Although no definitive treatment exists mortality without supportive care has been reported as high as 91% with reports of 4-48% mortality with supportive care. The parvovirus is transmitted by the fecal oral route and can persist in the environment for 5-7 months; fecal shedding of virus is variable and short lived, typically less then 2 weeks following infection. It almost excusively affects puppies between the ages of approximately 6 weeks to 6 months. Risk factors include unsanitary over crowded conditions, endoparasitism and breed.
In dogs greater then 2 weeks of age lymphoid tissue, intestinal epithelium, and bone marrow are primarily affected a neurologic form characterized by diffuse leukoencephalomalacia. After ingestion viral replication begins in the oropharynx and local lymphoid tissue, the virus then reaches the intestinal mucosa by way of the blood stream and, subsequent villous loss results in collapse of the intestinal epithelium, loss of absorptive cavity and the development of hemorrhagic diarrhea 4-5 days after the initial ingestion. Lymphopenia, and in sever cases, panleukopenia occur secondary to lymphoid necrosis and destruction of myeloproliferative cells in the bone marrow.
Initial signs of CPV enteritis are nonspecific and include anorexia, depression and fever, with most developing small bowel diarrhea and vomiting 24-48 hours after the initial signs. Large fluid and protein losses through the gastrointestinal may result in severe dehydration and hypovolemic shock. Classic sign associated with impairment in tissue perfusion, including changes in mentation, prolonged CRT, tachycardia, poor pulse quality/hypotension, cool extremities, and low rectal temperature may be present. Abdominal pain secondary to acute gastroenteritis or intussusception may also be evident, intestinal intussusception warrants immediate surgical intervention.
Diagnosis of CPV infection can be made by it classic presentation, acute onset of enteritis, fever and leucopenia. An ELISA as also readily available for in-office to demonstrate CPV in the feces from approximately 3 days after infection, false positives may occur 3-10 days after vaccination with modified live CPV vaccine.
The coroner stone of management of CPV enteritis remains supportive care. Mildly infected puppies may be treated as out patients, receiving subcutaneous fluids and dietary restriction. Puppies that fail outpatient management due to persistent or recurrent diarrhea and /or vomiting, and puppies that initially present to the veterinarian with more sever clinical signs, including severe dehydration/hypoperfusion, fever, abdominal pain, and protracted diarrhea and/or vomiting should be hospitalized immediately and managed aggressively.
Re-establishment of effective circulating blood volume inpuppies that present in hypovolemic shock and fluid replacement for losses secondary to ongoing diarrhea and vomiting is mandatory in severly affected puppies. The initial fluid of choice is a balanced electrolyte solution (i.e. LRS) with fluids deficits being replace in 1-2 hours in dogs with hypovolemic shock, while animals that are dehydrated but not in shock should be rehydrated over a period of 6-24 hours. Once perfusion has been restored and deficits corrected the IV rate is decreased to 4-10 mL/kg/hr, adjusted to account for ongoing losses.
Puppies with ongoing anorexia, vomiting, and diarrhea are prone to the development of hypokalemia, which can result in profound muscle weakness/paralysis, gastrointestinal ileus, cardiac arrhythmias and polyuria. Potasium chloride is added to the fluids as needed to prevent the development or worsening of hypokalemia, the rate should not exceed 0.5mEq/kg/hr because it may adversely affect normal cardiac function. After rehydration IV supplementation of 2.5-5% dextrose may be added to combat hypoglycemia secondary to ongoing vomiting and anorexia. A sever PLE may accompany CPV enteritis and the addition of a nonprotein colloid to the fluid plan should be added it the albumin decrease below 2g/dL, the TP decrease below 4g/dL or if the patient develops evidence of third spacing fluids. Daily COP measurements are warranted as during colloidal therapy as over-supplementation can blunt endogenous hepatic albumin production. Packed RBC’s should be administered for anemia resulting from blood loss secondary to hemorrhagic diarrhea or concurrent endoparastism, this should be based on clinical signs of anemia not on the absolute hematocrit. Plasma transfusions can be added as adjunctive treatment for CPV enteritis, for its ability to provide albumin, immunoglobulins, and serum protease inhibitors tht may help to neutralize circulating virus and diminish the accompanying systemic inflammatory response.
Disruption of the mucosal barrier can lead to bacterial translocation, endotoxemia, or sepsis and neutropenia. Severly effected dogs may require aggressive combination antibiotic therapy with a B lactam antibiotic (ampicillin) with and aminoglycosied (gentamicin). Antibiotic therapy may increase the release of endotoxin and exacerbate any ongoing systemic inflammatory response, and may also lead to the over growth of Clostridium perfringens, resulting in bloody diarrhea. Antiemetic therapy may be used in cases of severe vomiting the most common being chlorpromazine and metoclopramide. Immunothearpy to combat the leucopenia secondary to destruction of hematopoetic progenitor cells in the bone marrow have been disused however at this time remain controversial. Nutritional support must not be over looked, and enteral feeding has been shown to help maintain mucosal integrity and decrease risk of bacterial translocation. This can be accomplished via syringe/forced feedings or via a feeding tube.
