Each year, more than 15 million new cases of sexually transmitted infections (STIs) are diagnosed. Almost half of these cases are in adolescents and young adults. Despite the fact that 15- to 24-year-olds make up only one quarter of the sexually active population, they carry a heavy burden of disease. The National Health and Nutrition Examination Survey found that 25.6% of adolescents contracted at least one STI within 1 year after the start of sexual activity.1 Surveillance data from the Centers for Disease Control and Prevention reveal that young adults aged 20 to 24 had the highest incidence of chlamydia, gonorrhea, and syphilis, and highest prevalence of human papillomavirus (HPV) in 2011.2 For the majority of these infections, teens aged 15 to 19 years followed closely behind in the incidence and prevalence of STIs.
The incidence of STIs among youth has increased over the past decade. A combination of biological, behavioral, and socioeconomic factors have been cited as reasons adolescents are disproportionately affected by STIs. Higher risk has been attributed to early age at onset of sexual activity, higher number of sexual partners, and multiple concurrent partners, all leading to more exposures over time. Lack of condom use, barriers to accessing preventive services for STIs, lack of health insurance or inability to pay, confidentiality concerns, and discomfort with adult-designed healthcare services are also contributors.1,2
Disparities by sex, race, ethnicity, and sexual behavior are also present within the adolescent population. Rates of gonococcal and chlamydial infections are consistently higher in women than men. This difference is attributable to increased screening of women as well as to the often asymptomatic presentation of disease in men. Young men who have sex with men (YMSM) have higher incidence rates of HIV and primary and secondary syphilis and make up a disproportionate number of the new cases of syphilis, chlamydia, and gonorrhea. Data from 2005 to 2011 showed that men who have sex with men (MSM) were 60 times more likely than men who have sex with women to be diagnosed with syphilis and 95 times more likely than women.3 Racial and ethnic minorities also have disproportionately higher STI prevalence rates. According to the National Longitudinal Study of Adolescent to Adult Health study, African American adolescents had chlamydia rates 6 times higher than white adolescents, and gonorrhea prevalence was 36 times higher in African American males and 14 times higher in African American females compared to their respective Caucasian peers.1 Similar discrepancies exist for trichomoniasis, chlamydia, herpes simplex virus (HSV), and syphilis. Of note, African American adolescents have actually been found to have lower risk behavior scores (number of reported partners, use of alcohol, tobacco, and drugs, etc.) than their Caucasian counterparts, and yet are still up to 29 times more likely to have an STI.1 More work is needed to determine the source for these disparities, which are clearly not based on individual risk behavior alone.
The long-term sequelae of STIs in youth are also significant public health issues. Adolescents can be affected by complications such as pelvic inflammatory disease, infertility, ectopic pregnancy, and chronic pelvic pain, in addition to mental health issues associated with the shame, stigma, discrimination, and stress that may result from these diagnoses.3,4 It is important that health care providers understand the epidemiology of STIs, common signs and symptoms, most effective modes for testing and treatment, indications for hospitalization, need for sensitive history-taking, and the best interventions for prevention in the adolescent population.
While psychosocial and behavioral factors are contributors to the high prevalence of STIs in youth, there is also a biologic basis for the increased burden of disease in adolescents. Differences in anatomy, immunology, and the role of co-infections all contribute to high rates of STIs in this age group.
Changes in the cervical epithelium make young women increasingly susceptible to STIs. During puberty, the cervical columnar epithelium undergoes squamous metaplasia, during which a transformation zone is formed in the junction between the endocervical columnar and ectocervical squamous cells.5 As a result, columnar cells, which are more vulnerable to infection with bacteria such as Chlamydia trachomatis and Neisseria gonorrhoeae are present in greater numbers on the exposed ectocervix. In addition, the area of higher cell turnover in the transformation zone is a prime host for viruses such as HPV.5 Comparatively, in the adult cervix, the ectocervix is predominately composed of squamous cells, which are less susceptible to infection.
In addition to having an anatomy more vulnerable to infection, youth also have fewer immunologic defenses against STIs. Depending on the age at onset of sexual activity, adolescents’ exposures to STIs are the initial introduction for their urogenital system to these pathogens. Lack of prior exposure means a lack of immunity, rendering youth more susceptible to infection.6 Having an STI also places an individual at increased risk for subsequent and concurrent infections. When STIs are present, disruptions in the skin and mucous membranes, such as genital ulcers, serve as entry points for pathogens. Thus presence of an STI makes an individual two to five times more likely to acquire HIV through unprotected sex.3 The inflammatory state of the infected cells also renders them easier targets for bacteria and viruses. Youth are also more likely to transmit HIV when another STI is present due to increased viral shedding through genital secretions.3 Treatment of STIs has been shown to decrease the risk of HIV acquisition. The role of STIs in HIV transmission underscores the importance of early detection and treatment of STIs in youth.
Although most sexually transmitted infections in adolescents are asymptomatic, some specific clinical syndromes present with the following signs and symptoms.
Typically presents with vaginal odor, discharge, vulvar irritation, and/or pruritis. Trichomonas vaginalis is the most common sexually transmitted cause of vaginitis. This protozoa classically causes a frothy yellow-green discharge and foul odor. While gonorrhea and chlamydia may cause vaginitis in prepubescent females, in post-menarchal females these organisms are associated with cervicitis.
Pain and burning with urination, with or without urethral discharge, are the cardinal features of urethritis. As with cervicitis, gonococcus and C. trachomatis are the chief causative organisms. Other less common causes of urethritis include T. vaginalis, Herpes simplex, Mycoplasma genitalium, Ureaplasma urealyticum, and Mycoplasma hominis.7 Enteric organisms may also lead to urethritis via insertive anal sex.
Ascending infection from the urethra in males can lead to epididymitis, typically presenting as unilateral testicular pain, swelling, tenderness, and palpable swelling of the epididymis. There may be accompanying hydrocele. Symptoms of urethritis often accompany or precede epididymitis, and the causative organisms are typically the same.8
A number of sexually transmitted pathogens can cause anogenital ulcerative lesions, with or without inguinal adenopathy. In the United States, HSV is the predominant pathogen. The lesions of HSV are classically painful, shallow, and often multiple, and associated with lymphadenopathy that may be bilateral. However, some patients may be asymptomatic, even with active lesions. Primary HSV infection often presents with systemic symptoms including fever, myalgias, headache, and malaise. Recurrent episodes tend to have a milder presentation.9
The chancre of primary syphilis is typically solitary, painless, deep, and indurated. Other important ulcer-forming infections include chancroid (Hemophilus ducreyi), lymphogranuloma venereum (LGV), and granuloma inguinale (Klebsiella granulomatis). Chancroid may present with single or multiple papules which evolve into painful genital ulcers with ipsilateral tender adenopathy. LGV is an invasive lymphatic disease caused by C. trachomatis serovars L1–L3. It is characterized by an initial ulcerative genital lesion with subsequent tender, unilateral, suppurative inguinal or femoral lymphadenopathy. Granuloma inguinale, a rare entity in the United States, is characterized by progressive beefy, red, painless ulcerative genital or perineal lesions without lymphadenopathy.9,10
Anogenital warts (condylomata acuminata) are skin-colored flat, papillary, or pedunculated lesions with a cauliflower- or frond-like appearance. They can appear throughout the anogenital region. Condyloma acuminata are caused by the Human papilloma virus, with 90% caused by the non-oncogenic types 6 or 11. While these lesions are typically asymptomatic, they may cause itching, burning, or bleed easily when irritated. Condyloma latum are a highly infectious, characteristic lesion of secondary syphilis. These grey-white, coalescent plaques of wart-like lesions are typically painless and occur in intertriginous areas.
Patients who engage in receptive anal intercourse may present with anorectal infection.
This inflammation limited to the rectum is associated with anorectal pain, bleeding and/or discharge, with accompanying tenesmus. It is commonly caused by gonococci, C. trachomatis, Treponema pallidum, and HSV.
This inflammation of the colonic mucosa, extending to 12 cm above the anus, has the additional symptoms of diarrhea and bloating. In addition to the above organisms, Campylobacter species, Shigella species, and Entamoeba histolytica may cause proctocolitis. LGV can be a cause of hemorrhagic proctocolitis and may lead to anal fistulas and stricture mimicking inflammatory bowel disease (IBD).
This manifests as abdominal cramping and diarrhea without evidence of proctitis or proctocolitis. It is often caused by Giardia lamblia in patients who engage in oral–anal sexual practices.10
This is characterized by purulent or mucopurulent cervical exudates and cervical friability which may manifest as vaginal bleeding, particularly postcoitally. The most common causes of cervicitis in adolescent females are N. gonorrhoeae and C. trachomatis.10
Pelvic inflammatory disease (PID) is an important cause of pelvic pain in sexually active females. PID involves the upper genital tract in females and manifests as any combination of endometritis, salpingitis, tubo-ovarian abscess, peritonitis, or perihepatitis (Fitz-Hugh–Curtis syndrome). While PID is most often caused by untreated ascending chlamydial and gonococcal infections, in two-thirds of cases no pathogen is isolated from the lower genital tract.11 Other known pathogens include endogenous vaginal flora (Gardnerella vaginalis, Haemophilus influenzae, group B streptococci), Mycoplasma hominis, M. genitalium, and Ureaplasma urealyticum. PID is a clinical diagnosis that can be difficult to make because of the wide range of symptoms, which may be absent, vague, or nonspecific. The diagnostic criteria for PID are provided in Table 45-1.
| Minimal Criteria | Additional Criteria | Definitive Criteria |
|---|---|---|
Lower abdominal tenderness and No other identifiable source and ≥1 of the following: | Those listed under “Minimal” plus ≥1 of the following: | |
Uterine tenderness Adnexal tenderness | Fever (>38.3°C) | Histopathologic evidence of endometritis on endometrial biopsy |
| Cervical motion tenderness | Abnormal vaginal or cervical discharge | |
Elevated ESR or CRP Laboratory evidence of gonococcal or Chlamydia trachomatis cervicitis | Tranvaginal ultrasound or MRI that demonstrates thickened, fluid-filled fallopian tubes or tubo-ovarian abscess Laparoscopic abnormalities consistent with PID |
A number of STIs can present with oropharyngeal symptoms. Gonococcal infection of the pharynx is most commonly asymptomatic, but may cause an exudative pharyngitis. HSV infection may cause an ulcerative pharyngitis. Genital–oral transmission of HPV can lead to respiratory papillomatosis in the pharynx and upper airway.10,12 In secondary syphilis, oropharyngeal mucous patches may occur as painless, silvery plaques with an erythematous border.
Several STIs can present with disseminated symptoms, including N. gonorrheae infections, syphilis, and HSV.
DGI occurs via hematogenous seeding of distant sites from a preceding gonococcal bacteremia. The most common manifestation is the arthritis and dermatitis syndrome which presents with asymmetric polyarthralgias and arthritis of distal joints (typically knees, ankles, elbows, and/or wrists), tenosynovitis, and dermatitis. The classic skin findings are papules and pustules on an erythematous base that are tender and may show evidence of necrosis. Rarely, DGI may cause endocarditis, meningitis, and hepatitis.
These infections often present with systemic symptoms including fever, malagias, headache, and/or photophobia. Severe HSV outbreaks may also disseminate, leading to hepatitis, pneumonitis, or meningoencephalitis.
Caused the spirochete T. pallidum, syphilis can present in any of the three symptomatic phases of the illness (primary, secondary, and tertiary) or may be detected during the asymptomatic latent phase. During the latent phase, patients are noninfectious except for transplacental transmission from mother to fetus. Neurosyphilis, characterized by cranial neuropathy, meningitis, stroke, altered mental status, auditory or ophthalmic abnormalities, and loss of vibratory sense, can occur at any of the stages of disease. The clinical findings in the different stages of syphilis and the treatment based on stage are provided in Table 45-2.
| Primary | Secondary | Tertiary | Latent | Neurosyphilis | |
|---|---|---|---|---|---|
| Time course | Incubation period: 1–4 wk Lesion resolves in 3–6 wk | Begins after 6–12 wk Resolution in 1–3 mo | Cardiac occurs 10–40 y after infection Destructive gummas form after 1–10 y | Early latent: acquired within the past year Late latent: acquired >1 y ago | Can occur at any stage of syphilis |
| Symptoms | Painless ulcer or chancre at inoculation site | Rash: salmon-pink macules progress to copper-colored papules; evolves centrifugally, involves palms and soles Adenopathy: generalized, painless Mucosa: grayish patches Condyloma latum: broad, flat macules, especially on vulva, scrotum, anus, axilla Constitutional: fever, malaise Other: patchy alopecia, arthritis, osteitis, gastritis, hepatitis, splenomegaly, nephrotic syndrome myalgias, sore throat | Cardiac: aneurysm of ascending aorta ± aortic insufficiency Gummas (granulomas) may involve skin, respiratory tract, gastrointestinal tract, bones | Asymptomatic infection with positive serology | Meningeal: cranial neuropathies, sensorineural deafness Meningovascular: endarteritis, stroke Tabes dorsalis: demyelination of posterior columns, Charcot joint, incontinence, ataxia General paresis Asymptomatic CSF abnormalities Uveitis, iritis |
Reiter syndrome (arthritis, urethritis, and bilateral conjunctivitis) is a reactive inflammatory condition that may follow chlamydial infection.
Hepatitis B and HIV can also present systemically. HIV is discussed in detail in Chapter 108.
Careful history-taking and physical examination can help distinguish STIs from other common illnesses with similar symptomatology.
In patients presenting with vaginitis, one might also consider candidiasis, bacterial vaginosis, foreign body, or irritant vaginitis from bubble baths, soaps, or detergents.
While it may be difficult to distinguish urethritis from UTI on clinical presentation alone, hematuria, fever, and urgency are less common in urethritis.
It is crucial to distinguish epididymitis from testicular torsion, which is a true surgical emergency. A positive Prehn sign (relief of pain with elevation of the affected testis), normal testicular position, and present cremasteric reflex all suggest epididymitis instead of torsion. However, imaging with Doppler ultrasound to rule out torsion is always warranted when the diagnosis is uncertain, in order to preserve the testicle in cases of torsion.10
Ulcerative disease of the anogenital region and mucous membranes can also be caused by EBV, Behçet’s disease, Crohn’s disease, drug eruption, and varicella zoster virus.
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