This is a 17 year old female who presents to the ER with a chief complaint of abdominal pain and vaginal discharge. She noticed a yellow-green vaginal discharge approximately three days prior, with cramping. She is experiencing worsening lower abdominal pain beginning yesterday, which is now 5/10 in intensity. She is having some nausea, but no vomiting or changes in bowel movements. LMP was two weeks ago. She recently began dating a college senior whom she met at a university party 4 months ago. She admits to having unprotected sex with him three times in the last month. She also recalls that he had some burning with urination a few days ago. Her past surgical history is significant for a previous ITOP (intentional termination of pregnancy) at age 16. Otherwise, she does not have any medical problems or take any medications.
Exam: VS T 38.7, P 95, R 20, BP 130/86. HEENT, neck, cardiac, and lung exams are unremarkable. Abdominal exam is significant for mild right upper quadrant tenderness and moderately severe lower abdominal (pelvic region) tenderness. Pelvic exam reveals mucopurulent vaginal discharge, right adnexal tenderness, and severe cervical motion tenderness. A urine sample tests negative for beta-hCG and it is sent for a DNA amplification assay for Chlamydia. A cervical swab and gram stain of the vaginal discharge demonstrates many WBCs and multiple intracellular gram negative cocci. Transvaginal ultrasound shows thick, fluid filled fallopian tubes with free fluid in the cul-de-sac. She is hospitalized and treated with IV cefotetan and oral doxycycline.
Sexually transmitted infections (STI), also known as sexually transmitted diseases (STDs), are a significant cause of morbidity and mortality in the world, particularly in adolescents who are prone to adopting high-risk behaviors. Epidemiologic studies show teenagers initiating sexual activity earlier than before, with nearly half of all adolescents sexually active by age 17 (1). Adolescents who initiate sexual intercourse at younger ages are more likely to have multiple partners, thus increasing their chances of becoming infected. Experimentation with alcohol and drugs may compromise an adolescent's ability to make sound judgments about sex and contraception. Those particularly at risk for STIs include homosexual males, street youth, incarcerated adolescents, teens engaged in prostitution, and injection drug users (1,2). Adolescents, in particular, face obstacles in utilizing health care services. Embarrassment about discussing sexuality with health care providers may discourage adolescents from seeking care. Limited financial independence and transportation barriers for teenagers may also reduce access to health care. Consequently, the incidence of STIs among adolescents is increasing with 3 million American teenagers infected each year (3). These numbers are difficult to estimate accurately, but suffice it to say, that STIs are common and a major health care concern.
Primary prevention of STIs is the chief goal for health care providers, with emphasis on safe sexual practices or abstinence. When condoms are used correctly and consistently, they are highly effective in preventing spread of STIs. However, condoms may not provide complete protection against human papillomavirus, herpesvirus type 2, and C. trachomatis (3). As younger adolescents engage in high-risk sexual activity, early recognition of the various clinical syndromes may further decrease the long-term health consequences associated with STIs. The number of identified STIs has increased to more than 20 pathogens, 8 of which have been newly recognized since 1980 (1,3). Fortunately, there is a limited set of clinical presentations. Genital ulcers occur with both Treponema pallidum (syphilis) and herpes simplex type 2 (genital herpes), as well as the rarer Haemophilus ducreyi (chancroid) and Calymmatobacterium granulomatis (granuloma inguinale). Certain serotypes of human papillomavirus cause nonulcerative genital warts (condyloma acuminata). Pubic lice, caused by Phthirus pubis, manifest as pruritus and may demonstrate eggs at the base of pubic hairs. Vaginal discharge may be noted with Candida albicans (vulvovaginal candidiasis, white cottage cheese discharge) and Gardnerella vaginalis (bacterial vaginosis, fishy foul odor), which are not considered to be sexually transmitted, but also with Trichomonas vaginalis (trichomoniasis), which is. Urethritis in the male and cervicitis or PID in the female can result from infection with Neisseria gonorrhoeae (gonorrhea) and/or Chlamydia trachomatis (chlamydia) (2). The Centers for Disease Control and Prevention (CDC) also require physicians in every state to report syphilis, gonorrhea, chlamydia, and AIDS.
STIs with serious long-term sequelae include: 1) human papillomavirus (HPV) infection, which leads to an increased prevalence of cervical neoplasia in adolescents and cervical cancer in adults; 2) chlamydia and 3) gonorrhea, which are the leading causes of pelvic inflammatory disease, tubal infertility, and infant pneumonia; 4) herpes simplex, which can result in recurrent painful episodes and subsequent neonatal infection; and 5) syphilis, which can be passed to offspring, resulting in congenital syphilis (1).
Of note, STIs diagnosed in preadolescent children (beyond the neonatal period) suggests sexual abuse. Acquisition of HIV, gonorrhea, chlamydia, and syphilis in the post-neonatal period is almost indisputably indicative of sexual contact (2). Other diseases are not as clearly connected, but sexual abuse should be suspected in infants and prepubertal children with trichomoniasis, genital herpes, and condyloma acuminata. Findings should be confirmed, and evidence should be reported to the appropriate community agency for child abuse or neglect (2).
Human Papillomavirus (HPV)
Papillomaviruses are members of the papovavirus family. They are non-enveloped, have an icosahedral virion capsid, and contain a double-stranded DNA genome. It is postulated that the virus gains entry into the body through microscopic abrasions of the surface epithelium, leading to transformation of basal cells. The natural history of HPV infection ranges from spontaneous regression to persistent infection and/or neoplastic progression (4). HPV transmission is very common, perhaps the most common sexually transmitted infection among young, sexually active people in the United States (5,6). There are multiple subtypes, e.g., subtypes 6 and 11 cause 90% of genital warts (condyloma acuminata). Nearly all cases of cervical cancer or squamous intraepithelial neoplasia are associated with HPV, particularly subtypes 16, 18, 31, 33, and 35 (5).
HPV produces subclinical infection in 70% of cases and overt infection in 30% (4). Condyloma acuminata or genital warts are the most widely recognized manifestation of HPV infection, often described as cauliflower-like in gross appearance. The most common sites of these lesions are the posterior fourchette, adjacent labia and perineum, introitus, vagina, and cervix (4). Depending on the size and location, genital warts can be painful, friable, and pruritic (2). Conversely, cervical intraepithelial dysplasia is asymptomatic, but can be detected by a Pap smear.
Traditionally, the diagnosis of HPV in sexually active adolescents is made by visual inspection, often with colposcopy. Tissue infected with HPV often undergoes epithelial hyperplasia and has a shiny white appearance (acetowhitening) after being soaked with acetic acid (4). Biopsy of lesions can be sent for light microscopy or DNA subtyping (4). The use of DNA testing of vaginal swabs to detect HPV in high risk individuals is being evaluated in screening for cervical cancer (5). Cytology of cervical scrapings (Pap smear) permits the detection of cervical neoplasia, widely believed to be triggered by certain serotypes of HPV. However, screening with the Pap smear results in a significant number of false negatives. For patients who have a Pap test indicative of low-grade SIL (squamous intraepithelial lesion) or ASCUS (atypical squamous cells of undetermined significance), follow-up with repeat Pap tests every 6 months for 2 years may be acceptable without colposcopy. If repeat tests show persistent abnormalities or if compliance is an issue, colposcopy and directed biopsy may be indicated (2).
HPV spontaneously resolves in many patients (4). Therefore, the goal of therapy should target symptomatic manifestations. In general, there are patient-applied and provider-applied modalities of treatment. Patients may apply podofilox solution or gel or imiquimod cream to visible lesions. Alternatively, condyloma can be managed by topical application of trichloroacetic acid (TCA), cryotherapy, or podophyllin by a health professional. Surgical removal is indicated if topical therapy fails, for extensive lesions, or for a young patient who requires general anesthesia (4). No clear evidence exists to determine whether treatment of genital warts will reduce transmission (2). All adolescent women with anogenital warts should have a Pap smear, with follow-up recommended every 6 months (4).
C. trachomatis is an obligate intracellular organism that does not gram stain. Infected cells contain cytoplasmic Giemsa stain-positive inclusions. C. trachomatis has at least 15 different immunotypes. Types D through K are responsible for the majority of genital infections, including mucopurulent cervicitis, urethritis, proctitis, epididymitis, salpingitis, endometritis, and perihepatitis. Types L1 through L3 are associated with lymphogranuloma venereum. Ocular trachoma (a chronic follicular keratoconjunctivitis which is a common cause of acquired blindness in other countries), is caused by types A-C (4).
Chlamydia is one of the most prevalent bacterial STIs in the United States, accounting for an estimated 3-4 million new cases each year, more frequently diagnosed in adolescents than gonorrhea (4,6). Up to 85% of women and 40% of men who are infected with chlamydia are asymptomatic (3). Yet if recognition and treatment are inadequate, pelvic inflammatory disease (PID) will develop in 20-40% of women with chlamydia (3). As with some other inflammatory STIs, transmission of HIV can be facilitated by chlamydial infection.
C. trachomatis infects the endocervix most often, in addition to the urethra, anus, Bartholin's glands, and fallopian tubes. The most common signs of C. trachomatis cervicitis include yellow/green mucopurulent endocervical discharge and an edematous, friable cervix (hypertrophic ectropion) which may present with abnormal vaginal bleeding (4). A wet-mount or gram stain of the discharge usually reveals greater than 30 polymorphonucleocytes (PMN) per high power field and absence of gonococci (although the presence of gonorrhea does not rule out concurrent chlamydia infection). Chlamydia urethritis should be suspected in sexually active females with prolonged dysuria (greater than 7-10 days) unresponsive to traditional treatment for bacterial cystitis (J). In males, chlamydial infection can also cause non-gonococcal urethritis, acute epididymitis, or proctitis. Chlamydial pharyngitis or conjunctivitis can occur in both males and females.
Chlamydia is diagnosed by cervical culture, antigen detection techniques (e.g., enzyme immunoassay, direct fluorescent antibody test), or DNA based testing (e.g., nucleic acid hybridization probe, DNA amplification). Although cervical culture for chlamydia is costly and technically difficult (it requires cell media culture because it is an obligate intracellular organism similar to a virus), it remains the gold standard and the procedure against which new diagnostic methods are measured (4). Tests for detecting chlamydial antigen have a sensitivity of approximately 60-80% (7). DNA amplification tests are the most recent development, including polymerase chain reaction (PCR) and ligase chain reaction (LCR). Both PCR and LCR are highly sensitive and specific with endocervical, urethral, and urine specimens from men and women (5,7,8). The U.S. Preventive Services Task Force strongly recommends that "all sexually active women 25 years and younger and other asymptomatic women at increased risk of infection" be routinely screened for chlamydial infection. This was based on evidence that screening women at risk reduces the incidence of PID (9). Urine-based home testing for chlamydia is expected to increase availability of low-cost screening (7). Shafer et al. reported that urine-based LCR screening, rather than routine pelvic examinations, was the most cost-effective strategy in asymptomatic sexually active adolescent girls because of greater acceptance of urine testing (10).
A single dose of azithromycin (1 gram) has been shown to be equally effective in treating chlamydia but at a modestly greater cost than a 7-day course of doxycycline (100 mg BID) (5). Azithromycin is an alternative regimen for pregnant women or patients for whom compliance is an issue (2). Either regimen is recommended for children older than 8 years of age (2). Patients should be encouraged to refer their sexual partners for diagnosis and treatment to prevent reinfection (2). A test of cure should be performed approximately 6 weeks after completion of treatment (7).
Pelvic inflammatory disease (PID) results from ascension of infection from the endocervix to the upper genital tract (e.g., endometritis, salpingitis). This is suggested by the triad of: 1) abdominal pain, 2) uterine/adnexal tenderness on bimanual exam, and 3) cervical motion tenderness. Symptoms often begin a few days after menstruation. Empiric treatment should be initiated if no other cause for these symptoms can be identified. Other findings that support the diagnosis (2) include: fever, abnormal cervical/vaginal mucopurulent discharge, presence of WBCs on saline microscopy of vaginal secretions, elevated acute phase reactants (WBC, ESR, CRP), laboratory documentation of cervical infection with N. gonorrhea or C. trachomatis.
If necessary, the diagnosis can be confirmed by: a) endometrial biopsy showing endometritis; b) transvaginal sonography demonstrating fluid-filled fallopian tubes, free pelvic fluid, or a tubo-ovarian complex (abscess); or c) laparoscopy. Differential diagnosis may include acute appendicitis, ectopic pregnancy, ruptured corpus luteum cyst with hemorrhage, diverticulitis, septic abortion, adnexal torsion, leiomyoma degeneration, endometriosis, or ulcerative colitis.
Criteria for hospitalization (2) include: surgical emergencies (e.g., appendicitis) cannot be ruled out, pregnancy, failure to respond to outpatient treatment, suspected noncompliance or intolerance to outpatient treatment, nulligravid status, severe illness (including nausea, vomiting, or high fever), suspected tubo-ovarian or other pelvic abscess. Aggressive antibiotic usage for at least 24 hours is warranted as PID accounts for 15% of female infertility and increases the risk of ectopic pregnancy and chronic pelvic pain (3). A common regimen includes cefotetan (2 g IV every 12 hours) or cefoxitin (2 g IV every 6 hours); plus doxycycline (100 mg PO or IV every 12 hours) (2). A combination of clindamycin, gentamicin, and doxycycline is an alternative regimen (2). Mild PID is often treated as an outpatient with single dose IM/IV ceftriaxone and PO doxycycline or azithromycin.
Neisseria gonorrhoeae, a gram-negative intracellular diplococcus, is a commonly found co-infection with chlamydia. Gonorrhea infects the urethra, Bartholin glands, Skene's glands, cervix, epididymis, prostate, anus, pharynx, and conjunctiva. Hematogenous dissemination to joints, skin, meninges, and endocardium may occur (4).
Gonorrhea is one of the most commonly reported bacterial STIs in adolescents (chlamydia is more common, but chlamydia is not a true bacteria). Estimates of 600,000 new infections occur in the U.S. each year in all age groups (2). Overall, the rates of diagnosis are declining, but still remain high among adolescents aged 15 to19 of all racial and ethnic groups (2). In addition to its role in pelvic inflammatory disease, gonorrhea infection also facilitates HIV transmission (2).
Males infected with gonorrhea often present with symptomatic urethritis within 2 to 5 days of exposure, with urethral discharge or dysuria (7). Other manifestations in the male include epididymitis, lymphangitis, or prostatitis. In young women, the endocervical canal and urethra are the primary sites of infection. However, like chlamydia, they are often asymptomatic. If left untreated, it can lead to PID or disseminated infection. Only 10-20% of infected females are likely to present with increased vaginal discharge, dyspareunia, abnormal vaginal bleeding, or signs and symptoms of ascending infection (4). Physical exam may reveal mucopurulent discharge, erythema of the ectropion, and a friable cervix. Ten to 20% of females with acute gonococcal infection will develop PID (7). Individuals with gonococcal salpingitis, as compared to non-gonococcal salpingitis, are more likely to appear more ill, have a fever, and present within 3 days of symptom onset (7). Peritonitis and perihepatitis (right upper quadrant pain and elevated liver enzymes) characterize the Fitz-Hugh-Curtis syndrome, commonly associated with gonorrhea-caused PID.
Disseminated gonococcal infection (DGI) occurs in 0.5 % to 3% of untreated patients (4). DGI is often manifested by polyarticular septic arthritis (joint pain, swelling, tenderness) and skin lesions. Most commonly, the wrist, ankle, knee, and metacarpophalangeal (MCP) joints are involved in an asymmetric and/or migrating fashion. Skin lesions present as a tender, necrotic pustule on an erythematous base over the distal extremities (7).
Gonorrhea can be confirmed by culture, immunochemical, or DNA testing. Gram stain of cervical or urethral discharge generally reveals gram-negative diplococci within or closely associated with PMN leukocytes. Gram stain has a high sensitivity and specificity for males, but the test has a poor sensitivity for females at 30% to 60% because of vaginal bacterial contamination (2,4). Culture is the gold-standard, using antibiotic-containing selective media (e.g., Thayer-Martin medium), which has sensitivities from 80 to 90% (7); however, gonorrhea is fastidious, requiring a special transport and incubation conditions. The non-amplified DNA probe is reported to have sensitivities and specificity up to 97% and 99%, respectively (7). The LCR amplification assay is found to have sensitivities of 95% (7). A test of cure should be performed at approximately 6 weeks after completion of treatment (7).
As gonorrhea has become increasingly resistant to penicillin, quinolone-resistant N. gonorrhoeae (QRNG) is becoming more common in parts of Asia and the Pacific, including Hawaii (2). The CDC's 2002 STD Treatment Guidelines recommend that quinolones no longer be used to treat gonorrhea for infections acquired in Hawaii and California (2). The CDC recommends second- and third-generation cephalosporins such as cefixime (400 mg PO, single dose) or ceftriaxone (125 mg IM, single dose). Partners of patients suspected of having gonorrhea should also be treated to prevent re-infection.
Because patients with gonorrhea are often concomitantly infected with chlamydia, many physicians treat women with mucopurulent cervicitis with an additional regimen of doxycycline or azithromycin to prevent sequelae such as PID. The best prevention of PID is prevention of lower genital tract infection by C. trachomatis and N. gonorrhea (4).
Herpes simplex virus (HSV) is a member of the herpesvirus family which includes the Epstein-Barr virus, varicella-zoster virus, and cytomegalovirus. HSV-2 is responsible for most of the genital infections. HSV-1 primarily causes oral infections, but it has been isolated in 10-25% of genital lesions with first-episode genital herpes. HSV infections are transmitted by viral shedding through a peripheral site, mucosal surface, or in genital or oral secretions. Between recurring episodes, HSV virus ascends peripheral sensory nerves and enters nerve root ganglia (7), persisting in a dormant state. The frequency of recurrence of genital lesions after a symptomatic first-episode of genital herpes is high for HSV-2 and less for HSV-1 (2).
At least 50 million people in the U.S. have genital HSV infection (2). In a major study published in the New England Journal of Medicine, 22% of Americans over 12 years old have positive test results for antibodies against HSV-2, the major cause of genital herpes (3,11). This represents a 30% overall increase in the prevalence of HSV-2 since the late 1970s. Furthermore, individuals with HSV-2 are more susceptible to contracting HIV from a HIV-positive partner (3). Most individuals with genital herpes have not been diagnosed (2). Therefore, the disease is often transmitted from asymptomatic individuals, even those who have never had any symptoms (3).
Genital herpes is a life-long, recurring infection. Yet, symptoms vary greatly, both on an individual basis as well as between episodes for the same individual. The primary episode of herpes infection may present with vulvar pain, dysuria, and occasionally urinary retention (4). Systemic symptoms are common such as flu-like symptoms, with malaise, headache, fever, and body aches. Severe complications such as herpes meningitis/encephalitis are rare (4), except in neonates when the risk is much higher.
The most frequent presenting sign of infection is an exquisitely painful pustular, vesicular or ulcerative lesion that spreads rapidly over the external genitalia. In females, lesions may be hidden intravaginally, and patients may not even be aware of its existence. HSV cervicitis occurs in 70-90% of women with their first episode of HSV infection (7). Examination may reveal cervical erythema and friability. Ulcerative lesions may last up to two weeks until crusting or re-epithelialization occurs.
Adolescents should be counseled that genital herpes transmission can occur even when they are asymptomatic. Asymptomatic individuals may shed the virus at the same rate as symptomatic individuals. Recurring infections are generally localized to the genitalia with fewer systemic symptoms.
Diagnosis of herpes infection is best confirmed by viral culture of the lesions (1). However, the sensitivity of the culture declines within a few days of onset as lesions begin to crust and heal. HSV antigen detection tests do not distinguish between HSV-1 and HSV-2 (2). Cytologic detection via the Tzank smear of the ulcer discharge may demonstrate multinucleated giant cells, though the test itself is not highly sensitive and also does not distinguish between viral types.
During the first several weeks of a primary infection, both type-specific and nonspecific antibodies develop. Type-specific antibodies to HSV-2 are virtually indicative of sexual transmission. Serologic tests may show that the current infection is primary, suggested by a rise in IgM antibodies followed by a rise in IgG antibodies. Because false-negative HSV cultures are common, HSV-2 type-specific serologic tests are useful in determining a diagnosis of genital herpes (2). However, serologic screening for genital herpes in the general population is not indicated (2).
Systemic antiviral drugs partially control the symptoms of herpes episodes for both primary and recurrent disease. Antivirals such as acyclovir, valacyclovir, and famciclovir have demonstrated decreased shedding when taken regularly. However, these medications do not permit a lasting effect. Once the treatment stops, the disease resumes typical pre-treatment frequency and severity of recurrences (2).
Patients with first-episode herpes may eventually develop severe or prolonged symptoms, so treatment is indicated. Recommended regimens include acyclovir, famciclovir, or valacyclovir for 7 to 10 days (2). Treatment for recurrent disease may be administered episodically or continuously as suppressive therapy. Episodic therapy requires initiation within 1 day of lesion onset. Suppressive therapy reduces the frequency of genital herpes recurrences by 70 to 80% for patients normally with 6 or more recurrences a year (2). Thus, quality of life is often improved in these patients. Suppressive therapy reduces subclinical viral shedding, but does not eliminate the risk.
Counseling is also critical to the management of herpes, to help patients cope and to prevent sexual and perinatal transmission. Patients should be informed that transmission of HSV can occur during asymptomatic periods. Condoms may help reduce the risk, especially when infected areas are covered (2).
Syphilis is caused by Treponema pallidum (subspecies pallidum), a spirochete that cannot be seen by light microscopy. It is identified by darkfield microscopy examination by its characteristic corkscrew motility (4). T. pallidum is transmitted via breaks in the skin or mucus membranes, perinatal transmission, or rarely blood transfusion.
Though syphilitic disease has been significantly curtailed by its sensitivity to penicillin, the incidence has been rising since the 1980s (4). In addition, the rate in adolescent females has increased since the 1990s (4). This is of particular concern considering the high teen pregnancy rates in today's population. Syphilis may be passed to the fetus, resulting in congenital syphilis, which affects brain development and growth. Furthermore, genital ulcer disease increases the risk of HIV transmission (4).
Syphilitic disease is divided into three symptomatic stages: primary, secondary and tertiary syphilis. Primary syphilis presents as a chancre, approximately 1 to 3 weeks after inoculation. A chancre is a highly infectious, painless, ulcerative lesion with well-defined raised borders and an indurated base. It contains large numbers of spirochetes that cannot be visualized by gram stain, but can be seen by darkfield microscopy (4).
Secondary syphilis develops between 4 and 10 weeks after the primary chancre appears. Infected individuals may have systemic complaints such as low-grade fever, malaise, myalgia, arthralgia, and generalized adenopathy. A nonpruritic maculopapular rash may develop on the trunk or extremities, especially the palms and soles. Other anogenital lesions include condyloma lata, which are highly infectious, flat, beefy-like lesions with a broad base (4).
Latent syphilis describes the period after which these systemic symptoms resolve. This period is further divided into early and late phases. Early latent syphilis is defined as less than a year, whereas late latent is longer than 1 year (4). Infectivity is thought to be significantly decreased during the late latent phase, and prolonged antibiotic therapy may be required to adequately manage the slower replicating treponemes (2).
Tertiary syphilis is rarely encountered in adolescents, but serious complications may occur in approximately one-third of patients who enter late latency even though they may no longer be contagious (4). Tertiary syphilis may present with cardiovascular, gummatous and/or neurologic manifestations. Common cardiovascular manifestations of tertiary syphilis include thoracic aortic aneurysm, aortic insufficiency, and coronary ostial occlusion. Chronic inflammatory lesions of tertiary syphilis, called gummas, affect the skin, subcutaneous tissue, and bones. Neurosyphilis, which can occur during any stage, usually includes tabes dorsalis, affecting the spinal tracts controlling proprioception and vibratory sense, and is associated with the Argyll-Robertson pupil (accommodation reflex is intact, but there is no response to direct light).
Diagnosis of early syphilis is done clinically, serologically, or most accurately, by direct visualization on darkfield microscopy. T. pallidum is best visualized by darkfield microscopy of the lesion exudate. Alternatively, direct fluorescent antibody tests can also be used to visualize the treponemes in ulcer smears (2).
During primary and secondary stages, nonspecific serologic tests for non-treponemal (cardiolipin) antibody such as the RPR (rapid plasma reagin) or VDRL (Venereal Disease Research Laboratory) are used as screening tests (RPR has now largely replaced the VDRL test for serum, but not for CSF). Positive results are confirmed with more specific antibody tests including the fluorescent treponemal antibody absorption (FTA-Abs) test, the microhemagglutination-T. pallidum test (MHA-TP), or the hemagglutination treponemal test for syphilis (HATTS). False positive results may occur in patients with various medical problems (e.g., false positive VDRL/RPR occurs with systemic lupus). The differential diagnosis of a positive specific treponemal antibody test includes other treponemal diseases such as pinta, yaws, and endemic syphilis. Yaws is an infection with Treponema pallidum pertenue (T. pallidum, subspecies pertenue), while syphilis is an infection with Treponema pallidum pallidum (T. pallidum, subspecies pallidum). Thus, even the MHA-TP (a specific test for T. pallidum) can be positive in yaws, making the definitive diagnosis of syphilis in yaws endemic areas (e.g., Micronesia), very difficult. According to the CDC, all patients diagnosed with syphilis should be tested for HIV (2).
Diagnosis of neurosyphilis may be difficult as the VDRL test for CSF is high in specificity but low in sensitivity (more false-negatives). In other words, a reactive test would indicate syphilis, but the test may not be reactive in a mildly affected person. Some specialists recommend performing an FTA-Abs test for CSF which is higher in sensitivity (2).
Penicillin is the treatment of choice for syphilis, even for pregnant women (2). Standard treatment for primary, secondary, and early latent syphilis includes parenteral (longer acting) benzathine penicillin G. Late latent and tertiary syphilis requires a longer course of therapy. A test for cure (with the same serologic test) should be performed 3, 6, and 12 months after treatment with a four-fold decline in titer considered to be clinically significant (e.g., from 1:16 to 1:4) (4). Furthermore, patients should be cautioned about the Jarisch-Herxheimer reaction after treatment for early syphilis, due to the sudden rupture of cells containing T. pallidum. Patients may experience self-limiting symptoms such as fever, myalgias, chills, headache, and postural hypotension for the first 24 hours. Management consists of hydration and NSAIDs (4). Identification of sexual partners at risk for contracting syphilis should be directed for serologic testing and/or treatment.
1. What is the triad of symptoms that suggests pelvic inflammatory disease?
2. What is likely to be the most common STI in adolescents in the United States?
3. Why are adolescents more susceptible to acquiring STIs than adults?
4. What treatment regimen would not be appropriate for an adolescent in Hawaii with confirmed gonococcal cervicitis?
. . . . . a. doxycycline 100mg PO BID x 7 days
. . . . . b. ceftriaxone 125mg IM x 1 day
. . . . . c. cefixime 400mg PO x 1 day; plus azithromycin 1g PO x 1 day
. . . . . d. ciprofloxacin 500mg PO x 1 day
5. True/False: Suppressive therapy for genital herpes with acyclovir effectively eliminates viral shedding.
6. Which test is more specific for syphilis? RPR, VDRL, or FTA-Abs (fluorescent treponemal antibody absorption)?
7. What are the criteria for hospitalization of a patient with suspected pelvic inflammatory disease?
1. American Academy of Pediatrics Committee on Adolescence. Sexually Transmitted Diseases. Pediatrics 1994;94:568-572.
2. Centers for Disease Control and Prevention (CDC). Sexually Transmitted Diseases Treatment Guidelines, 2002. Morbidity and Mortality Weekly Report. May 10, 2002, vol 51:1-77.
3. McIlhaney JS. Sexually Transmitted Infection and Teenage Sexuality. Am J Obstet Gynecol 2000;183(2):334-339.
4. Muram D. Chapter 22 - Sexually Transmitted Diseases in Adolescents. In: Sanfilippo JS, et al (eds). Pediatric and Adolescent Gynecology, second edition. 2001, Philadelphia: W.B. Saunders Company, pp. 357-378.
5. Gilson RJ, Mindel A. Recent Advances: Sexually Transmitted Infections. BMJ 2001;322(7295):1160-1164.
6. Division of STD Prevention, National Center for HIV, STD, and TB Prevention. Tracking the Hidden Epidemics. Trends in STDs in the United States 2000. Atlanta: Center for Disease Control and Prevention. (CDC), pp. 1-32. http://www.cdc.gov/nchstp/dstd/Stats_Trends/Trends2000.pdf
7. Amador L, Eyler AE. Diagnosis and Treatment of Sexually Transmitted Diseases in Adolescence: A Practical Clinical Approach. Clinics in Family Practice 2000;2(4):967-991.
8. Biro FM. New Developments in Diagnosis and Management of Adolescents with Sexually Transmitted Disease. Curr Opin Obstet Gynecol 1999:11(5):451-455.
9. US Preventive Services Task Force. Recommendations and Rationale: Screening for Chlamydial Infection: Recommendations and Rationale. Am Fam Phys 2002;65(4):673-676.
10. Shafer MA, et al. Is the routine pelvic examination needed with the advent of urine-based screening for sexually transmitted diseases? Arch Pediatr Adolesc Med 1999;153:119-125.
11. Fleming DT, McQuillan GM, Johnson RE, et al. Herpes simplex virus type 2 in the United States, 1976-1994. N Engl J Med 1997;337:1105-1111.
Answers to questions
1. Abdominal pain, adnexal tenderness on bimanual exam, and cervical motion tenderness.
2. Human papillomavirus (HPV) is estimated to be the most common STI among young, sexually active people in the United States, though many HPV infections are asymptomatic. According to the CDC, an estimated 5.5 million people of all ages contract HPV each year in the United States. On the other hand, chlamydia is the most commonly reported infectious disease in the United States.
3. Adolescents adopt high risk behaviors including early onset of sexual activity, multiple sexual partners, or drug/alcohol use which may impair judgment. Adolescents generally are less able to access health care due to embarrassment about their condition, financial constraints, or transportation barriers.
4. d. Quinolones are no longer recommended for the treatment of gonorrhea in Hawaii or infections acquired in Asia. In 2000, the CDC collected 5,461 isolates for its Gonococcal Isolate Surveillance Project (GISP). 14.3% of the GISP isolates in Hawaii were found to be quinolone-resistant N. Gonorrhoeae (QRNG), compared to 0.2% of samples collected within the continental United States and Alaska. Furthermore, since QRNG is becoming more common in West Coast areas, the use of fluoroquinolones in California is probably inadvisable.
5. False. Acyclovir and other antivirals only reduce viral shedding, but they do not eliminate the risk of transmission. Suppressive therapy reduces the frequency of symptomatic genital herpes recurrences by 70% to 80% for patients with 6 or more recurrences a year.
6. FTA-Abs is more specific, but it is still not totally diagnostic of syphilis since patients with yaws will still have a positive FTA-Abs. Other false positive results of FTA-Abs may occur with patients with various medical problems. The differential diagnosis of a positive treponemal antibody test includes other treponemal diseases such as pinta, yaws, and endemic syphilis.
7. Criteria for hospitalization include: surgical emergencies (e.g., appendicitis) that cannot be excluded, pregnancy, failure to respond to outpatient treatment, suspected noncompliance or intolerance to outpatient treatment, nulligravid status, severe illness (including nausea, vomiting, or high fever), suspected tubo-ovarian or other pelvic abscess.