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Sexually Transmitted Infections
Clifton S. Hall MD
Jason S. Reichenberg MD
Dayna Diven MD
Sexually transmitted infections (STIs) are a very common problem throughout the world. Those having sex with multiple partners are the most at risk, and men and women are more likely to have sex with multiple partners between ages 18 and 24, so it is not surprising that two thirds of all cases of STIs occur in people less than 25 years of age. All people who are sexually active are at risk, regardless of socioeconomic status. Carriers of STIs are often asymptomatic and spread their infections unknowingly.
There are at least 20 different types of STIs. Many STIs produce erosions and ulcers on the perineum and lymphadenopathy during one of the stages in their development (Table 26-1
), which makes obtaining a detailed skin examination critical to their diagnosis. The types of STIs in this chapter have been grouped into these categories: viruses, bacteria, parasites, and fungi.
Herpes simplex virus (HSV) subtypes 1 and 2 can result in oral or genital lesions. HSV-2 is the most common culprit for genital herpes, and is much more likely to cause recurrent outbreaks. HSV-1, which most commonly causes oral lesions, is associated with about 30% of HSV primary genital ulcers. Transmission via oral-genital sex is often implicated in these cases. The virus initially infects the contacted area, then travels to the sensory root ganglia, where it lies dormant. A recurrence occurs when the dormant virus in the ganglia travels back down the nerve to the skin.
TABLE 26-1 ▪ STIs with Genital Ulcers
Groups of vesicles, erosions, and ulcers on a red base
Bilateral, tender, discrete, nonsuppurative, and nonindurated
Clinical, PCR, Tzanck, culture
HSV-2 > HSV-1
Vesicle or shallow ulcer that heals rapidly
Mostly unilateral, becomes violaceous and tender before fistula formation
Chlamydia trachomatis serovariants L1, L2, and L3
Papule that ulcerates with overhanging edges
Giemsa stain of smear
Calymmatob acterium granulomatis
Ulcer with firm indurated border
Painless, regional, nonsuppurative, and rubbery
Serology, dark field microscopy
Papule that becomes a friable, shallow, nonindurated ulcer
Mostly unilateral, painful, and suppurative
Culture, rule out other causes of ulcers
HSV lesions present as groups of discrete vesicles of clear fluid on an erythematous base that develop into erosions and then crust over time (Fig. 26-1
). The lesions are painful because there is inflammation of the affected nerves. The lesions are neither suppurative nor indurated.
After initial exposure, symptomatic “primary” herpes occurs after a 3- to 14-day incubation period. The vesicular lesions of primary herpes last 10 to 14 days, and new vesicles will continue to form over a 1- or 2-week period. There can be extensive bilateral inguinal lymphadenopathy. Overall, a
primary infection lasts about 3 weeks. Only a slight majority (57%) of primary HSV-2 infections are symptomatic. With so many asymptomatic primary infections, an outbreak of recurrent herpes may often be confused with a primary infection.
FIGURE 26-1 ▪ Genital herpes erosions and crusts.
A recurrent episode of herpes will usually be preceded by a prodrome of burning, itching, or tingling in the affected area. Usually herpetic vesicles follow in less than 24 hours. The duration of recurrent herpes is much shorter than that of primary herpes. Recurrent outbreaks usually last about 1 week. Herpes can recur for years, but typically becomes less frequent over time.
Genital herpes is spread by direct physical contact. The virus is fragile and does not survive long outside of its host. Active vesicles and erosions have high viral titers and are the most contagious. Asymptomatic viral shedding and transmission is extremely common. As a result, patients who have asymptomatic primary or recurrent infections may unknowingly transmit the virus to others. Among monogamous couples, an uninfected partner will acquire the virus at a rate of 5% to 10% annually. Chronic suppression of the infected partner can halve this rate.
The diagnosis is based on the characteristic lesions and/or the history of recurrent vesicles and erosions in the perineal area. To confirm a diagnosis, the gold standard is a viral culture from a vesicle or moist erosion. Culturing dry, crusted lesions should be avoided as they are frequently negative. More rapid diagnostic methods such as direct fluorescent antibody test and polymerase chain reaction (PCR) assays are also available. The Tzanck smear is a rapid diagnostic test, where the base of a vesicle is gently scraped with a scalpel, smeared onto a glass slide, and stained with Wright or Giemsa stain. A positive Tzanck has large, multinucleated keratinocytes (Fig. 26-2
). A positive result, however, cannot distinguish between HSV-1, HSV-2, or varicella-zoster virus.
FIGURE 26-2 ▪ Positive Tzanck smear with Giemsa stain demonstrates giant multinucleated keratinocytes.
At this time, there is no cure for genital herpes. The goal of treatment is to decrease the frequency, duration, and severity of outbreaks. Treatment can also decrease, but not eliminate asymptomatic shedding. To decrease transmission of the virus, sex should be avoided when there are vesicles and moist erosions. Also, condoms should be used to decrease transmission during asymptomatic shedding. The antiviral medications currently available to treat herpes are acyclovir, famciclovir, and valacyclovir. These medications are relatively safe and are preferentially absorbed by infected cells. Valacyclovir and famciclovir offer the advantage of less frequent dosing.
Patients with a primary or initial genital herpes eruption should be treated to help avoid developing severe or prolonged symptoms. They should be treated for 7 to 10 days using any of the following: acyclovir 400 mg orally three times a day, acyclovir 200 mg orally five times a day, famciclovir 250 mg orally three times a day, or valacyclovir 1 g orally twice a day.
Patients with recurrent genital herpes can be treated either episodically or continually for suppressive therapy. Chronic suppressive therapy is generally used in patients with greater than six outbreaks a year or for those whose outbreaks are symptomatically severe. Suppressive therapy can reduce outbreaks by 70% to 80%. Twenty percent of suppressed patients have no visible outbreaks. As the frequency of recurrences decreases with time, a “drug holiday” can be tried every year to assess whether the patient still requires suppressive therapy. The recommended dosages for suppressive therapy are acyclovir 400 mg orally twice a day, famciclovir 250 mg orally twice a day, valacyclovir 500 mg orally once a day, or valacyclovir 1 g orally once a day.
Episodic treatment of recurrent genital herpes entails that the patient start treatment as soon as prodromal symptoms are noticed, in order to obtain maximum benefit. Once a skin eruption begins, only mild symptomatic improvement occurs. The dosage for episodic treatment is usually a 5-day course of acyclovir 400 mg three times a day or 800 mg twice a day; famciclovir 125 mg twice a day; or valacyclovir 1 g once a day. Shorter treatment durations include acyclovir 800 mg for 2 days, famciclovir 1,000 mg twice daily for 1 day, or valacyclovir 500 mg twice daily for 3 days.
Venereal Warts (Condylomata Acuminata)
Venereal warts are the most common STI in the world. Half of all sexually active young adults in Europe and the United States have been infected. Venereal warts are caused by the human papillomavirus (HPV). HPV is a circular, double-stranded DNA virus. There are greater than 200 different types of HPV. The HPV types can be grouped as either low risk or high risk, depending on their risk for causing cervical cancer. Fortunately, the most common types, HPV-6 and HPV-11, are low risk. The most common high-risk types are 16, 18, 31, and 33.
Venereal warts, also known as condylomata acuminata, are multiple, painless, cauliflower-shaped, soft, lobulated papules located in moist anogenital regions (Fig. 26-3
). In females, they are typically found on the vulva, cervix, perineum, or anus. In males, they are usually on the penis or perianal area. Warts are less common on the scrotum, unless the immune system is deficient. Bowenoid papulosis is a rare phenotype of venereal wart that is more often associated with the high-risk HPV types. These warts are less prominent flat papules that may have hyperpigmentation.
The incubation period can vary from several weeks to over a year. Most infections, particularly the low-risk visible warts of HPV types 6 and 11, are transient, lasting 1 to 2 years on average. Most “recurrent” warts are actually areas that were subclinical at the time of treatment. High-risk HPV types can not only lead to cervical cancer but also increase the risk of developing cancers of the vulva, vagina, glans penis, and anus.
FIGURE 26-3 ▪ Large perianal condylomata acuminata.
HPV spreads via direct skin-to-skin contact and fomites. Men are more at risk for genital warts if they have sex before they are 17, have greater than six sexual partners, have sex with prostitutes, or are not circumcised. Genital warts in children less than 2 years old do not necessarily signify abuse, since warts can spread during delivery, from autoinoculation, and from nonsexual contact.
Most venereal warts can be diagnosed clinically. Flat or sessile warts may occasionally warrant a biopsy for bowenoid papulosis given its higher association with cancer. PCR and in situ hybridization tests are also available and frequently used for cervical warts. These tests can differentiate between high- and low-risk HPV types.
There are a large number of treatment options for genital warts. These treatments can be grouped into those that physically destroy the wart, those that kill infected cells, and those that stimulate the immune system to destroy the wart.
Liquid nitrogen cryotherapy is the most commonly used in-office destructive method. It is quick, effective, and inexpensive. The warts and 2 mm of surrounding skin are frozen white once or twice with a liquid nitrogen dispenser or cotton swab.
Electrofulguration and electrocautery are slightly more effective than cryotherapy and work well for large warts. However, fewer physicians are using these methods because the smoke plume can theoretically cause warts in the respiratory tract. In response to this theory, many wear masks or use smoke evacuators. Other disadvantages of these modalities include the need for anesthesia and frequent scarring. Other in-office treatment options are trichloroacetic acid and podophyllin.
Imiquimod 5% cream is less effective (~50% efficacious) and often slow (sometimes taking 10 or more weeks of treatment); however, it has a low recurrence rate and can be done at home. The cream is applied three times a week at bedtime for up to 16 weeks. The cream causes mild to moderate irritation and has been reported to flare concomitant psoriasis.
5-Fluorouracil 5% cream twice a day can be effective and works well for intraurethral warts, but it can cause inflammation and painful scrotal erosions. Another effective option is podophyllotoxin 0.5% solution applied to the warts at home twice daily for 3 consecutive days per week for 1 to 4 weeks. It is contraindicated in pregnancy and can cause erythema and erosions in treated areas.
Gardasil, a quadrivalent vaccine against HPV types 6, 11, 16, and 18 is very effective at preventing warts caused by the four most common high- and low-risk HPV types. No therapeutic vaccine currently exists.
Hepatitis B Virus
Hepatitis B virus (HBV) is an enveloped double-stranded DNA virus of the Hepadnaviridae family. It is unrelated to any other human virus. Chronic carriers are most commonly found in the Far East, where it is often spread from mother to child perinatally. In the United States, half of all cases arise from sexual contact.
HBV does not produce any genital lesions. Nevertheless, HBV can cause jaundice, urticaria, and vasculitis.
HBV has an average incubation time of 10 weeks before an acute infection becomes clinically apparent. Patients complain of fevers, anorexia, nausea, diarrhea, right upper quadrant pain, and general malaise. Few (<1%) acute infections go on to liver failure. About one fifth of acute infections develop a serum sickness-like infection 1 to 6 weeks before clinical liver disease. These patients typically have urticaria and arthralgias and occasionally vasculitis, arthritis, and glomerulonephritis. This sickness gradually resolves spontaneously. Polyarteritis nodosa develops in 7% to 8% of cases, usually within the first 6 months. A chronic liver infection develops in 10% of patients, a quarter of whom go on to develop cirrhosis and/or hepatocellular carcinoma.
The virus is found in body fluids such as blood, saliva, semen, and cervical fluid. The disease typically spreads via close physical contact, intravenous drug use, and perinatally.
The diagnosis of an HBV infection is typically made serologically. Acute infections are diagnosed by finding elevated liver tests and IgM antibodies against hepatitis B core antigen, which is almost always positive when jaundice is present. Chronic infections are diagnosed by finding HBV surface antigens in the blood. If antibodies to the surface antigen are present, the patient has eliminated the virus and does not have a chronic infection.
Acute infections generally require only supportive care, as most cases resolve on their own. Chronic infections are treated with α2b-interferon, lamivudine, or adefovir dipivoxil. HBV-associated polyarteritis nodosa is typically treated with systemic steroids, lamivudine, and rarely plasma exchange. A vaccine is available to prevent infections, and it is recommended for health care workers and children.
Hepatitis C Virus
Hepatitis C virus (HCV) is the most common cause of cirrhosis in the United States. It is a single-stranded RNA flavivirus. Other notable flaviviruses are yellow fever and dengue fever.
There are no acute genital lesions. The stigmata of liver cirrhosis such as jaundice, caput medusa, palmar erythema, and telangiectasias develop with chronic infections.
Most acute infections are asymptomatic; however, 55% to 85% of those infected develop a chronic infection that can lead to liver cirrhosis. Chronic HCV has also been associated with polyarteritis nodosa, sporadic porphyria cutanea tarda, lichen planus, necrolytic acral erythema, and cutaneous necrotizing vasculitis.
Sexual transmission of HCV is uncommon. A majority of cases in developed nations are acquired from intravenous illicit drug use, now that blood and blood products are screened for HCV.
Diagnosis is made via PCR for HCV RNA in the blood.
Chronic HCV infections are treated with a combination of interferon-α and ribavirin, which is effective half of the time. Eczema and pruritus are common side effects, which start 2 to 4 months after starting treatment. These side effects can be controlled with oral antihistamines, moisturizers, and topical steroids.
The human immunodeficiency virus (HIV) was first recognized in the United States in 1981, but it is thought to have been present in Africa for decades before the virus was discovered. HIV causes an immunodeficient state principally by depleting the body of CD4+ helper T cells. Acquired immunodeficiency syndrome (AIDS) is a term used to describe the later stages of HIV infection, in which the CD4 count has dropped below 200 cells/mL. Patients with AIDS usually present with an opportunistic infection (characteristic viral or fungal pneumonia), malignancy (Kaposi’s sarcoma or one of several lymphomas), or chronic fatigue syndrome (encephalopathy, wasting). A great majority of HIV-infected individuals develop skin disorders related to their immunocompromised status.
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