Human Papillomavirus: Anogenital Infections
ICD-9: 079.4 ○ ICD-10: B97.7
Mucosal human papilloma virus (HPV) infections are the most common sexually transmitted infection (STIs) seen by the dermatologist. Only 1–2% of HPV-infected young, sexually active persons have any visibly detectable clinical lesion.
HPV present in the birth canal can be transmitted to a newborn during vaginal delivery and can cause external genital warts (EGW) and respiratory papillomatosis.
Warts. Barely visible papules to nodules to confluent masses occurring on anogenital skin or mucosa and oral mucosa. EGW: External genitalia, perineum. Cervix. Oropharynx.
Dysplasia of anogenital and oral skin and mucosa ranging from mild to severe to squamous cell carcinoma (SCC) in situ (SCCIS). Invasive SCC can arise within SCCIS. Most commonly in cervix, anal canal
Etiology and Epidemiology
HPV is DNA papovavirus that multiplies in the nuclei of infected epithelial cells (see Section 27). More than 20 types of HPV can infect the genital tract: types 6, 11 most commonly. Types 16, 18, 31, 33, and 35 are strongly associated with anogenital dysplasia and carcinoma. In persons with multiple sexual partners, subclinical infection with multiple HPV types is common.
Risk Factors for Acquiring HPV Infection
Number of sexual partners/frequency of sexual intercourse. Sexual partner with HPV anogenital infection. Infection with other STIs.
Through sexual contact: genital– genital, oral–genital, genital–anal. Microabrasions occur on epithelial surface allowing virions from infected partner to gain access to basal cell layer of noninfected partner.
Most sexually active individuals are subclinically infected with HPV; most HPV infections are asymptomatic, subclinical, or unrecognized. 1% of sexually active adults (15–19 years of age) develop clinical lesions.
“Low-risk” and “high-risk” HPV types both cause anogenital infections. HPV infection may persist for years in a dormant state and becomes infectious intermittently. Exophytic warts are probably more infectious than subclinical infection. Immunosuppression may result in new extensive HPV lesions, poor response to treatment, increased multifocal intraepithelial neoplasia. All HPV types replicate exclusively in host’s cell nucleus. In benign HPV-associated lesions, HPV exists as a plasmid in cellular cytoplasm, replicating extrachromosomally. In malignant HPV-associated lesions, HPV integrates into host’s chromosome, following a break in the viral genome (around E1/E2 region). E1 and E2 function is deregulated, resulting in cellular transformation.
Usually asymptomatic, except for cosmetic appearance. Anxiety of having STI. Obstruction if large mass is uncommon.
Four clinical types of genital warts occur:
Small papular (Fig. 30-1...