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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.

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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.

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 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.

Blood smear. Photo courtesy of Dr. Garret Pachtinger

IVF. Photo courtesy of Dr. Garret Pachtinger

Treatment

Treatment of the CPV patient involves fluid therapy, antibiotic therapy, nutritional support, gastrointestinal support and ancillary supportive care.

1. Fluid therapy One of the most common causes of illness as a result of CPV infection is fluid loss from the gastrointestinal tract resulting in dehydration and eventual hypovolemia/hypovolemic shock. Neonates and pediatric patients have higher fluid requirements; therefore, gastrointestinal losses (vomiting and/or diarrhea), along with lack of intake (anorexia), can quickly result in dehydration and hypovolemia. Intravenous and/or intraosseous routes of fluid administration are recommended routes for fluid therapy. Shock fluid therapy is commonly provided using an isotonic crystalloid, 20-40 ml/kg as a bolus. Following the bolus, patient re-assessment is required to evaluate the need for further fluid resuscitation. Careful attention is also needed for additional supplementation, including potassium and/or dextrose. The use of hypertonic saline and/or synthetic colloids can also be considered for the patient that presents in shock.

2. Hypoglycemia Neonates and pediatric patients that present with lack of intake (anorexia) and/or gastrointestinal losses (vomiting, diarrhea) are prone to not only dehydration/hypovolemia but hypoglycemia as well. Intravenous dextrose is recommended for these patients (0.5-1.0 g/kg or 0.5-1.5 ml/kg IV of 50% dextrose, diluted 1:4). Oral dextrose can be considered if IV or IO access is not available. Hypoglycemic patients should also receive isotonic crystalloid fluids supplemented with 2.5-5% dextrose as a CRI until they are able to maintain their glucose level without supplementation.

3. Antibiotic Therapy Although CPV itself is not susceptible to antibiotics, antibiotics are generally indicated in parvovirus patients due to the concern for bacterial translocation — due to the damaged villi and diminished gut mucosal barrier from viral damage — along with immunosuppression caused by the virus resulting in leukopenia. Beta lactam antimicrobials are commonly used, as they are generally considered to be safe in pediatric patients. The Colorado State University Outpatient Parvo Protocol (see below) also discusses the use of cefovecin (Convenia©).

4. Gastrointestinal Support Anti-emetics (e.g. maropitant, ondansetron) are commonly used to treat nausea, vomiting and patient discomfort. The author prefers maropitant at a dose of 1 mg/kg IV every 24 hours.

5. Analgesia As discussed earlier, abdominal pain is a common finding in CPV patients. While some avoid opioids due the possibility of slowing intestinal transit time, when it comes to dogs with visceral pain, the author recommends using buprenorphine (0.01 - 0.02 mg/kg IV, IM, SQ). NSAIDs and corticosteroids should not be used due to their GI effects.

Finally, the outpatient protocol has gained attention since publication, "Evaluation of an outpatient protocol in the treatment of canine parvoviral enteritis" in the Journal of Veterinary Emergency and Critical Care.

Although this study was small (20 in-patient puppies were compared to 20 modified "outpatient" puppies), the study showed an 80% survival in the outpatient group compared to 90% in the in-patient group. While this protocol was not developed to be a substitute for the gold standard of care (hospitalization and administration of fluids/medications intravenously), it proves outpatient care can be considered as an alternative for clients that cannot afford the recommended in-hospital treatment protocol.

In this outpatient protocol study, both groups received initial intravenous fluid and dextrose support, and they were only released for outpatient care once stabilized. Following the initial in-hospital therapy, outpatient treatment included subcutaneous fluids, cefovecin antibiotic therapy and maropitant as an antiemetic. Other considerations in these patients included dextrose and potassium supplementation and nutritional support. While hospitalization may be best for many patients, a

significant number will survive with a carefully planned and implemented outpatient parvo protocol (OPP).

Conclusion While CPV remains a common disease in young patients, the prognosis for canine parvovirus infection is good with treatment. When financial limitations exist, the clinician can consider the outpatient protocol. While the survival rate (80%) is slightly lower compared to in-patient care (90%), this outpatient protocol can be offered as a reasonable option for clients that cannot afford in-patient care.

References 1. Decaro N, Crescento G, Desario C, et al. Long-term viremia and fecal shedding in pups after modified–live canine parvovirus vaccination. Vaccine. 2014;32:3850–3853.

2. Desario C, Decaro N, Campolo M, et al. Canine parvovirus infection: which diagnostic test for virus? 2005;126(1–2):179–185. 3. Glickman LT, Domanski LM, Patronek JG, et al. Breed-related risk factors for canine parvovirus enteritis. J Am Vet Med Assoc. 1985;187:589.

4. Goddard A, Leisewitz AL, Chistopher MM, et al. Prognostic usefulness of blood leukocyte changes in canine parvoviral enteritis. J Vet Intern Med. 2008;22:309–316.

5. Houston DM, Ribble CS, Head LL. Risk factors associated with parvovirus enteritis in dogs: 283 cases (1982-1991). J Am Vet Med Assoc. 1996;208:542.

6. Lawler DF. Neonatal and pediatric care of the puppy and kitten. Theriogenol. 2008;70:384-392. 7. Lenberg J, Sullivan L, Boscan P, et al. The effects of maropitant versus ondansetron on the clinical recovery of dogs with parvoviral gastroenteritis. J Vet Intern Med. 2012;26(3):795 (abstract).

8. Li R, Humm KR. Canine parvovirus infection. In: Silverstein DC, Hopper K, eds. Small Animal Critical Care Medicine, 2nd ed. Saint Louis, MO: Elsevier-Saunders; 2015:509-513.

9. Macintire DK. Pediatric fluid therapy. Vet Clin North Am Small Anim Pract. 2008;38:621-627. 10. Mantione NL, Otto CM. Characterization of the use of antiemetic agents in dogs with parvoviral enteritis treated at a veterinary teaching hospital: 77 cases. J Am Vet Med Assoc. 2005;227(11):1787–1793.

11. Mohr AJ, Leisewitz AL, Jacobson LS, et al. Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis. J Vet Intern Med. 2003;17(6):791–798.

12. Otto CM, Drobatz KJ, Soter C. Endotoxemia and tumor necrosis factor activity in dogs with naturally occurring parvoviral enteritis. J Vet Intern Med.1997;11:65–70.

13. Preisner K, Sullivan L, Boscan P. Evaluation of an outpatient protocol in the treatment of canine parvoviral gastroenteritis. J Vet Intern Med. 2013;27(3):721 (abstract).

14. Proksch AL, Unterer S, Speck S, et al. Influence of clinical and laboratory variables on faecal antigen ELISA results in dogs with canine parvovirus infection. Vet J. 2015;204:304–308.

15. Savigny MR, Macintire DG. Use of oseltamivir in the treatment of canine parvoviral enteritis. J Vet Emerg Crit Care. 2008;20(1):132–142. 16. Venn EC, Preisner K, Boscan PL, et al. Evaluation of an outpatient protocol in the treatment of canine parvoviral enteritis. J Vet Emerg Crit Care.2017;27(1):52-65.

Dr. Garret Pachtinger is a boardcertified veterinary specialist in emergency critical care and a member of the ACVECC Board of Regents. Dr. Pachtinger graduated from the University of Pennsylvania School of Veterinary Medicine. He then pursued an internship, emergency fellowship and emergency residency at the Ryan Veterinary Hospital at the University of Pennsylvania. He is currently an associate, internship director and trauma center medical coordinator at the Veterinary Specialty and Emergency Center in Levittown, Pennsylvania. Dr. Pachtinger has been published in numerous veterinary journals, textbooks and peer-reviewed learning tools and is on the editorial board of Today’s Veterinary Practice. Dr. Pachtinger lectures throughout the world on emergency and critical care and is the co-founder of VETgirl, a subscription-based service offering veterinary continuing education (CE).

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