Sexually Transmitted Infections

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89 Sexually Transmitted Infections

Sexually transmitted infections (STIs) present a significant source of morbidity among adolescents, especially young women. According to 2007 surveillance data, adolescents represent 25% of the sexually active population but account for 50% of new STIs. The high incidence of STIs is associated with greater susceptibility of the adolescent female reproductive tract, poor access to STI prevention services, inconsistent use of barrier prophylaxis, and high prevalence among sexual partners.

STIs present with a wide range of symptoms and physical findings. Moreover, many infections are asymptomatic. Thus, regular screening among sexually active adolescents is highly recommended.

This chapter focuses on the most common clinical syndromes among adolescents: vaginitis, urethritis, cervicitis, human papillomavirus (HPV) infection, herpes genitalis, chlamydia, gonorrhea, and syphilis.

Vaginitis

Vaginitis is one of the most common symptoms among adolescent females. It typically presents as increased or malodorous vaginal discharge and vulvovaginal erythema or edema. Although this can be caused by chemical or physical irritation, infectious causes include Trichomonas vaginalis, bacterial vaginosis (caused by Gardnerella vaginalis, genital Mycoplasmas, anaerobic bacteria) and Candida spp. In postpubertal women, normal vaginal flora is dominated by lactobacilli, which decrease the pH within the vaginal canal and prevent colonization by pathogens. However, any change to the genital environment can alter this balance and result in infection. Except T. vaginalis vaginitis, infectious vaginitis is not an STI. However, vaginitis is frequently diagnosed as part of the evaluation for STIs. The signs, symptoms, diagnostic criteria, and treatments for each infection are shown in Table 89-1.

Table 89-1 Infectious Causes of Vaginitis

Urethritis and Cervicitis

Epidemiology and Pathophysiology

Urethritis and cervicitis are most often caused by Neisseria gonorrhoeae and Chlamydia trachomatis. Gonorrhea and chlamydia are the most common reportable diseases in the United States, with approximately 360,000 cases of gonorrhea and 1.1 million cases of chlamydia reported in 2007. Adolescents are overrepresented: 50% of gonorrhea cases occur in individuals 15 to 24 years of age, and chlamydia infection among 15- to 19-year-old young women is 10 times the national average (3004 cases vs. 370 cases per 100,000 population). The transmission rate for each pathogen is much higher from males to females. Transmission occurs by oral, vaginal, or anal sexual contact. Each organism may be transmitted vertically to a newborn via passage through an infected birth canal.

N. gonorrhoeae is a gram-negative, oxidase-positive diplococcus, with 70 different strains. Its virulence is associated with the presence of pili and an outer membrane protein that increase adhesion of gonococci to tissues. C. trachomatis circulates as an elementary body. At epithelial cell attachment, it is ingested and then transforms into a reticulate body. It then reproduces within the infected cell, producing several elementary bodies, which are released. C. trachomatis also has a predilection for columnar epithelial cells, which are prevalent in the adolescent ectocervix.

Clinical Presentation

The clinical presentations of urethritis and cervicitis and their associated infections are detailed in Table 89-2 and Figure 89-1.

Figure 89-1 Cervicitis and urethritis.

Pelvic Inflammatory Disease

Pelvic inflammatory disease (PID) is an important complication of cervicitis, most commonly caused by N. gonorrhoeae and C. trachomatis. Other vaginal and enteric pathogens may be involved, including Bacteroides spp., Ureaplasma urealyticum, and Mycoplasma hominis. Gonococcus, C. trachomatis, and other organisms may ascend into the uterus and fallopian tubes. Infected material in the fallopian tubes may result in tubo-ovarian abscess, and overflow may lead to peritonitis or perihepatitis. The risk of PID is associated with young age at first intercourse, multiple partners, vaginal douching, and use of intrauterine devices.

The presenting symptoms of patients with PID are described in Table 89-2. Some patients may have subclinical infection that is not diagnosed until evaluation for infertility reveals fallopian tube scarring. On examination, patients usually have lower abdominal tenderness. Pelvic examination may reveal cervical discharge; an inflamed cervix; cervical, adnexal, or uterine tenderness; or an adnexal mass. Timely diagnosis of PID is important to prevent infertility. Because the signs and symptoms of infection are not specific, the Centers for Disease Control and Prevention developed criteria to guide diagnosis and empiric treatment (Table 89-3). Fulfillment of minimal criteria indicates presumptive treatment.

Table 89-2 Signs and Symptoms of Urethritis, Cervicitis, and Associated Syndromes in Men and Women

	Men	Women
Urethritis

Dysuria

Purulent urethral discharge

Epididymitis develops in 10%-30% of untreated men

Urethral discharge or dysuria

Scrotal pain, swelling, erythema

Inguinal or flank pain

Pain or swelling of epididymis or spermatic cord

Endocervicitis

Increased vaginal discharge

Dyspareunia

Cervical erythema, edema, friability

Endometritis or salpingitis (PID)

Develops in 10%-20% of acute urogenital infection

Abdominal pain

Intermenstrual bleeding

Menorrhagia

Dyspareunia

Cervical motion tenderness

Anorectal gonorrhea

Proctitis or anal discharge

Rectal bleeding

Anorectal pain

Tenesmus or constipation

Usually asymptomatic

Purulent exudate

Erythema or edema of rectal mucosa

Perihepatitis (Fitz-Hugh-Curtis syndrome)

Usually associated with salpingitis

PID, pelvic inflammatory disease; RUQ, right upper quadrant.

Table 89-3 Signs and Symptoms of Pelvic Inflammatory Disease

Minimal Criteria	Additional Criteria	Definitive Criteria
Uterine or adnexal tenderness or Cervical motion tenderness	Temperature >38.3°C Abnormal cervical or vaginal discharge WBCs on microscopic evaluation of vaginal discharge Elevated ESR and CRP Laboratory documentation of gonorrhea or chlamydial infection	Evidence of endometritis from endometrial biopsy Transvaginal sonography showing thickened fluid-filled tubes, free pelvic fluid, or tubo-ovarian complex Laparoscopic abnormalities

CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; WBC, white blood cell.

Other Manifestations of Gonococcal and Chlamydial Infection

Nongenitourinary manifestations of gonococcal and chlamydial infection include pharyngitis, conjunctivitis, and disseminated infection. Gonococcal pharyngitis should be considered for exudative pharyngitis in a sexually active adolescent. Disseminated gonococcal infection often manifests as arthritis, tenosynovitis, and dermatitis. Chlamydia is associated with Reiter’s syndrome (urethritis, spondylitis, uveitis). Both chlamydia and gonorrhea can also cause neonatal infection (see Chapter 105).

Evaluation and Management

Gonorrhea can be diagnosed by gram stain and culture from urethral and endocervical swabs. Chlamydia, as an intracellular organism, is difficult to grow in culture and has therefore been more difficult to diagnose. Newer and more rapid diagnostic methods include nucleic acid amplification techniques that have greatly increased the ease and sensitivity of testing. They can be performed on urine samples in addition to urethral or endocervical swabs. The other bacterial causes of urethritis—cervicitis and PID—are not generally isolated from cultures.

Patients with gonorrhea or chlamydia are at risk for co-infection. Therefore, treatment guidelines recommend covering for both pathogens when treating urethritis, cervicitis, or PID (Table 89-4). This is critical in PID, in which cervical culture results are often negative. Recommendations for PID also include anaerobic coverage because of the polymicrobial nature of the infection.

Table 89-4 Treatment Recommendations for Urethritis, Cervicitis, and Pelvic Inflammatory Disease *

	Treatment	Special Considerations
Nongonococcal urethritis or cervicitis	Azithromycin Doxycycline Erythromycin Ofloxacin Levofloxacin

Patients should abstain from sexual intercourse for 7 days from starting treatment.

Partners should be notified and treated.

Gonococcal urethritis or cervicitis

Ceftriaxone or

Cefixime

Spectinomycin

Cefoxitin IM + Probenecid PO

Fluoroquinolones are no longer recommended for treatment because of resistance.

Unless chlamydia is definitely ruled out (i.e., by use of NAAT), include coverage for chlamydia.

Pelvic inflammatory disease

Parenteral regimen

Cefotetan or cefoxitin plus

Doxycycline PO or IV for 14 d

Plus clindamycin or metronidazole if TOA

Outpatient regimen

Ceftriaxone IM or

Cefoxitin IM + probenecid PO

plus doxycycline PO for 14 d ± metronidazole

IV antibiotics until 24 h after improvement; then continue PO doxycycline to complete 14-d course.

As above, patients should abstain from sexual intercourse for 7 days from initiation of treatment.

Partners should be evaluated and treated.

Epididymitis

Ceftriaxone IM plus

Doxycycline PO

IM, intramuscular; IV, intravenous; NAAT, nucleic acid amplification test; PO, oral; TOA, tubo-ovarian abscess.

* Additional alternate regimens for special populations or for those with allergies are available at www.cdc.gov/std/treatment.

Anogenital Lesions

The most common causes of anogenital lesions in adolescents include herpes genitalis, HPV, and syphilis. The differential diagnosis should also include chancroid caused by Haemophilus ducreyi. Although only 23 cases of chancroid were reported in the United States in 2007, it is prevalent in certain regions and groups. In general, painful ulcerative lesions are associated with herpes genitalis and chancroid. Painless ulcers are associated with syphilis, and HPV causes painless anogenital growths.

Syphilis

Syphilis is a systemic infection caused by the spirochete Treponema palladium. The agent is usually transmitted via sexual contact but can also be transmitted in utero, through blood transfusions, or through direct contact with infectious lesions. After the organism enters the body, infection spreads through the blood and lymphatic systems, infiltrating cells and causing granuloma formation and endarteritis. If left untreated, the infection is chronic and can be transmitted for up to 4 years.

The overall incidence of syphilis has significantly declined since the 1970s, and in contrast to other STIs, the incidence of syphilis is lower among adolescents compared with other age groups. Most new cases occur among 20- to 30-year-old young adults. However, recent outbreaks of syphilis have occurred among adolescents who participate in commercial sex trades or illicit drug use.

The protean clinical manifestations of syphilis depend on the stage of infection, as shown in Table 89-5 and Figure 89-2.

Table 89-5 Clinical Manifestations of Syphilis

	Timing	Clinical Manifestations
Primary syphilis	9-90 days after exposure

1- to 2-cm painless chancre or ulcerative lesion on external genitalia

Typically single lesion but can have multiple

Heals in 3-6 wk

Secondary syphilis

6-8 wk (after exposure)

4-10 wk (after chancre)

Generalized macular, papular, or papulosquamous rash of trunk and extremities, including palms and soles

Any type of rash can appear

Rash is bilateral and symmetric, follows line of cleavage, and can involve mucous membranes

General or regional painless lymphadenopathy

Flulike syndrome with malaise, sore throat, fever, and so on

Rash lasts few weeks to 12 months

Latent syphilis

Early (within first year) vs. late (after first year)

No clinical signs or symptoms of syphilis

Persistently positive serologic test results (VDRL and FTA-ABS)

Negative syphilis test results from CSF

Late syphilis

2-10 years after infection

Gummas (hypersensitivity reaction)

Cardiovascular syphilis

Has not been reported in adolescents

Neurosyphilis

Within 2 years

Asymptomatic: CSF pleocytosis, increased protein, and positive CSF VDRL results

Acute meningitis with cranial nerve palsies

Meningovascular syphilis: local infarction resulting in headache, memory loss, hemiparesis, Argyll-Robertson pupils, tabes dorsalis; Rare in adolescents

CSF, cerebrospinal fluid; FTA-ABS, fluorescent treponemal antibody absorption test; VDRL, Venereal Disease Research Laboratory.

Figure 89-2 Syphilis.

Diagnosis

The diagnosis of syphilis should always be considered in the presence of any ulcerative anogenital or oral lesion. Breasts and fingers can also be affected. Because primary infection can present with either a small lesion or asymptomatically, regular screening for syphilis is recommended for sexually active adolescents and pregnant women.

Diagnosis uses screening nontreponemal antibody tests (rapid plasma reagin [RPR] and Venereal Disease Research Laboratory [VDRL]) and confirmatory specific treponemal antibody tests (fluorescent treponemal antibody absorption [FTA-ABS]). The RPR is a qualitative test that requires confirmation by the FTA-ABS. The VDRL is a quantitative test used to monitor treatment. The treponemal-specific antibody test also yields antibody titers, but levels do not change in response to treatment; the FTA-ABS result will remain positive for life. The sensitivity of these tests depends on the timing after infection: they are most sensitive 4 weeks after infection but before the onset of late syphilis. There is also a high likelihood of false-positive results, particularly for the nontreponemal tests. False-positive results can occur with viral, spirochetal, mycoplasmal, other bacterial infections, and autoimmune vasculitides. Although screening test results are confirmed with the FTA-ABS, definitive diagnosis is made through dark-field examination of transudate from lesions or through direct fluorescent antibody.

Treatment

The mainstay of treatment for syphilis is penicillin. Although other regimens are available to treat primary and secondary syphilis for patients who are allergic to penicillin, their efficacy has not been well demonstrated. The treatment regimens are shown in Table 89-6. Follow-up should include repeat nontreponemal quantitative antibodies (VDRL) at 6, 12, and 24 months after completion of therapy. If initially high titers have not decreased fourfold or if the titers have increased, treatment should be repeated. Further detail is available at www.cdc.gov/std/treatment.

Table 89-6 Treatment of Syphilis

Primary or secondary syphilis	Benzathine penicillin G IM Other preparations of penicillin are not appropriate for treatment.	In the setting of penicillin allergy, doxycycline or tetracycline can be used.
Early latent syphilis	Benzathine penicillin G	Alternate: doxycycline
Late latent or tertiary syphilis	Benzathine penicillin G	LP should be performed to look for neurosyphilis
Neurosyphilis	Aqueous crystalline penicillin G or Procaine penicillin + probenecid	LP should be repeated every 6 months until pleocytosis has resolved

IM, intramuscular; LP, lumbar puncture.

Herpes Genitalis

Epidemiology and Pathophysiology

The most common cause of anogenital ulcerative lesions is herpes simplex virus (HSV). HSV has two serotypes: HSV 1 is primarily associated with herpes labialis, and HSV2 is primarily associated with herpes genitalis (although ≤50% of primary genital herpes lesions are caused by HSV-1). Overall, herpes is responsible for 90% of anogenital ulcerative lesions, and it is the second most prevalent STI across all age strata. The prevalence is highest among young adults ages 20 to 29 years but has been increasing among adolescents. Overall, 20% of individuals in the United States are HSV-2 positive, and 6% of adolescents ages 12 to 19 years are positive.

The virus is transmitted through genital–genital or oral–genital sexual contact. Viral shedding is highest in the presence of lesions, but asymptomatic shedding also occurs, especially within the first 3 months after primary infection. Shedding occurs in salivary, cervical, and seminal secretions. After infection, the virus replicates in skin or mucosal cells and then spreads via sensory nerves. After primary infection in herpes genitalis, the virus becomes latent, remaining in sacral dorsal root ganglia until reactivation. During reactivation, the virus spreads along peripheral sensory nerves back to skin or mucosal surfaces, resulting in recrudescence of skin lesions. Recurrence occurs in 70% to 90% of individuals with HSV-2.

Clinical Presentation

Primary infection usually begins with a burning sensation in the genital area followed by the development of small (1-2 mm) vesicular lesions with an erythematous base that erode and become ulcers. The distribution of lesions can be extensive, involving the labia, vagina, perineum, cervix, and penis (Figure 89-3). The lesions are almost always painful. In primary infection, regional tender lymphadenopathy, fever, and malaise occur. Patients may also have dysuria, urinary retention, or dyspareunia. Lesions typically last from 4 to 15 days before crusting, and systemic symptoms usually peak in the first 3 to 4 days and then resolve.

Figure 89-3 Lesions of herpes simplex.

Recurrent episodes are usually less severe and involve fewer lesions. Overall, the episodes last approximately 1 week compared with 3 weeks for primary infection, and the virus sheds for 2 to 7 days. There may be paresthesias or pain in the anogenital region before the appearance of ulcers but mild systemic symptoms can occur. The likelihood and frequency of recurrence varies; recurrences are more frequent in the first year after infection. Although herpes results in chronic infection, episodes are usually self-limited. Complications can occur, including secondary bacterial infection of lesions, labial adhesions, sacral radiculopathy, proctitis, encephalitis, and meningitis. Another important complication is neonatal herpes (see Chapter 105).

Diagnosis and Management

If the clinical history and appearance of lesions suggest herpes genitalis, the most rapid and inexpensive test is a Tzanck smear of scrapings from the base of the lesions, looking for multinucleated giant cells. It has a sensitivity of only 30% to 80%. Other diagnostic tests are available; the historic gold standard is viral culture, which is most sensitive when samples are obtained from vesicles, pustules, or ulcers. HSV can grow in 1 to 7 days. Immunofluorescence microscopy, DNA probes, and polymerase chain reaction are highly sensitive and specific assays. HSV type-specific serologic tests exist but may be falsely negative in early infection.

Treatment will not clear infection but may decrease the duration of symptoms and viral shedding in both primary and recurrent infection. To be effective, episodic treatment should begin within 1 day of lesion appearance. In severe infection, patients require intravenous acyclovir, 5 to 10 mg/kg every 8 hours for 2 to 7 days until improved followed by oral therapy to complete a 10-day course. Topical therapy has not been shown to be effective for herpes genitalis. Long-term suppressive antiviral therapy can also be given to decrease the frequency of recurrences. See Table 89-7 for treatment of HSV infections.

Table 89-7 Treatment of Herpes Simplex Virus

Primary Infection	Suppressive Therapy	Episodic Therapy
Acyclovir: 400 mg TID or 200 mg five times a day for 7-10 d Famciclovir: 250 mg TID for 7-10 d Valacyclovir: 1 g PO BID for 7-10 d

Acyclovir: 400 mg BID

Famciclovir: 250 mg BID

Valacyclovir: 500 mg or 1 g/d

Acyclovir: 500 mg TID or 800 mg BID for 5 d

Famciclovir: 125 mg BID for 5 d or 1000 mg BID for 1 d

Valacyclovir: 500 mg BID for 3 d or 1000 mg QD for 5 d

BID, twice a day; PO, oral; QD, every day; TID, three times a day.

Human Papillomavirus

HPV is the most common STI in the United States, affecting at least 80% of women and men at some point during their lives. Similar to other STIs, adolescent and young adult women are most likely to be affected. In the United States, a recent study found that 25% of 14- to 19-year-old individuals and 45% of 20- to 24-year-old individuals were infected with at least one type of HPV. HPV is usually acquired shortly after sexual initiation, and the number of partners is the most important risk factor for HPV infection.

Epidemiology and Pathophysiology

HPV is a double-stranded DNA virus of which there are 130 known genotypes. Approximately 40 of these genotypes infect the anogenital region and are divided into low- and high-risk types based on their association with clinical disease. Although most HPV infections are asymptomatic and self-resolve, infection with low-risk types can cause anogenital warts, and high-risk types can cause precancerous anogenital lesions (i.e., cervical dysplasia) and anogenital cancers. Low-risk types 6 and 11 cause approximately 90% of anogenital warts. High-risk types 16 and 18 cause approximately 50% of high-grade cervical dysplasia and 70% of cervical cancers. Generally, HPV is thought to cause all cervical cancers.

Transmission of HPV is primarily through sexual contact; however, genital lesions can also be caused by autoinoculation from skin warts. There is also evidence that HPV types that cause skin warts are transmissible via fomites, although such evidence does not exist for genital HPV types. HPV infect rapidly dividing basal epithelial cells that predominate in the cervical transformation zone and genital areas during sexual intercourse (Figure 89-4).

Figure 89-4 Human papillomavirus.

Clinical Presentation

Four different types of genital warts can develop: condyloma acuminata, papular warts, keratotic warts, and flat-topped warts (Figure 89-5). The lesions are usually pinkish, red, gray, or white and are usually painless. They can, however, sometimes be associated with burning, itching, or bleeding.

Figure 89-5 Genital warts.

Cervical dysplasia is either low- or high-grade squamous intraepithelial dysplasia (LSIL and HSIL) or cervical intraepithelial neoplasia (CIN). Annually, 2 million women in the United States and 3% to 14% of adolescent females younger than the age of 19 years develop dysplasia. Although most are LSIL that spontaneously regress, some young women develop HSIL or CIN, which are considered precancerous, requiring more aggressive intervention. Although the cervix is the most affected anogenital region, HPV can also cause vulvar or vaginal intraepithelial neoplasia and cancer.

Diagnosis and Management

The diagnosis of genital warts is generally made by visual inspection. If external genital lesions are found in women, an internal examination of the genital tract is warranted. Anoscopy and urethroscopy may be indicated. Cervical dysplasia is diagnosed by Pap smear testing. Currently, Pap smears are recommended within 3 years of sexual initiation or by age 18 years. Testing should be performed yearly until a patient has three consecutive normal tests. Screening can then be performed every 3 years unless the patient is engaging in any high-risk sexual behavior or has had other STIs.

Treatment of genital warts includes multiple patient- and clinician-directed methods (Table 89-8). Treatment of an abnormal Pap smear depends on the degree of cervical dysplasia. For the most recent updates regarding cervical cancer screening, refer to www.asccp.org.

Table 89-8 Management of Human Papillomavirus Infections

External genital warts
For treatment of vaginal, cervical, or urethral warts, see www.cdc.gov/std/treatment

Patient administered:

Podofilox 0.5% solution or gel

Imiquod 5% cream

Provider administered:

Cryotherapy with liquid nitrogen or cryopulse every 1-2 wk until lesions resolve

Podophyllin resin 10%-25%

TCA or BCA 80%-90%

ASCUS

Repeat Pap smear in 4-6 months. If results remain abnormal, refer for colposcopy. If results are normal, repeat again in 6 months. If the patient has two consecutive normal smear results, can continue routine screening.

HPV DNA typing: if high-risk HPV type isolated, refer for colposcopy.

LSIL

If good, follow-up can repeat Pap every 4-6 months. If the patient develops HSIL or if LSIL persists, refer to colposcopy.

If follow-up unreliable, refer directly for colposcopy.

HSIL

Refer for colposcopy.

ASCUS, atypical squamous cells of undetermined significance; BCA, bichloracetic acid; CIN, cervical intraepithelial neoplasia; HPV, human papillomavirus; HSIL, high-grade squamous intraepithelial dysplasia; LSIL, low-grade squamous intraepithelial dysplasia; TCA, trichloroacetic acid.

In addition to current cervical cancer screening, a quadrivalent HPV vaccine was approved in 2006 for the prevention of genital lesions and cervical cancers caused by HPV types 6, 11, 16 and 18. The vaccine is recommended for routine administration to 11- and 12-year-old girls and for catch-up vaccination to 13- to 26-year-old girls and women. It has been shown to be highly effective in girls and young women who have not yet been exposed to any of the HPV vaccine types.