Dr. Sinan Doğantürk

Ankara

ADOLESCENT MEDICINE

SEXUALLY TRANSMITTED DISEASES IN ADOLESCENTS

 

 

 

Section of Adolescent Medicine, St. Christopher's Hospital for Children, and the Department of Pediatrics, MCP-Hahnemann University, Philadelphia, Pennsylvania

Address reprint requests to
Paula K. Braverman, MD
Adolescent Medicine
St. Christopher's Hospital for Children
Front Street and Erie Avenue
Philadelphia, PA 19134

Sexually transmitted diseases (STDs) are among the top 10 reportable diseases in the United States. Of the more than 12 million cases annually, approximately 3 million occur in adolescents. An estimated two thirds of cases occur in individuals younger than age 25. ^[10] Almost half of adolescents report ever being sexually active, ^{[4] [8]} and approximately one third are currently sexually active. ^[6] For a number of biologic and psychosocial reasons, sexually active adolescents have the highest rate of STDs of any sexually active age group. ^{[9] [10]} They suffer from the acute manifestations of these diseases as well as complications that place them at risk for some significant long-term negative sequelae, such as infertility, chronic pelvic pain, and cancer. This article reviews the reasons for this increased risk and provides updates on the common STDs that affect adolescents.

OVERVIEW

There are at least 25 infections that are sexually transmitted (Table 1) . ^[10] The infections cause various symptoms ranging from genital lesions (ulcers, blisters, papules), to vaginal or penile discharge, to systemic manifestations, such as rash, arthralgia or arthritis, fever, and myalgia. Associated symptoms include genital itching, burning, dysuria, urinary frequency, abdominal pain, and tender inguinal lymphadenopathy. Even more concerning is the fact that STDs can be completely asymptomatic, and long-term sequelae, such as liver cancer (hepatitis B), cervical cancer (human papillomavirus [HPV]), and acquired immunodeficiency syndrome (AIDS) (human immunodeficiency virus [HIV]) may not be manifested for years after the primary exposure. ^[9]

 

 

Primary prevention of STDs would be the ideal. Short of that, prompt diagnosis and treatment are key in the management of these diseases. Recognition of the signs and symptoms of STDs is far from adequate among the lay public and health professionals, ^[10] especially when addressing the magnitude of asymptomatic infection and the need for screening and treatment regardless of symptoms. Burstein et al ^[1] recommended that sexually active adolescent girls be screened every 6 months for Chlamydia trachomatis because of the high rate of infection and the inability to predict most of the subjects who tested positive.

 

PSYCHOSOCIAL ISSUES

In some surveys, adolescents have shown more knowledge about STDs than adults. ^[10] Knowledge alone is not sufficient, however. There must be the inclination and the means available to access health services when an STD is suspected. As part of normal psychosocial development, younger adolescents are concrete thinkers who understand current experiences but may not understand the future consequences of their actions. Adolescents may also believe that they will not suffer any negative consequences. Although they may know all of the facts, knowledge is not translated into self-protective behavior, such as abstinence or consistent use of condoms. ^{[9] [10] [16]}

Several steps are needed to engage in protective behavior. Acknowledgment of the decision to become sexually active and understanding the consequences of this decision are prerequisites to having condoms available and engaging a partner in a discussion about condom use. The next step after acknowledgment of sexual activity is the belief that there is risk for STDs. Adolescents frequently say that they can tell their partner is clean and do not consider the fact that their partner may have other risky partners--past and present. Adolescents are more likely than older individuals to have multiple sequential partners over a relatively short period, increasing the chances of exposure to a risky partner. ^{[9] [10]} In the 1997 Youth Risk Behavior Surveillance, ^[6] 16% of adolescents reported having four or more lifetime partners. Reinfection with STDs is higher among adolescents than adults, in large part because the partner is not treated. ^{[9] [10]} Discussing STDs with a partner and confronting the issues of monogamy and trust in relationships is hard for anyone and particularly challenging for less experienced adolescents.

Once there is acknowledgment of sexual activity and the risk of STDs, proper condom use depends on several factors, including the belief that condoms help prevent STDs, assertiveness in demanding that a condom is used, and positive feelings of self-efficacy in the proper techniques of condom use and the ability to say no to sex if a partner refuses to use a condom. Having adolescents practice proper condom use on models is helpful in reinforcing proper techniques concretely. Practicing how to talk with a partner about condom use by using role plays gives adolescents the vocabulary and techniques needed in these difficult interactions. ^{[9] [10]} It is important to be sensitive to acculturation issues when considering condom use negotiation between men and women. In some cultural contexts, the imbalance of power between the sexes may make it impossible for a woman to negotiate use successfully and maintain a relationship with her partner. ^[10] Another factor that has an impact on STD risk is substance use, in particular, drugs and alcohol. Risk-taking behaviors tend to cluster together, and adolescents who are sexually active are also more likely to be abusing drugs and alcohol. These substances may impair an individual's ability to have good judgment about their choice of partners or to negotiate safe sex successfully. ^{[9] [10]} Although condom use among adolescents has increased, according to the 1997 Youth Risk Behavior Surveillance, ^[6] only 57% of adolescents used condoms the last time they had sex. More work is needed.

 

HEALTH CARE ACCESS

Access to health care is a major barrier faced by adolescents even when they reach the point of acknowledging the importance of STD screening. Many adolescents lack health insurance and cannot pay for services out-of-pocket. Even those with insurance face issues of co-pays and deductibles. Not all private insurances provide adequate coverage for STD services. Although publicly funded clinics provide free STD screening and treatment services, many adolescents are not aware of their existence or lack transportation to access these facilities. Even when these issues are resolved, some adolescents feel uncomfortable in environments designed mainly for adults. ^{[9] [10]}

 

CONFIDENTIALITY

Confidentiality becomes a concern for many adolescents, who are unaware that they are legally entitled to confidential STD diagnostic and treatment services. Because some states have age limits of 12 or 14 years, clinicians should check the laws in their particular state. Providers need to be careful to consider the information that is sent home by insurance companies when insurance is billed for STD-related services. Some of the details in the explanation of benefits may reveal the purpose of the visit. ^{[9] [10] [16]} It is also important to remind adolescents that many STDs must be reported to city and state health departments. If the health department cannot verify treatment with a clinician, case workers may attempt to locate them to ensure proper treatment. ^[16] If the clinician suspects that an STD represents a case of sexual abuse, reporting to child protective services is required. This situation is more likely in a younger adolescent, and it is recommended that the adolescent be informed ahead of time that the protective service agency will be involved.

 

ETHNIC AND RACIAL DIFFERENCES

Certain groups seem to be at particular risk for STDs, including some racial and ethnic minority groups. African-Americans and Hispanics tend to have higher rates of disease, particularly chlamydia, gonorrhea, and syphilis. Data showed that 15- to 19-year-old African-American adolescents were 24 times more likely to have gonorrhea than their white counterparts. Overall the rate of gonorrhea in African-Americans is 31 times greater than in whites, and the rate of syphilis is 44 times greater than in whites. Although Hispanics were only three times more likely than whites to have syphilis, there is still a significant difference, with 34.6 per 100,000 cases of congenital syphilis among live births to Hispanics as compared with 3.3 per 100,000 for whites. These differences may reflect other markers for health status, including socioeconomic status, access to health care, and living in communities with a high rate of STDs among sexual networks. There may also be some element of reporting bias because these minority populations are more likely to access publically funded clinics, which have higher rates of disease reporting to health departments. ^{[9] [17]}

 

BIOLOGIC FACTORS

The biologic factors related to STDs tend to affect women more than men, although lack of circumcision may increase the risk of HIV infection and ulcerative diseases such as chancroid in men. ^[9] In both sexes, prior exposure to STDs seems to provide some immunity for future exposures to the same pathogen. Adolescents who are inexperienced with STDs lack this immunity. ^{[9] [10] [13] [14]} Women of all ages are at higher risk for STDs and some of the long-term sequelae. Studies of transmission suggest that gonorrhea and chlamydia are more likely to be transmitted from men to women than from women to men, and HIV transmission studies in the United States have yielded similar results. ^{[9] [10]}

The anatomy of the female reproductive tract may contribute to STD infections, especially in younger women. Adolescent women commonly have a normal cervical anatomic finding known as the ectropion. The ectropion represents the border of the squamocolumnar junction known as the transformation zone. In adolescents, the squamocolumnar junction is on the exocervix exposed to the vaginal environment. The columnar cells recede into the endocervical canal over time; however, the presence of the ectropion in adolescents is postulated to place them at higher risk for infection. C. trachomatis infects columnar cells, and Neisseria gonorrhoeae has more affinity for these cells than squamous cells. Ectopy may also be related to increased chances of acquiring and shedding HIV. The squamocolumnar junction is the transformation zone where cervical cancer originates. In adolescents, this area is actively undergoing squamous metaplasia. HPV may be incorporated during cell replication, making adolescents more susceptible to the consequences of this infection. ^{[8] [9] [10] [13] [14]} Finally, as a result of the hormonal changes occurring during maturation of the hypothalamic-pituitary axis, cervical mucus becomes thicker. The thinner mucus found in younger adolescents, who have a predominance of anovulatory cycles, which are deficient in progesterone, may allow STD pathogens to ascend more readily to the upper tracts, placing them at higher risk for pelvic inflammatory disease (PID). ^{[8] [13]}

 

SPECIFIC SEXUALLY TRANSMITTED DISEASES

Chlamydia trachomatis

C. trachomatis is an obligate intracellular parasite. ^[9] It is the most prevalent STD in the United States with more than 0.5 million cases reported in 1997. The rate of infection is highest for individuals younger than age 20, and in 1997, women aged 15 to 19 had rates of 2044.3 per 100,000 compared with 1633.5 per 100,000 for women aged 20 to 24. State-specific data from 15- to 24-year-old women screened at family planning clinics ranged from 2% to 11.2% positivity. ^[17] In the Job Corps, which screens 16- to 24-year-old economically disadvantaged women, the positive chlamydia rates were 4% to 18.1%. ^[17] Screening of men has shown higher rates for those younger than age 25, with a prevalence of 5% to 10%. ^[9] Chlamydia causes 35% to 50% of nongonococcal urethritis in men. ^[9] Reported rates for women tend to exceed those for men in many data sets, in part, because of screening bias. Many screening programs have focused on women, and many men are treated without diagnostic testing. ^{[9] [17]}

The clinical spectrum of the disease includes urethritis, epididymitis, proctitis, prostatitis, cervicitis, bartholinitis, and conjunctivitis. Chlamydia is commonly asymptomatic, and when symptoms do occur, they are often milder and slower in onset than gonorrhea infection. In women, chlamydia can result in PID and perihepatitis (Fitz-Hugh-Curtis syndrome). Even when chlamydia causes PID, the symptoms can be mild enough to be ignored despite the fact that the organism can cause severe tubal scarring, leading to infertility, ectopic pregnancy, and chronic pelvic pain. Reiter's syndrome (urethritis, conjunctivitis, and arthritis) has been associated with chlamydia, with more than 80% of cases having evidence of past or concurrent infection. Perihepatitis, which can result in adhesions between the liver capsule and anterior abdominal wall, is more likely to be associated with chlamydia than gonorrhea. It should be suspected when a sexually active patient presents with right upper quadrant pain, which may be accompanied by fever, nausea, and vomiting. ^{[8] [9]}

There are various treatment options available for uncomplicated chlamydia infection. Single-dose orally administered azithromycin, 1 g, is equivalent to 1 week of doxycycline, 100 mg twice a day. Even though only a single dose is required, however, patients should be abstinent for 1 week after taking azithromycin. Although clinician-observed single-dose therapy should theoretically increase compliance, the cost of azithromycin is significantly greater than doxycycline. Use of this more expensive option should be considered within the framework of the clinical practice setting. Single-dose therapy should be used for noncompliant adolescents. Test of cure is not needed, unless symptoms persist or history is suggestive of reinfection. Erythromycin and ofloxacin are alternatives, but erythromycin can have significant gastrointestinal effects, and ofloxacin is more expensive than the other alternatives and does not have any advantages. Test of cure should be conducted after therapy with erythromycin. Neither doxycycline nor ofloxacin can be used in pregnancy. Although there are data suggesting that azithromycin is safe in pregnancy, routine use is not currently recommended. The recommended therapies for pregnant patients are erythromycin base or amoxicillin. Studies in pregnant women have shown that amoxicillin is effective, although this medication is not recommended in nonpregnant patients. To date, no significant resistance has developed to the established chlamydia treatment regimens (Table 2) . ^{[5] [9]}

 

 

Neisseria gonorrhoeae

N. gonorrhoeae is a fastidious gram-negative diplococcus that infects mucous membranes. ^[9] In 1997, 324,901 cases were reported in the United States. The rate of gonorrhea in the United States has decreased by 74% since 1975, although the rate of decline has been less dramatic for adolescents than for adults. In 1997, the rate of infection for 15- to 19-year-olds was 530.3 per 100,000, which represented a decrease from the previous year. This age group, however, has the highest rate of any sexually active group. The rates for 20- to 24-year-olds increased during the 1996-1997 period. ^[17]

The clinical spectrum for gonorrhea includes urethritis, proctitis, pharyngitis, conjunctivitis, epididymitis, prostatitis, and infection or abscess of Bartholin's and Skene's glands. Complications include PID, perihepatitis, and disseminated infection. In men, the penile discharge is generally more copious and purulent in appearance than the discharge of chlamydia. Although gonorrhea can be asymptomatic in women 80% of the time, fewer than 5% of men remain asymptomatic. Women are more likely to harbor the organism for longer periods before treatment, placing them at higher risk for developing a complication, such as PID. ^{[8] [9]}

Disseminated gonococcal infection occurs 0.5% to 3% of the time, presenting with arthritis, tenosynovitis, and dermatitis (tender necrotic pustules). The arthritis usually involves the knee, wrist, ankle, or metacarpophalangeal joints, and the skin lesions are concentrated on the distal extremities. Although the organism can be identified on mucous membranes more than 80% of the time, recovery from joint fluid, blood, or skin lesions is more difficult and varies throughout the course of the illness. Disseminated gonococcal infection is more common in women, with pregnancy, pharyngeal infection, and complement deficiency being other risk factors for dissemination. Disseminated gonococcal infection occurs within 1 week of menses in half of women. ^{[8] [9]}

Oral cefixime, ciprofloxacin, ofloxacin, or an intramuscular dose of ceftriaxone are the recommended regimens for treatment. Ceftriaxone and ciprofloxacin are more effective than cefixime, and ofloxacin is slightly more effective than cefixime. Only the quinolones and ceftriaxone are recommended for pharyngeal infection. ^[5] More than one third of isolates are resistant to penicillin or tetracycline. Although the penicillinase-producing isolates have declined to 3.9%, the chromosomally mediated penicillin-resistant strains have increased to 4%, with chromosomally mediated tetracycline resistance at 8.3%. Decreased susceptibility to ciprofloxacin is currently at 0.5%, with absolute resistance at 0.1%. Quinolones can still be used with confidence in the United States, although resistance levels in Asia are high enough to recommend nonquinolone regimens in that area of the world. ^{[9] [17]} Quinolones cannot be used in pregnancy and theoretically are not approved in children because of adverse effects on cartilage in animals. Ciprofloxacin has been used in children with cystic fibrosis without apparent problems. Disseminated infection is treated initially with intravenous or intramuscular therapy, which is then followed by oral therapy within 24 to 48 hours of clinical improvement (Table 3) . ^[5]

 

 

Pelvic Inflammatory Disease

PID represents infection in the upper genital tract and is a complication of chlamydia and gonorrhea. Although infection with gonorrhea or chlamydia may initiate the process, organisms from the lower genital tract gain ascent, leading to a polymicrobial infection including facultative and anaerobic organisms. ^{[8] [9] [13]} Chlamydia and gonorrhea are found in 25% to 40% of patients with PID, whereas 25% to 60% of cases represent mixed aerobic and anerobic infections. ^[8] PID associated with gonorrhea and chlamydia tends to occur within a week of menses, suggesting that loss of the mucous plug and blood as a culture media may play a role in ascent. By comparison, PID occurring more than 2 weeks after menses is associated with nongonococcal and nonchlamydia organisms two thirds of the time. ^{[8] [13]} Gonorrhea produces relatively rapid severe symptoms, whereas chlamydia seems to cause less severe symptoms but more severe scarring. ^{[8] [13]} Douching is considered by some women to be an important part of feminine hygiene. Studies have shown, however, that this practice increases the risk of PID. ^{[8] [9] [13]} Studies have also suggested an association between bacterial vaginosis (BV) and upper tract disease, although more studies are needed to clarify this relationship. ^{[8] [9] [13]} (See later section on BV.)

Adolescent women are at much higher risk for acquiring PID than adults. A sexually active 15-year-old has a 1:8 chance of developing PID, as compared with 1:80 for a 24-year-old. ^[13] The high rates of gonorrhea and chlamydia in the younger age group are major reasons for this difference. The biologic factors mentioned previously, however, including the cervical ectropion, immaturity of the menstrual cycle, and lack of antibodies to STDs, are also believed to play a role. ^{[8] [9] [13]} One study showed that on average, adolescents seek care 2 days later than adults. ^[15] This delay is concerning when considering the significant complications of PID, including infertility, tubo-ovarian abscess, perihepatitis, chronic pelvic pain, and ectopic pregnancy.

PID is a clinical diagnosis, and even in experienced hands, one third of women are diagnosed incorrectly (Table 4) . ^[9] The accompanying box lists differential diagnoses for PID and its complications. ^{[8] [9] [13]} The complete differential diagnosis should always be considered, and patients should be followed closely for expected improvement within 48 to 72 hours of initiating therapy. ^{[8] [9] [13]} Patients who do not improve or worsen should be investigated for other clinical entities, such as appendicitis; ectopic pregnancy; a ruptured, bleeding, or torsed ovarian cyst as well as other pelvic, gastrointestinal, and urinary tract disease entities. ^{[8] [9] [13]}

 

 

Therapy can be initiated as an inpatient or an outpatient. Because of noncompliance and concern over the significant sequelae, adolescents were previously automatically admitted to the hospital and begun on intravenous therapy. The inpatient admission allowed for education about PID and the need for partner treatment as well as close observation to ensure that the patient was responding appropriately to therapy. Pressure from insurance companies has made this practice more difficult. However, a patient who has an unclear diagnosis, cannot tolerate oral medication, is pregnant, has severe illness including a tubo-ovarian abscess, has failed outpatient therapy, or is not compliant should be hospitalized for initial therapy. If a patient is treated as an outpatient, she must receive close follow-up within 48 to 72 hours. If symptoms have not improved or have worsened, hospitalization and further evaluation are indicated. Both of the regimens in Table 5 are equally effective. Doxycycline can be given orally because it is well absorbed. Intravenous administration of doxycycline can be associated with significant pain. Oral therapy usually is begun within 24 hours of clinical improvement. ^{[5] [8] [9] [13]}

 

 

Syphilis

Syphilis is caused by the spirochete Treponema pallidum. ^[9] Since 1990, the rates of primary and secondary syphilis have fallen dramatically, but the disease is not evenly distributed throughout the United States. Syphilis is concentrated in the South, and 413 counties in the United States account for 80% of the reported cases of primary and secondary syphilis. Twenty-eight counties and the cities of Baltimore, St. Louis, and the District of Columbia account for half of the cases. The disease is 44 times more common in non-Hispanic blacks than non-Hispanic whites, although, as mentioned previously, some of this difference could be reporting bias. ^[17] Although the extent of the problem in the adolescent population depends on the area of the United States in which the clinician is practicing, it is important to recognize this entity because syphilis facilitates transmission of HIV infection. ^[9]

Untreated syphilis evolves through several clinical stages, the symptoms of which resolve on their own without treatment. The first stage is a generally nontender ulcer at the site of inoculation, which occurs within approximately 3 weeks of exposure. The second stage, which occurs a few weeks to months later, represents systemic dissemination and is characterized by fever, malaise, headache, adenopathy, generalized body rash, and mucosal lesions (condylomata lata). The rash of secondary syphilis can be confused with pityriasis rosea, and one should always consider this differential diagnosis in a sexually active adolescent. The disease then enters the latent stage, which can last for years, followed by late syphilis, which can result in neurologic, cardiovascular, and skeletal disease. ^[9]

Diagnosis is made by serologic testing. A rapid plasma reagin (RPR) or Venereal Disease Research Laboratory (VDRL) test is confirmed with a microhemagglutination assay for T. pallidum (MHA-TP) or fluorescent treponemal antibody absorbed (FTA-ABS) test. The RPR and VDRL can be falsely positive in conditions such as lupus. RPR or VDRL titers are followed every 6 months after treatment to document disease resolution, whereas confirmatory tests are not repeated because they can remain positive for life. A fourfold change in titer is considered significant in assessing clinical activity of the disease. It is important to use the same nontreponemal test in following titers after treatment. Although most patients revert to negative titers, a small proportion may continue to have low-level titers for life. ^{[5] [9]}

The interpretation of serologic titers may be more difficult in patients with HIV infection because in some cases the titers vary or are unusually low. Patients with HIV infection are more likely to develop neurosyphilis even after receiving appropriate treatment. It is recommended that anyone with syphilis be tested for HIV infection, and in areas of the United States where syphilis rates are high, the test should be repeated in 3 months if the initial test was negative. It is also recommended that HIV-positive patients have nontreponemal titers followed every 3 months after treatment to ensure adequate clinical response to therapy. ^{[5] [9]}

The treatment of choice for syphilis is penicillin. Doxycycline and tetracycline are alternatives in penicillin-allergic individuals, but strict compliance with these regimens is crucial. Desensitization to penicillin is recommended if compliance cannot be ensured. In the case of HIV infection, penicillin is the recommended regimen, and some clinicians suggest three doses of benzathine penicillin for primary and secondary syphilis because of possible treatment failures. Examination of the cerebrospinal fluid is recommended in all cases of treatment failure. Because of the prevalence of central nervous system abnormalities in HIV-positive patients, however, some clinicians recommend evaluation of the cerebrospinal fluid in these patients before treatment even in cases of primary or secondary syphilis (Table 6) . ^{[5] [9]}

 

 

Trichomonas vaginalis

Trichomoniasis is caused by the protozoan Trichomonas vaginalis. ^[9] There are no comprehensive surveillance data for this infection, but studies have shown a prevalence of 5% to 10% of the general population and 18% to 50% of women with vaginal complaints. One study in high-risk adolescent boys showed a prevalence of 58%. ^[9] Although this disease can be asymptomatic in men and women, lack of symptoms is more common in men. Clinical presentation includes vaginal discharge, vulvar irritation, urethritis, and strawberry cervix (punctate cervical hemorrhages and ulceration). Some data suggest that trichomoniasis may be associated with premature rupture of membranes and preterm delivery. ^{[8] [9]}

The diagnosis in women is frequently made by evaluating wet mount of vaginal secretions or urine in men to identify the motile organism. This method misses the diagnosis 30% to 50% of the time in women and is even less reliable in men. Although the organism may be identified on Papanicolaou (PAP) smear, confirmation with another test is recommended because of the rate of false-positive and false-negative results. Culture is recommended when wet mount evaluations are negative. ^[9] A new culture system, In-Pouch TV (Biomed Diagnostics, San Jose, CA), may provide some alternatives to more standard culture techniques because it is easily stored and transported. Studies of this method have yielded favorable results in men and women. ^{[2] [3] [7]}

The only oral medication available for the treatment of trichomoniasis in the United States is metronidazole. The recommended dose is metronidazole, 2 g orally in a single dose. ^[5] Single-dose treatment with 2 g has a cure rate of 90% to 95%. The seven-dose regimen is recommended only if single-dose therapy fails. Topical treatment with metronidazole is not as effective because there is not adequate penetration into the urethra and perivaginal glands. Patients should be reminded not to drink alcohol while taking metronidazole because it causes nausea and flushing. In cases of treatment failure not resulting from reinfection, higher doses of metronidazole may be effective. Patients who persistently fail treatment should be seen by an infectious disease specialist. The current Centers for Disease Control and Prevention treatment guidelines say that single-dose metronidazole can be used in pregnancy. ^{[5] [9]}

Bacterial Vaginosis

BV is a disruption of the normal vaginal microbial ecosystem with a decrease or absence of lactobacilli and a predominance of gram-variable coccobacilli, including Gardnerella vaginalis and Bacteroides species as well as other facultative bacteria and genital mycoplasmas. This entity is not a true vaginitis in the sense that is does not present with significant inflammation. G. vaginalis is present in women with no vaginal symptoms. Up to one third of adolescent girls who have not been sexually active harbor this organism. The current thinking is that G. vaginalis may interact with the anaerobes and mycoplasmas to cause the clinical entity BV. Although there is evidence suggesting that sexually active women are more likely to carry organisms related to BV and one study showed that sex partners of BV patients harbor the same biotype strains of G. vaginalis, other studies have failed to uphold the role of sexual transmission. Treatment of sex partners does not appear to prevent recurrence. Recurrence is common--up to 70% of patients are diagnosed with BV during the 3 months after a recommended treatment regimen. Some investigators believe that the lack of H₂ O₂ producing lactobacilli in the vaginal flora may contribute to recurrence because these bacteria appear to inhibit the overgrowth of bacteria, which contributes to the disrupted flora pattern seen in BV. ^[9]

Women with BV can present with a malodorous, thin white vaginal discharge characterized by having an elevated pH (>4.5), a fishy odor when mixed with 10% potassium hydroxide (whiff test), and clue cells on wet mount that represent vaginal cells covered with bacteria. The fishy odor is thought to be secondary to amines present in the vaginal fluid. As a single clinical diagnostic procedure, the presence of clue cells on wet mount is probably most useful. Accuracy of diagnosis can be increased, however, using the Amsel criteria, in which three of four signs are present, including the homogeneous white adherent discharge, elevated vaginal pH, positive whiff test, and presence of at least 20% clue cells. ^[9]

BV was traditionally thought to be a benign condition. Data have shown, however, that there is an increased risk of preterm and low-birth-weight deliveries, chorioamnionitis, intra-amniotic fluid infection, postpartum endometritis, and postabortion PID. There have been conflicting data on whether treatment of pregnant women for BV prevents these complications. A study in women undergoing abortion suggested that PID could be decreased by treatment of BV. The relationship between BV and PID in patients not undergoing abortion procedures or other uterine instrumentation is also unclear. Studies have found that the bacteria present in the upper tracts of women with PID resemble the vaginal flora of women with BV. One study found that symptoms of endometritis, such as intermenstrual bleeding, have resolved after treatment for BV. To date, however, treatment of asymptomatic nonpregnant women is not recommended as standard clinical practice. There are also some studies suggesting that BV may increase the risk of acquiring HIV infection. ^[9]

Current treatment regimens include oral or topical metronidazole or clindamycin. One week of therapy with metronidazole is generally a more effective cure than a single dose of 2 g. The intravaginal therapy appears to be as effective as the week of oral therapy. Clindamycin orally and vaginally is as effective as metronidazole. The vaginal preparations may have fewer systemic side effects, but they are more expensive than a 7-day course of metronidazole. There is a concern that vaginal clindamycin may be associated with an increase in preterm delivery, and it is not recommended in pregnancy. One disadvantage of clindamycin cream is that it is oil based and may weaken latex condoms. Treatment of partners is not recommended because recurrence rates are not changed. There is controversy over what to do in pregnancy. Women who have a previous preterm delivery may benefit from treatment in the early second trimester with a lower metronidazole dose (250 mg three times a day) for 1 week. Low-risk women who have not had a premature delivery can be treated to relieve symptoms. Treatment is not currently a standard recommendation for nonpregnant asymptomatic women (Table 7) . ^{[5] [9]}

 

 

Herpes Simplex Virus Infection

Genital herpes simplex virus (HSV) infection is a DNA virus. The strains that infect the genital tract are HSV-1 and HSV-2. Studies in 12- to 19-year-olds have shown HSV-2 seroprevalence rates of 4.3% to 11.7%. Although HSV-2 is more commonly found in the lower genital tract, both strains can cause lower tract disease. Recurrent disease is possible with both types, but HSV-2 is more commonly recurrent in the genital area, and HSV-1 is more likely to recur in the oral area. Some protection is afforded by prior infection with HSV-1. Oral HSV-1 protects against subsequent HSV-1 disease in the genital area, and although it does not provide complete protection against HSV-2, it does seem to ameliorate the symptoms. ^[9]

The initial infection with HSV can last for several weeks and is frequently accompanied by systemic symptoms, including fever, headache, malaise, and myalgia. The lesions are classically painful groups of small vesicles and ulcers; however, atypical clinical presentations, including small linear ulcerations, are possible. These atypical lesions can be confused with trauma or yeast infections. Because the virus retreats to the nerve root ganglion rather than being eradicated, recurrences are possible. Recurrent infections are usually less extensive and of shorter duration, and symptoms are generally confined to the genital area. Subclinical infection with viral shedding in the absence of lesions is most common in the first 6 months after primary infection. Transmission is still possible with subclinical infection, and patient education about infectivity is extremely important. Complications include aseptic meningitis; transverse myelitis; extragenital lesions; bacterial superinfection; and blood-borne dissemination, including hepatitis, meningitis, pneumonitis, arthritis, and cutaneous dissemination. Risk of transmission to a neonate is highest in women who develop primary herpes in the third trimester. Maternal antibodies seem to protect the neonate such that the risk of transmission from a mother with recurrent HSV-2 is less than 1%. ^[9]

HSV is easily cultured, then subtyped. Viral titers are not clinically useful because the currently available assays do not distinguish well enough between HSV-1 and HSV-2. Although the presence of multinucleated giant cells in a Tzanck preparation of lesions suggests HSV, it is not diagnostic because Tzanck preparation is positive for all herpes viruses, including varicella. Finding a positive culture is most likely early in the illness when a fresh lesion is sampled. ^[9]

Treatment for initial and recurrent infection includes oral acyclovir, valacyclovir, and famciclovir. Systemic therapy should be used because topical acyclovir does not seem to have significant clinical benefit. Valacyclovir has the advantage of twice-a-day dosing for initial infection. If the patient suffers frequent recurrent episodes--defined as six or more recurrences in 1 year--episodic therapy initiated by the patient at the beginning of a prodrome or daily suppressive therapy can reduce recurrences significantly. Although the use of acyclovir in recurrent disease has been studied most extensively, all three drugs can be used. One advantage of valacyclovir is that it can be used once a day rather than twice a day for daily suppressive therapy. The higher dose of 1000 mg of valacyclovir appears to be more effective than 500 mg for patients with more than 10 recurrences per year. Suppressive therapy does not eliminate completely recurrences or infectivity--25% of patients experience breakthrough approximately every 3 months. Intravenous therapy should be instituted in the case of severe or systemic disease. There are currently no recommendations on the use of these agents during pregnancy (Table 8) . ^{[5] [9]}

 

 

Human Papillomavirus

HPV is a DNA virus of which there are approximately 75 different types. More than 30 types have been found to infect the genital tract, and some types, in particular, 16, 18, 31, and 45, cause neoplastic lesions. ^[9] Type 16 has been found in association with 50% of cervical cancers, whereas types 6 and 11 are low risk. ^{[9] [14]} The cervix and anus are most vulnerable to squamous intraepithelial lesions (SIL). Studies looking for HPV DNA in adolescents have found rates of approximately 15% to 57%. ^[14] Clinical presentation of HPV ranges from overt lesions known as condylomata acuminata to subclinical infection, which is detected through cytology and visualized by application of acetic acid and viewed with the aid of a colposcope. ^{[9] [14]} Acetic acid causes coagulation of protein in abnormal cells, producing an acetowhite reaction on the mucosal surface. Condylomata acuminata usually contain viral types that are not oncogenic, whereas subclinical infection is more commonly caused by the aggressive HPV types. Vulvar and penile cancers are much less common, and the rest of this discussion focuses on cervical infection. ^{[9] [14]}

The major risk factor for HPV is sexual activity, and rates of infection increase with the number of sexual partners. Younger age also is a risk factor, and this is most likely related to poorer use of condoms and having more and riskier partners. ^{[9] [14]} Studies of the natural history of HPV infection show that 70% of adolescents with high-risk types and 90% with low-risk types clear the infection within 30 months. ^[9] Some patients show persistent infection, and host immune response related to cell-mediated immunity is considered an important factor. Patients with persistent high-risk viral types have an increased risk of high-grade SIL. Although 90% of adolescents with low-grade SIL show regression, those with persistent infection tend to have persistence of low-grade SIL as well. As previously mentioned, adolescents may have increased risk from consequences of HPV because of the cervical ectropion. Older women may have more immunity to the infection and are able to clear the virus more quickly. ^[14]

Routine PAP smears are the best screen for cervical abnormalities in sexually active adolescent women. Screening for HPV using DNA testing is not a standard of care because the virus is so prevalent and the likelihood of high-grade disease is so low in adolescents. ^[14] The Bethesda system (see the accompanying box ) is the standard used to describe the cytologic abnormalities found on PAP smears. ^{[8] [16]} Abnormal PAP smears have been found in 3% to 17% of adolescents, with the wide variation due, in part, to the degree of abnormality included in the study and the population being studied. ^[8] PAP smears are not perfect, and false-negative rates are 20% to 60%. ^[8] New techniques have been developed to improve cytologic readings, including the ThinPrep (CYTYC Corporation, Marborough, MA) and PapNet (Neuromedical Systems, Suffern, NY). The ThinPrep method involves the collection of cells in a liquid transport medium and preparation of a cell monolayer that should eliminate problems with fixation and obscuring of cells by inflammation or blood. The PapNet is an automated screener that is supposed to decrease technician error. The PapNet and the PapNet techniques are not currently being widely used because they have not been shown to improve dramatically on standard PAP smear techniques, and they have not proved to be more cost-effective. ^{[9] [14]}

 

 

The follow-up for abnormal PAP smears is controversial. Those with atypical squamous cells of undetermined significance can be followed with a repeat smear in 3 to 6 months, and patients with repeat abnormal smears are referred for colposcopy. Patients with low-grade SIL lesions could be followed similarly if they are compliant. If the patient is not compliant, which may be a significant issue for adolescents, referral for colposcopy and biopsy if appropriate should be considered with the first abnormal PAP result. All patients with high-grade lesions should be referred immediately for colposcopy. Treatment of significant cervical lesions confirmed by biopsy includes cryocautery, carbon dioxide laser treatment, and loop electrosurgical excision procedure. ^[9]

Treatment of external condylomata acuminata includes patient-administered therapies, such as podofilox and imiquimod cream, and clinician-applied therapies, such as podophyllin, trichloroacetic acid (TCA), and bichloroacetic acid (BCA), and surgical removal. Imiquimod works by enhancing the local immune system, activating interferon and cytokines. Podofilox is an antimitotic drug. Imiquimod, podophyllin, and podofilox cannot be used during pregnancy. Even with successful resolution of the initial lesions, recurrences are possible, especially in the first 3 months, so patients should be counseled about that possibility (Table 9) . ^{[5] [9]}

 

NEW TESTS FOR SEXUALLY TRANSMITTED DISEASES

Advances in testing for STDs include nucleic acid amplification techniques, which have changed the landscape for STD screening. DNA amplification, including ligase chain reaction (LCR, LC_x , Abbott laboratories, Abbott Park, IL) and polymerase chain reaction (PCR, Amplicor, Roche Diagnostics, Branchburg, NJ), and ribosomal RNA amplification (transcription-mediated amplification [TMA], GenProbe Amplified, Gen-Probe Inc, San Diego, CA) are now available. LCR can be used on cervical, urethral, and first-voided urine specimens in men and women to test for gonorrhea and chlamydia. PCR and TMA can be used on cervical, urethral, and first voided urine for chlamydia, although PCR testing of urine is currently limited to males. Culture had been the traditional gold standard, but this method frequently is subject to problems related to transport and storage. In many studies, the amplification tests, particularly for chlamydia, are more sensitive than culture, and the urine-based testing is sensitive enough to provide a noninvasive alternative for screening. Urine-based testing is much less threatening to adolescents and opens up the possibility of more extensive screening, including use in nontraditional settings, such as schools and recreation centers. Because these amplification tests are so sensitive, test of cure should not be done for at least 3 weeks after completion of treatment to prevent false-positive reporting. Only culture tests are permitted in cases of abuse because it is not possible to have a false-positive test. ^[9]

 

CONCLUSION

STDs are a major concern for the sexually active adolescent. Although the problem may seem overwhelming at first glance, a few points are important to remember. Sexuality education is key to ensuring that adolescents have the correct information on these diseases. Multiple studies have shown that sex education does not cause adolescents to become sexually active. ^[16] Some programs have been successful in delaying the onset of sexual activity. ^[12] Adolescents who are given comprehensive information, which includes abstinence messages as well as information on use of condoms and other methods of contraception, are more likely to protect themselves if they become sexually active. ^{[11] [12] [16]} Intervention with adolescents needs to address more than just knowledge. It is essential to include interactive teaching methods, practicing techniques of proper condom usage and partner negotiation and communication, and reinforcement of individual as well as group values. ^{[9] [11]} Adolescents need to become familiar with the clinical services available to them for STD-related care, and clinicians must become more creative in reaching out to adolescents in less traditional settings. Community education on the extent of the problem and mobilization to improve access to care must not be forgotten because they are essential elements in addressing the STD epidemic. ^{[9] [10]}

References

1. Burstein GR, Gaydos CA, Deiner-West M, et al: Incident Chlamydia trachomatis infections among inner-city adolescent females. JAMA 280:521-526, 1998  abstract

2. Borchardt KA, al-Haraci S, Maida N: Prevalence of Trichomonas vaginalis in a male sexually transmitted disease clinic population by interview, wet mount microscopy, and the InPouch TV test. Genitourin Med 71:405-406, 1995  abstract

3. Borchardt KA, Smith RF: An evaluation of an InPouch TV culture method for diagnosing Trichomonas vaginalis infection. Genitourin Med 67:149-152, 1991  abstract

4. Centers for Disease Control, National Center for Health Statistics: Fertility, Family Planning, and Women's Health: New Data From the 1996 National Survey of Family Growth. Vital and Health Statistics Series 23, No. 19. Hyattsville, MD, DHHS, 1997  

5. Centers for Disease Control: 1998 Guidelines for the treatment of sexually transmitted diseases. MMWR Morb Mortal Wkly Rep 47:1-118, 1997  

6. Centers for Disease Control: Youth Risk Behavior Surveillance--United States, 1997. Morb Mortal Wkly Rep CDC Surveill Summ 47:1-89, 1998  

7. Draper D, Parker R, Patterson E, et al: Detection of Trichomonas vaginalis in pregnant women with the InPouch TV culture system. J Clin Microbiol 31:1016-1018, 1993  abstract

8. Emans SJ, Laufer MR, Goldstein DP (eds): Pediatrics and Adolescent Gynecology, ed 4. Philadelphia, Lippincott-Raven, 1998  

9. Holmes KK, Sparling PF, Mardh P-A, et al (eds): Sexually Transmitted Diseases, ed 3. New York, McGraw-Hill, 1999  

10. Institute of Medicine: The Hidden Epidemic: Confronting Sexually Transmitted Diseases. Washington, DC, National Academy Press, 1997  

11. Jemmott JB, Jemmott LS, Fong G: Abstinence and safer sex HIV risk reduction interventions for African American adolescents: A randomized controlled trial. JAMA 279:1529-1536, 1998  abstract

12. Kirby D, Short L, Collins J, et al: School-based programs to reduce sexual risk behaviors: A review of effectiveness. Public Health Rep 109:339-360, 1994  abstract

13. Lawson MA, Blythe MJ: Pelvic inflammatory disease in adolescents. Pediatr Clin North Am 46:767-782, 1999  full text

14. Moscicki A-B: Human papillomavirus infection in adolescents. Pediatr Clin North Am 46:783-807, 1999  full text

15. Spence MR, Adler J, McLellan R: Pelvic inflammatory disease in the adolescent. J Adolesc Health Care 11:304-309, 1990  abstract

16. Stasburger VC, Brown RT: Adolescent Medicine: A Practical Guide, ed 2. Philadelphia, Lippincott-Raven, 1998  

17. U.S. Department of Health and Human Services: Sexually Transmitted Disease Surveillance 1997. Atlanta, CDC, 1998  

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