Agent. Canine parvoviruses are non-enveloped DNA viruses which require rapidly divided cells to reproduce. Currently, most worldwide cases with clinical diseases are infected with CPV-2b or CPV-2c. The small animal parvoviruses are quite resistant to environmental destruction but are susceptible to bleach. Infections in dogs came from feline panleukopenia virus and emerged in the late 1970s. The primary means of transmission is horizontal transmission via oronasal—fecal transmission. Vertical transmission via in utero infection can occur and can leads to myocarditits. CPV-2b and CPV2c can also infect cats.

CPV-2 first enters the oronasal cavity and infects lymphoid tissue followed by viremia for at least 1–5 days. Rapidly dividing cells of the gastrointestinal tract, myocardium, CNS, skin, kidney and other organs are targeted. Most notably, CPV-2 infects the crypt epithelial cells causing villus blunting. Decreased absorption (manifested as diarrhea), necrosis (sloughing of blood) and inflammation result. Lack of gastrointestinal integrity allows normal GI flora to penetrate into the blood stream and can lead to bacteremia with or without sepsis. Canine parvoviruses are shed primarily in feces for 3 to 14 days post infection, often starting before clinical signs appear. Clinical signs usually develop starting 5 to 12 days after exposure. Dogs with maternal or vaccinal antibodies can usually limit viremia and fully immunized dogs have sterilizing immunity.

Clinical findings. Any dog can be infected, but disease is thought to be more severe in some breeds like the American pit bull terrier and Rottweilers. Severity of disease depends on virulence of the strain, size of inoculum, age, breed, and host’s defenses. Clinical signs of CPV infection are most severe in pups less than 12 weeks that do not have prior immunity. Most dogs have enteritis characterized by foul-smelling bloody diarrhea and vomiting. Leukopenia and fever are also common. Dogs may also have signs of sepsis like red mucous membranes and some dogs will develop disseminated intravascular coagulation. CPV-2 can infect the primary CNS with resultant hemorrhage into brain or spinal cord. In utero infection or infection in pups less than 8 weeks can lead to myocarditis and result in sudden death or congestive heart failure. Depending on the presence of prior immunity, some dogs may have subclinical infections.

Diagnostic evaluation. Dogs under two years of age with acute bloody diarrhea should be considered at high risk for CPV-2, particularly if the vaccine history is incomplete. Another differential diagnosis in dogs with appropriate clinical signs is salmonellosis; this should be considered in dogs that look clinically like parvovirus, but are well vaccinated. The clinical diagnosis is usually supported by documenting parvovirus antigen in feces by ELISA or PCR assays which are commonly part of diagnostic PCR panels in the United States. However, the PCR assays are so sensitive, CPV-2 DNA can be amplified from feces of dogs vaccinated with modified live strains of the virus. At least one of the ELISA antigen tests (SNAP®Parvo; IDEXX Laboratories) has a cut point for a positive test result that excludes most vaccinated dogs. Thus, the ELISA may be superior to PCR for screening dogs and can also be performed in the veterinary clinic. Some dogs will have completed the shedding period by the time the test is run, leading to false negative results. Electron microscopy, virus isolation and seroconversion can also be used to document active or recent infection.

Treatments. Greater than 90% of dogs with CPV-2 enteritis will survive if administered supportive care shortly after clinical signs develop. Fluid replacement, electrolyte balance (particularly potassium), control of hypoglycemia, control of oncotic pressure (hypoalbuminemia can develop), treatment of bacteremia and sepsis (antibiotics), control of nausea and vomiting, and “feeding the gut” as early as possible are paramount to success.

Fluid therapy should be designed to correct losses, hyponatremia and hypokalemia. Oncotic pressure should be maintained with plasma transfusions, hetastarch, or related compounds. Broad spectrum antibiotics with like a first generation cephalosporins are often used in routine cases with therapy escalated to include drugs with a better gram-negative spectrum in dogs showing signs of sepsis. Injectable enrofloxacin or amikacin can be added to the protocol to enhance the gram-negative spectrum. Many clinics use second generation cephalosporins like cefoxitin as their primary antibiotic as this drug has an enhanced gram-negative spectrum compared to first generation cephalosporin. Recently it has been shown that maropitant can be used successfully as an antiemetic agent, but also lessens abdominal pain. It is important to “feed the gut” early in cases with enteritis and so at Colorado State University, nasoesophageal or nasogastric tubes are often used to start to deliver elemental diets as soon as possible. Highly digestible diets with or without probiotics are often used in the recovery phase.

A new gastrointestinal recuperation diet, rebound recuperation (Virbac), was found to be palatable, as determined by acceptance and preference testing, in healthy dogs during the preoperative and postoperative phases of routine sterilization (Forbes et al., 2015). In a follow-up study, rebound recuperation was used successfully in the management of canine parvovirus infections in a clinical trial performed at Colorado State University (Tenne et al., 2016).

Many different adjunctive therapies like passive immune therapy (hyperimmune serum infections), colony stimulating factors, oseltamivir (Tamiflu) are used to attempt to improve survival but not all have been shown to be effective in controlled studies. Interferon omega has been beneficial in some puppies and is labeled for this purpose in some countries. Prognosis is variable. Intussusception may occur as a sequel to severe enteritis and so all parvovirus puppies should be palpated daily.

Not all clients can afford hospitalization and intensive care. Thus, researchers at Colorado State University evaluated an out-patient protocol that had equivalent success rates to hospitalization (Venn et al., 2017)

References

1.  Armenise A, Trerotoli P, Cirone F, et al. Use of recombinant canine granulocyte-colony stimulating factor to increase leukocyte count in dogs naturally infected by canine parvovirus. Vet Microbiol. 2019;231:177–182.

2.  Boscan P, Monnet E, Mama K, et al. Effect of maropitant, a neurokinin 1 receptor antagonist, on anesthetic requirements during noxious visceral stimulation of the ovary in dogs. Am J Vet Res. 2011;72:1576–1579.

3.  Bragg RF1, Duffy AL, DeCecco FA, et al. Clinical evaluation of a single dose of immune plasma for treatment of canine parvovirus infection. J Am Vet Med Assoc. 2012;240:700–704.

4.  Decaro N, Buonavoglia C. Canine parvovirus—a review of epidemiological and diagnostic aspects, with emphasis on type 2c. Vet Microbiol. 2012;155:1–12.

5.  Forbes JM, Bell A, Twedt DC, Martin LE, Lappin MR, Mathis JC, Sullivan LA. Palatability assessment of an oral recuperation fluid in healthy dogs during the perioperative period. Top Companion Anim Med. 2015;30:35–38.

6.  Hodge D 3rd, Delgado-Paredes C, Fleisher G. Intraosseous infusion flow rates in hypovolemic “pediatric” dogs. Ann Emerg Med. 1987;16:305–307.

7.  Li SF, Zhao FR, Shao JJ, et al. Interferon-omega: Current status in clinical applications. Int Immunopharmacol. 2017;52:253–260.

8.  Prittie J. Canine parvoviral enteritis: a review of diagnosis, management, and prevention: J Vet Emerg Crit Care. 2004;4:167–176.

9.  Reineke EL, Walton K, Otto CM. Evaluation of an oral electrolyte solution for treatment of mild to moderate dehydration in dogs with hemorrhagic diarrhea. J Am Vet Med Assoc. 2013;243:851–857.

10.  Savigny MR, Macintire DK. Use of oseltamivir in the treatment of canine parvoviral enteritis. J Vet Emerg Crit Care (San Antonio). 2010;20:132–42.

11.  Tenne R, Sullivan LA, Contreras ET, et al. Palatability and clinical effects of an oral recuperation fluid during the recovery of dogs with suspected parvoviral enteritis. Top Companion Anim Med. 2016;31:68–72.

12.  Van Nguyen S, Umeda K, Yokoyama H, et al. Passive protection of dogs against clinical disease due to canine parvovirus-2 by specific antibody from chicken egg yolk. Can J Vet Res. 2006;70:62–64.

13.  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 (San Antonio). 2017;27:52–65.