Infections of the Genital Tract
Sangini Sheth
Jean M. Keller
INFECTIONS OF THE LOWER GENITAL TRACT
Symptoms caused by infections of the lower genital tract are among the most common presenting complaints of gynecologic patients. This chapter reviews the following: vulvar infections, parasitic infections, ulcerative lesions, vaginitis, cervicitis, and pelvic inflammatory disease (PID). Urinary tract infections are covered in Chapter 16.
Vulvar Infections
Human Papillomavirus
Human papillomavirus (HPV) infection is the most common sexually transmitted disease (STD) in the United States, with an estimated 80% of sexually active women having acquired genital HPV by the age of 50 years. Most HPV infection is asymptomatic or subclinical, with the majority of patients clearing the infection within 2 years.
There are over 100 types of HPV, of which approximately 30 are mucosal and can infect the lower genital tract in women. HPV types 6 and 11 cause condyloma acuminata or genital warts. HPV can be classified as low-, intermediate-, and highrisk for the development of squamous cell carcinoma, with the majority of cervical cancer caused by HPV types 16 and 18 (see Chapter 45).
HPV prevalence is highest among 20- to 24-year-olds. Risk factors for HPV infection include number of sexual partners, history of other sexually transmitted infections (STIs), smoking, and immune deficiency such as HIV or use of immunosuppressive medications.
Signs and symptoms of genital warts include soft, sessile, and/or verrucous lesions on any mucosal or dermal surface that range in size and formation. Lesions are
usually multifocal and asymptomatic, although itching, burning, bleeding, vaginal discharge, and pain can occur.
Diagnosis: Genital warts are usually diagnosed by gross inspection, and colposcopic examination may aid in the identification of cervical or vaginal lesions. HPV testing is not warranted for the diagnosis of genital warts and results would not alter management. Biopsy is recommended if there is no response to standard therapy; the lesions worsen with therapy; there are hyperpigmented, indurated, fixed, ulcerated, bleeding, or atypical lesions; if the patient is immunocompromised; or if the diagnosis is uncertain. Condyloma acuminatum must be differentiated from the lesion of secondary syphilis, condyloma lata.
Treatment: Treatment is indicated for cosmetic benefit and to address symptoms. There are multiple modalities for the treatment of genital warts, including surgical excision, application of topical cytotoxic or keratolytic agents, cytodestructive techniques, and immune modulators. No single treatment method has been shown to be optimal and therefore treatment should be based on patient preference and provider experience. Clinical factors to consider in choosing a treatment modality include anatomic location, size, morphology, and number of lesions. Additional factors that might influence treatment choice include cost of treatment, convenience, and side effects. Lesions may spontaneously regress and recur. A combination of approaches may be required. No therapy can ensure complete eradication of the virus and it remains unclear whether treatment reduces further transmission (Table 28-1). Most lesions resolve within 3 months of treatment; however, recurrence rates range from 30% to 70%.
Complications from treatment include hypo- or hyperpigmentation of treated areas with ablative or immune-modulating modalities. Rarely, abnormal scarring or chronic pain can occur.
Prevention: Two types of HPV vaccine are licensed by the U.S. Food and Drug Administration (FDA). Cervarix is a bivalent vaccine that protects against HPV types 16 and 18, which accounts for 70% of all cervical cancer. Gardasil is a quadrivalent vaccine against types 16 and 18, as well as types 6 and 11 found in 90% of genital warts. The HPV vaccine is recommended for female patients 9 to 26 years old and male patients 9 to 21 years old but can be given up to 26 years of age. Vaccination does not replace routine cervical cancer screening. See also Chapters 45 and 46.
Molluscum Contagiosum
Molluscum is a benign poxvirus infection of the skin found worldwide but is most common in the developing world. It is spread by skin contact (sexual or nonsexual), autoinoculation, and fomites. The incubation period ranges from several weeks to months.
Signs and symptoms include the appearance of dome-shaped papules with central umbilication ranging from 2 to 5 mm in diameter. Multiple lesions may arise but generally are fewer than 20. The lesions are usually asymptomatic but occasionally pruritic and may become inflamed and swollen. They are usually self-limited, lasting for 6 to 12 months, but may take as long as 4 years to resolve.
Diagnosis: The characteristic appearance of molluscum contagiosum lends itself to clinical diagnosis by gross inspection. When in doubt, a crush preparation (i.e., microscopic examination of white, waxy material expressed from a nodule) can be performed. Intracytoplasmic eosinophilic inclusion bodies (molluscum bodies) inside keratinocytes confirm the diagnosis. Immunocompromised patients with HIV/AIDS or other conditions can develop giant lesions (>15 mm in diameter) and large numbers of lesions that may be resistant to standard therapy.
TABLE 28-1 Treatment Options for Genital Warts
Therapy
Application
Clearance Rate (%)
Recurrence Rate (%)
Use in Pregnancy
Patient applied
Imiquimod 5% cream
Apply three times a week at bedtime for up to 16 wk. Wash the area with soap and water 6-10 hr after application.
40-77
5-19
Contraindicated
Podofilox 0.5% solution or gel
Apply bid for 3 d, no treatment for 4 d; repeat the cycle for up to four times. Do not exceed 10 cm2 area of treatment or 0.5 mL volume of podofilox per day.
68-88
16-34
Contraindicated
Sinecatechins 15% ointment
Apply three times daily (0.5 cm strand to each wart) until complete resolution of warts (do not exceed 16 wk of treatment). Do not use in immunosuppressed patients or those with clinical genital herpes or open wounds.
54-57
10
Contraindicated
Provider administered
Podophyllin resin at 10%-25% in benzoin
Can be repeated one or two times weekly, as needed
38-79
21-65
Contraindicated
5-Fluorouracil epinephrine gel
Intralesion injection weekly for up to 6 wk
61
50-60
Interferons
Inject at the edge of and beneath the wart with a 26- to 32-gauge needle.
36-53
21-25
Not recommended
Topical trichloroacetic acid or bichloroacetic acid (80%-90% solution)
Apply small amount one or two times weekly until the wart sloughs off. Typical course is six treatments.
81
36
Permitted
Excisional procedures
Electrocautery or sharp excision may be employed.
89-93
19-22
Only if obstructing vaginal delivery
Cryotherapy with liquid nitrogen
Can be repeated one or two times weekly until resolved
70-96
25-39
Permitted
CO2 laser excision
72-97
6-49
Not recommended
bid, twice a day.
From Workowski KA, Berman S; Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2010. MMWR Recomm Rep 2010;59(RR-12):1-110, with permission.
Treatment: Molluscum contagiosum is usually self-limited. Multiple regimens have been evaluated in clinical trials, with none being convincingly efficacious. Many practitioners employ watchful waiting. Treatment should be considered, however, in immunosuppressed individuals and those with sexually transmitted lesions that risk infecting their partners. Lesion visibility and patient preference may prompt therapy, which consists of evacuation of the core material with cryofreezing, curettage, or laser ablation.
Parasites
Pediculosis Pubis
An ectoparasite, Phthirus pubis is usually restricted to the pubic, perineal, and perianal areas but may infect the eyelids and other body parts. It can be transmitted sexually or via close contact through shared bedding or clothing. The parasite deposits eggs at the base of the hair follicle. The incubation period is 1 week and the crab louse lives for about 6 weeks but dies within 24 hours without blood.
Symptoms of infection include intense pruritus in the affected area, sometimes accompanied by maculopapular lesions. Occurrence of a large number of bites over a short period may lead to systemic manifestations, such as mild fever, malaise, or irritability.
Diagnosis is made by gross visualization of lice, larvae, or nits in the pubic hair or microscopic identification of crablike lice under oil.
Scabies
Scabies is caused by the mite Sarcoptes scabiei var. hominis. It is transmitted via prolonged close contact (sexual or nonsexual) and may infect any part of the body, especially flexural surfaces of the elbows, wrists, finger webs, axilla, genitals, and buttocks.
Fomite transmission is considered possible through clothing, bedding, or towels. The adult female burrows beneath the skin, lays eggs, and travels quickly across the skin. Crusted or Norwegian scabies is highly infectious and is an aggressive infestation in immunodeficient, debilitated, or malnourished persons, and is associated with increased treatment failure.
Symptoms include the insidious onset of severe intermittent pruritus approximately 3 to 6 weeks after the initial exposure. Subsequent infections can become symptomatic within 24 hours of reinfection. The intense pruritus may worsen at night and include most of the body. The characteristic lesion is the burrow, a 1- to 10-mm curving track that serves to house the mite. Other lesions include papules and vesicles.
Diagnosis can often be made clinically based on history and gross appearance of the burrows. Skin scrapings can be obtained for microscopic examination under oil.
Treatment (Table 28-2) for pediculosis pubis and scabies requires an agent that kills both adult organisms and eggs. Treatment should include decontamination of clothing and bed linens with dry cleaning or machine washing and drying with hot cycle. Treat pruritus with antihistamines.
Toxic effects of lindane include seizures and aplastic anemia. This agent is not recommended for use in pregnant or lactating women, children younger than age 2 years, or patients with extensive dermatitis.
TABLE 28-2 Treatment Options for Parasites | ||||||||||||||||||||||||||||||
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Genital Ulcers
The most common infectious causes of genital ulcers in young, sexually active women are herpes simplex virus (HSV) and Treponema pallidum (syphilis). Less common causes include chancroid and donovanosis. Genital herpes is the most prevalent. All of these lesions are associated with increased risk of HIV acquisition. A patient presenting with genital ulcers should be evaluated for syphilis, herpes, and Haemophilus ducreyi in areas where chancroid is prevalent, as well as HIV if status is unknown.
Genital Herpes
At least 50 million people in the United States have HSV-2 genital herpes, a chronic STI. Multiple types of herpesvirus have been identified. Historically, HSV-2 accounts for the majority of genital infections; however, HSV-1 now accounts for up to 50% of first-episode cases. HSV-1 genital infections are less likely to recur
and less commonly result in asymptomatic viral shedding. The majority of persons infected with HSV-2 remain undiagnosed and intermittent viral shedding accounts for most HSV transmission.
Clinical diagnosis of genital herpes is both insensitive and nonspecific. The classic presentation of multiple, painful, vesicular, or ulcerative lesions is absent in many patients. Herpetic outbreaks can last as long as 2 to 6 weeks in a first-episode primary infection and up to 7 days in recurrent outbreaks. Classically, lesions are preceded by vulvar paresthesias or pruritus, followed by the formation of multiple vesicles that coalesce into ulcerations, which may be painful. Outbreaks are selflimiting, and lesions heal without scar formation. The prodrome of itching or burning in the affected area is important for counseling patients on when to start antiviral therapy because systemic symptoms are usually absent. The majority of patients with HSV-2 will experience recurrent outbreaks in the first year with declining frequency over time. Patients should be counseled that asymptomatic shedding of virus with possible transmission to sexual partners can occur in the absence of outbreaks.
Diagnosis: Clinical suspicion is based on history and the appearance of lesions. Obtain laboratory confirmation with type-specific virologic and serologic testing. Documentation of HSV-1 or HSV-2 is useful for prognosis and counseling.
Virology: Cell culture and polymerase chain reaction (PCR) testing are preferred for diagnosis of HSV. Sensitivity of cell culture is low, especially with recurrent lesions or those that have begun to heal. PCR is becoming more common due to its increased sensitivity. Viral culture isolates should be typed to determine HSV-1 or HSV-2; lack of HSV detection by culture or PCR does not prove absent infection because viral shedding is intermittent.
Serology can confirm clinical suspicion in the absence of a positive culture; antibodies develop within weeks of infection. Type-specific assays that differentiate glycoprotein 1 (HSV-1) from glycoprotein 2 (HSV-2) are recommended. The presence of HSV-2 antibodies is predominantly seen in genital infections and patients should therefore be counseled as such. HSV-1 antibodies, however, may be the result of childhood transmission although genital transmission is growing.
Treatment (Table 28-3)
Systemic antiviral therapy for HSV may reduce symptoms and complications of infection. Medical management does not eradicate the virus or reduce the frequency or severity of recurrences after medication is stopped. Primary genital herpes outbreaks should be treated with antiviral therapy, as patients are at increased risk for severe or prolonged symptoms.
Episodic treatment for recurrent herpes should be initiated within 1 day of lesions or during prodromal period.
Suppressive therapy can reduce recurrence in up to 80% of patients. Daily suppressive therapy with valacyclovir 500 mg a day has been shown to decrease HSV-2 transmission in discordant, heterosexual couples.
Recurrences will decrease over time regardless of suppressive therapy, so providers should address continued suppressive therapy yearly.
Severe or complicated disease should be treated with intravenous acyclovir (5 to 10 mg/kg every 8 hours for 2 to 7 days or until clinical improvement is observed followed by oral therapy to complete 10-day course).
Topical antiviral therapy has not shown any benefit and is not recommended.
The virus cannot be completely eradicated and remains latent in the cell bodies of sacral nerves S2, S3, and S4.
TABLE 28-3 Treatment for Genital Herpes
Stage
Treatment
Duration
Primary outbreak— outpatient
Acyclovir, 400 mg PO tid
Acyclovir, 200 mg PO five times a day
Famciclovir, 250 mg PO tid
Valacyclovir, 1 g PO bid
7-10 d
Episodic recurrences (begin treatment with prodrome or within 1 d of lesion outbreak)
Acyclovir, 400 mg PO tid
Acyclovir, 800 mg PO tid
Acyclovir, 800 mg PO bid
Famciclovir, 125 mg PO bid
Famciclovir, 1 g PO bid
Valacyclovir, 1 g PO qd
Valacyclovir, 500 mg PO bid
5 d
2 d
5 d
5 d
1 d
5 d
3 d
Daily suppression therapy
Acyclovir, 400 mg PO bid
Famciclovir, 250 mg PO bid
Valacyclovir, 500 mg PO qd
Valacyclovir, 1 g PO qd
Per day
Recommended regimens in persons with HIV
Acyclovir, 400 mg PO tid
Famciclovir, 500 mg PO bid
Valacyclovir, 1 g PO bid
5-10 d
5-10 d
5-10 d
PO, orally; tid, three times a day; bid, twice a day; qd, every day.
From Workowski KA, Berman S; Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2010. MMWR Recomm Rep 2010;59(RR-12):1-110, with permission.
An effective HSV vaccine is not yet available.
All women with genital herpes should be counseled on the natural history of HSV, sexual and perinatal transmission risks, and ways to reduce transmission.
Complications include herpes encephalitis (rare but potentially life-threatening) and urinary tract infection (which can cause urinary retention or severe pain).
Counseling: Patients should be advised to remain abstinent from the onset of prodromal symptoms until complete reepithelialization of lesions. Couples should discuss the role of suppressive therapy in decreasing transmission risk. Counseling should be appropriate to the HSV type.
During pregnancy, women with primary HSV should be treated with antiviral therapy. Perinatal transmission is possible, and therefore, cesarean delivery is recommended for women with active lesions or prodromal symptoms of genital HSV at delivery. The risk of perinatal HSV transmission is high among women who acquire HSV near time of delivery and low for those with recurrent herpes. Many providers prescribe suppressive therapy for pregnant women with a history of genital herpes beginning at 36 weeks’ gestation. Also see Chapter 11.
Syphilis
The spirochete T. pallidum causes the systemic disease syphilis. The disease is contagious only when mucocutaneous lesions are present. This occurs through contact with a chancre, condyloma lata, or mucosal lesion. The organism can penetrate skin
or mucous membranes, incubating over a period of 10 days to 3 months. Syphilis has a complex course characterized by the immunologic response to the spirochete.
Syphilis is divided into overlapping stages: primary, secondary, neurologic, and tertiary based on clinical findings to guide treatment and follow-up. Latent infections without clinical manifestations is detected with serologic testing and characterized as early latent, infection acquired in the previous year or late latent, and infection of greater than 1 year duration or latent syphilis of unknown duration. Determination of early latent versus late latent or latent infection of unknown duration guides duration of therapy.
Primary syphilis usually presents as a hard, painless, solitary chancre appearing on the vulva, vagina, or cervix, although extragenital lesions may occur. Lesions that occur on the cervix or in the vagina often go unrecognized. Nontender inguinal lymphadenopathy is frequently present. The primary chancre resolves spontaneously within 2 to 6 weeks.
Secondary syphilis occurs after hematogenous spread of the spirochete and is characterized by protean manifestations including generalized nonpruritic papulosquamous rash typically on the palms and soles, irregular rash, mucous patches, patchy alopecia, condyloma lata, and generalized lymphadenopathy. Systemic symptoms such as fever, headache, and malaise also occur.
Latent syphilis is defined by seropositivity without evidence of clinical manifestations. Latent syphilis documented as acquired during the previous year is referred to as early latent. All other latent syphilis is either late latent or latent syphilis of unknown duration. The late latent phase (>1 year) is not infectious by sexual transmission, but the spirochete may transplacentally infect the fetus.
Tertiary syphilis develops in up to one third of the untreated or inadequately treated patients and refers to gummas, locally destructive lesions of the bone, skin, or other organs. Cardiovascular involvement in tertiary syphilis includes aortic aneurysm and aortic valvular insufficiency.
Neurosyphilis can occur during any stage of syphilis and is not synonymous with tertiary syphilis. All patients with clinical evidence of central nervous system involvement, evidence of active tertiary syphilis, or serologic treatment failure should have examination of the cerebrospinal fluid (CSF) performed. CSF should be tested for fluorescent treponemal antibody absorption (FTA-ABS) reactivity.
Diagnosis: T. pallidum cannot be cultured in vitro. The diagnosis is made definitively by identifying the spirochete through dark-field microscopy or by direct fluorescent antibody tests of lesion exudate or tissue. The majority of syphilis infection is diagnosed presumptively with nontreponemal serologic tests, such as the Venereal Disease Research Laboratory (VDRL) or rapid plasma reagin (RPR) and treponemal tests. A positive VDRL or RPR requires confirmation with treponemal testing. These are FTA-ABS, T. pallidum passive particle agglutination assay (TP-PA assay), various enzyme immunoassays, and chemiluminescence immunoassays. False-positive nontreponemal tests are associated with pregnancy, autoimmune disorders, chronic active hepatitis, intravenous drug use, febrile illness, and immunization. Serologic tests become positive 4 to 6 weeks after exposure, usually 1 to 2 weeks after the appearance of the primary chancres. The specific FTA-ABS test remains positive indefinitely. Some laboratories have begun screening with treponemal tests which will be positive in individuals with previously treated syphilis as well as those with untreated or incompletely treated syphilis. A positive result must be followed by a nontreponemal test with titer. If the nontreponemal test is negative,
a different treponemal test should be performed to verify the results of the first test. If the second treponemal test is positive, those without a history of prior treatment should be offered treatment.
The diagnosis of neurosyphilis cannot be made with a single test but requires a combination of reactive serologic tests, CSF analysis, and reactive VDRL-CSF with or without clinical symptoms.
The diagnosis of syphilis should prompt HIV testing and if negative repeated again in 3 months for those living in high HIV-risk areas (prevalence >1% of the population).
Pregnancy: All women should be screened for syphilis in early pregnancy, and this is mandated in most states. In high-risk patients or in high-prevalence areas, syphilis testing should be repeated twice in the third trimester (i.e., at 28 to 32 weeks’ gestation and again at delivery).
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