Sexually Transmitted Infections

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Chapter 114 Sexually Transmitted Infections

When controlled for sexual activity, age-specific rates of many sexually transmitted infections (STIs) are highest among sexually experienced adolescents. Some STI pathogens present as STI syndromes with a specific constellation of symptoms, but most are asymptomatic and only detected by a laboratory test. The approach to prevention and control of these infections lies in education, screening, and early diagnosis and treatment.

Etiology

The risk of contracting an STI exists in any adolescent who has had oral, vaginal, or anal sexual intercourse. Physical, behavioral, and social factors contribute to the adolescent’s higher risk (Table 114-1). Adolescents who initiate sex at a younger age are at higher risk for STIs, along with youth residing in detention facilities, youth attending sexually transmitted diseases (STD) clinics, young men having sex with men (YMSM), and youth who are injecting-drug users (IDUs). Adolescence-increased STI risk may in part be attributed to risky behaviors, such as sex with multiple concurrent partners or multiple sequential partners of limited duration, failure to use barrier protection consistently and correctly, and increased biological susceptibility to infection. Although all 50 states and the District of Columbia explicitly allow minors to consent for their own sexual health services, many adolescents encounter multiple obstacles to accessing this care. Adolescents who are victims of sexual assault may not consider themselves “sexually active,” given the context of the encounter, and need reassurance, protection, and appropriate intervention when these circumstances are uncovered.

Table 114-1 CIRCUMSTANCES CONTRIBUTING TO ADOLESCENTS’ SUSCEPTIBILITY TO SEXUALLY TRANSMITTED INFECTIONS

PHYSICAL

Younger age at puberty

Cervical ectopy

Smaller introitus leading to traumatic sex

Asymptomatic nature of sexually transmitted infection

Uncircumcised penis

BEHAVIOR LIMITED BY COGNITIVE STAGE OF DEVELOPMENT

Early adolescence: have not developed ability to think abstractly

Middle adolescence: develop belief of uniqueness and invulnerability

SOCIAL FACTORS

Poverty

Limited access to “adolescent friendly” health care services

Adolescent health-seeking behaviors (forgoing care because of confidentiality concerns or denial of health problem)

Sexual abuse and violence

Homelessness

Young adolescent females with older male partners

From Shafii T, Burstein G: An overview of sexually transmitted infections among adolescents, Adolesc Med Clin 15:207, 2004.

Epidemiology

In the USA, STI prevalence varies by age, gender, and race/ethnicity. Adolescents and young adults less than 25 yr of age have the highest reported prevalence of gonorrheal (Chapter 185) and chlamydial (Chapter 218) infection; among females, rates are highest in the 15-19 yr old age group, and among males, rates are highest for 20-24 yr olds. In 2008, females 15-19 yr of age had the highest reported chlamydia rate (3,275.8 per 100,000 population), followed by females 20 to 24 years of age (3,179.9 per 100,000 population) (Fig. 114-1). The reported 2008 chlamydia rate for 15-19 yr old females was almost 5 times higher than for 15-19 yr old males. Chlamydia is common among all races and ethnic groups; however, African-American, Native American/Alaska Native, and Hispanic women are disproportionately affected. In 2008, black females 15-19 yr of age had the highest chlamydia rate of any group (10,513.4), followed by black females 20-24 yr of age (9,373.9). Data from the 1999-2002 National Health and Nutrition Examination Survey estimate the prevalence of chlamydia among the U.S. population was highest among African-Americans across all ages, including adolescents (Fig. 114-2).

Figure 114-1 Reported Chlamydia trachomatis cases among females by age, USA, 2008.

(Adapted from the Centers for Disease Control and Prevention: Sexually transmitted diseases in the United States, 2008 [website]. www.cdc.gov/std/stats08/trends.htm. Accessed June 22, 2010.)

Figure 114-2 Chlamydia trachomatis prevalence by age group and race/ethnicity from a national survey, 1999-2002. Error bars indicate 95% confidence intervals.

(Adapted from Centers for Disease Control and Prevention: Chlamydia. Sexually transmitted disease surveillance 2008 (slide presentation). www.cdc.gov/std/stats08/slides/chlamydia.ppt. Accessed June 22, 2010.)

Reported rates of other bacterial STIs are also high among adolescents. In 2008, 15-19 yr old females had the highest (636.8 per 100,000 population) and 20-24 yr old females had the second highest gonorrhea rates (608.6 per 100,000 population) compared to any other age/sex group (Chapter 185). Gonorrhea rates among 15-24 yr old females have increased for the past 5 years. Primary and secondary (P&S) syphilis rates among 15-19 yr old females have increased annually since 2004 from 1.5 cases per 100,000 population to 3.0 per 100,000 population in 2008 (Chapter 210). Rates in women have been the highest each year in the 20-24 yr age group (5.1 cases per 100,000 population in 2008). P&S syphilis rates among 15-19 yr old males are much lower than those in older males. However, these rates have increased since 2002 from 1.3 cases per 100,000 population to 5.3 in 2008. Pelvic inflammatory disease (PID) rates are highest in females aged 15-24 yr when compared to older women.

Adolescents also suffer from a large burden of viral STIs. Young people in the USA are at persistent risk for HIV infection (Chapter 268). This risk is especially notable for youth of minority races and ethnicities. In 2004 in the 35 areas with long-term, confidential name-based HIV reporting, an estimated 4,883 young people aged 13-24 yr received a diagnosis of HIV infection or AIDS, representing about 13% of the persons given a diagnosis during that year. As of April 2008, all 50 states, the District of Columbia, and 5 dependent areas use the same confidential name-based reporting system to collect HIV and AIDS data. Surveillance data on HIV infections provide a more complete picture of the HIV/AIDS epidemic and the need for prevention and care services than does the picture provided by AIDS data alone.

The STI with the highest estimated incidence in the USA is HPV. The 2003-2004 National Health and Nutrition Examination Survey (NHANES) found a third of females aged 14-24 yr were actively infected with HPV. The highest HPV infection prevalence was among females aged 20-24 yr (44.8%; 95% CI, 36.3-55.3%) (Chapter 258). Among sexually active females, half of 20-24 yr olds were HPV-infected. Although HPV infection is common, studies suggest approximately 90% of infections clear within 2 years.

Herpes simplex virus-2 (HSV-2) is the most prevalent viral STI (Chapter 244). HSV-2 prevalence rates among adolescents in the USA and young adults appear to be decreasing. The 2005-2008 NHANES estimates that 1.4% (95% CI, 1.0-2.0) of adolescents age 14-19 yr are infected with HSV-2, which is about a 76% decrease observed from the 1988-1994 NHANES and 10.5% (95% CI, 9.0-12.3) of 20-29 yr olds are HSV-2 seropositive, which is about a 39% decrease compared to the 1988-1994 NHANES (Fig. 114-3).

Figure 114-3 Estimated incidence of sexually transmitted infections among American youth ages 15 to 24 years, 2000.

(Adapted from Weinstock H, Berman S, Cates W: Sexually transmitted diseases among American youth: incidence and prevalence estimates, 2000, Perspect Sex Reprod Health 36:6–10, 2004.)

Pathogenesis

During puberty, increasing levels of estrogen cause the vaginal epithelium to thicken and cornify and the cellular glycogen content to rise, the latter causing the vaginal pH to fall. These changes increase the resistance of the vaginal epithelium to penetration by certain organisms (including Neisseria gonorrhoeae) and increase the susceptibility to others (Candida albicans and Trichomonas, Chapter 276). The transformation of the vaginal cells leaves columnar cells on the ectocervix, forming a border of the 2 cell types on the ectocervix, known as the squamocolumnar junction. The appearance is referred to as ectopy (Fig. 114-4). With maturation, this tissue involutes. Prior to involution, it represents a unique vulnerability to infection for adolescent females. A 15 yr old sexually active girl with endocervical colonization has a 1:8 chance of developing PID compared to the 1:80 chance for a 24 yr old. As a result of these physiologic changes, gonococcal infection becomes primarily cervical and susceptibility to ascending infection is greatest during menses, when the pH is 6.8-7.0. The association of early sexual debut and younger gynecologic age with increased risk of sexually transmitted infections supports this explanation of the pathogenesis of infection in young adolescents.

Figure 114-4 Cervical ectopy.

(From the Seattle STD/HIV Prevention Training Center at the University of Washington: Claire E. Stevens.)

STI Screening

Early detection and treatment are the primary STI control strategies. Some of the most common STIs in adolescents, including HPV, HSV, chlamydia, and gonorrhea, are usually asymptomatic and if undetected can be spread inadvertently by the infected host. Screening initiatives for chlamydial infections have demonstrated reductions in PID cases by up to 40%. Although federal and professional medical organizations recommend annual chlamydia screening for sexually active females 24 yr and younger, in 2007, less than half (42%) of the sexually active females enrolled in commercial and Medicaid health plans were screened. The lack of a dialogue about STIs or the provision of STI services at annual preventive service visits to adolescents who are sexually experienced are missed opportunities for screening and education. Comprehensive, confidential, reproductive health services including STI screening should be offered to all sexually experienced adolescents (Table 114-2).

Table 114-2 ROUTINE LABORATORY SCREENING RECOMMENDATIONS FOR SEXUALLY TRANSMITTED INFECTIONS IN SEXUALLY ACTIVE ADOLESCENTS AND YOUNG ADULTS

Chlamydia trachomatis AND Neisseria gonorrhoeae

• Routinely screening for C. trachomatis and N. gonorrhoeae of all sexually active females aged ≤25 yr is recommended annually

• Routinely screening for asymptomatic C. trachomatis infection in young men has not been recommended because studies have not yet demonstrated efficacy in decreasing prevalence or preventing disease outcomes in women by screening for chlamydial infection in men. Screening of sexually active young men should be considered in clinical settings with a high chlamydia prevalence rates (e.g., adolescent or school-based clinics, correctional facilities, Job Corps, and STD clinics).

HIV

• HIV screening should be discussed with all adolescents and encouraged for those who are sexually active and injection drug using

SYPHILIS

• Syphilis screening should be offered to sexually active adolescents reporting risk factors

• The majority of U.S. syphilis cases occurring among YMSM and many early syphilis cases are identified from correctional facilities

• Providers should consult with their local health department regarding local syphilis prevalence and associated risk factors that are associated with syphilis acquisition

HEPATITIS C VIRUS

• Screening adolescents for hepatitis C virus who report risk factors, i.e., injection drug use, MSM, received blood products or organ donation before 1992, received clotting factor concentrates before 1987, long term hemodialysis, or high prevalence setting, i.e., correctional facilities or STD clinics

NO RECOMMENDATIONS

• Although prevalent among adolescent populations, currently there are no recommendations to routinely screen adolescents who are asymptomatic for infections, such as trichomoniasis, bacterial vaginosis, genital herpes infection, HPV, HAV, or HBV

• Young MSM and pregnant adolescent females may require more thorough evaluations and assessments

STD, sexually transmitted diseases; HIV, human immunodeficiency virus; YMSM, young men who have sex with men; HPV, human papillomavirus; HAV, hepatitis A virus; HBV, hepatitis B virus.

From Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines, 2010, MMWR 59(No. RR-12):1-110, 2010.

Definitions, Etiology, and Clinical Manifestations

STI syndromes are generally characterized by the location of the manifestation (vaginitis) or the type of lesion (genital ulcer). Certain constellations of presenting symptoms suggest the inclusion of a possible STI in the differential diagnosis.

Urethritis

Urethritis is an STI syndrome characterized by inflammation of the urethra, usually due to an infectious etiology. Urethritis may present with urethral discharge, urethral itching, dysuria, or urinary frequency. Urgency, frequency of urination, erythema of the urethral meatus, and scrotal pain are less common clinical presentations. Many patients are completely asymptomatic at the time of diagnosis. On examination, the classic finding is mucoid or purulent discharge from the urethral meatus (Fig. 114-5). If no discharge is evident on exam, providers may attempt to express discharge by applying gentle pressure to the urethra from the base distally to the meatus 3-4 times. Chlamydia trachomatis and N. gonorrhoeae are the most commonly identified pathogens. Mycoplasma genitalium and Ureaplasma urealyticum are considered potential pathogens in nongonococcal urethritis (NGU) when chlamydia is not confirmed. NGU caused by these pathogens may be less responsive to usual NGU therapy. Trichomonas vaginalis and HSV should also be considered in the NGU differential diagnosis. Sensitive diagnostic tests for these NGU pathogens are not available but should be considered when NGU is not responsive to treatment. Noninfectious causes of urethritis include urethral trauma or foreign body. Unlike in females, urinary tract infections are fairly rare in males who have no past genitourinary medical history. In the typical sexually active adolescent male, dysuria and urethral discharge suggest the presence of an STI unless proven otherwise. Laboratory evaluation is essential to identify the involved pathogens to determine treatment, partner notification, and disease control.

Figure 114-5 Gonococcal urethral discharge.

(From the Seattle STD/HIV Prevention Training Center at the University of Washington: Connie Celum and Walter Stamm.)

Epididymitis

The inflammation of the epididymis in adolescent males is most often associated with an STI, most frequently C. trachomatis or N. gonorrhoeae. The presentation of unilateral scrotal swelling and tenderness, often accompanied by a hydrocele and palpable swelling of the epididymis, associated with the history of urethral discharge, constitute the presumptive diagnosis of epididymitis. Testicular torsion, a surgical emergency usually presenting with sudden onset of severe testicular pain, should be considered in the differential diagnosis (Chapter 539). Males who practice insertive anal intercourse are also vulnerable to Escherichia coli infection.

Vaginitis

Vaginitis is a superficial infection of the vaginal mucosa frequently presenting as a vaginal discharge, with or without vulvar involvement (Chapter 543). Bacterial vaginosis, vulvovaginal candidiasis (VVC), and trichomoniasis are the predominant infections associated with vaginal discharge. Bacterial vaginosis is replacement of the normal H₂O₂–producing Lactobacillus sp. vaginal flora by an overgrowth of anaerobic microorganisms as well as Gardnerella vaginalis, Ureaplasma, and Mycoplasma. Although bacterial vaginosis is not categorized as a STI, sexual activity is associated with increased frequency of vaginosis. VVC, usually caused by C. albicans, can trigger vulvar pruritus, pain, swelling, and redness and dysuria. Findings on vaginal exam include vulvar edema, fissures, excoriations, or thick curdy vaginal discharge. Trichomoniasis is caused by the protozoan T. vaginalis. Infected females may present with symptoms characterized by a diffuse, malodorous, yellow-green vaginal discharge with vulvar irritation or may be diagnosed by screening an asymptomatic patient. Cervicitis can sometimes cause a vaginal discharge. Laboratory confirmation is recommended because clinical presentations may vary and patients may be infected with more than 1 pathogen.

Cervicitis

The inflammatory process in cervicitis involves the deeper structures in the mucous membrane of the cervix uteri. Vaginal discharge can be a manifestation of cervicitis, if the cervical discharge is profuse. Less subtle clinical manifestations of cervicitis are irregular or postcoital bleeding, mucopurulent discharge from the os, and a friable cervix. The cervical changes associated with cervicitis must be distinguished from cervical ectopy in the younger adolescent to avoid the over diagnosis of inflammation (Fig. 114-6; see Fig. 114-4). The pathogens identified most commonly with cervicitis are C. trachomatis and N. gonorrhoeae, although no pathogen is identified in the majority of cases. HSV is a less common pathogen associated with ulcerative and necrotic lesions on the cervix.

Figure 114-6 Inflamed cervix due to gonococcal cervicitis.

(From Centers for Disease Control and Prevention: STD clinical slides (website). www.cdc.gov/std/training/clinicalslides/slides-dl.htm. Accessed June 12, 2009.

Pelvic Inflammatory Disease

PID encompasses a spectrum of inflammatory disorders of the female upper genital tract, including endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis, usually in combination rather than as separate entities. N. gonorrhoeae and C. trachomatis predominate as the involved pathogenic organisms in younger adolescents, although PID should be approached as multiorganism etiology, including pathogens such as anaerobes, G. vaginalis, Haemophilus influenzae, enteric gram-negative rods, and Streptococcus agalactiae. In addition, cytomegalovirus (CMV) (Chapter 247), Mycoplasma hominis, U. urealyticum, and Mycoplasma genitalium (Chapter 216), may be associated with PID.

PID is difficult to diagnose because of the wide variation in the symptoms and signs. Many females with PID have subtle or mild symptoms resulting in many unrecognized cases. Health care providers should consider the possibility of PID in young sexually active females presenting with vaginal discharge and/or abdominal pain.

The clinical diagnosis of PID is based on presence of at least 1 of the minimal criteria, either lower abdominal tenderness, adnexal tenderness, or cervical motion tenderness, to increase the diagnostic sensitivity and reduce the likelihood of missed or delayed diagnosis. In addition, the majority of females with PID have either mucopurulent cervical discharge or evidence of WBC on a microscopic evaluation of a vaginal fluid saline preparation. If the cervical discharge appears normal and no WBCs are observed on the wet prep of vaginal fluid, the diagnosis of PID is unlikely, and alternative causes of pain should be investigated. Specific, but not always practical, criteria for PID include evidence of endometritis on biopsy, transvaginal sonography or MRI evidence of thickened, fluid-filled tubes, or Doppler evidence of tubal hyperemia or laparoscopic evidence of PID.

Genital Ulcer Syndromes

An ulcerative lesion in a mucosal area exposed to sexual contact is the unifying characteristic of infections associated with these syndromes. These lesions are most frequently seen on the penis and vulva, but also occur on oral and rectal mucosa depending on the adolescent’s sexual practices. HSV, Treponema pallidum (syphilis), and Haemophilus ducreyi (chancroid) are the most common organisms associated with genital ulcer syndromes.

Genital herpes, the most common ulcerative STI among adolescents, is a chronic, life-long viral infection. Two sexually transmitted HSV types have been identified, HSV-1 and HSV-2. The majority of cases of recurrent genital herpes are caused by HSV-2. Most HSV-2–infected persons are unaware of their diagnosis because they experience mild or unrecognized infections but continue to shed virus intermittently in the genital tract. Therefore, the majority of genital herpes infections are transmitted by asymptomatic persons who are unaware of their infection.

Although the initial herpetic lesion is a vesicle, by the time the patient presents clinically, the vesicle most often has ruptured spontaneously, leaving a shallow, painful ulcer. Up to 50% of first genital herpes episodes are caused by HSV-1, but recurrences and subclinical shedding are much more frequent for genital HSV-2 infection.

Syphilis and chancroid are less common causes of genital ulcers in adolescents than in adults. Lymphogranuloma venereum due to C. trachomatis serovars L1-L3, and donovanosis are rare infections in the USA and other industrialized countries, although outbreaks of lymphogranuloma venereum do occur in MSM. In these circumstances, genital ulcerations with inflamed inguinal lymph nodes (buboes) are unusual; proctitis or proctocolitis is the usual manifestation. HIV is present in affected men.

Clinical characteristics differentiating the lesions of the most common infections associated with genital ulcers are presented in Table 114-3, along with the required laboratory diagnosis to identify the causative agent accurately. The differential diagnosis includes Behçet disease (Chapter 155), Crohn disease (Chapter 328), and acute genital ulcers (AGU) due to Epstein-Barr virus (Chapter 246). AGU often follows a flu or mononucleosis-like illness in an immunocompetent female and is unrelated to sexual activity. The lesions are 0.5-2.5 cm in size, bilateral, symmetric, multiple, painful and necrotic, and are associated with inguinal lymphadenopathy. This primary infection is also associated with fever and malaise. The diagnosis may require EBV titers, or PCR testing. Treatment is supportive care including pain management.

Table 114-3 SIGNS, SYMPTOMS, AND PRESUMPTIVE AND DEFINITIVE DIAGNOSES OF GENITAL ULCERS

Genital Lesions and Ectoparasites

Lesions that present as outgrowths on the surface of the epithelium and other limited epidermal lesions are included under this categorization of syndromes. HPV can cause genital warts and genital cervical abnormalities that can lead to cancer. Genital HPV types are classified according to their association with cervical cancer. Infections with low-risk types, such as HPV types 6 and 11, can cause benign or low-grade changes in cells of the cervix, genital warts, and recurrent respiratory papillomatosis. High-risk HPV types can cause cervical, anal, vulvar, vaginal, and head and neck cancers. High-risk HPV types 16 and 18 are detected in approximately 70% of cervical cancers. Persistent infection increases the risk of cervical cancer. Molluscum contagiosum and condyloma lata associated with secondary syphilis complete the classification of genital lesion syndromes. As a result of the close physical contact during sexual contact, common ectoparasitic infestations of the pubic area occur as pediculosis pubis or the papular lesions of scabies (Chapter 660).

Hiv Disease and Hepatitis B

HIV and hepatitis B present as an asymptomatic, unexpected occurrences in most infected adolescents. Risk factors identified in the history or routine screening during prenatal care are much more likely to result in suspicion of infection, leading to the appropriate laboratory screening, than are clinical manifestations in this age group (Chapters 268 and 350).

Diagnosis

Most adolescents infected with viral and bacterial STI pathogens usually do not report symptoms suggestive of infection. With the increased use of very sensitive, noninvasive, nucleic acid amplification tests (NAAT), providers are finding that most genital infections in females as well as many males are asymptomatic. Therefore, a good sexual history is key to identifying adolescents who should be screened for STIs and for identifying those who require a laboratory diagnostic evaluation for an STD syndrome.

When eliciting a sexual health history, discussions should be appropriate for the patient’s developmental level. In addition to questions regarding vaginal or urethral discharge, genital lesions, and lower abdominal pain among females, one should ask about prior treatment of any STI symptoms, including self-treatment using over-the-counter medications. Dyspareunia is a consistent symptom in adolescents with PID. Providers must ask about oral or anal sexual activity to determine sites for specimen collection.

Urethritis should be objectively documented by either (1) mucoid or purulent urethral discharge, (2) ≥5 WBC per high-power field on microscopic examination of a urethral secretions Gram stain, (3) ≥10 WBC per high-power field on microscopic examination of first-void urine (FVU) specimen, or (4) positive FVU leukocyte esterase test. The presence of gram-negative intracellular diplococci on microscopy confirms the diagnosis of gonococcal urethritis. Patient complaint without objective clinical or laboratory evidence does not fulfill diagnostic criteria. All patients with complaints, whether or not diagnostic criteria are fulfilled, should be tested for gonorrhea and chlamydia.

An essential component of the diagnostic evaluation of vaginal, cervical or urethral discharge is a chlamydia and gonorrhea NAAT. NAATs are the most sensitive chlamydia tests available and allow for noninvasive STI testing via urine and self-collected vaginal swabs in addition to testing endocervical and urethral specimens (Table 114-4). Gonorrhea and chlamydia NAATs perform well on rectal and oropharyngeal specimens and can be performed by most commercial laboratories.

Table 114-4 AMPLIFIED GONORRHEA AND CHLAMYDIA TESTS AND APPROVED SPECIMENS FOR TESTING *

TEST TECHNOLOGY AND NAME (MANUFACTURER)	SPECIMENS APPROVED FOR TESTING
POLYMERASE CHAIN REACTION
COBAS AMPLICOR (CT/NG) Test (Roche Diagnostics, Indianapolis, IN)	Female: cervical, urine (NOT approved for Neisseria gonorrhoeae female urine testing) Male: urethral (NOT approved for asymptomatic N. gonorrhoeae male urethral swab testing), urine

Abbott RealTime CT/NG Assay (Abbott Laboratories, Abbott Park, IL) Female: cervical, urine, vaginal (including self-collected in health-care setting)
Male: urethral, urine TRANSCRIPTION MEDIATED AMPLIFICATION APTIMA COMBO 2 Assay (GenProbe, San Diego, CA)

Female: cervical, urine, vaginal (including self-collected in health-care setting), liquid pap specimen

Male: urethral, urine

STRAND DISPLACEMENT AMPLIFICATION BDProbeTec ET Chlamydia trachomatis and N. gonorrhoeae Amplified DNA Assays

Female: cervical, urine

Male: urethral, urine

BDProbeTec CT/GC Q^x Amplified DNA Assays (Becton Dickinson, Sparks, MD)

Female: cervical, urine, vaginal (including self-collected in health care setting)

Male: urethral, urine

NUCLEIC ACID HYBRIDIZATION WITH SIGNAL AMPLIFICATION digene HC2 CT/GC DNA Test (QIAGEN, Gaithersburg, MD) Female: swab, cytobrush

* Specimens approved for testing as of June 22, 2010.

Evaluation of adolescent females with vaginitis includes laboratory data. The cause of vaginal symptoms usually can be determined by pH and microscopic examination of the discharge. Using pH paper, an elevated pH (i.e., >4.5) is common with BV or trichomoniasis. For microscopic exam, a slide can be made with the discharge diluted in 1-2 drops of 0.9% normal saline solution and another slide with discharge diluted in 10% potassium hydroxide (KOH) solution. Examining the saline specimen slide under a microscope may reveal motile or dead T. vaginalis or clue cells (epithelial cells with borders obscured by small bacteria), which are characteristic of bacterial vaginosis. WBCs without evidence of trichomonads or yeast are usually suggestive of cervicitis. The yeast or pseudohyphae of Candida species are more easily identified in the KOH specimen (Fig. 114-7). The sensitivity of microscopy is approximately 60-70% and requires immediate evaluation of the slide for optimal results. Therefore, lack of findings does not eliminate the possibility of infection. T. vaginalis culture is more sensitive than microscopy. Objective signs of vulvar inflammation in the absence of vaginal pathogens, along with a minimal amount of discharge, suggest the possibility of mechanical, chemical, allergic, or other noninfectious irritation of the vulva (Table 114-5).

Figure 114-7 Common normal and abnormal microscopic findings during examination of vaginal fluid. KOH, potassium hydroxide solution; PMN, polymorphonuclear leukocyte; RBC, red blood cell.

(From Adolescent medicine: state of the art reviews, vol 14, no 2, Philadelphia, 2003, Hanley & Belfus, pp 350–351.)

Table 114-5 PATHOLOGIC VAGINAL DISCHARGE

INFECTIVE DISCHARGE	OTHER REASONS FOR DISCHARGE
COMMON CAUSES	COMMON CAUSES
Organisms	Retained tampon or condom Chemical irritation Allergic responses Ectropion Endocervical polyp Intrauterine device Atrophic changes
Candida albicans Trichomonas vaginalis Chlamydia trachomatis Neisseria gonorrhoeae
Conditions
Bacterial vaginosis Acute pelvic inflammatory disease Postoperative pelvic infection Postabortal sepsis Puerperal sepsis
	LESS COMMON CAUSES
	Physical trauma Vault granulation tissue Vesicovaginal fistula Rectovaginal fistula Neoplasia Cervicitis
LESS COMMON CAUSES
Mycoplasma genitalium Ureaplasma urealyticum Syphilis Escherichia coli

From Mitchell H: Vaginal discharge—causes, diagnosis, and treatment, Br Med J 328:1306–1308, 2004.

In settings where microscopy is not available, alternative tests may be used to diagnose vaginitis. The OSOM Trichomonas Rapid Test (Genzyme Diagnostics, Cambridge, MA), an immunochromatographic capillary flow dipstick technology, is Clinical Laboratory Improvement Amendments (CLIA)-waived and results are available in 10 min. The Affirm VPIII (Becton Dickenson, San Jose, CA), a nucleic acid probe test that evaluates for T. vaginalis, G. vaginalis, and C. albicans, is a moderate complexity laboratory test and results are available within 45 min. Both tests have a sensitivity >83% and a specificity >97% and are point-of-care diagnostics.

The definitive diagnosis of PID is difficult based on clinical findings alone. Clinical diagnosis is imprecise and no single historical, physical, or laboratory finding is both sensitive and specific for the diagnosis of acute PID. Clinical criteria have a positive predictive value of only 65-90% compared with laparoscopy. Although health care providers should maintain a low threshold for the diagnosis of PID, additional criteria to enhance specificity of diagnosis, such as transvaginal ultrasonography, can be considered (Table 114-6).

Table 114-6 EVALUATION FOR PELVIC INFLAMMATORY DISEASE (PID)

2010 CENTERS FOR DISEASE CONTROL AND PREVENTION DIAGNOSTIC CRITERIA

Minimal Criteria

Additional Criteria to Enhance Specificity of the Minimal Criteria

• Oral temperature >101°F (>38.3°C)

• Abnormal cervical or vaginal mucopurulent discharge *

• Presence of abundant numbers of white blood cells on saline microscopy of vaginal secretions *

• Elevated ESR or C-reactive protein

• Laboratory documentation of cervical Neisseria gonorrhoeae or Chlamydia trachomatis infection

Most Specific Criteria to Enhance the Specificity of the Minimal Criteria

• Transvaginal sonography or MRI techniques showing thickened, fluid-filled tubes, with or without free pelvic fluid or tubo-ovarian complex, or Doppler studies suggesting pelvic infection (e.g., tubal hyperemia)

• Endometrial biopsy with histopathologic evidence of endometritis

• Laparoscopic abnormalities consistent with PID

DIFFERENTIAL DIAGNOSIS (PARTIAL LIST)

GI: appendicitis, constipation, diverticulitis, gastroenteritis, inflammatory bowel disease, irritable bowel syndrome

GYN: ovarian cyst (intact, ruptured, or torsed), endometriosis, dysmenorrhea, ectopic pregnancy, mittelschmerz, ruptured follicle, septic or threatened abortion, tubo-ovarian abscess

Urinary tract: cystitis, pyelonephritis, urethritis, nephrolithiasis

SR, erythrocyte sedimentation rate; GI, gastrointestinal; GYN, gynecologic; WBC, white blood cell.

* If the cervical discharge appears normal and no WBCs are observed on the wet prep of vaginal fluid, the diagnosis of PID is unlikely and alternative causes of pain should be investigated.

Adapted from Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines, 2010, MMWR 59(No. RR-12):1-110, 2010.

Isolation of HSV in cell culture is the preferred virologic test for genital ulcers, but culture sensitivity is low and false negatives do occur due to intermittent viral shedding. HSV PCR assays are more sensitive and can be used instead of viral culture. The Tzanck test is insensitive and nonspecific and should not be relied on.

Accurate type-specific HSV serologic assays are based on the HSV-specific glycoprotein G2 (HSV-2) and glycoprotein G1 (HSV-1). Both laboratory-based and point-of-care tests are available. Because nearly all HSV-2 infections are sexually acquired, the presence of type-specific HSV-2 antibody implies anogenital infection. The presence of HSV-1 antibody alone is more difficult to interpret because of the frequency of oral HSV infection acquired during childhood. Type-specific HSV serologic assays might be useful in the following scenarios: (1) recurrent genital symptoms or atypical symptoms with negative HSV cultures; (2) a clinical diagnosis of genital herpes without laboratory confirmation; and (3) a partner with genital herpes, especially if considering suppressive antiviral therapy to prevent transmission.

For syphilis screening more laboratories are now using treponemal enzyme immunoassay (EIA) tests. A positive treponemal EIA test identifies both previously treated and untreated or incompletely treated syphilis. False-positive results can occur, particularly among populations with low syphilis prevalence. Persons with a positive treponemal screening test should have a standard nontreponemal test with titer, such as an RPR or VDRL to guide patient management decisions.

Adolescents with STIs should be offered HIV testing. Rapid HIV testing with the availability of results in 10-20 min can be useful in settings in which the likelihood of adolescents returning for their results is low. Point-of-care, CLIA-waived tests for whole blood finger-stick and oral fluid specimen testing are available. Clinical studies have demonstrated that the rapid HIV test performance is comparable to those of EIAs. Because some reactive test results may be false-positive, every reactive rapid test must be confirmed by a more specific test, such as a Western blot.

Treatment

See Part XVI for chapters on the treatment of specific microorganisms and Tables 114-7 to 114-9. Treatment regimens using over-the-counter products for candida vaginitis and pediculosis reduce financial and access barriers to rapid treatment for adolescents, but there are potential risks for inappropriate self-treatment and complications from untreated more serious infections that must be considered before using this approach. Minimizing noncompliance with treatment, finding and treating the sexual partners, addressing prevention and contraceptive issues, offering available vaccines to prevent STIs and making every effort to preserve fertility are additional physician responsibilities. Repeat testing in 3-4 mo is recommended for patients with chlamydial and gonorrheal infections. Some experts also recommend repeat testing for trichomonas infection. Once an infection is diagnosed, partner evaluation, testing, and treatment are recommended for sexual contacts within 60 days of symptoms or diagnosis or the most recent partner if sexual contact was >60 days, even if the partner is asymptomatic. Abstinence is recommended for at least 7 days after both patient and partner are treated. A test for pregnancy should be performed for all females with suspected PID, since the test outcome will affect management.

Table 114-7 MANAGEMENT GUIDELINES FOR UNCOMPLICATED BACTERIAL STIS IN ADOLESCENTS AND ADULTS

PATHOGEN	RECOMMENDED REGIMENS	ALTERNATIVE REGIMENS AND SPECIAL CONSIDERATIONS
Chlamydia trachomatis	Azithromycin 1 g orally once OR Doxycycline 100 mg orally twice daily for 7 days

For pregnancy:

Azithromycin 1 g orally once

Amoxicillin 500 mg orally 3 times a day for 7 days

Neisseria gonorrhoeae (cervix, urethra, and rectum)

Ceftriaxone 250 mg IM in a single dose

OR, IF NOT AN OPTION

Cefixime 400 mg orally in a single dose

Single-dose injectable cephalosporin (e.g., ceftizoxime 500 mg IM, cefoxitin 2 g IM with probenecid 1 g orally, and cefotaxime 500 mg IM)

PLUS

Treatment for Chlamydia infection if not ruled out with NAAT

Alternative: Cefpodoxime 400 mg orally in a single dose

Cephalosporin allergy: Azithromycin 2 g orally in a single dose

Neisseria gonorrhoeae (pharynx)

Ceftriaxone 250 mg IM in a single dose

PLUS

Treatment for Chlamydia infection if not ruled out with NAAT

Gonococcal conjunctivitis Ceftriaxone 1 g IM in a single dose Treponema pallidum (primary and secondary syphilis or early latent syphilis, i.e., infection <12 mo) Benzathine penicillin G 2.4 million units IM in 1 dose Penicillin allergy: Doxycycline 100 mg orally twice daily for 14 days OR Tetracycline 500 mg 4 times daily for 14 days. Some experts recommend ceftriaxone 1 g daily either IM or IV for 8-10 days or azithromycin 2 g orally in a single dose Treponema pallidum (late latent syphilis or syphilis of unknown duration) Benzathine penicillin G 7.2 million units total, administered as 3 doses of 2.4 million units IM each at 1 wk intervals Penicillin allergy: Doxycycline 100 mg orally twice daily or Tetracycline 500 mg orally 4 times daily, both for 28 days in conjunction with close serologic and clinical follow-up Haemophilus ducreyi (chancroid: genital ulcers, lymphadenopathy)

Azithromycin 1 g orally in a single dose

Ceftriaxone 250 mg IM in a single dose

Ciprofloxacin 500 mg orally twice a day for 3 days

Erythromycin base 500 mg orally 3 times a day for 7 days

Chlamydia trachomatis serovars L1, L2, or L3 (lymphogranuloma venereum) Doxycycline 100 mg orally twice daily for 21 days

Alternative: Erythromycin base 500 mg orally 4 times a day for 21 days

Azithromycin 1.0 g orally once weekly for 3 wk

Calymmatobacterium granulomatis (donovanosis or granuloma inguinale)

Doxycycline 100 mg orally twice daily for at least 3 weeks and until all lesions have healed

Alternative regimens should be taken at least until all lesions have completely healed: Azithromycin 1 g orally once per week for at least 3 weeks

Ciprofloxacin 750 mg orally twice a day for at least 3 wk

Erythromycin base 500 mg orally 4 times a day for at least 3 wk

Trimethoprim-sulfamethoxazole 1 double-strength (160 mg/800 mg) tablet orally twice a day for at least 3 wk

IM, intramuscular; IV, intravenous; NAAT, nucleic acid amplification test.

Adapted for Centers for Disease Control and Prevention: 2010 Sexually transmitted diseases treatment guidelines, 2010 MMWR 59(No. RR-12):1-110, 2010.

Table 114-8 MANAGEMENT GUIDELINES FOR UNCOMPLICATED MISCELLANEOUS SEXUALLY TRANSMITTED INFECTIONS IN ADOLESCENTS AND ADULTS

PATHOGEN	RECOMMENDED REGIMENS	ALTERNATIVE REGIMENS
Trichomonas vaginalis	Metronidazole 2 g orally in a single dose OR Tinidazole 2 g orally in a single dose	Metronidazole 500 mg orally twice daily for 7 days
Phthirus pubis (pubic lice)	Permethrin 1% cream rinse applied to affected areas and washed off after 10 min OR Pyrethrins with piperonyl butoxide applied to affected areas and washed off after 10 min Launder clothing and bedding	Malathion 0.5% lotion applied for 8-12 hr and washed off OR Ivermectin 250 µg/kg PO, repeat in 2 wk
Sarcoptes scabiei (scabies)	Permethrin 5% cream applied to all areas from the neck down, washed off after 8-14 hr OR Ivermectin 200 µg/kg orally, repeated in 2 wk Launder clothing and bedding	Lindane (1%) 1 oz of lotion or 30 g of cream in thin layer to all areas of body from neck down; wash off in 8 hr

Adapted for Centers for Disease Control and Prevention: 2010 Sexually transmitted diseases treatment guidelines, 2010 MMWR 59(No. RR-12):1-110, 2010.

Table 114-9 MANAGEMENT GUIDELINES FOR UNCOMPLICATED GENITAL WARTS AND GENITAL HERPES IN ADOLESCENTS AND ADULTS

PATHOGEN	RECOMMENDED REGIMENS	ALTERNATIVE REGIMENS
Human papillomaviruses external genital warts	Patient-applied: Podofilox 0.5% solution or gel self-applied to warts twice daily for 3 consecutive days each wk followed by 4 days of no therapy. May be repeated for up to 4 cycles. OR Imiquimod 5% cream self-applied to warts once daily at bedtime 3 times wkly for up to 16 wk; washed off after 6-10 hr OR Sinecatechins 15% ointment self-applied 3 times daily for up to 16 wk. Does not need to be washed off. Provider-administered: Cryotherapy with liquid nitrogen or cryoprobe. Repeat applications every 1-2 weeks. OR Podophyllin resin 10-25% in a compound tincture of benzoin. A small amount should be applied to each wart and allowed to air dry. Can be repeated weekly, if necessary. May wash off 1-4 hr after application to reduce irritation. OR Trichloroacetic acid (TCA) or bichloroacetic acid (BCA) 80-90%. A small amount should be applied only to the warts and allowed to dry, at which time a white “frosting” develops. Can be repeated weekly, if necessary. OR Surgical removal either by tangential scissor excision, tangential shave excision, curettage, or electrosurgery	Intralesional interferon OR Photodynamic therapy and topical ciclovir Safety of podofilox, imiquimod, sinecatechins or podophyllin resin during pregnancy has not been established.
Human papillomaviruses Cervical warts	Refer to specialist for oncologic evaluation
Human papillomaviruses Vaginal warts	Cryotherapy with liquid nitrogen. Avoid use of a cryoprobe. OR TCA or BCA 80-90% applied to warts. A small amount should be applied only to warts and allowed to dry, at which time a white “frosting” develops. Can be repeated weekly, if necessary.
Human papillomaviruses Urethral meatal warts	Cryotherapy with liquid nitrogen OR Podophyllin 10-25% in compound tincture of benzoin. Treatment area must be dry before contact with normal mucosa. Can be repeated weekly, if necessary.
Human papillomaviruses Anal warts	Cryotherapy with liquid nitrogen OR TCA or BCA 80-90% applied to warts. A small amount should be applied only to warts and allowed to dry, at which time a white “frosting” develops. Can be repeated weekly, if necessary. OR Surgical removal	Warts on the rectal mucosa should be managed in consultation with a specialist. Persons with anal warts should have rectal mucosa inspected by digital examination or anoscopy.
Herpes simplex virus (genital herpes): First clinical episode	Treat for 7-10 days with 1 of the following: Acyclovir 400 mg orally 3 times daily OR Acyclovir 200 mg orally 5 times daily OR Famciclovir 250 mg orally 3 times daily OR Valacyclovir 1 g orally twice daily	Consider extending treatment if healing is incomplete after 10 days of therapy.
Herpes simplex virus (genital herpes): Episodic therapy for recurrences	Acyclovir 400 mg orally 3 times daily for 5 days OR Acyclovir 800 mg orally twice daily for 5 days OR Acyclovir 800 mg orally 3 times daily for 2 days OR Famciclovir 125 mg orally twice daily for 5 days OR Famciclovir 1000 mg orally twice daily for 1 day OR Famciclovir 500 mg orally once then 250 mg twice daily for 2 days OR Valacyclovir 500 mg orally twice daily for 3 days OR Valacyclovir 1000 mg orally once daily for 5 days	Effective episodic treatment of recurrences requires initiation of therapy within 1 day of lesion onset or during the prodrome that precedes some outbreaks. The patient should be provided with a supply or a prescription for the medication with instructions to initiate treatment immediately when symptoms begin.
Herpes simplex virus (genital herpes): Suppressive therapy for recurrences	Acyclovir 400 mg orally twice daily OR Famciclovir 250 mg orally twice daily OR Valacyclovir 500 mg orally once daily or 1 g orally once daily	All patients should be counseled regarding suppressive therapy availability, regardless of number of outbreaks per year. Since the frequency of recurrent outbreaks diminishes over time in many patients, periodically, providers should discuss the need to continue therapy.