Genital lesions can be a cause of great alarm and anxiety in patients, especially when noticed after sexual intercourse for the first time or after sexual intercourse with a new partner. A good number of young men are obsessed with their genitals during puberty and will inspect their genitalia frequently. This can be a source of anxiety for the young adolescent who may be under the impression that he has been plagued by an STD.

Familiarity with normal genital anatomy and physiology is essential to be able to recognize normal anatomic variants and processes. Patients often present with worries about their own genitals, such as size, shape, retractibility of the prepuce and the distribution of pubic hair, as well as questions about vaginal/penile discharge. The normal variants of genital morphology are listed in Table 13-2 (Figs. 13-1 to 13-5).

Condyloma acuminatum (CA) derives its origin from the Greek word “kondylos” meaning knob or knuckle. It is the most common STD with a 1% incidence in sexually active adults. The CDC reports that at least 50% of sexually active
adults are affected at some point in their lives. The risk of disease increases with the number of lifetime sexual partners. CA is associated with infections by the human papilloma virus (HPV). In the 1970s, the association between HPV infections and cervical cancer was first recognized. However, more recently, it has become apparent that certain specific “high-risk” HPV types are more closely associated with the development of cervical cancer.

Similar to verruca vulgaris, CA is caused by infection with HPV. HPV infects the proliferating basal keratinocytes, causing upregulation of the cell cycle and dysregulated cellular proliferation. This results in the characteristic hyperkeratotic, exophytic lesions.

As mentioned, HPV types 16, 18, 31, 33, and 45 are “high-risk” HPV types, associated with an increased risk of cervical cancer. Of these types, HPV 16 and 18 are the most common cause of cervical cancer. It is not clear why these particular HPV types are oncogenic, although it is thought that when this HPV type DNA integrates into host DNA, it inhibits specific cellular proteins (E6 and E7 proteins). The E6 and E7 proteins normally regulate p53 and pRb genes; their inhibition results in dysregulated cell division and oncogenic potential.

CA are typically soft, papillated exophytic growths located in the anogenital region (perineum and perianally); the external genitalia (labia, shaft of the penis, scrotum) (Fig. 13-11); or the adjacent areas (inguinal fold, mons pubis). They are usually skin-colored or pink and lack the thick hyperkeratotic surface of common warts. Early small lesions may be easily missed during a routine examination; larger lesions can be easily recognized. Many patients have subclinical infection and may be unaware that they can spread HPV. Patients with a pre-existing sexually transmitted infection are at increased risk for disease. Although nonsexual transmission is possible (such as during the passage through an infected vaginal canal during birth), when found in children it is imperative to look for signs of sexual abuse.

Soft, moist, pink- or flesh-colored papular eruptions with normal surrounding skin are typically present. However larger nodular growths or plaques may also be seen. In males, the shaft of the penis and the prepuce are the most commonly affected sites. The labia and the posterior fornix are the most commonly affected sites in women. Individuals participating in anal intercourse may have warts around the anal region.

The diagnosis is based on clinical findings. However, if in doubt, 3% to 5% acetic acid can be applied with a cotton swab to look for whitening of the lesion. Aceto-whitening can also help to identify affected areas not easily apparent to the naked eye. If still uncertain, a biopsy can be performed for a more definitive diagnosis. A biopsy may also be indicated if there is any suspicion of malignant change. In women, a Papanicolaou smear should be performed. Anoscopy is recommended for patients with anal lesions. A workup for other STDs may be warranted depending on the clinical history and physical findings.

Many cases of CA are subclinical, with significant multifocal infection with HPV. As a result, high rates of recurrence are noted regardless of which therapeutic modality is utilized. Therapeutic options are broadly divided into locally destructive and immunomodulators.

Safe sexual practice is key in preventing CA, as skin-to-skin transmission is the main route of transmission. Male latex condoms confer some protection, but skin-to-skin transmission may still be possible. In 2006, a vaccine (Gardasil®) was approved for use in female patients between the ages of 9 and 26. The vaccine protects against HPV types 6, 11, 16, and 18 and is most effective if administered prior to initial engagement in sexual activity. HPV 6 and 11 have been shown to cause approximately 90% of all cases of benign CA. HPV 16 and 18 are associated with approximately 70% of all cervical cancers. Thus, this vaccine not only protects against the high-risk HPV types, but also the most common low-risk HPV types. The vaccine requires three injections over a 6-month period. Common side effects include injection site pain, bruising, fever, vomiting, and syncope. While the vaccine can help prevent primary infection in HPV naïve patients, it does not have a role in the treatment of patients previously infected with HPV.