Primary genital herpes is characterized by multiple painful, grouped vesicles or ulcerative and crusted external genital lesions on an erythematous base (see Table 116-2). Infemales the cervix is also involved. Symptoms may includeregional lymphadenopathy, discharge, and dysuria. Primaryillness lasts 10 to 20 days with recurrences in 50% to 80% ofpatients. Secondary, recurrent, or reactivation eruptions are not as dramatic and are not associated with systemicsymptoms. In primary infection, viral shedding lasts 1 to2 weeks, and the entire course from vesicle and ulcer onset resolves over 16 to 20 days. In recurrent disease, virus shedding lasts for less than 7 days, and the course resolves over8 to 10 days. Many persons experience five to eight recurrences per year. Some primary and many recurrent episodesare asymptomatic.
Viral cultures and PCR are the preferred methods of diagnosis; culture typically shows cytopathic effect in 1 to 3 days and seldom takes longer than 5 days. PCR assays have increased sensitivity over culture. Viral shedding is intermittent after primary infection, so both culture and PCR can fail to detect latent infection. Serologic testing is useful for primary infection only (to show seroconversion between acute and convalescent sera), and positive serologies persist lifelong. Titers are not helpful in guiding management of recurrences.
Oral famciclovir and valacyclovir are effective treatments in reducing the severity and duration of symptoms in primary cases and may reduce recurrences. Once-daily suppressive therapy reduces the frequency of genital herpes recurrences by 70% to 80% among patients who have frequent recurrences (more than six recurrences per year). Local hygiene and sitz baths may relieve discomfort. The use of condoms provides some protection against sexual transmission of HSV.
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Trichomoniasis is caused by the protozoan T. vaginalis and often is associated with other STIs such as gonorrhea and Chlamydia. Infection is asymptomatic in as many as 90% of men and 85% of women. Symptomatic males can have urethritis. Symptomatic females have vaginitis with thin, malodorous, frothy yellow-green discharge, vulvar irritation, and cervical “strawberry hemorrhages” (see Table 116-3). Diagnosis is based on visualization of motile, flagellated protozoans in the urine or in a saline wet mount, which has a sensitivity of only 60% to 70% among symptomatic women. Culture is the most sensitive method of diagnosis. Treatment of both sexual partners with oral metronidazole or tinidazole in a single dose is recommended.
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HPV, the cause of genital warts (condylomata acuminata), is the most common STI in the United States with the highest prevalence rates among 15to 24-year-olds. Most HPV infections are asymptomatic or subclinical. HPV types 6 and 11 cause 90% of genital warts and are nononcogenic. HPV types 16 and 18 are associated with 70% of cases of cervical cancer. HPV types 31, 33, and 35 are also oncogenic.
Genital warts can occur on the squamous epithelium or mucous membranes of the genital and perineal structures of females and males (see Table 116-4). Genital warts are usually multiple, firm, gray-to-pink excrescences. Untreated genital warts may remain unchanged, increase in size or number, or resolve spontaneously. They can become tender if macerated or secondarily infected. The diagnosis usually is established by appearance without biopsy. The differential diagnosis includes condylomata lata (secondary syphilis) and tumors.