Epidemiology

Gynecologic infections are often asymptomatic in women, and the majority of these infections are transmitted sexually. In 2009, the Centers for Disease Control and Prevention (CDC) reported approximately 19 million new sexually transmitted infections with an estimated cost of $16.4 billion annually.¹ Many cases of sexually transmitted diseases in the United States, such as human papillomavirus (HPV) and genital herpes, are not reported to the CDC.

Epidemiology

The number of reported cases of chancroid in the United States has varied for the past 10 years but remains very low. Only 28 cases were reported domestically in 2009.¹

Pathophysiology

Chancroid, a sexually transmitted disease caused by the short gram-negative bacillus Haemophilus ducreyi, is characterized by painful genital ulcers and painful lymphadenopathy.² The incubation period is 4 to 7 days.

H. ducreyi infection occurs through loss of integrity of the epithelial layer of the skin, most commonly following minor trauma such as sexual intercourse. Once the bacteria have breached the integument, secretion of a cytologically lethal toxin causes apoptosis and necrosis of cells, which results in the characteristic ulcer formation seen with chancroid.

Presenting Signs and Symptoms

H. ducreyi forms a vesicopustule that progresses to a painful ulcer with a necrotic base and surrounding erythema. Because of autoinoculation, multiple lesions may develop.

The adenitis is generally unilateral and tender with overlying erythema. The lesions may become fluctuant and rupture spontaneously. Fever, chills, and malaise may accompany the lymphadenitis. Women may have adenitis without external ulcerative lesions.

Differential Diagnosis and Medical Decision Making

Chancroid must be differentiated from other genital ulcers based on clinical findings. The chancre of syphilis, for example, is clean and painless with a hard base. The diagnosis of chancroid is established by culturing a swab of the lesion onto a specific medium.

The presence of more than one sexually transmitted disease is very common (including syphilis, HSV infection, and human immunodeficiency virus [HIV] infection), as is infection of the ulcer with fusiforms, spirochetes, and other organisms.

Treatment

Several treatment regimens have been recommended and are listed in Box 126.1.^3,4

Epidemiology

The incidence of granuloma inguinale is low, with less than 100 cases reported in the United States per year. The peak demographic of occurrence is in people between the ages of 20 and 40 years who are sexually active.

Pathophysiology

Granuloma inguinale is a chronic granulomatous anogenital infection caused by Calymmatobacterium granulomatis. Granuloma inguinale is primarily a sexually transmitted disease, but gastrointestinal transmission is possible. Its onset is insidious, with a median incubation period of about 50 days.

Presenting Signs and Symptoms

The lesions, which can occur on the skin and mucous membranes of the genitalia or perineal area, are relatively painless nodules that transform into shallow, sharply demarcated ulcers with a red base. The lesions spread by contiguity, and the ulcer then becomes purulent, painful, and foul smelling.

Differential Diagnosis and Medical Decision Making

C. granulomatis is difficult to culture because it is an intracellular parasite. Identification is usually made from scraped material or a biopsy specimen obtained from the periphery of the lesion. Bipolar-staining bacteria are best identified within mononuclear cells (Donovan bodies) by Wright or Giemsa staining. Note that genital ulcers are also caused by syphilis, chancroid, and LGV.

Treatment

See Box 126.2 for treatment.

Follow-up, Next Steps in Care, and Patient Education

Risk for relapse remains a concern for up to 18 months after treatment. Carcinoma (squamous and basal cell variants) is the most concerning sequela of granuloma inguinale and occurs in 0.25% of patients. Lymphatic destruction may result in elephantiasis of the genitals. Increased risk of acquiring HIV infection exists when granuloma inguinale is present.

Epidemiology

HSV is widespread in the United States, with approximately 50 million people infected,⁵ and it is the most common cause of genital ulcers. The overall domestic seroprevalence of subtype 2 (HSV-2) is 16.2%, but infection rates are considerably higher (39.2%) in African Americans.¹ HSV-2 is the most common variant causing genital infections, but subtype 1 (HSV-1) is the causative agent in up to 10% to 15% of all cases.¹

Pathophysiology

Two types of HSV may cause genital herpes: HSV-1 and HSV-2. Once acquired, genital herpes becomes a lifelong infection. Herpes simplex is a DNA virus with an incubation period ranging from 2 to 7 days.⁵ Transmission occurs through exposure to infectious secretions of mucosal surfaces or through skin microabrasions during sexual contact.

Presenting Signs and Symptoms

Of all HSV-2 infections studied, 81.1% were reported to be asymptomatic or were not recognized.⁵ Symptoms usually begin with painful lesions that are often described as burning (Fig. 126.1). These lesions begin as vesicles and then rupture to expose an ulcerated base that persists for 1 to 2 weeks before crusting over and healing without scars. The vesicles and ulcers contain many highly infectious virus particles, and viral shedding occurs until the lesions disappear. Vulvar lesions may last for 3 or more weeks before complete healing. The cervix and vagina may also be involved, with a gray, necrotic cervix and profuse leukorrhea. External dysuria is common, and bilateral inguinal lymphadenopathy is usual.

Fig. 126.1 Primary herpes simplex.

A, Scattered erosions covered with exudate. B, Numerous erosions appeared 4 days after contact with an asymptomatic carrier.

(From Habif TP. Clinical dermatology. 4th ed. Philadelphia: Mosby; 2004.)

The primary episode, defined as genital herpes without antibodies to HSV-1 and HSV-2, is typically associated with systemic symptoms, including headache, fever, malaise, and other flulike symptoms in about two thirds of the cases.

Following primary infection, latent HSV usually localizes in the sacral ganglion and perhaps the dermis. Recurrent attacks tend to be more subtle and are the most frequently seen outbreaks in the emergency department (ED). Recurrence can be precipitated by immunodeficiency, trauma, fever, or sexual intercourse.

Differential Diagnosis and Medical Decision Making

A significant number of patients with the typical signs and symptoms of herpesvirus infection are later found to have syphilis; therefore, screening for treponemal antibodies is an important part of the ED evaluation. The diagnosis of HSV infection can be made clinically if the typical, painful, shallow multiple vulvar ulcers are present. Laboratory confirmation is best attained by polymerase chain reaction (PCR) testing.

Treatment

Treatment of HSV infection is dependent on the onset of clinical symptoms (acute versus recurrent) and their frequency, which determines the need for suppressive therapy (Box 126.3).

Follow-up, Next Steps in Care, and Patient Education

Timely outpatient referral to gynecology should be made. Patients should be informed of the potential for recurrent episodes, as well as the potential for transmission of HSV even when symptoms are not present. Sexual activity should be avoided when active genital lesions or prodromal symptoms are present. In pregnant patients, immediate referral to obstetrics for potential cesarean section to avoid transmission of the virus from mother to fetus should be made if rupture of membranes has occurred. HSV serves as a cofactor in the transmission of HIV.

Epidemiology

LGV is rarely reported in developed countries—perhaps in part because of the lack of a standardized diagnostic test or surveillance requirements. However, outbreaks have been reported in populations of homosexual men in Western Europe and North America since 2003, with the largest cluster of case reports occurring in the United Kingdom and New York City.⁶

Pathophysiology

LGV is an acute or chronic sexually transmitted disease caused by Chlamydia trachomatis types L1, L2, and L3. The disease is acquired during intercourse or through contact with contaminated exudates from active lesions. C. trachomatis enters the system through loss of skin integrity (breaks and abrasions) or by crossing the epithelial cells of mucous membranes and multiplies in regional lymph nodes after lymphatic dissemination. The primary mode of transmission is sexual; however, spread by fomites, nonsexual personal contact, and laboratory accidents has been documented.

Presenting Signs and Symptoms

The most common clinical manifestation of LGV in heterosexuals is tender inguinal or femoral lymphadenopathy (or both), which is typically unilateral. The initial vesicular or ulcerative lesion is transient and often goes unnoticed. Inguinal buboes appear 1 to 4 weeks after exposure and have a tendency to fuse, soften, and break down to form multiple draining sinuses with extensive scarring. In women, genital lymph drainage is to the perirectal glands. Early anorectal manifestations include proctitis with tenesmus and bloody purulent discharge; late manifestations are chronic inflammation of rectal and perirectal tissue. These changes can lead to obstipation, rectal stricture, and occasionally, rectovaginal and perianal fistulas.

Differential Diagnosis and Medical Decision Making

The early lesion of LGV must be differentiated from the lesions of syphilis, genital herpes simplex, chancroid, and granuloma inguinale; lymph node involvement must be distinguished from that caused by tularemia, tuberculosis, plague, neoplasm, or pyogenic infection; and rectal stricture must be distinguished from that secondary to neoplasm and ulcerative colitis.

The complement fixation test may be positive, but cross-reaction with other chlamydiae occurs. Although a positive reaction may reflect remote infection, high titers usually indicate active disease. Specific immunofluorescence tests for immunoglobulin M are more specific for acute infection.

Treatment

Box 126.4 details the treatment regimen for LGV.

Follow-up, Next Steps in Care, and Patient Education

Appropriate treatment should resolve all symptoms and result in no significant sequelae. Patients should be advised to notify sexual contacts to be evaluated for possible infection. Complications of LGV include cervicitis, perimetritis, salpingitis, fistula development, and rectal stricture.

Epidemiology

Rates in women increased from 0.8 case per 100,000 in 2004 to 1.4 cases per 100,000 in 2009 despite a previously decreasing incidence.¹

Pathophysiology

Syphilis is a systemic, sexually transmitted disease caused by the spirochete Treponema pallidum. It can also be acquired congenitally. The risk for transmission following sexual exposure depends on many factors and is estimated to be about 30%.⁷ T. pallidum causes infection after traversing mucous membrane surfaces or denuded skin and then extending systemically through hematogenous and lymphatic routes.

Presenting Signs and Symptoms

Syphilis can be seen in the ED in any of the four stages through which untreated syphilis can pass. Primary infection is manifested as a single, painless ulcer, usually within 3 weeks but sometimes 2 to 3 months after infection. The labia and vaginal walls are most often affected; however, lesions can also occur on the cervix (Fig. 126.2). Secondary syphilis is associated with a characteristic maculopapular generalized rash on the palms and soles and may include components of arthralgia, pharyngitis, and lymphadenopathy. This stage is typically seen 4 to 10 weeks after the initial appearance of a chancre. Infectivity can occur in the first two stages (up to 2 to 4 years following infection).

Fig. 126.2 Primary syphilis with a chancre in the vagina.

The lesions are painless and may never be detected.

The third stage—the asymptomatic latent phase—may last many years. It is defined as syphilis characterized by seroreactivity without other evidence of disease.

The fourth stage—tertiary syphilis—has numerous neurologic, cardiovascular, and other systemic effects and develops in about 25% of untreated patients.⁶

Differential Diagnosis and Medical Decision Making

The diagnosis of syphilis should be considered in any patient with an ulcerative lesion in the genital area, as well as in patients with unexplained rashes, arthralgia, and neurologic or systemic complaints.

Screening includes the rapid plasma reagin and Venereal Disease Research Laboratory tests, which must be followed by confirmatory testing when positive. If the serologic results are nonreactive and spirochetes cannot be demonstrated by darkfield examination, the serologic tests should be repeated in 1 month.

Treatment

Penicillin remains the mainstay of treatment across the board (Box 126.5). According to the CDC guidelines, parenteral penicillin is considered to be the only treatment documented to be efficacious in pregnancy.³ Treatment with penicillin is the same as for the corresponding stage of syphilis in nonpregnant women. For pregnant patients who are allergic to penicillin, tetracycline and doxycycline are contraindicated. Pregnant patients who are allergic to penicillin should be skin-tested and desensitized.

The Jarisch-Herxheimer reaction, caused by massive release of treponemal antigens and manifested by fever, headache, and myalgias, can occur in any patient in the first 24 hours following initiation of therapy and is observed most often in patients with early syphilis (frequently in those with secondary syphilis). Because this reaction in pregnant women may precipitate early labor or cause fetal distress, these patients should be hospitalized for monitoring. Concern for this reaction should not prevent or delay therapy. Systemic glucocorticoids administered 12 hours before or concurrent with antibiotics may minimize the effects, and antipyretics have been used for supportive care.

Follow-up, Next Steps in Care, and Patient Education

Quantitative serologic tests should be performed in patients with syphilis to monitor the results of treatment. Sexual contacts must be notified and evaluated for possible infection. All patients with syphilis should be tested for HIV to assess for possible coinfection. Delay in diagnosis during pregnancy past 20 weeks’ gestation should prompt fetal ultrasound to rule out congenital syphilis.

Epidemiology

Although the range is wide, depending on the population, prevalence rates for bacterial vaginosis (BV) have been estimated to be 4% to 40%. However, because Gardnerella vaginalis is present in 50% to 70% of asymptomatic women, the exact incidence of BV is difficult to estimate.⁸

Pathophysiology

BV is a polymicrobial infection that results from replacement of the normal Lactobacillus species in the vagina by high concentrations of the anaerobic G. vaginalis, Mycoplasma hominis, and Mobiluncus curtisii. It can be a precursor infection to upper genital tract extension, including cervicitis and pelvic inflammatory disease (PID). Infection is related to the Lactobacillus concentration and changes in pH within the vaginal vault but remains primarily multifactorial.

Presenting Signs and Symptoms

Clinical signs include a thick, homogeneous, milky vaginal discharge sometimes with a fishy odor. Usually, no other symptoms are present.