Genital herpes is caused by infection with the herpes sim-plex virus (HSV), a DNA virus. This condition affects more than 50 million persons in the United States, and as many as 75% of primary infections go unrecognized by either patient or provider. Herpes simplex infections are highly contagious. There are two types of HSV—HSV-1, which is associated with cold sore lesions of the mouth but may also cause genital lesions, and HSV-2. Most HSV genital infections are caused by HSV-2, but genital HSV-1 infec-tions are becoming increasingly common, particularly among adolescent and young women. Up to 80% of new gen-ital infections among women may be due to HSV-1, with the highest rates occurring in adolescents and young adults. Womeninfected with HSV-1 remain at risk for acquiring HSV-2 infection.
Suggested Criteria for Hospitalization for Pelvic Inflammatory Disease
· Surgical emergencies (e.g., appendicitis) cannot be excluded.
· The patient is pregnant.
· The patient does not response clinically to oral antimicrobial therapy.
· The patient is unable to follow or tolerate an outpatient oral regimen.
· The patient has a severe illness, nausea and vomiting, or high fever.
· The patient has a tuboovarian abscess.
Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep. 2006;55 (RR-11):1–94. http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5511a1.htm. Accessed October 20, 2008.
First episode infections, which represent new acquisition of HSV, usually are most severe, and recurrent infections may be milder. First episode infections often are accompanied by sys-temic symptoms, including a prominent flu-like syndrome and frequent neurologic involvement, which occur within 2 to 3 days following infection. Painful vesicular and ulcerated lesionsappear on the vulva, vagina, cervix, or perineal and perianal skin, often extending onto the buttocks, 3 to 7 days after exposure and usually resolving in approximately 1 week (Fig. 27.3). These vesicles lyse and progress to shallow, painful ulcers with a red border. The lesions of herpes sim-plex infections are distinguishable from the ulcers found in chancroid, syphilis, or granuloma inguinale by their appear-ance and extreme tenderness. Dysuria caused by vulvar lesions or urethral and bladder involvement may lead to uri-nary retention. Patients with primary lesions may require hospitalization for pain control or management of urinary complications. Aseptic meningitis with fever, headache, and meningismus occurs in some patients 5 to 7 days after the appearance of the genital lesions.
After primary infection, the HSV migrates via nerve fibers to remain dormant in the dorsal root ganglia. Recurrences are triggered by unknown stimuli, resulting in the virus traveling down the nerve fiber to the affected area. Recurrent lesions are usually milder in severity than lesions asso-ciated with primary infection and persist for a shorter duration, generally lasting 2 to 5 days. Recurrent lesions may be unilat-eral rather than bilateral and present as fissures or vulvar irritation, as opposed to being vesicular in appearance. Infections with HSV-1 are less likely to cause recurrences than HSV-2, a fact that should be considered when a patient is considering suppressive therapy.
Most HSV-1 and HSV-2 infections are asymptomatic in women. The classic presentation of a painful cluster of vesi-cles and ulcers occurs in a small proportion of women, and most women will have atypical lesions, such as abrasions, fissures, or itching without obvious lesions. Viral shedding can occur forup to 3 weeks after lesions appear. Definitive diagnosis must be confirmed with reliable laboratory testing.
The laboratory test used most often has been viral culture. Culture is highly specific; however, it is not very sensitive, with a false-negative rate of 25% with primary infection and as high as 50% in a recurrent infection. PCR testing has a higher sensitivity and will most likely replace culture in the future as the definitive test for HSV infec-tion. In addition to viral detection methods, the detection of type-specific antibodies to HSV-1 and HSV-2 also can help to establish the diagnosis. These tests may yield false-negative test results when administered in the early stages of infection, as the median time from infection to serocon-version is 22 days. Approximately 20% of patients may remain seronegative after 3 months, particularly if they have received antiviral therapy. Type-specific testing may be useful in the following scenarios: (1) recurrent genital or atypical symptoms with negative HSV cultures, (2) clin-ical diagnosis of genital herpes in the absence of labora-tory diagnosis, and (3) a partner with genital herpes.
Antiviral drugs are the mainstay of treatment. Oral med-ication can reduce the duration of viral shedding and shorten the initial symptomatic disease course, but it does not affect the long-term course of the disease. Treatments for first episode genital herpes include acyclovir, famciclovir, or valacyclovir. Treatment is usually prescribed for 7 to 10 days, but can be given longer if new lesions persist. These therapies do not decrease the likelihood of recurrence. Lesions should be kept clean and dry. In addition, anal-gesics should be provided as needed (e.g., acetaminophen or ibuprofen). Warm water baths often are helpful during the first few days. Topical lidocaine also is occasionally beneficial, but it can result in local allergic reactions. Severe episodes may require hospitalization for parenteral analgesia and intravenous antiviral therapy. Such therapy is generally recommended for immunosuppressed or other-wise compromised patients.
Recurrences may also be treated with oral antiviral therapy. Episodic therapydecreases the duration of the episode(lesion, pain, and viral shedding) and is most effective when the patient initiates the therapy at prodrome, or at the beginning of the episode. Treatment regimens for recurrences are usu-ally of a shorter duration than those administered for first episodes (3 to 5 days). Episodic therapy is recommended for patients with infrequent symptomatic recurrences. Suppressive therapy for genital herpes (in which the medica-tion is taken daily) prevents approximately 80% of recurrences and results in a 48% reduction in viral transmission between sexual partners as a result of decreased viral shedding. It may be most effective for patients with frequent occurrences. It shouldalso be recommended for women with HSV-2 whose sex-ual partner does not have HSV or who has HSV-1 infec-tion. Such discordant couples should also be advised that consistent use of condoms decreases, but does not elimi-nate the risk of transmission.
Pregnant women with a history of genital herpes should be carefully screened throughout the prenatal course for evi-dence of outbreaks. Cesarean delivery is indicated for womenwith active lesions or a typical herpetic prodrome at the time of delivery to prevent neonatal transmission.
Human papillomavirus (HPV) is extremely common,occurring in up to 80% of sexually active women by age 50. Transmission occurs through contact with infected genital skin, mucous membranes, or body fluids from a partner with either overt or subclinical HPV infections. HPV is species-specific and only infects humans. Most infections are transient, but the proportion of women whose infec-tions resolve decreases with age. Unlike other STDs, seque-lae of HPV infection may take years to develop. More than 100 HPV subtypes have been identified, with at least 40 identified in genital infections. HPV viral types are rou-tinely classified into low-risk and high-risk categories. Low-risk subtypes, such as 6 and 11, are typically associated with genital condyloma. High-risk subtypes, such as 16, 18, 31, 33, and 45, are so classified because of their association with cervical dysplasia and cervical cancer. Of the high-risk subtypes, HPV16 and 18 together account for approximately two-thirds of cervical cancer cases, whereas low-risk HPV subtypes rarely lead to cancer.
Condyloma acuminata (genital or venereal warts) aresoft, fleshy growths that may arise from the vulva, vagina, cervix, urethral meatus, perineum, and anus (Fig. 27.4). They may occasionally also be found on the tongue or oral cavity. These distinctive lesions may be single or multiple and generally cause few symptoms. They are often accom-panied by other STDs. Because HPV is spread by direct skin-to-skin contact, symmetrical lesions across the mid-line are common.
The diagnosis of condyloma acuminata is based on physical examination, but may be confirmed through biopsy of the warts.
Thorough inspection of the external genitalia and anogenital region should be performed during the routine gynecologic examination, especially in patients with known cervical or vaginal lesions. Because the condyloma lata of syphilis may be confused with gen-ital warts, the clinician must be able to distinguish the two types of lesions in patients at high risk for both infections (see Fig. 27.5 photo of syphilis).
Management options include chemical treatments, cautery, and immunologic treatments. Patient-applied products include podofilox and imiquimod; these treat-ments should not be used during pregnancy. Treatments that are administered by a healthcare provider include application of trichloroacetic acid, application of podo-phyllin resin in tincture of benzoin, cryosurgery, surgical excision, laser surgery, or intralesional interferon injec-tions. Lesions exceeding 2 cm respond best to cryother-apy, cautery, or laser treatment.
Lesions are more resistant to therapy in patients who are pregnant, have diabetes, smoke, or are immunosup-pressed. In patients with extensive vaginal or vulvar lesions, delivery via cesarean section may be required, to avoid extensive vaginal lacerations and problems with suturing tissues with these lesions. Cesarean delivery also decreases the possibility of transmission to the infant, which can cause subsequent development of laryngeal papillomata, although the risk is small and is not considered an indica-tion for cesarean delivery.
The relationship between infection by high-risk subtypes and cervical dysplasia and cancer is now well-established. A quadri-valent HPV vaccine protects against HPV genotypes 6, 11, 16, and 18 (the strains of HPV that cause 90% of genital warts and 70% of cervical cancers). Additional vaccines are also beinginvestigated.
ACOG currently recommends that all girls and women aged 9 to 26 years be immunized against HPV. The vaccine isa protective tool and is not a substitute for cancer screen-ing; women should be advised to follow current cervical cytologic screening guidelines regardless of their vaccina-tion status.
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