ISSN 2398-2969      

Mouth: viral papilloma

icanis
Contributor(s):

David Godfrey

John Munday

Synonym(s): Oral papillomatosis; canine oral warts


Introduction

  • Cause: canine papillomavirus type 1 (formerly canine oral papillomavirus).
  • Signs: multiple exophytic discrete papillomas (warts) in the mouth.
  • Diagnosis: clinical diagnosis, histology rarely required.
  • Treatment: surgical excision of larger lesions if causing clinical signs. No medical treatment has proven efficacy.
  • Prognosis: excellent. Papillomas in overwhelming majority of dogs spontaneously resolve within 6 weeks. Occasional cases can take longer. Very rarely papillomas are persistent and there are isolated reports that oral papillomas could progress to oral squamous cell carcinoma.

Pathogenesis

Etiology

Predisposing factors

General
  • Exposure to dogs with oral papillomas may predispose to disease, although this is usually only observed in larger dog colonies.
  • Dogs that have recovered from oral papillomas are protected from further papilloma development and this disease is seen in young dogs that have not been previously exposed to the papillomavirus.
  • Immunosuppression will not usually predispose to disease development, but may allow the development of a greater number and size of the lesions and may delay spontaneous regression.

Pathophysiology

  • Microtrauma in the oral cavity allows canine papillomavirus type 1 access to the basal cells of the epithelium.
  • The papillomavirus infects basal cells and, as part of a productive infection, stimulates massive hyperplasia of keratinocytes.
  • This hyperplasia causes marked thickening of the epidermis.
  • The thickened epidermis folds resulting in an exophytic lesion within the mouth.
  • The characteristic 'cauliflower' appearance of the papillomas is caused by the irregular folding of the hyperplastic epithelium.
  • Early in the infection, the dog produces antibodies against canine papillomavirus type 1. Although these antibodies prevent additional papilloma development, they do not cause papilloma regression.
  • Papilloma regression is dependent on a cell-mediated immune response which develops after a variable amount of time.
  • Once the cell-mediated immune response has been initiated, papilloma regression is rapid.
  • The dog is subsequently protected from papilloma development, although some evidence suggests a high proportion of dogs continue to have sub-clinical infection by canine papillomavirus type 1.

Timecourse

  • Experimental infection reveals the incubation period is 4-8 weeks.
  • The typical time to regression of the papillomas is also 4-8 weeks.
  • However, regression in some cases can take as long as 6 months.
  • In humans, around a quarter of cutaneous viral papillomas take over a year before spontaneous regression and even when persistence of the papillomas is prolonged, eventual regression should still be expected.

Epidemiology

  • The epidemiology of infection is poorly understood.
  • Currently it is believed that both dogs with oral papillomas and those without visible papillomas can shed the infectious virus particles.
  • The rate of shedding of papillomavirus from a dog with visible papillomas is much higher than a dog without oral papillomas.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Lange C E, Favrot C (2011) Canine papillomaviruses. Vet Clin North Am Small Anim Pract 41 (6), 1183-1195 PubMed.
  • Lange C E, Zollinger S, Tobler K et al (2011) Clinically healthy skin of dogs is a potential reservoir for canine papillomaviruses. J Clin Microbiol 49 (2), 707-709 PubMed.
  • Favrot C, Olivry T, Werner A H, Nespecca G, Utiger A, Grest P, Ackermann M (2005) Evaluation of papillomaviruses associated with cyclosporine-induced hyperplastic verrucous lesions in dogs. Am J Vet Res 66 (10), 1764-1769 PubMed.
  • Ghim S, Newsome J, Bell J et al (2000) Spontaneously regressing oral papillomas induce systemic antibodies that neutralize canine oral papillomavirus. Exp Mol Pathol 68 (3), 147-151 PubMed.
  • Nicholls P K, Klaunberg B A, Moore R A et al (1999) Naturally occurring, nonregressing canine oral papillomavirus infection: host immunity, virus characterization, and experimental infection. Virology 265 (2), 365-374 PubMed.
  • Bell J A, Sundberg J P, Ghim S J et al (1994) A formalin-inactivated vaccine protects against mucosal papillomavirus infection: a canine model. Pathobiology 62 (4), 194-198 PubMed.
  • Sundberg J P, Smith E K, Herron A J et al (1994) Involvement of canine oral papillomavirus in generalized oral and cutaneous verrucosis in a Chinese Shar Pei dog. Vet Pathol 31 (2), 183-187 PubMed.
  • Watrach A M, Small E, Case M T (1970) Canine papilloma: progression of oral papilloma to carcinoma. J Natl Cancer Inst 45 (5), 915-920 PubMed.

Other sources of information

  • Head K W, Else R W, Dubielzig R R (2002)Tumors of the alimentary tract.In: Meuten D J ed.Tumors in Domestic Animals. 4th edn. Iowa State Press, United States of America.

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