Genital ulcer disease manifests as a breach in the skin or mucosa of the genitalia, usually caused by a sexually transmitted infection. Of these infections, herpes simplex virus type 2 (HSV-2) is the most common etiology in most geographic areas, followed by syphilis and chancroid. The most important noninfectious cause is Behçet’s disease.
The mechanisms by which ulcers are produced by pathogens are incompletely understood, and there are different mechanisms of injury depending on the pathogen. In chancroid, a cytotoxin secreted by Haemophilus ducreyi may be important in epithelial cell injury.
Although the various lesions may have a characteristic appearance, it is important to note that local epidemiology is an important consideration because lesions may appear in an atypical fashion. The appearance of the ulcer, whether it is painful, and the nature of the associated lymphadenopathy may be clues in the etiology of the ulcer. Figure 74–1 shows several vesicles on the shaft of the penis of a patient with genital herpes. The vesicular lesions are typically painful. The vesicles can then progress to form shallow ulcers. Figure 74–2 shows the chancre of primary syphilis. It is a painless lesion with a shallow base and a firm, rolled edge. Table 74–1 describes the important clinical features of genital ulcer lesions, their diagnostic procedures, and treatment.
Genital herpes caused by herpes simplex virus 2. Note group of vesicles on shaft of penis. (Reproduced with permission from Wolff K, Johnson R, Saavedra A. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology. 7th ed. New York, NY: McGraw-Hill Education; 2013.)
Chancre of primary syphilis caused by Treponema pallidum. Note shallow ulcer with clean base and rolled edge. (Reproduced with permission from Kang S, Amagai M, Bruckner AL, et al. Fitzpatrick’s Dermatology in General Medicine. 9th ed. New York, NY: McGraw-Hill Education; 2019.)
TABLE 74–1Genital Ulcers: Clinical Features, Diagnosis, and Treatment ||Download (.pdf) TABLE 74–1 Genital Ulcers: Clinical Features, Diagnosis, and Treatment
|Syndrome ||Pathogen ||Appearance of Ulcer ||Pain ||Adenopathy ||Diagnosis ||Treatment |
|Genital herpes ||HSV-2 (more common than HSV-1) ||Multiple, small vesicles and ulcers with an erythematous base ||Painful ||Tender lymphadenopathy ||Direct fluorescent antibody (DFA) testing and/or viral culture; sample taken from the base of the ulcer; Tzanck smear shows multinucleated giant cells; nucleic acid amplification test (NAAT) may be useful ||Acyclovir, famciclovir, valacyclovir |
|Syphilis ||Treponema pallidum ||Single (usually) indurated ulcer with a clean base; self-resolves and may not be observed ||Painless ||Painless, regional lymphadenopathy; lymph nodes feel “rubbery” ||Serologic screening with nontreponemal test (e.g., rapid plasma reagin [RPR] or Venereal Disease Research Laboratory [VDRL]); treponemal test (e.g., fluorescent treponemal antibody absorption [FTA-ABS]) for confirmation; dark field examination of fluid from the lesion if possible ||Benzathine penicillin G |
|Chancroid ||Haemophilus ducreyi ||Multiple, nonindurated ulcers with a gray or yellow exudate at the base ||Very painful ||Tender, unilateral inguinal lymphadenopathy; lymph nodes may rupture ||Difficult to diagnose; special culture media, if available, or polymerase chain reaction (PCR) ||Azithromycin |
|Lymphogranuloma venereum ||Chlamydia trachomatis serovars L1–3 ||Small, shallow ulcers that self-resolve and are not usually observed ||Painless ||Characteristic appearance of lymph nodes is key feature; may be bilateral, large, and painful; presents with fluctuant “buboes” and sinus tracts ||NAAT; serology can also be used ||Doxycycline |
|Granuloma inguinale (donovanosis) ||Klebsiella granulomatis ||Marked, beefy red, vascular ulcer with granulomatous appearance and rolled edges ||Painless ||Not a major feature; subcutaneous granulomas, “pseudobuboes” may occur ||Difficult to diagnose; PCR if available; may also see dark-staining oval organisms on Giemsa staining (Donovan bodies) of biopsy specimen ||Doxycycline |
Common infectious etiologies of genital ulcer disease include HSV-2 (causing genital herpes) and T. pallidum (causing primary syphilis) primarily, as well as H. ducreyi (causing chancroid). Less common causes of genital ulcers include C. trachomatis serovars L1–3 (causing lymphogranuloma venereum) and Klebsiella granulomatis (causing granuloma inguinale, also known as donovanosis).
A thorough sexual and medical history, followed by the physical examination, are important for diagnosis. Although clinical characteristics can be very helpful, there is often overlap in presentation, and there may also be multiple syndromes copresenting. Therefore, diagnostic testing is highly recommended. This typically includes the following tests at the initial visit: direct fluorescent antibody (DFA) test for HSV antigens, viral culture for HSV, or nucleic acid amplification methods for HSV DNA using a specimen taken from the base of the ulcer, and syphilis serologic testing (e.g., rapid plasmin reagin, RPR) using a serum sample. Testing for other sexually transmitted diseases including human immunodeficiency virus (HIV) is also important because there is often cotransmission of multiple pathogens (see Table 74–1).
The drug of choice for genital herpes is acyclovir or one of its derivatives, famciclovir or valacyclovir. Primary and secondary syphilis are treated with a long-acting penicillin, benzathine penicillin G. The drug of choice for chancroid is azithromycin, whereas for lymphogranuloma venereum, it is doxycycline (see Table 74–1).
Empiric treatment is often used before diagnostic tests return. As for most sexually transmitted infections, treatment that involves one dose and that is observed is preferred if possible.
Consistent use of condoms is an important measure that can prevent genital ulcers. In some cases, primary prevention of HSV infection can be undertaken by treatment of the negative partner in serodiscordant couples with acyclovir or one of its derivatives. Prophylaxis with these drugs can be effective in preventing recurrences of HSV outbreaks in patients who have had frequent occurrences, especially among those who are immunosuppressed. Partner notification and treatment are important prevention strategies as well. There is no vaccine against any of the organisms that cause genital ulcer disease.