Porth's Essentials of Pathophysiology, 4e

1050

Genitourinary and Reproductive Function

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Infections of the External Genitalia

producing the various HPV-proliferative lesions. 5 The incubation period for HPV-induced genital warts ranges from 6 weeks to 8 months, with a mean of 2 to 3 months. Genital warts typically present as soft, raised, fleshy lesions on the external genitalia, including the penis (Fig. 41-1), vulva, scrotum, perineum, and perianal skin. External warts may appear as small bumps, or they may be flat, rough surfaced, or pedunculated. Less commonly, they can appear as smooth reddish or brown raised papules or as dome-shaped lesions on keratinized skin. Internal warts are cauliflower-shaped lesions that affect the mucous membranes of the vagina, urethra, anus, or mouth. They may cause discomfort, bleeding, or painful intercourse. 6 Although warts can be a disturbing clinical feature of HPV infection, subclinical infection is common. Approximately 70% of women with HPV become HPV DNA negative within 1 year, and as many as 91% of them become negative within 2 years. 1 Many women with transient HPV infections develop atypical squa- mous cells of undetermined significance (ASC-US) or low-grade squamous intraepithelial lesions (LSILs) of the cervix as detected on a Pap test, colposcopy, or biopsy (see Chapter 40). In men, transient HPV infection may be associated with intraepithelial neoplasia of the penis and anus. 1 Although many individuals will clear the virus and become negative within 1 to 2 years, it is unclear if development of an effective immune response completely clears the infection. In some individuals the virus may remain dormant for years and reactivate at a later time. While some of these later lesions may be reactivations, others may be re-infections from an affected partner.

Sexually transmitted infections can selectively infect the mucocutaneous tissues of the external genitalia, rectum, and oral pharynx, or produce both genitourinary and systemic effects. These infections include condylomata acuminata, genital herpes, chancroid, and lymphogran- uloma venereum. Human Papillomavirus Infection and Genital Warts Genital warts (condylomata acuminata) are caused by the human papillomavirus (HPV) that infects epithelial cells and can cause a number of benign and malignant growths. 2–8 Although recognized for centuries, HPV- induced genital warts have become one of the fastest- growing STIs of the past decade. The Centers for Disease Control and Prevention (CDC) estimates that 360,000 million Americans are currently infected with the HPV. 3 Etiology and Pathogenesis Transmission of HPV is usually through skin-to-skin contact, most often through penetration (oral–genital, manual–genital, and genital–genital contact). HPV can also be transmitted though nonsexual routes including mother to newborn (vertical transmission) and fomites (objects such as clothing, towels, or utensils that har- bor the agent). Prevention of HPV transmission through condom use has not been adequately demonstrated. Most HPV infections are asymptomatic and transient, and resolve without treatment. In some cases, how- ever, HPV infection results in genital warts, abnormal Papanicolaou (Pap) test abnormalities, or, rarely, cervical cancer. Human papillomaviruses are nonenveloped dou- ble-stranded deoxyribonucleic acid (DNA) viruses that cause proliferative lesions of the squamous epithelium. 1,2 Human papillomavirus is species specific, meaning it only affects humans. 2 More than 100 distinct HPV subtypes have been identified, over 40 of which affect the ano- genital area. 2–6 These subtypes are routinely classified into low-risk and high-risk categories. Low-risk types such as HPV 6 and 11 are typically associated with genital warts. Types 16, 18, 31, 33, and 45 are considered to be high risk because of their association with cervical dysplasia and cervical cancer. Of the high-risk types, HPV 16 and 18 account for approximately two thirds of cervical can- cer. 2 Only a subset of women infected with HPV go on to develop cervical cancer, however, suggesting that even the most virulent HPV strains may vary in terms of their oncogenic potential. Cofactors that may increase the risk for cancer include smoking, immunosuppression, and exposure to hormonal alteration (e.g., pregnancy, oral contraceptives). 2 Human papillomavirus infection begins with viral inoculation into squamous epithelial cells, where infec- tion stimulates replication of the squamous epithelium,

FIGURE 41-1. Condylomata of the penis. Raised circumscribed lesions are seen on the shaft of the penis. (From Damjanov I, McCue PA.The lower urinary tract and male reproductive system. In: Rubin R, Strayer DS, eds. Rubin’s Pathology: Clinicopathologic Foundations of Medicine. 6th ed. Philadelphia, PA:Wolters Kluwer Health | LippincottWilliams &Wilkins; 2012:825.)