Getting the Right Info on PO: What's New With Parvovirus
Garret Pachtinger, VMD, DACVECC Canine parvovirus (CPV) infection is a common problem in small animal medicine, both in general practice and in the emergency room. Although CPV is not new, as it was originally discovered in 1967, our treatment options and medicine have advanced. CPV remains a common pathogen affecting young dogs that are either unvaccinated or under-vaccinated. Although CPV can be life threatening, this article will focus on pathophysiology and important treatment strategies to reduce morbidity and mortality. This article will also review the use of outpatient protocol compared to in-hospital treatment, including the recent findings from Colorado State University.
Clinical Signs
CPV patients present with non-specific signs of illness including anorexia, lethargy, hypersalivation, vomiting, diarrhea and/ or hematochezia. The lack of intake (anorexia) along with gastrointestinal loss (vomiting and diarrhea) results in dehydration, hypovolemia and, subsequently, shock. As a result, dogs often present with abnormal perfusion parameters, including abnormal mucous membrane color, prolonged capillary refill time, weak or poor femoral pulses, lethargy, tachycardia and potentially altered mentation. Other examination findings include abdominal pain and potentially secondary signs of illness resulting from vomiting, notably respiratory signs due to concurrent aspiration pneumonia.
bone marrow, as well as consumption of peripheral neutrophils. Lymphopenia may also be seen and has been demonstrated to be more severe in those that die from CPV. While continued lymphopenia is a poor prognostic indicator, a rebound in lymphocyte count was positively associated with survival. Other CBC abnormalities can include a nonregenerative anemia secondary to gastrointestinal hemorrhage and acute blood loss and thrombocytopenia following systemic inflammation and platelet consumption. Venous blood gas findings often include metabolic acidosis as a result of hyperlactatemia and poor perfusion. Prerenal azotemia may also be seen, also a result of poor perfusion. Hyponatremia and hypochloremia are also common as a result of severe gastrointestinal loss (diarrhea and vomiting) and lack of intake (anorexia). Hypoglycemia may also develop as a result of excessive glucose utilization, decreased intake and decreased gluconeogenesis.
Diagnosis
The most common test for diagnosis of CPV is the enzymelinked immunosorbent assay (ELISA) test. The ELISA is a rapid, bed-side, inexpensive test for CPV antigen. The CPV ELISA test detects viral antigen in rectal swabs/feces for all CPV type-2 variants. While polymerase chain reaction (PCR) assays are available, this is not commonly chosen for initial CPV evaluation. Ancillary diagnostic tests for CPV patients may include a blood smear, complete blood count (CBC), serum biochemistry profile including electrolytes, venous blood gas, coagulation panel and fecal flotation. As CPV infection results in destruction of hematopoietic progenitor cells, a common CBC finding is leukopenia. Neutropenia is a result of myeloblast destruction within the
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Blood smear.
Photo courtesy of Dr. Garret Pachtinger
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