Disease Genital Ulcer.

Essentials of Diagnosis of Disease  Genital Ulcer.
 Diagnosis is based on the finding of one or more mucocutaneous ulcers involving the genitalia, perineum, or anus.
 Careful inspection of all genital mucosa is important, as lesions may be inside the foreskin, labia, vagina, or rectum, and may be painless.
 Genital herpes is the most common cause, followed by syphilis.
 A specific pathogen often cannot be identified based on clinical findings alone; laboratory testing should include culture or polymerase chain reaction (PCR) amplification for herpes simplex virus (HSV), and serologic testing for syphilis.
 Despite appropriate testing, no pathogen is identified in up to 50% of patients.

General Considerations
Genital ulcer disease (GUD) is a syndrome characterized by ulcerating lesions on the penis, scrotum, vulva, vagina, perineum, or perianal skin. In general usage the term refers to genital ulcerations from a sexually transmitted disease (STD), which is the most common etiology; however, nonsexually acquired illnesses, including infectious (bacterial skin infections, fungi) or noninfectious etiologies (fixed drug eruption, Behçet syndrome, sexual trauma), can present with similar ulcers. The clinician should bear in mind that nonvenereal dermatoses (eg, psoriasis) resulting from a variety of causes also can present with anogenital lesions.

The annual global incidence of GUD probably exceeds 20 million cases. The most commonly identified pathogens are HSV types 1 and 2 (HSV-1, HSV-2), syphilis, and chancroid. As recently as 20 years ago, the predominant causes of GUD in much the developing world were bacterial pathogens, especially Haemophilus ducreyi, the etiologic agent of chancroid. However, since the early 1990s the prevalence of chancroid in sub-Saharan Africa has decreased dramatically, while HSV-2 infection has increased. Although this change may be related to more widespread use of antibiotics and syndromic treatment of STDs, the HIV epidemic and behavioral changes in response may have played an equally important role. As a result, genital herpes now constitutes the most common infectious cause of GUD worldwide.

Regardless of the cause, GUD has assumed increased importance in view of its well-recognized role in facilitating HIV transmission. Surveys of HIV prevalence among patients seeking treatment for STDs have found a higher prevalence of coexisting HIV infection in those with genital ulcers than in those without, both in the United States and in the developing world. The presence of GUD in an individual not infected with HIV makes that person more susceptible to HIV infection by breaching the integumentary barrier and by recruiting macrophages and T-helper cells to the genital tract, where they may more readily be infected. Conversely, GUD in an HIV-infected individual increases his or her likelihood of transmitting HIV to a sex partner. HIV-infected patients with GUD who present for care at STD clinics actually have a higher plasma HIV viral load than similar patients without GUD. In a 2001 study of 174 HIV-serodiscordant couples in Uganda, the presence of GUD was associated with an almost fourfold increase in the probability of HIV transmission. A similar magnitude of increased risk of HIV acquisition (hazard ratio of 3.8) was associated with new onset of HSV-2 infection in the prior 6 months in a cohort of over 2700 patients in Pune, India.

Gray RH, Wawer MJ, Brookmeyer R, et al. Probability of HIV-1 transmission per coital act in monogamous, heterosexual, HIV-1-discordant couples in Rakai, Uganda. Lancet 2001; 357:1149–1153. (The landmark study documenting the role of GUD and HIV viral load in transmission risk.) [PMID: 11323041]

 
Paz-Bailey G, Rahman M, Chen C, et al. Changes in the etiology of sexually transmitted diseases in Botswana between 1993 and 2002: Implications for the clinical management of genital ulcer disease. Clin Infect Dis 2005;41:1304–1312. (A good account of the changes in GUD etiology over a 10-year period in a representative sub-Saharan African county.) [PMID: 16206106]

 
 
Prevention

Risk Counseling
The mainstay of prevention of GUD, as for prevention of STDs in general, is risk reduction counseling. Topics of counseling include limiting the number of sex partners, use of condoms (either male or female), and regular testing for asymptomatic disease. However, there are some ways in which GUD differs from other STDs. For example, condom use is somewhat less efficacious in preventing GUD. Because causative pathogens may be transmitted by skin-to-skin contact, contact with skin that is not covered by a condom may transmit infection. Furthermore, patients may only put on a condom preparatory to penetrative sex, whereas transmission may occur via nonpenetrative contact. Finally, despite counseling messages, few patients routinely use condoms for oral sex. Some patients engage more frequently in oral sex than in anal or vaginal penetrative sex, perceiving oral sex as a lower risk activity. However, the three most common pathogens implicated in GUD (HSV-2, HSV-1, and Treponema pallidum) can be transmitted efficiently by oral sex, a fact that may be underappreciated by patients.

Chemoprophylaxis
Among other potential prevention strategies, chemoprophylaxis is available for genital herpes in the form of daily suppressive medication such as acyclovir. Daily suppressive therapy not only reduces the frequency and severity of herpes outbreaks, but also reduces asymptomatic viral shedding and transmission. This strategy may be appropriate for many patients and is discussed in more detail in Chapter 14. In many parts of the developing world where bacterial pathogens are prevalent, mass anti-infective treatment of populations has been attempted as a prevention strategy.

Circumcision
Interest has recently been raised in circumcision as a possible strategy for prevention of HIV infection, and large, well-controlled studies in Africa have demonstrated significant reductions in infection rates among circumcised versus uncircumcised adults. Because some ulcerative diseases (eg, chancroid) are more common in uncircumcised men and tend to occur in the preputial sulcus and inside surface of the prepuce, circumcision may also provide some protection against these diseases; however, this hypothesis has not been studied, and the magnitude of any protective effect is unknown.
 
Clinical Findings

History
In the diagnosis of GUD, the first consideration is whether or not the condition is sexually acquired; that is, whether a potential sexual exposure has occurred. Thus, an accurate sexual history is essential to diagnosis and management. Many clinicians may not readily elicit a sexual history in busy clinical practices, and many patients are unwilling to broach the subject of their sexual practices if they are not fully comfortable with their health care provider. Nevertheless, because accurate information about potential sexual exposures is essential to a diagnosis, it is incumbent on any health care provider who sees sexually active patients to become proficient in this area of history taking. Details about obtaining an accurate sexual history are found in Chapter 31.

Once a potential sexual route of infection has been established, the history can sometimes help differentiate between different pathogens. The interval between a high-risk sexual exposure and the onset of symptoms may suggest the diagnosis. A primary genital herpes infection most often produces symptoms within a week of exposure. Symptoms of primary syphilis generally appear after 2–3 weeks, and more uncommon pathogens may have a longer incubation period. The patient's description of the initial stages of the lesion (eg, as small blisters [vesicles]) may be helpful; however, these earlier stages may not have been noticed by the patient, particularly if the lesions are in an area that is difficult for the patient to inspect, such as the perineum, labia majora or minora, or perianal region. In addition, patients may not reliably distinguish an initial lesion as papular, vesicular, or pustular; thus, the patient's description is frequently not contributory. A history of travel to an endemic area may increase the likelihood of a more exotic pathogen, such as chancroid or donovanosis.

If sexually acquired GUD has been ruled out, a more detailed history may be helpful in pointing toward certain less common diagnoses. An appropriate exposure history in an endemic area, for example, may suggest tularemia; likewise, a history of oral ulcers can suggest Behçet syndrome, an uncommon disease of unknown etiology whose hallmarks are recurrent oral and genital ulcers. However, most of the nonvenereal causes of genital ulceration are less common than sexually transmitted GUD. As a general rule, whenever there is doubt as to the etiology, it is safest to assume that genital ulcers are sexually acquired. Even a highly experienced provider with expertise at obtaining an accurate sexual history will frequently be given unreliable information about sexual risk.

Symptoms and Signs

Description of Ulcer(s)
Classic textbook descriptions would have the clinician believe that herpes, syphilis, and chancroid can be easily distinguished on the basis of physical presentation and symptoms. In fact, diagnosis of specific etiologies of GUD on the basis of clinical presentation alone is often impossible. Nevertheless, it is helpful to be familiar with the "textbook" distinguishing characteristics, which are summarized in Table 4–1. Important findings to note include whether the ulcer is single or multiple, painless or painful, tender or nontender, and indurated or soft. The base of the ulcer may be necrotic (as in chancroid) or clean (as in a syphilitic chancre); it may appear shallow or have raised or rolled margins. The location of the ulcers also should be noted, because conditions such as chancroid are most often confined to the prepuce and glans in men and the labia majora and minora in women. Ulcers seen on the scrotum in men or the cervix in women should raise suspicion for herpes or syphilis. 

Lymphadenopathy
The presence of inguinal lymphadenopathy can provide a clue to the etiology of GUD. Enlarged inguinal lymph nodes are a common finding in many ulcerating conditions. In primary genital herpes the enlarged lymph nodes are frequently tender, whereas the classic adenopathy of syphilis is firm and nontender. Less common diseases such as chancroid and lymphogranuloma venereum usually present with tender, fluctuant inguinal lymph nodes (buboes). In lymphogranuloma venereum the primary ulcer may be transient, and lymphadenopathy, most often unilateral, is the predominant finding. The lymph nodes in patients with lymphogranuloma venereum become large and matted, and may erode through the skin to produce draining sinus tracts. Donovanosis, described in more detail below (see Differential Diagnosis), is one of the few causes of genital ulcer disease that does not characteristically include inguinal lymphadenopathy, although it can produce firm subcutaneous swellings called pseudobuboes.

Systemic Findings
Physical examination should include a thorough inspection of the oral cavity and a general skin examination. The presence of fever, malaise, headaches, or other constitutional findings in conjunction with a genital ulcer strongly suggests either primary genital herpes or a nonvenereal systemic disease such as Behçet syndrome or tularemia. In general, primary syphilis, chancroid, donovanosis, and the ulcerative stage of lymphogranuloma venereum are not associated with systemic symptoms. Rarely, a chancre will persist until the onset of secondary syphilis.

Laboratory Testing
Because clinical findings are not reliable for diagnosis of GUD, the appropriate choice of diagnostic tests and collection of samples is critical. Even in optimal circumstances, however, laboratory testing may fail to produce a diagnosis. In fact, in research studies of GUD, laboratory investigation fails to identify a pathogen in up to one third of cases.

Darkfield Microscopy
The most reliable way of diagnosing a syphilitic chancre at the time of presentation is to identify live treponemes in a microscopic examination of the ulcer exudate, using darkfield microscopy. The organisms are abundant and have a characteristic appearance and motility. Visualizing spirochetes from a genital ulcer is pathognomonic for primary syphilis; darkfield examination of oral or intrarectal ulcers must be interpreted with more caution, because they may be contaminated by commensal spirochetes that are part of the resident flora.

Although visual inspection using darkfield examination is a mainstay of classic venereology, this test is no longer practical for most clinicians, because accurate visual identification of treponemes requires some experience, and most clinicians have not performed enough of these examinations to be proficient. Additionally, most clinical practices do not have access to darkfield microscopy.

Serology
Serologic testing for syphilis is the major method by which syphilis is diagnosed and comprises a generally inexpensive nontreponemal screening test (eg, rapid plasma reagin, RPR), with reactive tests confirmed by a more specific treponemal assay, such as the fluorescent treponemal antibody absorbed (FTA-ABS) or T pallidum particle agglutination (TP-PA) assay. Although highly sensitive for syphilis in secondary and early latent disease, syphilis serologies may be nonreactive in a large proportion of acute, primary infections. Furthermore, previous syphilis infection can confound the diagnosis, because positive findings on both the RPR and treponemal tests can persist for long periods of time despite successful treatment. Finally, syphilis may coexist with other causes of GUD; therefore, serologic testing for syphilis should be performed in all patients presenting with GUD, even if an alternative diagnosis is strongly suspected, unless such testing has been done recently.

The measurement of changes in syphilis serologic responses is helpful in differentiating recurrent from chronic infections. Individuals in whom serial syphilis serologies do not decrease by at least fourfold within 6 months after appropriate clinical treatment may be diagnosed with recurrent infection, if the clinical history is corroborative. In some individuals serologic responses remain reactive more than 6 months after successful antitreponemal therapy, a condition referred to as "serofast." These individuals are generally at low risk for recurrent infection and may have other predisposing conditions (eg, HIV infection or autoimmune diseases).

Serologic testing for type-specific HSV antibodies can be helpful in supporting a diagnosis of genital herpes. However, because 30–40% of genital herpes infections are caused by HSV-1, the absence of HSV-2 antibodies does not rule out such infections. Furthermore, although the presence of HSV antibodies can support the diagnosis, it cannot rule out other proximate causes or distinguish between active genital herpes and prior history of genital herpes. HSV antibody testing thus plays very little role in the etiologic diagnosis of GUD.

Viral Culture
HSV-1 and HSV-2 are easily grown in cell culture, and with current technology a presumptive positive culture can be read in as little as 2 days. However, viral culture is of limited sensitivity in later disease and is not likely to be positive after crusting or scabbing of lesions has occurred. Nevertheless, given its ease of performance and high positive predictive value, viral culture should be considered a test of first choice for diagnosis of genital herpes, especially in patients in whom the etiology is not obvious.

Nucleic Acid Amplification Tests
A PCR assay has been developed for the detection of HSV DNA from a genital ulcer swab. This assay can be performed in real time, with results often available within hours, and can distinguish HSV-1 from HSV-2. PCR is at least as sensitive as viral culture and is clearly superior to culture later in the course of genital herpes disease after lesions have ulcerated. Drawbacks of the test include cost and availability; although most commercial laboratories perform HSV PCR.

Biopsy
If an etiology has not been determined by other laboratory testing and an ulcer has failed to respond to empiric antimicrobial therapy directed against the most likely pathogens, a biopsy may be appropriate. Besides identifying a causative agent, a biopsy of a nonhealing ulcer should be pursued to rule out cancer. When donovanosis is suspected, a crush preparation can be examined to look for the characteristic Donovan bodies in cells from the ulcer base. For this purpose, a scraping, curettage, or excisional biopsy specimen is crushed between two glass slides, then air-dried and stained.

Bacterial Culture
H ducreyi is fastidious and not easily grown in culture; however, a bacterial culture using select media is still recommended if chancroid is suspected, because isolation of H ducreyi in culture establishes the diagnosis with certainty. Although antibiotic resistance is not common in chancroid, bacterial culture also permits confirmation of antimicrobial susceptibility. Nevertheless, a negative culture should not be relied upon to exclude chancroid. Other bacterial causes of GUD (syphilis, lymphogranuloma venereum, donovanosis) are not routinely diagnosed by culture.

Gram Stain
A swab of the exudative base of a suspected chancroid ulcer can also be examined with Gram stain for the presence of typical gram-negative coccobacilli. This test is also less useful for the practicing clinician than might be hoped; Gram-negative bacilli of a variety of morphologies may be seen from superficially colonized or secondarily infected wounds, and the textbook "school of fish" arrangement that is considered suggestive of chancroid on Gram stain requires interpretation by a microscopist familiar with the disease.

Tzanck Preparation
A Tzanck preparation is a scraping from the base of a skin lesion, smeared on a slide and stained with Giemsa or Wright stain. The presence of multinucleated giant cells establishes the causative agent as a herpesvirus. In real-world settings most clinical practices are not set up for same-day preparation and interpretation of Tzanck smears. In addition, the sensitivity of a Tzanck smear diminishes considerably after vesicular lesions have ulcerated. For these reasons, and with the availability of technologies such as shell vial culture and PCR, which permit rapid diagnosis of genital herpes, the Tzanck preparation has no role in the diagnosis of GUD.
 
Differential Diagnosis

The differential diagnosis of GUD includes the previously described sexually transmitted pathogens, as well as several other causes of ulcerative disease.

Genital Herpes
A history of similar episodes of genital ulcers in the past suggests a diagnosis of genital herpes, as does a sex partner with known genital herpes. Most often the ulcers of genital herpes are tender and shallow; they also may be multiple and clustered. If the typical clusters of small vesicles are seen on external genital skin or mucosa the diagnosis is obvious; however, patients often present for care after ulceration has occurred. Men with penile or scrotal herpes are more likely to present with vesicles still intact, whereas in women, vaginal or vulvar disease is often ulcerative and frequently associated with discharge. Primary genital herpes is often significantly painful and accompanied by constitutional symptoms such as fever, malaise, and headaches, but these symptoms are usually absent from recurrent episodes. The diagnosis of GUD resulting from HSV may be made by a positive viral culture or PCR test.

Syphilis
As mentioned, a disproportionate number of cases of primary and secondary syphilis occur among men who have sex with men (MSM), particularly among those who are infected with HIV. Indeed, virtually all of the increase in primary and secondary syphilis incidence in the United States over the past decade is probably attributable to infection among MSM; the rate of primary and secondary syphilis has actually decreased among women. Thus, a history of male-male sexual activity or HIV infection in a patient with GUD increases the likelihood of syphilis.

The classic chancre of primary syphilis is a single painless, nontender, indurated ulcer, with a clean base, a heaped-up or "rolled" margin, and accompanying inguinal adenopathy. Although all of these descriptors are true in general, many cases are atypical in appearance. For instance, multiple chancres may occur, especially in HIV-infected patients. Furthermore, up to 30% of chancres are described as painful. It is also important to remember that many causes of GUD are relatively painless when the vagina or cervix is involved, and supposedly painless ulcers can become secondarily infected with staphylococci or other bacteria and become tender when first brought to clinical attention. The clinician who has access to a darkfield microscope can examine ulcer exudate after abrading the ulcer (the preferred diagnostic test for primary syphilis). Otherwise he or she must rely on clinical impression and serologic testing, which is negative in approximately 30% of patients with chancres. Finally, a patient with GUD from another cause may have a positive serologic response for syphilis because of preexisting undiagnosed latent syphilis.

Chancroid
Chancroid is rare in the United States (54 cases were reported in 2003, mostly in the Southeast), and it usually occurs in the setting of a sporadic outbreak. It shows a striking male-to-female predominance, on the order of 10:1, although this may be due to greater identification of disease in men. In the developing world, chancroid is associated with intercourse with commercial sex workers. In contrast to genital herpes and syphilis, untreated chancroid ulcers can persist for many months.

In the United States, patients with chancroid typically seek care for an ulcer that has been present for 1–3 weeks. Chancroid ulcers are usually painful, generally larger than chancres or herpes lesions, and likely to be multiple. The "soft chancre" of chancroid is classically described as well circumscribed and nonindurated, with ragged edges and a necrotic base with purulent exudate, which bleeds when scraped. If the constellation of a painful genital ulcer with associated tender lymphadenopathy is seen, the diagnosis of chancroid can be made with some confidence. In fact, this "classic" presentation occurs in fewer than half of patients. Diagnosis is best established by obtaining a swab for culture on selective medium (notify the testing laboratory that chancroid is suspected), or presumptively in patients with a typical presentation in the setting of a local outbreak.

Lymphogranuloma Venereum
Lymphogranuloma venereum is caused by three serotypes (L1, L2, and L3) of Chlamydia trachomatis, and its presentation varies depending on the site of infection. Rectal lymphogranuloma venereum was recently reported in MSM in the Netherlands and has now been identified in some gay communities in the United States. However, rectal lymphogranuloma venereum almost never presents with external ulcers. Infection on the male external genitalia is characterized by a small, transient ulcer in the earliest phase of illness; subsequently very large, tender inguinal lymphadenopathy and constitutional symptoms predominate. In cases of rectal or female genital involvement, the infection drains to pelvic lymph nodes, and inguinal lymphadenopathy is usually not apparent.

Only about 10% of patients with lymphogranuloma venereum present with a complaint of a genital ulcer, which has usually resolved by the time the patient seeks care. Diagnosis can be made by a positive culture or molecular testing of appropriate clinical specimens for C trachomatis in the setting of an appropriate syndrome. Some laboratories can analyze an isolate to confirm that it is a lymphogranuloma serotype or genotype, but a presumptive diagnosis can be made merely by isolating C trachomatis from a lesion in a patient with a typical presentation.

Donovanosis
Donovanosis, a rare condition also known as granuloma inguinale, is caused by infection with the gram-negative bacterium Calymmatobacterium granulomatis. It is endemic to certain geographic "hot spots," most notably Papua New Guinea and parts of South Africa, as well as Australia, Brazil, and parts of the Caribbean. Donovanosis is rarely reported in the United States. The typical ulcerative form of donovanosis is beefy red and bleeds easily when touched. The lesions of donovanosis may also be hypertrophic, often raised above the surrounding skin, and can become dry and verrucous in appearance. In its exuberant hypertrophic form, donovanosis can be mistaken for carcinoma, tuberculosis, or condylomata lata. It is generally not painful. "Kissing lesions" (ie, on areas of the skin in contact with each other, such as bilateral labia) or autoinoculation of other body sites may occur. The lesions of donovanosis do not resolve unless treated appropriately.

O'Farrell N. Donovanosis. Sex Transm Infect 2002;78:452–457. (An excellent review of an uncommon disease.) [PMID: 12473810]

 

Cancer
Although the vast majority of genital ulcers are not neoplastic, cancers and premalignant lesions may present as GUD and can carry considerable morbidity and mortality if not diagnosed early. Thus, all practitioners should be able to recognize a suspicious lesion. A large percentage of squamous cell carcinomas of the vulva, vagina, and penis are associated with human papillomavirus infection, as are virtually all cervical and anal squamous cell cancers. Thus, the patient with a history of sexually transmitted infections may be at increased risk of genital malignancy. A prior history of an abnormal Pap smear or anogenital warts may be helpful but is not always present in such cases. Physical findings suggestive of cancer include hyperpigmentation, tenderness, and induration. If the provider does not have the capability of performing a detailed examination under high magnification (ie, colposcopy) and biopsy in the office, patients with these findings should be referred to an experienced surgeon expeditiously.

Other Causes of Genital Ulcers

Fixed Drug Eruption
A fixed drug eruption is a localized skin lesion that occurs in response to a medication, generally an oral medication that is used intermittently. Fixed drug eruptions may involve any part of the skin, and the genitalia are sometimes affected They are most often solitary, well-circumscribed plaques, but they occasionally become ulcers, which may be painful and may mimic genital herpes. The most common genital sites of involvement are the glans and shaft of the penis. Tetracyclines and nonsteroidal anti-inflammatory drugs have been implicated in this regard, as have less commonly used medications such as hydroxyurea and foscarnet.

Behcet Syndrome
Behcet syndrome is an idiopathic inflammatory multisystem disease characterized by oral and genital ulcerations and ocular disease. The genital lesions of Behçet syndrome are painful except when the vagina or cervix is involved, and they tend to heal with scarring. Although these lesions may be confused with genital herpes, the diagnosis can be made by taking note of the multisystem nature of the disease.

Other Genital and Systemic Infections
Severe candidiasis can lead to skin breakdown and should be considered in the differential diagnosis. In addition to specific genital infections, several systemic illnesses can present with genital ulcers, including infections such as tuberculosis, histoplasmosis, and tularemia. Tularemia acquired from a tick bite may present with an ulcer in the genital region, perineum, or lower trunk (reflecting the site of inoculation) and inguinal adenopathy. The ulcer of tularemia is frequently tender and has a raised border. When it occurs on the genitalia it can be confused with syphilis, lymphogranuloma venereum, or chancroid. Genitourinary tuberculosis is well known historically but rarely presents with lesions mimicking STDs; in women, an ulcerating mass may be seen on the cervix, and in men, a painful mass in the scrotum may be associated with a draining sinus.

Primary HIV Infection
Patients with primary HIV infection frequently present with a constellation of symptoms that may include oral and genital ulcers in up to 15% of cases. Although the presence of mucocutaneous ulcers in the setting of a recent exposure to an HIV-infected source is considered highly predictive of acute HIV disease by some experts, ulcers are not the predominant manifestation of this disease. More common signs and symptoms are most often present in acute HIV infection, including fevers, sweats, malaise, lymphadenopathy, and an evanescent maculopapular eruption.

Sexual Trauma
External genital ulcers occur occasionally in men due to sexual trauma (eg, vigorous masturbation, biting during fellatio, etc) or nonsexual injury. The etiology may be obvious to the patient and can often be elicited by taking a sensitive and thorough history. Likewise, women may have internal genital ulcerations after a traumatic sexual assault.
 
Complications
Although genital ulcers are not generally life-threatening, some of the pathogens of GUD are associated with significant complications if untreated. The sequelae of untreated syphilis are considered elsewhere (see Chapter 19). Perhaps the gravest complication of GUD, overall, is its role in facilitating HIV infection. Given the high prevalence of HIV coinfection in patients with GUD, all such patients should be strongly counseled to undergo testing for HIV.

Scarring, Strictures, and Genital Deformity
Untreated chancroid can result in phimosis, balanoposthitis, and formation of fistulous tracts or nonhealing ulcers from draining buboes. Lymphogranuloma venereum that is not treated early in the course of the infection can progress to scarring, rectal strictures, genital deformity and fistula formation. Donovanosis is a progressive destructive granulomatous infection that can result in considerable tissue destruction and deformity if untreated.

Systemic Complications

Both lymphogranuloma venereum and donovanosis can spread systemically if not treated promptly. Systemic spread of lymphogranuloma venereum is most common in women and may result in arthritis, ocular disease, aseptic meningitis, hepatitis or perihepatitis, or pulmonary disease. Donovanosis can involve multiple organs, including viscera and bone.
 
Treatment
When no pathogen has been identified, the provider may have to resort to empiric treatment. It is probably wisest to treat for both HSV and syphilis in such circumstances. Additional coverage for the more exotic pathogens should be added only if suggested by the patient's history. Table 4–2 summarizes preferred and alternative treatments for the most common causes of GUD. Laboratory "test of cure" is not required except for syphilis, where the RPR should be repeated to confirm a decline in titer (if positive initially). However, it is advisable to follow up cases of chancroid, lymphogranuloma venereum, and donovanosis clinically to confirm an appropriate response to therapy.

 ^aFirst-line treatment.

When to Refer to a Specialist

Evaluation by a dermatologist or infectious disease specialist is warranted when diagnostic tests for HSV, T pallidum, and H ducreyi have been negative, particularly if the patient has failed to respond to empiric anti-infective therapy directed toward these common pathogens. Early referral is particularly important if cancer is suspected; a patient with an ulcerating lesion that is raised or indurated, especially if also painful, should be referred promptly for biopsy if the lesion does not respond to anti-infective treatment.
 
Prognosis

With appropriate treatment, GUD is always either treatable or curable. Some causes of GUD (syphilis, lymphogranuloma venereum, chancroid, and donovanosis) may have long-term complications if untreated.
 
Practice Points

 As a general rule, whenever there is doubt as to the etiology, it is safest to assume that genital ulcers are sexually acquired.
 When no pathogen has been identified, the provider may have to resort to empiric treatment. It is probably wisest to treat for both HSV and syphilis in such circumstances. 

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