Sexually Transmitted Diseases in Adolescents
Sexually Transmitted Diseases in Adolescents
Author: Eileen M. Duffy, MD, FAAP, FACEP, Assistant Professor, Department of Surgery, Division of Emergency Medical Services, Loyola University Medical Center, Maywood, IL.
Peer Reviewer: Maureen McCollough, MD, MPH, FACEP, Assistant Professor of Medicine, UCLA School of Medicine; Director of Pediatric Emergency Medicine, OliveView-UCLA Medical Center, Sylmar, CA.
Sexually transmitted diseases (STDs) are occurring in epidemic proportions in sexually active adolescents. This age group accounts for approximately 25% of the 12 million cases of STDs occurring annually in the United States.1 The prevalence of Neisseria gonorrheae, Chlamydia trachomatis, and possibly even human papilloma virus (HPV) infections are highest among the adolescent age group. In 1996, of the 325,000 people infected with gonorrhea in the United States, about 60% of cases occured in young adults between the ages of 15 and 24.2 Approximately 4 million cases of chlamydia occur each year in the United States. Although age-specific rates are not available for chlamydial infections, a study from family planning clinics showed the prevalence to be three times higher in females younger than 18 years of age than in those older than 29 years of age.3 The rate of HPV infection is also reported to be 2-3 times higher in young women.4 This article comprehensively reviews a variety of STD syndromes, their clinical presentation, diagnostic evaluation, and management.
— The Editor
Introduction
In the 1997 Youth Risk Behavior Surveillance Survey, almost 50% of high school students polled had been sexually active.5 Several factors place these adolescents at increased risk for acquiring STDs. First, this age group is more likely to practice unprotected intercourse. According to the risk behavior survey, only 57% reported that either they or their partner had used a condom the last time they had intercourse. Adolescents are also biologically more susceptible to infection than adults. In addition, health care services are less readily accessible to adolescents.
Long-term sequelae may occur in up to 25% of patients with certain STDs,6 and management in an emergency department (ED) setting is frequently based on a presumptive diagnosis as results of definitive tests are not immediately available—making follow-up a critical aspect of ED care. The vulnerability of this age group mandates a careful, thorough ED evaluation and scheduled follow-up.
History and Physical Examination
Clinicians must appreciate the value adolescent patients place on confidentiality. In most states, they can consent to the diagnosis and treatment of STDs without parental knowledge. Likewise, adolescents can consent to HIV counselling and testing in many states. Familarity with state laws governing STDs and adolescents is essential to the ED physician’s ability to provide care.
Eliciting accurate information from adolescents can be challenging. The medical history should be obtained privately, without parents present. If the patient’s presentation may be consistant with an STD, information obtained should include date of last menstrual period, sexual activity, number of partners and their health, contraceptive use, history of STDs, and symptoms suggestive of STDs.
Since STDs may present with a wide variety of findings, the examination must include inspection of the skin, oropharynx, lymph nodes, abdomen, genitalia, and anorectal region. Cultures and serologic testing should be obtained as indicated, and all females should have a pregnancy test. Screening for syphilis and HIV should be considered in all patients with STDs.
Urethritis
Urethritis. N. gonorrheae. Urethritis is divided into gonococcal and non-gonococcal etiologies. N. gonorrheae is a gram-negative diplococcus that accounts for 15-32% of urethritis in symptomatic adolescent males. The incubation period is 3-7 days after exposure. Gonorrheal infections of the urethra are symptomatic in 85-90% of cases.8 Patients who practice oral or receptive ano-rectal sex may also develop gonorrheal pharyngitis or proctitis. As many as 20% of males with gonococcal urethritis are coinfected with chlamydia.9
Chlamydia trachomatis. Chlamydia trachomatis is an obligate intracellular parasite that accounts for 23-55% of non-gonococcal urethritis (NGU) in adult men.10 Chlamydia may be more prevalent in adolescents. Studies have isolated the organism in 83-89% of patients with urinalysis evidence of NGU.11 The incubation period to symptomatic disease is 7-14 days. Of note, approximately 5-10% of sexually active males are infected with chlamydia but remain asymptomatic.12
Other sexually transmitted organisms causing NGU include Ureaplasma urealyticum, Mycoplasma genitalium, and Trichomonas vaginalis.10 Herpes simplex virus (HSV) may also cause urethritis; however, this is usually accompained by typical skin lesions. In approximately 20% of cases, the cause of urethritis is unknown.13
The microbiology of sexually transmitted urethritis in females has not been extensively studied. It is thought to be similar to that seen in males.
Clinical Presentation. Urethritis in males most commonly presents as dysuria and/or urethral discharge. Other symptoms may include urinary urgency or frequency, scrotal pain, and meatal irritation. The differential includes other causes of urethral irritation such as foreign bodies, ulcers, or other lesions.
Urethritis may also occur in females, with symptoms simulating a urinary tract infection (UTI). Typically, concurrent signs and symptoms of a cervical infection are present when the etiology is due to a sexually transmitted organism.
It is difficult to differentiate gonococcal vs. non-gonococcal urethritis on exam alone. Classically, gonorrhea is associated with expression of a purulent urethral discharge, while a serous or mucoid discharge is usually associated with NGU.
Diagnosis. Urethritis may be diagnosed when any of the following is present:
1. Mucopurulent or purulent urethral discharge;
2. Gram stain of discharge with five or more white blood cells (WBCs) per oil immersion field. A presumptive diagnosis of gonorrhea can be made if intracellular gram-negative diplococci are present; or
3. Positive leukocyte esterase test or demonstration of more than 10 WBCs per high powered field on a first-void urine.10
Identifying the organism is important for infection control. The gold standard of using culture techniques to isolate gonorrhea and chlamydia are largely being replaced by non-culture tests. DNA amplification techniques using polymerase chain reaction (PCR) or ligase chain reaction (LCR) and nucleic acid hybridization (NAH) techniques have been shown to be more sensitive and nearly as specific in identifying these agents. NAH and LCR offer the advantage of requiring one swab to test for both gonorrhea and chlamydia. Specifically, studies have shown that PCR and LCR detect these agents in urine with more sensitivity than culture techniques, thus eliminating the need for urethral swabbing.7,14 Direct fluorescent antibody (DFA) staining and enzyme immunoassay (EIA) tests are also available to detect chlamydia.
Urethral cultures are still indicated in cases of abuse and rape as non-culture methods have a small potential for false-positive results. Swabs with cotton tips and wooden shafts should be avoided, as they may interfere with the culture. Specimens for gonorrhea are plated on chocolate agar and modified Thayer-Martin media and transported in CO2 containing systems. Culture of chlamydia is more difficult and requires a laboratory staff experienced in the technique and handling of specimens. Even in an experienced laboratory setting, the sensitivity is only about 70-90%.15
Treatment. Since it is difficult to distinguish gonococcal from non-gonococcal causes of urethritis on physical exam, treatment should include coverage for both gonorrhea and chlamydia in symptomatic patients.10 (See Table 1.) Single-dose regimens are strongly recommended given the high rate of compliance when administered under direct observation. Patients with HIV should be treated with the same regimen as those who are HIV negative. Quinolones are not approved for the treatment of patients younger than 18 years of age. Fluoroquinolone-resistant strains of gonorrhea are widespread in Asia but have only been reported sporadically in the United States and, therefore, have not altered current treatment recommendations.10 Patients should be advised to abstain from sexual intercourse until treatment is completed and clinical symptoms have resolved.
| Table 1. Treatment of Urethritis, Epididymitis, and Cervicitis |
| Recommended Regimens for the Treatment of Gonococcal Infections |
| Cefixime 400 mg po (single dose) |
| or |
| Ceftriaxone 125 mg IM (single dose) |
| or |
| Ciprofloxacin 500 mg po (single dose) |
| or |
| Cfloxacin 400 mg po (single dose) |
| Plus |
| Recommended Regimens for the Treatment of Chlamydia |
| Azithromycin 1 gm po (single dose) |
| or |
| Doxycycline 100 mg po bid for 7 days |
Complications. Left untreated, the symptoms of urethritis usually resolve spontaneously, although infectivity persists. Symptomatic complications of urethritis include epididymitis, Reiter’s syndrome, and disseminated gonococcal infection. Reiter’s syndrome consists of the triad of a reactive arthritis, NGU, and conjunctivitis. Although typically occuring after an enteric infection, Reiter’s syndrome has also been associated with chlamydial urethritis. The majority of patients are HLA-B27 positive and therefore genetically predisposed.16
Epididymitis
Etiology. Gonorrhea and chlamydia are responsible for 67% of cases of epididymitis in sexually active adolescents and young men. Gram-negative enteric organsims are a more common cause of epididymitis in men older than 35 years and in younger males who practice anal intercourse.17
Clinical Presentation. Scrotal pain and swelling are the most common symptoms associated with epididymitis. Onset may be acute or gradual, with the scrotum eventually becoming warm and erythematous. Symptoms of urethritis are usually present. Occasionally the patient will be febrile.
On examination, the scrotum is typically swollen, erythematous, and warm. Differentiating epididymitis from testicular torsion can be difficult. With epididymitis, palpation revels exquisite tenderness over the epididymus. Scrotal swelling may make it difficult to discern this structure. A urethral discharge may be present. The cremasteric reflex is usually preserved in epididymitis and absent in testicular torsion. However, 30% of normal males do not have an elicitable reflex.7
Diagnosis. As with urethritis, gonorrhea and chlamydia may be diagnosed by culture or non-culture methods. A mid-stream, clean-catch urine culture can identify infections caused by gram-negative enteric organisms. If testicular torsion cannot be ruled out on clinical exam, a testicular scan or Doppler ultrasound should be performed. A urologist should be notified as soon as the diagnosis of torsion has been made or if there is going to be any delay in getting a testicular scan or ultrasound.
Treatment. When the etiology is gonorrhea or chlamydia, treatment is the same as for urethritis.10 (See Table 1.) Partners should be notified and treated and patients should abstain from sexual intercourse until fully treated and asymptomatic.
Disseminated Gonococcal Infection
Left untreated, gonorrheal mucosal infection can spread hematologically, causing a disseminated disease in 0.5-3% of cases.18 The incubation period ranges from 7 to 30 days, and symptoms include a migratory asymmetric tenosynovitis of multiple joints, fevers, and skin lesions. The rash occurs in about 75% of cases and is characterized by papular lesions that may progress to pustular or purpuric lesions.9 In the early phase of disseminated gonococcal infection (DGI), blood cultures may be positive, however, joint aspirates are typically negative. As DGI progresses, septic arthritis will develop in one or more joints, most commonly the knee, followed by the elbow, ankle, wrist, foot, and hand. In patients younger than 45 years, gonorrhea is the most common etiology of septic arthritis.19 In this phase, blood cultures will be negative, whereas joint aspirates will reveal gonococcus. Cultures should also be obtained from the genital tract. Endocarditis and meningitis may complicate DGI. Patients with DGI are hospitalized for IV therapy.10 (See Table 2.) These patients should also be treated presumptively for chlamydial infection. Therapy is generally switched to an oral regimen 24-48 hours after clinical improvement is noted.
| Table 2. Treatment of Disseminated Gonococcal Infection |
| Recommended Initial Regimen |
| Ceftriaxone 1 g IV every 24 hours |
| Alternative Initial Regimen |
| Cefotaxime 1 g IV every 8 hours |
| or |
| Ceftizoxime 1 g IV every 8 hours |
| For Persons Allergic to Beta-lactam Drugs |
| Ciprofloxacin 500 mg IV every 12 hours |
| or |
| Ofloxacin 400 mg IV every 12 hours |
| or |
| Spectinomycin 2 g IM every 12 hours |
Cervicitis
Etiology. Gonorrhea and chlamydia are the most common infectious agents causing cervicitis. Symptomatic gonococcal cervicitis typically presents within 10 days of contact with an infected person. Approximately 25% of women infected with gonorrhea will be asymptomatic.20 As many as 50% of patients with gonococcal cervicits are coinfected with chlamydia.21 Chlamydia has an incubation period of 7-14 days to symptomatic disease. Approximately 30-80% cases of cervicitis due to chlamydia are asymptomatic.20
Clinical Presentation. Females with cervicitis typically present with vaginal discharge. Dysuria may be a predominent symptom if there is a concomittant urethritis. Presenting complaints may also include abnormal vaginal bleeding, post-coital vaginal bleeding, and dyspareunia.
On pelvic exam, a cervical discharge is usually noted. Traditionally, the discharge associated with gonorrhea is purulent while the discharge seen with chlamydia cervicitis is mucoid. In reality, it is usually difficult to distinguish the etiology based on physical examination alone. A positive Q-tip sign occurs when a sample of the discharge changes the color of the white cotton tip. Cervical edema, erythema, and friability may be present. It is not unusual to see vaginal spotting during culture collection.
The oropharynx and anorectal areas should be inspected as well. Gonorrhea may cause pharyngitis or proctitis with minimal symptomatology in patients who practice oral or anorectal receptive sex.
Diagnosis. Screening for both gonorrhea and chlamydia should be performed on any female suspected of having cervicitis. Culture specimens must be taken from the endocervical canal and plated as described in the section on urethritis. The specifity of culture techniques is 100%; however, the sensitivity for gonorrhea and chlamydia is less (80-95% and 70-80%, respectively).21 Although culture techniques remain the gold standard for diagnosis, they are more commonly reserved for cases where legal issues arise (i.e., rape and abuse). DFA, EIA, and NAH are both sensitive and specific for identifying gonorrhea and chlamydia from endocervical samples. Recent studies have demonstrated DNA amplification tests (LCR, PCR) on first-void urines to be as sensitive and specific as endocervical cultures.1,21
Treatment. Empiric treatment of cervicitis must cover both gonorrhea and chlamydia.10 (See Table 1.) In order to ensure compliance, single-dose regimens are recommended; however, quinolones are not recommended in patients younger than 18 years. Doxycycline and quinolones are contraindicated during pregnancy.10 (See Table 3.) HIV-infected patients are treated the same as HIV-negative patients. Sexual partners should be evaluated and tested as well.
| Table 3. Treatment of Cervicitis in Pregnant Women |
| Recommended Regimens for the Treatment of Gonorrhea |
| Cefixime 400 mg po (single dose) |
| or |
| Ceftriaxone 125 mg IM (single dose) or (if unable to tolerate cephalosporins) |
| Spectinomycin 2 g IM (single dose) |
| Plus |
| Recommended Regimens for the Treatment of Chlamydia |
| Erythromycin Base* 500 mg po qid for 7 days |
| or |
| Amoxicillin 500 mg po tid for 7 days |
| * erythromycin estolate is contraindicated in pregnancy |
Complications. Disseminated gonococcal infection (see prior section) and pelvic inflammatory disease (PID) are potential significant complications of untreated cervical infections.
Pelvic Inflammatory Disease
PID is a bacterial infection of the upper genital reproductive tract in females. Each year, more than 1 million cases occur in the United States, with adolescents comprising about 20% of the total.22 Significant, long-term sequelae occur in 25% of women with a history of PID.23 Adolescents are at particular risk for sequelae due to a delay in seeking treatment and non-compliance with therapy.
Etiology. Studies of direct cultures from the upper genital tract have shown PID to be polymicrobial in nature.24,25 The most important causative agents remain chlamydia and gonorrhea, which account for more than 50% of the cases.6 Other pathogens isolated represent microflora from the vagina and bowel, including Escherichia coli, Bacteroides species, anaerobic cocci, Mycoplasma hominis, and Ureaplasma urelyticum.6
Clinical Presentation. Lower abdominal pain is the most common presenting symptom. Typically, the pain is bilateral and sharp. Local peritoneal symptoms may cause patients to walk stooped over with a shuffling gait. An abnormal vaginal discharge is reported in up to 50% of patients. Other symptoms include dysfunctional uterine bleeding, dysuria, dyspareunia, nausea, vomiting, and fever. Women may have asymptomatic PID, which is not recognized until evaluation for infertility reveals tubal scarring and serum antibodies to chlamydia and gonorrhea.22
Pelvic examination typically shows signs of cervicitis, including a mucopurulent discharge. Uterine and/or adnexal tenderness may be present. Cervical motion tenderness is a hallmark of acute PID, although it is not reliably present in all cases. Peritoneal signs may be elicited on abdominal exam.
Diagnosis. Laparoscopy is considered the gold standard for diagnosing PID, but because of the expense and invasiveness of this procedure, it is not routinely used in the emergency diagnosis of PID. The Centers for Disease Control and Prevention (CDC) recommended criteria for diagnosing PID rely on clinical findings through a direct physical examination and selected lab tests.10 (See Table 4.) Endocervical cultures for gonorrhea and chlamydia should be obtained, although most cases of PID also involve other aerobic and anaerobic organisms. It is also important to obtain a pregnancy test, as this will affect treatment. An ultrasound study can aid in differentiating PID from other conditions with similar presentations, including appendicitis, ovarian torsion, and ovarian cysts. Ultrasound is mandatory in the symptomatic pregnant patient to exclude the diagnosis of ectopic pregnancy.
| Table 4. CDC Guidelines for the Diagnosis of PID |
| Minimum Criteria |
| Lower abdominal tenderness, |
| Adnexal tenderness, and |
| Cervical motion tenderness |
| Additional Criteria Supporting a Diagnosis of PID |
| Oral temperature > 101°F (38.3°C) |
| Abnormal cervical or vaginal discharge |
| Elevated erythrocyte sedimentation rate |
| Elevated C-reactive protein |
| Laboratory documentation of cervical infection with |
| N. gonorrhoeae or C. trachomatis |
Treatment. Empiric treatment for PID should be administered if the minimal CDC criteria are present without another identifiable etiology. Current CDC criteria for hospitalization no longer include mandatory admission of adolescent females; however, the clinician must have a low threshold for admitting adolescents if compliance or follow-up is in question.10 (See Table 5.) Due to the polymicrobial etiology of PID, treatment must include broad-spectrum antibiotics. Current guidelines for in-patient treatment are listed in Table 6.10 Patients admitted for parenteral therapy may be discharged 24 hours after showing clinical improvement on a regimen of doxycycline or clindamycin to complete a total of 14 days of treatment. Patients initally managed with an out-patient oral regimen should be reevaluated within 72 hours and admitted if no improvement is noted. (See Table 7.)10
| Table 5. CDC Criteria for Hospitalization to Treat PID |
| - Diagnosis is in question |
| - Pregnancy |
| - Patient fails outpatient treatment |
| - Patient is unable to follow or tolerate an outpatient oral regimen |
| - Patient has nausea, vomiting, or high fever |
| - Patient has a tubo-ovarian abscess |
| - Patient is immunodeficient (i.e., HIV with low CD4 counts) |
| Table 6. Parenteral Treatment of PID |
| Regimen A |
| Cefotetan 2 g IV every 12 hours |
| or |
| Cefoxitin 2 g IV every 6 hours |
| Plus |
| Doxycycline 100 mg IV or po every 12 hours |
| Regimen B |
| Clindamycin 900 mg IV every 8 hours |
| Plus |
| Gentamicin loading dose 2 mg/kg IV or IM followed by a maintenance of 1.5 mg/kg every 8 hours (single daily dosing may be substituted) |
| Table 7. Oral Treatment of PID |
| Regimen A |
| Ofloxacin 400 mg po twice a day for 14 days |
| Plus |
| Medtronidazole 500 mg po twice a day for 14 days |
| Regimen B |
| Ceftriaxone 250 mg IM (single dose) |
| or |
| Cefoxitin 2 g IM plus Probenecid 1 g po (single dose) |
| Plus |
| Doxycycline 100 mg po twice a day for 14 days |
Complications. Acute complications of PID include tubo-ovarian abscess (TOA) formation, peritonitis, and peri-hepatitis (Fitz-Hugh-Curtis syndrome). Patients with a TOA usually appear ill and typically present with fever and severe lower abdominal pain. Exam reveals localized tenderness over an adnexal mass. Ultrasound can be used to confirm the presence of an abscess. A ruptured TOA represents a surgical emergency. Treatment of an unruptured TOA is more controversial but generally involves conservative management with IV antibiotics in a regimen similar to that used for PID.
Peritonitis results when microorganisms exit the fallopian tubes and enter the peritoneal cavity. Infection that tracks up the paracolic gutter causing inflammation of the liver capsule is known as the Fitz-Hugh-Curtis syndrome. Patients typically present with sudden onset of severe right upper quadrant pain that may refer to the right shoulder. Pain in the right upper quadrant may overshadow pelvic pain, making the diagnosis more elusive. In a few cases, ultrasound was helpful in demonstrating peritoneal fluid around the liver and spleen and ruling out cholelithiasis.26
Significant long-term complications from PID result from tubal and intra-abdominal scarring and include chronic pelvic pain, infertility, and increased risk of ectopic pregnancies. The risk of infertility following the first episode of PID is 12% and increases following each subsequent episode.27 The risk for ectopic pregnancy is 7- to 10-fold greater in women with a history of PID.27
Vaginitis
Patients with vaginitis typically present with vaginal discharge accompanied by irritation, itching, burning, and/or dyspareunia. Candidiasis, trichomonas infection, and bacterial vaginosis are the most common causes of an abnormal vaginal discharge. Candidal infection will not be discussed here as it is not usually transmitted sexually.
Trichomonas Infection. Women infected with the protozoa T. vaginalis will usually complain of a malodorous discharge that is frequently accompanied by pruritus, dyspareunia, and post-coital bleeding. As many as 25-50% of infected women will be asymptomatic.28 On examination, the discharge is typically purulent, however, the classic "frothy" discharge is only seen in 12% of cases.28 Punctate hemorrhage of the cervix (strawberry cervix) is seen in only 2% of patients.28
Testing for the presence of amines by mixing a sample of secretions with a drop of 10% KOH will produce the characteristic fishy odor (Whiff test). Diagnosis is made by identifying motile, flagellated trichomonads by saline microscopy. The sensitivity for this test ranges around 60%.28 Culture techniques are available when a more definitive diagnosis is required. PCR tests may be available in the near future to further aid in the diagnosis.
Metronidazole is the only effective treatment for trichomonas vaginitis. The recommended regimen is 2 gm orally in a single dose. The alternative regimen is 500 mg twice a day for seven days.10 Patients who are allergic to metronidazole should be desensitized. HIV-infected patients should receive the same treatment protocol. Sexual partners should also be treated.
Bacterial Vaginosis. Bacterial vaginosis, formerly known as non-specific or Gardnerella vaginitis, is a polymicrobial infection of the vagina. Fifty percent of women will be asymptomatic.28 Symptoms that may be present include a thick, malodorous vaginal discharge that is associated with pruritus or irritation in up to 67% of cases.28 Meeting three of Amsel’s criteria is sufficient to make the diagnosis:
1. Homogeneous gray or white discharge on exam;
2. Vaginal pH greater than 4.5;
3. Positive whiff test; and/or
4. Clue cells on saline microscopy.29
Treatment regimens for bacterial vaginosis are listed in Table 8.10 HIV-positive patients are treated similarly. Routine treatment of sexual partners is not recommended.
| Table 8. Treatment of Bacterial Vaginosis |
| Recommended Regimen |
| Metronidazole 500 mg po twice a day for 7 days |
| or |
| Clindamycin cream 2%, one applicator full intravaginally for 7 days |
| or |
| Metronidazole gel 0.75%, one applicator full intra-vaginally twice a day for 5 days |
STDs Associated with Lesions
In the United States, herpes simplex virus (HSV) accounts for the majority of genital ulcers. Other disease processes that may be associated with lesions include syphilis and chancroid. In developing nations, chancroid and granuloma inguinale predominate. More than one infectious agent is found in 3-10% of cases.30 Of note, these infectious diseases are associated with an increased risk of HIV infection.
Herpes Simplex Virus. It is estimated that 20% of the United States population older than 12 years is infected with HSV.31 HSV1 is associated with oral or facial lesions, while HSV2 typically affects the genital area (however cross-over does occur). The organism is highly contagious, with an 80% transmission rate after a single sexual exposure to an individual actively shedding the virus.32
Primary infection with HSV follows an incubation period of 2-10 days after sexual contact. Manifestations include mucosal and/or cutaneous lesions as well as systemic symptoms. It is not uncommon for patients to experience a 1- to 2-day prodrome of localized tingling, burning, and irritation before lesions appear. Painful, itchy, vesicular, or ulcerated lesions with an erythematous base develop. Lesions may coalesce and cause significant swelling and pain. As a result, patients may present with urinary retention as a chief complaint.33 Extra-genital lesions due to self-innoculation may be seen on the buttocks, fingers, hands, or legs in 20% of cases.34 The sores and pain may last up to six weeks. Mucopurulent discharge occurs with urethral or cervical involvement. Dysuria occurs in males and females with HSV urethritis. As many as 50% of patients will also experience fever, myalgias, arthralgias, nausea, vomiting, and headache. Aseptic meningitis occurs in up to 8%.34 Often, tender, non-fluctuant lymphadenopathy is present. Pharyngitis is seen in 10-15% of cases.33 Herpes proctitis is associated with severe rectal pain, tenesmus, and rectal discharge. Immunosuppressed patients are at risk for more disseminated infection.
Following the primary infection, HSV travels to the dorsal root ganglia where it remains latent until reactivation occurs.35 Secondary outbreaks occur in up to 90% of patients with initial genital involvement.36 Reactivation may also be heralded by a prodrome of burning or paresthesias. These episodes tend to be less painful and of shorter duration than the primary infection. Lesions occur in the same nerve distribution as the primary infection but are fewer in number and last for only 5-10 days. Constitutional symptoms are uncommon with reactivation. Patients may have reactivation without a clear history of primary infection. Up to 25% of recurrent episodes are asymptomatic; however, viral shedding still occurs.34
The characteristic ulcerated lesion usually makes HSV an easy diagnosis on clinical grounds alone. A Tzanck test, whereby a vesicle is unroofed and material from the base is stained with Giemsa or Wright’s stain, can confirm the diagnosis by demonstrating multinucleated giant cells. This test is very specific for HSV but is only 30-50% sensitive.37 EIA and DFA tests are also available as well as viral cultures.
Some antivirals have been shown to reduce the duration of viral shedding and symptoms with primary infection when started within five days of symptom onset.35 If taken during the prodrome period or within one day after onset of lesions in a reactivation infection, the duration of symptoms may shorten by 1-2 days.38 Treatment does not prevent latency of the virus or reactivation of disease.38 Patients should be advised to avoid intercourse when an active herpetic infection is present.
Oral acyclovir, famciclovir, and valacyclovir are approved for the treatment of primary and reactivation herpes. (See Table 9.)10 The topical form of acyclovir is far less effective and therefore not recommended. Intravenous therapy is recommended for patients with more severe, systemic infection, including patients with disseminated infections, pneumonitis, hepatitis, or meningitis.
| Table 9. Genital Herpes: Recommended Regimens for Treatment |
| Recommended Regimen |
| Acyclovir 400 mg po three times a day for 7-10 days |
| or |
| Acyclovir 200 mg po five times a day for 7-10 days |
| or |
| Famciclovir 250 mg po three times a day for 7-10 days |
| or |
| Valacyclovir 1 g po twice a day for 7-10 days |
| Recommended Regimen for Recurrent Infection |
| Acyclovir 400 mg po three times a day for 5 days |
| or |
| Acyclovir 200 mg po five times a day for 5 days |
| or |
| Acyclovir 800 mg po twice a day for 5 days |
| or |
| Famciclovir 125 mg po twice a day for 5 days |
| or |
| Valacyclovir 500 mg po twice a day for 5 days |
| Severe Disease |
| Acyclovir 5-10 mg/kg IV every 8 hours for 5-7 days or until clinical resolution is noted |
Initial episodes of herpes proctitis and oral infections may require higher dosages of acyclovir (400 mg 5 times daily).10 Valacyclovir and famciclovir have not been adequately studied for these particular infections. HIV patients may require higher doses of antivirals as well.
Syphilis
Syphilis is caused by the spirochete Treponema pallidum, which is spread after contact with infectious lesions. The majority of cases are acquired by sexual exposure; however, syphilis can also be transmitted by kissing, transfusion of fresh blood from an infected person, and congenitally.39
Between 1985 and 1990 there was a 75% increase in the incidence of syphilis in the United States.39 An increase in the prevalence of HIV in the 1980s may have played a role. Approximately 15% of persons with syphilis are also HIV positive.40 Since 1990, rates of syphilis have declined.
Syphilis is divided into clinical stages (primary, secondary, latent, and late), although there is considerable overlap of symptoms between stages.
Primary syphilis occurs following an incubation period of 9-90 days, with an average of three weeks, following exposure.41 This stage manifests as one or more painless papules originating at the site of innoculation. The lesion(s) erode and develop into the classic chancre with a well-defined raised border and a hard, ulcerative base. Chancres are most commonly located on the external genitalia but, dependent on site of innocuation, may also occur on the cervix, the perianal area, or the oropharynx. These lesions are teeming with spriochetes. Chancres are accompanied by painless regional lymphadenopathy (LAN) in about 50% of patients.40 It is not uncommon for chancres to go unnoticed. They resolve spontaneously in 3-6 weeks without treatment.
Hematogenous and lymphatic spread of T. pallidum will cause more disseminated disease in untreated individuals. Secondary syphilis develops in 9-90 days, with an average of three weeks following the onset of the chancre.41 Rash, LAN, and flu-like symptoms characterize this stage. A painless, non-pruritc, generalized eruption is a prominent feature of secondary syphilis. This rash may mimic other dermatologic conditions, however, there are several characteristics that implicate syphilis as the cause. The rash may be macular, papular, pustular, or a combination of these but is not vesicular. The lesions tend to be pink or red in color, symmetric, discrete, and well demarcated. In addition, the rash is more prominent on the upper extremities and has a predilection for palms and soles. When hair follicles are involved, patients may develop patchy alopecia including loss of the lateral third of eyebrows. The rash may last a few weeks to several months.
Some patients with secondary syphilis may develop mucus patches. These shallow, painless ulcerations with slightly raised borders can develop on any mucosal surface. Mucus patches are packed with spirochetes.
Condyloma lata are raised, flat, grayish papular lesions which are found in moist areas of the body including the anus, vulva, and scrotum. These lesions are also teeming with T. pallidum.
Generalized LAN is a common finding in secondary syphilis. This painless lymph node enlargement usually precedes skin manifestations.
Constitutional symptoms including headaches, fever, malaise, nasal discharge, sore throat, and arthralgias are common. Aseptic meningitis occurs in 1-2% of infected patients.39 Cranial nerve involvement is occasionally seen.
Without treatment, the symptoms of secondary syphilis resolve spontaneously in 1-2 months and patients enter the latent phase. The latent phase is divided into early (less than 1 year duration) and late periods. Typically, patients are asymptomatic during this phase, however, relapses of secondary syphilis may occur, particularly in the first two years.
Late syphilis is rarely seen in the United States. Manifestations often occur 10-20 years following the primary infection and involve the CNS, cardiovascular system, skin, and/or bone.
Testing for syphilis should be considered in any patient with another STD as there is a 6% incidence of coinfection.42 In addition, patients with multiple partners, groin adenopathy, an unexplained generalized rash, or history of cocaine abuse in exchange for sex should undergo screening.
Scrapings of lesions seen in primary and secondary disease will reveal moving, corkscrew-like spriochetes under dark field microscopy. The non-specific serologic tests (VDRL, RPR) use reaginic, cardiolipin-lechithin-cholesterol antigens to detect antibodies to T. pallidum. These quantitative levels correlate with disease activity. They become detectable shortly after patients enter the primary stage and remain elevated through the early latent stage if left untreated. During the late latent period, levels will decrease even without treatment. In the absence of reinfection, properly treated patients with primary syphilis will become seronegative within one year. Patients treated with secondary syphilis will become seronegative within two years. Those with late syphilis should convert in five years following successful treatment. False-positive results may occur with collagen vascular disorders, pregnancy, other spirochete infections, and some viral illnesses.
The treponemal specific tests (FTA-ABS, MHA-TP, and TPI) are more expensive and technically demanding. They are generally reserved to confirm positive non-treponemal tests. Once a patient becomes positive, they are generally positive for life despite adequate treatment.
Parenteral penicillin G is the first-line therapy for all stages of syphilis.10 (SeeTable 10.) Patients who are allergic to penicillin may be tried on doxycycline or tetracycline with close follow-up for treatment failure. For patients with neurosyphilis or syphilis during pregnancy, parenteral penicillin G is the only proven treatment. If these patients are penicillin allergic, they should be desensitized and then treated with penicillin. The Jarisch-Herxheimer reaction, characterized by acute onset of fever, rigors, and possibly hypotension may occur within 24 hours of initiating treatment for syphilis. There is no natural immunity to syphilis so reinfection is possible despite appropriate treatment. Sexual partners should be identified and evaluated serologically for syphilis.
| Table 10. Primary and Secondary Syphilis |
| Recommended Regimen |
| Benzathine penicillin G 2.4 million units IM (single dose) |
| Regimen for Penicillin Allergic Patients |
| Doxycycline 100 mg po twice a day for 2 weeks |
| or |
| Tetracycline 500 mg po four times a day for 2 weeks |
Chancroid
Chancroid, which is caused by the bacteria Haemophilus ducreyi, is endemic in tropical and semi-tropical regions but is uncommon in the United States. Symptoms of infection appear 1-21 days following exposure and present as a papule or pustule at the site of innoculation that eventually erodes into one or more deep, soft, painful ulcers with ragged edges. A yellow-gray exudate usually covers the base of the ulcer. Lesions are usually located on the penis in males and vaginally in females. Painful unilateral or bilateral inguinal lymphadenopathy is present in about 50% of patients.30 These nodes may suppurate and form large bubos in up to 25%.30
Generally, the diagnosis of chancroid is based on a clinical presentation and exclusion of HSV and syphilis. Gram stain of an aspirated bubo or swab of an ulcer may reveal gram-negative coccobacilli in clusters or chains. Culture of H. ducreyi is difficult and requires special media not available in all laboratories. Sensitivity for cultures is less than 80%.10 Recent studies have shown PCR to be sensitive and specific for detecting H. ducreyi.
Treatment is usually based on clinical presentation after considering the more common causes of genital ulcers, including syphilis and HSV. (See Table 11.)10 Resistance to ceftriaxone has been reported in Africa but not in the United States.43 HIV-positive patients can receive the same treatment as HIV-negative patients. All sexual contacts should be treated regardless of symptomatology. Successful treatment results in clinical improvement within three days. Ulcers and lymphadenopathy may take more than two weeks to completely resolve. Fluctuant nodes should be drained by aspiration.
| Table 11. Treatment of Chancroid |
| Recommended Regimen |
| Azithromycin 1 g po (single dose) |
| or |
| Ceftriaxone 250 mg IM (single dose) |
| or |
| Ciprofloxacin 500 mg po twice a day for 3 days |
| or |
| Erythromycin base 500 mg po four times a day for 7 days |
Lymphogranuloma Venereum
Lymphogranuloma venereum (LGV) is caused by Chlamydia trachomatis serotypes L1-3. It is rare in the United States. Following an incubation period of 3-30 days, infection is manifested by small, painless papules, vesicles, or ulcers that heal spontaneously in 2-3 days. Occasionally the primary lesion goes unnoticed. This is followed in 2-3 weeks by painful, typically unilateral, inguinal LAN. Systemic symptoms, including fever, malaise, and headache, may occur with the LAN. The nodes enlarge, coalesce, and eventually ulcerate. Open lesions may drain a purulent discharge. Diagnosis may be made by aspirating lymph nodes and testing for chlamydia by EIA or DFA techniques. Treatment involves a prolonged course of antibiotics due to poor penetration into the lymph nodes. (See Table 12.)10 Fluctuant nodes may be aspirated. All partners having sexual contact with the patient within 30 days of symptom onset must also be treated. HIV-infected patients are also treated as outlined in Table 12.
| Table 12. Treatment of Lymphogranuloma Venereum |
| Recommended Regimen |
| Doxycycline 100 mg po twice a day for 21 days |
| Alternative Regimen |
| Erythromycin base 500 mg po four times a day for 21days |
Granuloma Inguinale
Granuloma Inguinale (GI), another rare sexually transmitted disease in the United States, is caused by Calymmatobacterium granulomatis. Following an incubation period ranging from eight days to 12 weeks, the clinical symptoms of GI take on one of four possible forms. The most common presentation, the ulcerovegetative form, manifests as large, friable, painless ulcerations with a rolled border and beefy red base. There is usually no lymph node involvement. If left untreated, the infection may spread to surrounding tissue, causing extensive destruction of the genitalia. C. granulomatis cannot be readily cultured. Diagnosis depends on identifying the organism within cytoplasmic vacuoles of macrophages (Donovan bodies) in biopsy specimens taken from the advancing edge of the ulceration.
Prolonged antibiotic therapy is required and relapses are not uncommon. (See Table 13.)10 Persons having sexual contact with the patient within 60 days of the onset of symptoms must be treated as well. HIV patients are treated the same as HIV-negative patients.
| Table 13. Recommended Treatment of Granuloma Inguinale |
| Recommended Regimen |
| Trimethoprim-Sulfamethoxazole double-strength tablet po twice a day for 3 weeks |
| or |
| Doxycycline 100 mg po twice a day for 3 weeks |
| Alternative Regimen |
| Ciprofloxacin 750 mg po twice a day for 3 weeks |
| or |
| Erythromycin base 500 mg po four times a day for 3 weeks |
Human Immunodeficiency Virus (HIV)
AIDS was the seventh leading cause of death among persons 15-24 years of age in 1997.44 Although AIDS is a reportable disease in the United States and has reliable prevalence and incidence data, HIV infection is not. Given that the incubation period between HIV infection and manifestations of AIDS has a mean of 10 years, the true magnitude of HIV in adolescents may not be recognized until they are adults. Early diagnosis of HIV is important for several reasons. Therapy, which is available to delay the decline in immune function, is most effective early in the course of the disease. Prophylactic medications may be initiated, which can prevent the development of certain opportunistic infections. In addition, patients can be counselled on methods to prevent the transmission of infection to others.
Recent reports suggest that one in four new infections are occurring in persons younger than 21 years of age.45 HIV infection in adolescents is acquired primarily through heterosexual or homosexual encounters or through intravenous drug use. It is important to identify this group at risk for HIV infection, particularly patients presenting with other sexually transmitted diseases, in order to counsel them about high-risk activities and offer a means for testing for early identification of disease.
Informed consent must be obtained before HIV testing is performed. HIV is tested for using HIV-1 antibody tests. A positive screening test, such as the EIA, must be confirmed by a supplemental test such as the Western blot or immunofluorescence assay. Ninety-five percent of affected persons will have positive tests within six months of infection.45
HIV testing should only be offered in the setting where appropriate pretest and post-test counseling can be given.
Summary
Due to the prevalence of STDs in the adolescent age group, physicians caring for these patients must consider this in the differential diagnosis of patients who present with abdominal pain, dysuria, vaginal or penile discharge, arthralgias, pharyngitis, or a rash. Obtaining an accurate history may be difficult especially if parents are allowed to stay in the room. A thorough physical is essential as STDs can present with a wide variety of signs.
Chlamydia and gonorrhea are more prevalent in adolescents than adults. Symptomatic disease includes cervicitis, urethritis, and PID. However, a significant number may actually be asymptomatic and present with long-term complications such as infertility or after a partner has been diagnosed.
Herpes is the most common STD presenting with lesions and is diagnosed clinically by the characteristic vesicular or ulcerative lesion with an erythematous base. Although the prevalence of syphilis has declined recently, it must be considered in any patient with a diffuse rash, particularly those involving the hands and feet. Screening for syphilis is recommended for patients presenting with other STDs. Chancroid, lymphogranuloma venereum, and granuloma inguinale are rare in the United States.
Finally, any patient who is sexually active should be offered testing for HIV, particularly those presenting with other STDs. Since the emergency department is typically not a suitable setting for a formal discussion on HIV infections, adolescents at risk should be referred to the appropriate clinic.
References
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2. Centers for Disease Control and Prevention (CDC). Summary of Notifiable Diseases, US 1996. Morb Mortal Wkly Rep MMWR 1997;45(S3).
3. Centers for Disease Control and Prevention (CDC). Sexually Transmitted Disease Surveillance, 1995. Atlanta, GA; 1996.
4. Rosenfeld W, Vermund SH, Wentz SJ, et al. High Prevalence rate of human papillomavirus infection and association with abnormal papanicolaou smears in sexually active adolescents. Am J Dis Child 1989;143:1443-1447.
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7. Lappa S, Moscicki A. The pediatrician and the sexually active adolescent. Pediatr Clin North Am 1997; 44:1405-1445.
8. Stewart C, Bosker G. Common sexually transmitted diseases (STDs): Diagnosis and treatment of uncomplicated gonococcal and chlamydial infections. Emerg Med Reports 1999;20:173-182.
9. Sung L, MacDonald NE. Gonorrhea: A pediatric perspective. Pediatr Rev 1998;19:13-16.
10. Centers for Disease Control and Prevention (CDC). 1998 Guidelines for treatment of sexually transmitted diseases. Morb Mortal Wkly Rep MMWR 1998;47(RR-1).
11. Chambers CV, Shafer MA, Adger H, et al. Microflora of the urethra in adolescent boys: Relationships to sexual activity and non-gonococcal urethritis. J Pediatr 1987;110:314-321.
12. Shafer MA, Prager V, Shalwitz J, et al. Prevalence of urethral Chlamydia trachomatis and Neisseria gonorrhoeae among asymptomatic, sexually active adolescent boys. J Infect Dis 1987;156:223-224.
13. Janier M, Lassau F, Casin I, et al. Male urethritis with and without discharge: A clinical and microbiological study. Sex Transm Dis 1995;22:244.
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15. Darville T. Chlamydia. Pediatr Rev 1998;19:85-91.
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17. Berger RE, Alexander ER, Harnisch JR, et al. Etiology, manifestations and therapy of acute epididymitis: Prospective study of 50 cases. J Urol 1979;121:7500-754.
18. Zenilman JM. Update on bacterial sexually transmitted diseases. Urol Clin North Am 1992;19:25-34.
19. Cucurull E, Espinoza LR. Gonococcal arthritis. Rheum Dis Clin North Am 1998;24:305-322.
20. Golden NH. Vaginitis and cervicitis in adolescents. Emerg Office Pediatr 1997;10:44-48.
21. Gevelber MA, Biro FM. Adolescents and sexually transmitted diseases. Pediatr Clin North Am 1999;46:747-766.
22. Pletcher JR, Slap GB. Pelvic inflammatory disease. Pediatr Rev 1998;19:363-367.
23. Peterson HB, Galaid EI, Cates W Jr. Pelvic inflammatory disease. Med Clin North Am 1990;74:1603-1615.
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25. Sweet RL, Mills J, Hadley KW, et al. Use of laparoscopy to determine the microbiologic etiology of acute salpingitis. Am J Obstet Gynecol 1979;134:68-74.
26. Dinerman LM, Elfenbein DS, Cumming WA, et al. Clinical Fitz-Hugh-Curtis syndrome in an adolescent. Clin Pediatr 1990;29:532-535.
27. Labadie LL, Rhule RL. Management of genital infections. Emerg Med Clin North Am 1987;5:443.
28. Nyirjesy P. Vaginitis in the adolescent patient. Pediatr Clin North Am 1999;46:733-746.
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30. Rosen T, Brown TJ. Genital ulcers. Dermat Clin 1998;16:673-685.
31. Brown HP. Recognizing STDs in adolescents. Contemp Pediatr 1989;6:17-36.
32. Fleming DT, McQuillan GM, Johnson RE, et al. Herpes simplex virus Type 2 in the United States, 1976 to 1994. N Engl J Med 1997;337:1105-1111.
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Physician CME Questions
25. Factors placing adolescents at increased risk for STDs include which of the following?
A. This age group is likely to practice unprotected intercourse.
B. Adolescents are biologically more susceptible to infection than adults.
C. Health care services are less readily accessible to adolescents.
D. All of the above
26. Which of the following accounts for the majority of non-gonococcal urethritis?
A. Ureaplasma urealyticum
B. Chlamydia trachomatis
C. Mycoplasma genitalium
D. Trichomonas vaginalis
27. Gram-negative enteric organisms are the most common cause of epididymitis in:
A. young males practicing anal intercourse.
B. all men younger than age 35.
C. heterosexual adolescent males.
D. victims of sexual abuse.
28. Appropriate treatment for a 14-year-old female presenting with cervicitis includes:
A. azithromycin 1 gram orally plus ciprofloxacin 500 mg orally.
B. ceftriaxone 250 mg IM.
C. doxycycline 100 mg twice a day orally plus azithromycin 1 gram orally.
D. azithromycin 1 gram orally plus ceftriaxone 125 mg IM.
29. CDC criteria for the diagnosis of PID includes:
A. PID shuffle, cervical discharge, and fever.
B. adnexal mass, fever, and vomiting.
C. lower abdominal tenderness, cervical motion tenderness, and adnexal tenderness.
D. fever, lower abdominal tenderness, and anorexia.
30. Painful, itchy vesicular or ulcerated lesions with an erythematous base are characteristic of:
A. syphilis.
B. chancroid.
C. lymphogranuloma venereum.
D. herpes simplex virus.
31. A generalized painless rash, lymphadenopathy, and flu-like symptoms characterize which stage of syphilis?
A. Primary
B. Secondary
C. Latent
D. Late
32. Which of the following statements concerning HIV infection in adolescents is true?
A. The majority of infected persons have a positive HIV test within six months of exposure.
B. Having other STDs does not place the patient at increased risk for HIV infection.
C. There is no benefit to diagnosisng HIV infection before progression to AIDS occurs.
D. HIV infection is reportable in the United States.
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