 ml/kg/hr may be necessary to restore perfusion. If circulatory collapse prevents venous access, fluids can be administered initially via a 20 g 1.5 inch spinal needle placed in the intraosseous space in the shaft of the femur.
3) Colloid therapy: Puppies with CPV enteritis often experience severe protein losing enteropathy because of destruction of the intestinal villi. Administration of a colloid fluid is indicated to maintain intravascular oncotic pressure in the following circumstances: 1) If the albumin decreases below 1.5 g/dl. 2) If the total protein decreases below 3.5 g/dl. 3) If the dog develops pitting edema or cavity effusions.
- Hetastarch: 20 ml/kg IV over 3-4 hours each day.
- Plasma: 10-20 ml/kg IV through an in-line filter over 2-4 hours. It is not as good a colloid as hetastarch because the albumin in plasma will leak out the same big holes in the gut that the dog's own albumin is leaking out of, but it provides valuable clotting factors and antibodies.
- There is no contraindication to giving both hetastarch and plasma to same patient. General guidelines are to supply one third of fluid needs as a colloid and two thirds as a crystalloid solution.
4) Blood transfusion: If the pup is anemic because of parasitism or gastrointestinal blood loss, a transfusion of whole blood (preferably from a recovered animal with a high CPV antibody titer) is indicated. A dosage of 10-20 ml/kg can safely be administered to most puppies over a 4 hour period.
5) Dextrose: Many puppies, particularly toy breeds or septic animals, are prone to hypoglycemia with CPV enterits. Thus serum glucose needs to be closely monitored. If dextrose supplementation is necessary, only use it after the patient is appropriately rehydrated. Solutions of 2.5 to 5% dextrose can be used. Dextrose can be added to the balanced electrolyte solution (100 ml of 50% dextrose added to 1 liter will make a 5% solution). If the blood glucose is well within normal range, it may be best to not add dextrose to the fluids because glycosuria may result in an osmotic diuresis which contributes to the fluid losses.
6) Potassium: Hypokalemia often occurs because of lack of intake and loss via vomiting and diarrhea. Hypokalemia contributes to GI ileus. Serum potassium should be monitored daily until the signs resolve and the patient is eating.
- If potassium is in the normal range, 14-20 mEq KCl should be added to each
liter to prevent the levels from dropping. ect
ﾜｸﾁﾝの販売元
犬 MSD,ｲﾝﾀｰﾍﾞｯﾂ
犬 京都微研
犬 Zoetis(Pfizer)
犬 ﾒﾘｱﾙ
*Quotation from VIN
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