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Canine Viral Enteritis
Margaret C. Barr, DVM, PhD

College of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, USA

Dogs are susceptible to several viral diseases that present hematopoietic cells. Perinatal infection with CPV‐2 can
with gastrointestinal signs either as the primary com- result in cardiac myofiber lysis and multifocal necrosis.
plaint or as a component of multisystemic disease.
Canine parvovirus type 2 (CPV‐2) is the most common Epidemiology
cause of viral enteritis in dogs, but enteric canine coro-
navirus (CCoV) and canine distemper virus must also be
considered as possible viral etiologies. Canine rotavirus Canine parvovirus is closely related to feline parvovirus
causes diarrhea in neonatal puppies, similar to type A and similar viruses of wild carnivores, such as mink
rotaviruses in other animal species. A multitude of other enteritis virus and raccoon parvovirus. Since its emer-
viruses, including two newly discovered viruses of dogs, gence and worldwide spread in domestic and wild canids
canine kobuvirus and dog circovirus, have been identi- in the mid‐late 1970s, CPV‐2 has mutated to form anti-
fied in some cases of canine enteritis. genic variants CPV‐2a, CPV‐2b, and CPV‐2c, which are
Because CPV‐2 is the most clinically relevant of the all defined by amino acid changes in the major capsid
canine enteric viruses, this section will focus on its char- protein, VP2. Although CPV‐2 is unable to infect cats,
acteristics, pathogenesis, and management. Table 82.1 subsequent variants have expanded host ranges and can
provides a comparison of CPV‐2 with some of the other replicate in feline cells.
canine enteric viruses. The main route of infection for CPV‐2 (as with most
other enteric viruses) is through oral or nasal contact with
feces or feces‐contaminated material. In utero transmis-
sion of CPV‐2 can also occur. The small compact size and
Etiology/Pathophysiology nonenveloped structure of the virus make it highly resist-
ant to inactivation by environmental conditions and easily
Canine parvovirus is a small single‐stranded, nonenvel- transmitted on fomites. Infected animals shed the virus in
oped DNA virus that infects and replicates in a variety of high concentrations beginning around day 4 of infection
rapidly dividing cells. Entry into the host cells depends on and can continue to shed for several days after the resolu-
interaction between the major capsid protein of the virus, tion of clinical signs. Parvovirus is rarely detected in the
VP2, and the transferrin receptor on the cell surface. Initial feces of healthy dogs with no history of enteritis.
replication usually occurs in the oropharyngeal lymphoid At least in some regions, there is a distinct seasonality
tissues, followed by viremia and systemic replication in to the occurrence of parvovirus enteritis, usually peaking
other lymphoid tissues, leukocyte precursors in the bone in late summer to early fall.
marrow, and intestinal crypt epithelial cells. Clinical signs
may appear as early as four days after exposure but more
typically occur about a week after infection. Signalment
Pathologic findings include gastrointestinal inflamma-
tion and hemorrhage predominantly in the small intestine, While male and female dogs of all ages are susceptible
with characteristic crypt cell destruction and severe villous to infection, CPV‐2 is most significant as a cause of
atrophy. The virus also causes lymphoid depletion, thymic gastroenteritis in puppies 6 weeks to 6 months of age.
lymphocytolysis, and mitotic arrest of bone marrow Puppies become susceptible to infection as maternally
Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical