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Viral Papillomatosis
Margaret C. Barr, DVM, PhD

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

Dogs and cats, like many other species, are susceptible to Progression to malignant lesions occurs rarely in both
development of papillomatous growths (warts) on the dogs and cats, with some species differences in histologic
skin and mucous membranes. Most of the time, viral features and clinical presentation. Disregulation and
papillomas are benign and transient lesions but they can overexpression of two early genes, E6 and E7, have been
significantly affect the health of an animal if they pro­ linked to the development of PV‐associated squamous
gress to premalignant or malignant neoplastic lesions. cell carcinomas (SCCs).
Canine and feline papillomas and the viruses that cause In most animals, mild inflammation and a cell‐mediated
them share many features and will be discussed together immune response lead to spontaneous regression of papil­
in this chapter. lomas within 6–8 weeks. A humoral immune response
produces antibodies that protect against reinfection with
closely related types of PV. Immunocompromised animals
Etiology/Pathophysiology may develop persistent and generalized papillomatosis
with an increased risk of progression to malignant neo­
Papillomaviruses (PV) are small nonenveloped viruses plastic transformation.
with a circular double‐stranded DNA genome enclosed
in an icosohedral capsid. They belong to the large and
diverse viral family Papillomaviridae, which currently Epidemiology
includes over 280 types of papillomaviruses infecting
most (if not all) mammalian species and many nonmam­ Papillomaviruses infect domestic and wild canids and
malian species. Each PV type demonstrates a strong host felids throughout the world. Although only a few canine
and tissue/site preference, with only a few examples of and feline PV have been sequenced to date, almost 150
interspecies transmission. human PV types have been reported. In general, PVs are
Papillomaviruses replicate in epithelial cells of skin and highly host specific; however, bovine papillomavirus
mucous membranes, beginning their life cycle in the type 1 infection causes equine sarcoid tumors in horses,
basal layer and progressing as the cells mature. Viral and ruminant‐like PVs have been linked to the develop­
assembly and particle release are restricted to the stra­ ment of feline sarcoids.
tum granulosum and stratum corneum. This pattern of Papillomaviruses are transmitted through epidermal
replication is orchestrated by the complex expression of microabrasions or transepidermal inoculation of virus
a series of early and late genes. with contaminated fomites. Because the virus lacks an
Infections are often subclinical, with frequent detec­ envelope, it is relatively resistant to adverse environmen­
tion of papillomavirus DNA in normal skin of healthy tal conditions and difficult to kill with disinfectants.
dogs and cats. The typical presentation of papillomatosis These facts, along with the ubiquity and diversity of PVs,
(cutaneous or oral warts) occurs when high levels of PV make it likely that most animals will be infected at
early gene expression induce rapid expansion of the basal some point in their lives, but there is little information
epithelial cell population followed by cell differentiation, on the prevalence of PV infection in canine and feline
epithelial thickening, hyperkeratosis, and exophytosis. populations.

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