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STD Characterized by Urethritis and Cervicitis

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Author:    Julia Tortorice (RN, MBA, MSN, NEA-BC, CPHQ)

Objectives

After completing the course, the learner will be able to:

 

Identify signs and symptoms of STDs characterized by Urethritis and Cervicitis.

 

Identify recommended treatment, follow-up and partner referral for those diseases.

 

Identify special issues with STD in pregnant patients, infants and children.

 

 

Urethritis

Management of Male Patients Who Have Urethritis

Urethritis, or inflammation of the urethra, is caused by an infection characterized by the discharge of mucopurulent or purulent material and by burning during urination. Asymptomatic infections are common. The only bacterial pathogens of proven clinical importance in men who have urethritis are N. gonorrhoeae and C. trachomatis. Testing to determine the specific disease is recommended because both of these infections are reportable to state health departments, and a specific diagnosis may improve compliance and partner notification. If diagnostic tools (e.g., a Gram stain and microscope) are unavailable, patients should be treated for both infections. The extra expense of treating a person who has nongonococcal urethritis (NGU) for both infections also should encourage the health-care provider to make a specific diagnosis. New nucleic acid amplification tests enable detection of N. gonorrhoeae and C. trachomatis on first-void urine; in some settings, these tests are more sensitive than traditional culture techniques.

 

Etiology

NGU is diagnosed if Gram-negative intracellular organisms cannot be identified on Gram stains. C. trachomatis is the most frequent cause (i.e., in 23%-55% of cases); however, the prevalence differs by age group, with lower prevalence among older men. The proportion of NGU cases caused by chlamydia has been declining gradually. Complications of NGU among men infected with C. trachomatis include epididymitis and Reiter's syndrome. Documentation of chlamydia infection is important because partner referral for evaluation and treatment would be indicated.

 

The etiology of most cases of nonchlamydial NGU is unknown. Ureaplasma urealyticum and possibly Mycoplasma genitalium are implicated in as many as one third of cases. Specific diagnostic tests for these organisms are not indicated.

 

Trichomonas vaginalis and HSV sometimes cause NGU. Diagnostic and treatment procedures for these organisms are reserved for situations in which NGU is unresponsive to therapy.

Confirmed Urethritis

 

Clinicians should document that urethritis is present. Urethritis can be documented by the presence of any of the following signs:

a.      Mucopurulent or purulent discharge.

b.      Gram stain of urethral secretions demonstrating greater than or equal to 5 WBCs per oil immersion field. The Gram stain is the preferred rapid diagnostic test for evaluating urethritis. It is highly sensitive and specific for documenting both urethritis and the presence or absence of gonococcal infection. Gonococcal infection is established by documenting the presence of WBCs containing intracellular Gram-negative diplococci.

c.      Positive leukocyte esterase test on first-void urine, or microscopic examination of first-void urine demonstrating greater than or equal to 10 WBCs per high power field.

If none of these criteria is present, then treatment should be deferred, and the patient should be tested for N. gonorrhoeae and C. trachomatis and followed closely in the event of a positive test result. If the results demonstrate infection with either N. gonorrhoeae or C. trachomatis, the appropriate treatment should be given and sex partners referred for evaluation and treatment.

Empiric treatment of symptoms without documentation of urethritis is recommended only for patients at high risk for infection who are unlikely to return for a follow-up evaluation (e.g., adolescents who have multiple partners). Such patients should be treated for gonorrhea and chlamydia. Partners of patients treated empirically should be referred for evaluation and treatment.

 

Clinicians should document that urethritis is present. Urethritis can be documented by the presence of any of the following signs:

a.      Mucopurulent or purulent discharge.

b.      Gram stain of urethral secretions demonstrating greater than or equal to 5 WBCs per oil immersion field. The Gram stain is the preferred rapid diagnostic test for evaluating urethritis. It is highly sensitive and specific for documenting both urethritis and the presence or absence of gonococcal infection. Gonococcal infection is established by documenting the presence of WBCs containing intracellular Gram-negative diplococci.

c.      Positive leukocyte esterase test on first-void urine, or microscopic examination of first-void urine demonstrating greater than or equal to 10 WBCs per high power field.

If none of these criteria is present, then treatment should be deferred, and the patient should be tested for N. gonorrhoeae and C. trachomatis and followed closely in the event of a positive test result. If the results demonstrate infection with either N. gonorrhoeae or C. trachomatis, the appropriate treatment should be given and sex partners referred for evaluation and treatment.

Empiric treatment of symptoms without documentation of urethritis is recommended only for patients at high risk for infection who are unlikely to return for a follow-up evaluation (e.g., adolescents who have multiple partners). Such patients should be treated for gonorrhea and chlamydia. Partners of patients treated empirically should be referred for evaluation and treatment.

Management of Patients Who Have Nongonococcal Urethritis

Diagnosis

 

All patients who have urethritis should be evaluated for the presence of gonococcal and chlamydial infection. Testing for chlamydia is strongly recommended because of the increased utility and availability of highly sensitive and specific testing methods and because a specific diagnosis might improve compliance and partner notification.

 

Treatment

 

Treatment should be initiated as soon as possible after diagnosis. Single-dose regimens have the important advantage of improved compliance and of directly observed therapy. If multiple-dose regimens are used, the medication should be provided in the clinic or health-care provider's office. Treatment with the recommended regimen can result in alleviation of symptoms and microbiologic cure of infection.

Follow-Up for Patients Who Have Urethritis

 

Patients should be instructed to return for evaluation if symptoms persist or recur after completion of therapy. Symptoms alone, without documentation of signs or laboratory evidence of urethral inflammation, are not a sufficient basis for re-treatment. Patients should be instructed to abstain from sexual intercourse until therapy is completed.

 

Partner Referral

 

Patients should refer for evaluation and treatment all sex partners within the preceding 60 days. A specific diagnosis may facilitate partner referral; therefore, testing for gonorrhea and chlamydia is encouraged.

 

Recurrent and Persistent Urethritis

Objective signs of urethritis should be present before initiation of antimicrobial therapy. Effective regimens have not been identified for treating patients who have persistent symptoms or frequent recurrences after treatment. Patients who have persistent or recurrent urethritis should be re-treated with the initial regimen if they did not comply with the treatment regimen or if they were reexposed to an untreated sex partner. Otherwise, a wet mount examination and culture of an intraurethral swab specimen for T. vaginalis should be performed. Urologic examinations usually do not reveal a specific etiology.

 

Mucopurulent Cervicitis (MPC)

MPC is characterized by a purulent or mucopurulent endocervical exudate visible in the endocervical canal or in an endocervical swab specimen. Some experts also make the diagnosis on the basis of easily induced cervical bleeding. Although some experts consider an increased number of polymorphonuclear leukocytes on endocervical Gram stain as being useful in the diagnosis of MPC, this criterion has not been standardized, has a low positive-predictive value (PPV), and is not available in some settings. MPC often is asymptomatic, but some women have an abnormal vaginal discharge and vaginal bleeding (e.g., after sexual intercourse). MPC can be caused by C. trachomatis or N. gonorrhoeae; however, in most cases neither organism can be isolated. MPC can persist despite repeated courses of antimicrobial therapy. Because relapse or reinfection with C. trachomatis or N. gonorrhoeae usually does not apply to persistent cases of MPC, other non-microbiologic determinants (e.g., inflammation in an ectropion) could be involved.

 

Patients who have MPC should be tested for C. trachomatis and for N. gonorrhoeae by using the most sensitive and specific test for the population served. However, MPC is not a sensitive predictor of infection with these organisms, because most women who have C. trachomatis or N. gonorrhoeae do not have MPC.

 

Treatment

 

The results of sensitive tests for C. trachomatis or N. gonorrhoeae (e.g., culture or nucleic acid amplification tests) should determine the need for treatment, unless the likelihood of infection with either organism is high or the patient is unlikely to return for treatment. Empiric treatment should be considered for a patient who has a suspected case of gonorrhea and/or chlamydia if a) the prevalence of these diseases differs substantially (i.e., greater than 15%) between clinics in the geographic area and b) the patient might be difficult to locate for treatment. After the possibilities of relapse and reinfection have been excluded, management of persistent MPC is unclear. For such cases, additional antimicrobial therapy may be of little benefit.

 

Follow-Up

 

Follow-up should be as recommended for the infections for which the woman is being treated. If symptoms persist, women should be instructed to return for reevaluation and to abstain from sexual intercourse even if they have completed the prescribed therapy.

 

Management of Sex Partners

 

Management of sex partners of women treated for MPC should be appropriate for the identified or suspected STD. Partners should be notified, examined, and treated for the STD identified or suspected in the index patient.

 

Patients should be instructed to abstain from sexual intercourse until they and their sex partners are cured. Because a microbiologic test of cure usually is not recommended, patients should abstain from sexual intercourse until therapy is completed (i.e., 7 days after a single-dose regimen or after completion of a 7-day regimen).

 

Chlamydial Infections

Chlamydial Infection

 

In the United States, chlamydial genital infection occurs frequently among sexually active adolescents and young adults. Asymptomatic infection is common among both men and women. Screening sexually active adolescents for chlamydial infection should be routine during annual examinations, even if symptoms are not present. Screening women aged 20-24 years also is suggested, particularly for those who have new or multiple sex partners and who do not consistently use barrier contraceptives.

 

Chlamydial Infection in Adolescents and Adults

 

Several important sequelae can result from C. trachomatis infection in women; the most serious of these include PID, ectopic pregnancy, and infertility. Some women who have apparently uncomplicated cervical infection already have subclinical upper reproductive tract infection. A recent investigation of patients in a health maintenance organization demonstrated that screening and treatment of cervical infection can reduce the likelihood of PID.

 

Treatment

 

Treatment of infected patients prevents transmission to sex partners; and, for infected pregnant women, treatment might prevent transmission of C. trachomatis to infants during birth. Treatment of sex partners helps to prevent reinfection of the index patient and infection of other partners.

 

Coinfection with C. trachomatis often occurs among patients who have gonococcal infection; therefore, presumptive treatment of such patients for chlamydia is appropriate.

 

Follow-Up

 

Patients do not need to be retested for chlamydia after completing treatment with doxycycline or azithromycin unless symptoms persist or reinfection is suspected, because these therapies are highly efficacious.

 

Some studies have demonstrated high rates of infection among women retested several months after treatment, presumably because of reinfection. In some populations (e.g., adolescents), rescreening women several months after treatment might be effective for detecting further morbidity.

 

Management of Sex Partners

 

Patients should be instructed to refer their sex partners for evaluation, testing, and treatment. Because exposure intervals have received limited evaluation, the following recommendations are somewhat arbitrary. Sex partners should be evaluated, tested, and treated if they had sexual contact with the patient during the 60 days preceding onset of symptoms in the patient or diagnosis of chlamydia. Health-care providers should treat the most recent sex partner even if the time of the last sexual contact was greater than 60 days before onset or diagnosis.

 

Patients should be instructed to abstain from sexual intercourse until they and their sex partners have completed treatment. Because a microbiologic test of cure usually is not recommended, abstinence should be continued until therapy is completed (i.e., 7 days after a single-dose regimen or after completion of a 7-day regimen). Timely treatment of sex partners is essential for decreasing the risk for reinfecting the index patient.

 

Chlamydial Infection in Infants

 

Prenatal screening of pregnant women can prevent chlamydial infection among neonates. Pregnant women who are less than 25 years of age or who have new or multiple sex partners particularly should be targeted for screening. Periodic prevalence surveys of chlamydial infection can be conducted to confirm the validity of using these recommendations in specific clinical settings.

 

C. Trachomatis infection of neonates results from perinatal exposure to the mother's infected cervix. The prevalence of C. trachomatis infection among pregnant women usually is greater than 5%, regardless of race/ethnicity or socioeconomic status. Neonatal ocular prophylaxis with silver nitrate solution or antibiotic ointments does not prevent perinatal transmission of C. trachomatis from mother to infant. However, ocular prophylaxis with those agents does prevent gonococcal ophthalmia and should be continued for that reason.

 

Initial C. trachomatis perinatal infection involves mucous membranes of the eye, oropharynx, urogenital tract, and rectum. C. Trachomatis infection in neonates is most often recognized by conjunctivitis that develops 5-12 days after birth. Chlamydia is the most frequent identifiable infectious cause of ophthalmia neonatorum. C. Trachomatis also is a common cause of subacute, afebrile pneumonia with onset from 1 to 3 months of age. Asymptomatic infections also can occur in the oropharynx, genital tract, and rectum of neonates.

 

Ophthalmia Neonatorum Caused by C. trachomatis

 

A chlamydial etiology should be considered for all infants aged less than or equal to 30 days who have conjunctivitis.

 

Diagnostic Considerations

 

Sensitive and specific methods used to diagnose chlamydial ophthalmia in the neonate include both tissue culture and nonculture tests (e.g., direct fluorescent antibody tests and immunoassays). Giemsa-stained smears are specific for C. trachomatis, but such tests are not sensitive. Specimens must contain conjunctival cells, not exudate alone. Specimens for culture isolation and nonculture tests should be obtained from the everted eyelid using a dacron-tipped swab or the swab specified by the manufacturer's test kit. A specific diagnosis of C. trachomatis infection confirms the need for treatment not only for the neonate, but also for the mother and her sex partner(s). Ocular exudate from infants being evaluated for chlamydial conjunctivitis also should be tested for N. gonorrhoeae.

Infant Pneumonia Caused by C. trachomatis

 

Characteristic signs of chlamydial pneumonia in infants include a) a repetitive staccato cough with tachypnea and b) hyperinflation and bilateral diffuse infiltrates on a chest radiograph. Wheezing is rare, and infants are typically afebrile. Peripheral eosinophilia sometimes occurs in infants who have chlamydial pneumonia. Because clinical presentations differ, initial treatment and diagnostic tests should encompass C. trachomatis for all infants aged 1-3 months who possibly have pneumonia.

 

Diagnostic Considerations

 

Specimens for chlamydial testing should be collected from the nasopharynx. Tissue culture is the definitive standard for chlamydial pneumonia; nonculture tests can be used with the knowledge that nonculture tests of nasopharyngeal specimens produce lower sensitivity and specificity than nonculture tests of ocular specimens. Tracheal aspirates and lung biopsy specimens, if collected, should be tested for C. trachomatis.

 

The microimmunofluorescence test for C. trachomatis antibody is useful but not widely available. An acute IgM antibody titer greater than or equal to 1:32 is strongly suggestive of C. trachomatis pneumonia.

 

Because of the delay in obtaining test results for chlamydia, the decision to include an agent in the antibiotic regimen that is active against C. trachomatis must frequently be based on the clinical and radiologic findings. The results of tests for chlamydial infection assist in the management of an infant's illness and determine the need for treating the mother and her sex partner(s).

 

Infants Born to Mothers Who Have Chlamydial Infection

 

Infants born to mothers who have untreated chlamydia are at high risk for infection; however, prophylactic antibiotic treatment is not indicated, and the efficacy of such treatment is unknown. Infants should be monitored to ensure appropriate treatment if infection develops.

 

Chlamydial Infection in Children

 

Sexual abuse must be considered a cause of chlamydial infection in preadolescent children, although perinatally transmitted C. trachomatis infection of the nasopharynx, urogenital tract, and rectum may persist for greater than 1 year. Because of the potential for a criminal investigation and legal proceedings for sexual abuse, a diagnosis of C. trachomatis in a preadolescent child requires the high specificity provided by isolation in cell culture. The cultures should be confirmed by microscopic identification of the characteristic intracytoplasmic inclusions, preferably by fluorescein-conjugated monoclonal antibodies specific for C. trachomatis.

 

Diagnostic Considerations

 

Nonculture tests for chlamydia should not be used because of the possibility of false-positive test results. With respiratory tract specimens, false-positive results can occur because of cross-reaction of test reagents with Chlamydia pneumoniae; with genital and anal specimens, false-positive results occur because of cross-reaction with fecal flora.

 

Gonococcal Infection

Gonococcal Infection in Adolescents and Adults

 

In the United States, an estimated 600,000 new infections with N. gonorrhoeae occur each year. Most infections among men produce symptoms that cause them to seek curative treatment soon enough to prevent serious sequelae -- but this may not be soon enough to prevent transmission to others. Many infections among women do not produce recognizable symptoms until complications (e.g., pelvic inflammatory disease {PID}) have occurred. Both symptomatic and asymptomatic cases of PID can result in tubal scarring that leads to infertility or ectopic pregnancy. Because gonococcal infections among women often are asymptomatic, an important component of gonorrhea control in the United States continues to be the screening of women at high risk for STDs.

 

Dual Therapy for Gonococcal and Chlamydial Infections

 

Patients infected with N. gonorrhoeae often are coinfected with C. trachomatis; this finding led to the recommendation that patients treated for gonococcal infection also be treated routinely with a regimen effective against uncomplicated genital C. trachomatis infection. Routine dual therapy without testing for chlamydia can be cost-effective for populations in which chlamydial infection accompanies 20%-40% of gonococcal infections, because the cost of therapy for chlamydia (e.g., $0.50-$1.50 for doxycycline) is less than the cost of testing. Some experts believe that the routine use of dual therapy has resulted in substantial decreases in the prevalence of chlamydial infection. Because most gonococci in the United States are susceptible to doxycycline and azithromycin, routine cotreatment might hinder the development of antimicrobial-resistant N. gonorrhoeae.

 

Since the introduction of dual therapy, the prevalence of chlamydial infection has decreased in some populations, and simultaneous testing for chlamydial infection has become quicker, more sensitive, and more widely available.

 

Cases of gonorrhea caused by N. gonorrhoeae resistant to fluoroquinolones have been reported sporadically from many parts of the world, including North America, and are becoming widespread in parts of Asia. As of February 1997, however, Quinolone-Resistant N. gonorrhoeae (QRNG) occurred rarely in the United States: less than 0.05% of 4,639 isolates collected by CDC's Gonococcal Isolate Surveillance Project (GISP) during 1996 had minimum inhibitory concentrations (MICs) greater than or equal to 1.0 ug/mL to ciprofloxacin. The GISP sample is collected from 26 cities and includes approximately 1.3% of all reported gonococcal infections among men in the United States. As long as QRNG strains comprise less than 1% of all N. gonorrhoeae strains isolated at each of the 26 cities, the fluoroquinolone regimens can be used with confidence. However, importation of QRNG will probably continue, and the prevalence of QRNG in the United States could increase to the point that fluoroquinolones no longer reliably eradicate gonococcal infections.

 

Uncomplicated Gonococcal Infection of the Pharynx

 

Gonococcal infections of the pharynx are more difficult to eradicate than infections at urogenital and anorectal sites. Few antigonococcal regimens can reliably cure such infections greater than 90% of the time.

 

Although chlamydial coinfection of the pharynx is unusual, coinfection at genital sites sometimes occurs. Therefore, treatment for both gonorrhea and chlamydia is suggested.

 

Follow-Up

 

Patients who have uncomplicated gonorrhea and who are treated with any of the recommended regimens need not return for a test of cure. Patients who have symptoms that persist after treatment should be evaluated by culture for N. gonorrhoeae, and any gonococci isolated should be tested for antimicrobial susceptibility. Infections identified after treatment with one of the recommended regimens usually result from reinfection rather than treatment failure, indicating a need for improved patient education and referral of sex partners. Persistent urethritis, cervicitis, or proctitis also may be caused by C. trachomatis and other organisms.

 

Management of Sex Partners

 

Patients should be instructed to refer sex partners for evaluation and treatment. All sex partners of patients who have N. gonorrhoeae infection should be evaluated and treated for N. gonorrhoeae and C. trachomatis infections if their last sexual contact with the patient was within 60 days before onset of symptoms or diagnosis of infection in the patient. If a patient's last sexual intercourse was greater than 60 days before onset of symptoms or diagnosis, the patient's most recent sex partner should be treated. Patients should be instructed to avoid sexual intercourse until therapy is completed and they and their sex partners no longer have symptoms.

 

Disseminated Gonococcal Infection (DGI)

 

DGI results from gonococcal bacteremia. DGI often results in petechial or pustular acral skin lesions, asymmetrical arthralgia, tenosynovitis, or septic arthritis. The infection is complicated occasionally by perihepatitis, and rarely by endocarditis or meningitis. Strains of N. gonorrhoeae that cause DGI tend to cause minimal genital inflammation. In the United States, these strains have occurred infrequently during the past decade.

 

Treatment

 

Hospitalization is recommended for initial therapy, especially for patients who cannot be relied on to comply with treatment, for those in whom the diagnosis is uncertain, and for those who have purulent synovial effusions or other complications. Patients should be examined for clinical evidence of endocarditis and meningitis. Patients treated for DGI should be treated presumptively for concurrent C. trachomatis infection unless appropriate testing excludes this infection.

 

Management of Sex Partners

 

Gonococcal infection often is asymptomatic in sex partners of patients who have DGI. As with uncomplicated gonococcal infections, patients should be instructed to refer their sex partners for evaluation and treatment.

 

Gonococcal Infection in Infants

 

Gonococcal infection usually results from exposure to infected cervical exudate at birth. It is usually an acute illness that becomes manifest 2-5 days after birth. The prevalence of infection among infants depends on the prevalence of infection among pregnant women, on whether pregnant women are screened for gonorrhea, and on whether newborns receive ophthalmia prophylaxis.

The most serious manifestations of N. gonorrhoeae infection in newborns are ophthalmia neonatorum and sepsis, including arthritis and meningitis. Less serious manifestations include rhinitis, vaginitis, urethritis, and inflammation at sites of fetal monitoring.

 

Ophthalmia Neonatorum Caused by N. gonorrhoeae

 

Although N. gonorrhoeae is a less frequent cause of ophthalmia neonatorum in the United States than C. trachomatis and nonsexually transmitted agents, it is especially important because it may result in perforation of the globe of the eye and in blindness.

 

Diagnostic Considerations

 

Infants at increased risk for gonococcal ophthalmia are those who do not receive ophthalmia prophylaxis and those whose mothers have had no prenatal care or whose mothers have a history of STDs or substance abuse. Gonococcal ophthalmia is strongly suggested when typical Gram-negative diplococci are identified in conjunctival exudate, justifying presumptive treatment for gonorrhea after appropriate cultures for N. gonorrhoeae are obtained. Appropriate chlamydial testing should be done simultaneously. Presumptive treatment for N. gonorrhoeae may be indicated for newborns who are at increased risk for gonococcal ophthalmia and who have conjunctivitis but do not have gonococci in a Gram-stained smear of conjunctival exudate.

 

In all cases of neonatal conjunctivitis, conjunctival exudate should be cultured for N. gonorrhoeae and tested for antibiotic susceptibility before a definitive diagnosis is made. A definitive diagnosis is important because of the public health and social consequences of a diagnosis of gonorrhea. Nongonococcal causes of neonatal ophthalmia include Moraxella catarrhalis and other Neisseria species that are indistinguishable from N. gonorrhoeae on Gram-stained smear but can be differentiated in the microbiology laboratory.

 

Follow-Up

 

Infants who have gonococcal ophthalmia should be hospitalized and evaluated for signs of disseminated infection (e.g., sepsis, arthritis, and meningitis). One dose of ceftriaxone is adequate therapy for gonococcal conjunctivitis, but many pediatricians prefer to continue antibiotics until cultures are negative at 48-72 hours. The duration of therapy should be decided in consultation with experienced physicians.

 

Disseminated Gonococcal Infection and Gonococcal Scalp Abscess in Newborns

 

Sepsis, arthritis, meningitis, or any combination of these are rare complications of neonatal gonococcal infection. Localized gonococcal infection of the scalp might result from fetal monitoring through scalp electrodes. Detection of gonococcal infection in neonates who have sepsis, arthritis, meningitis, or scalp abscesses requires cultures of blood, CSF, and joint aspirate on chocolate agar. Specimens obtained from the conjunctiva, vagina, oropharynx, and rectum that are cultured on gonococcal selective medium are useful for identifying the primary site(s) of infection, especially if inflammation is present. Positive Gram-stained smears of exudate, CSF, or joint aspirate provide a presumptive basis for initiating treatment for N. gonorrhoeae. Diagnoses based on Gram-stained smears or presumptive identification of cultures should be confirmed with definitive tests on culture isolates.

 

Gonococcal Infection in Children

 

After the neonatal period, sexual abuse is the most frequent cause of gonococcal infection in preadolescent children. Vaginitis is the most common manifestation of gonococcal infection in preadolescent children. PID following vaginal infection is probably less common than among adults. Among sexually abused children, anorectal and pharyngeal infections with N. gonorrhoeae are common and frequently asymptomatic.

 

Diagnostic Considerations

 

Because of the legal implications of a diagnosis of N. gonorrhoeae infection in a child, only standard culture procedures for the isolation of N. gonorrhoeae should be used for children. Nonculture gonococcal tests for gonococci (e.g., Gram-stained smear, DNA probes, and EIA tests) should not be used alone; none of these tests have been approved by FDA for use with specimens obtained from the oropharynx, rectum, or genital tract of children. Specimens from the vagina, urethra, pharynx, or rectum should be streaked onto selective media for isolation of N. gonorrhoeae, and all presumptive isolates of N. gonorrhoeae should be identified definitively by at least two tests that involve different principles (e.g., biochemical, enzyme substrate, or serologic). Isolates should be preserved to enable additional or repeated testing.

 

All children who have gonococcal infections should be evaluated for coinfection with syphilis and C. trachomatis.

 

Ophthalmia Neonatorum Prophylaxis

 

Instillation of a prophylactic agent into the eyes of all newborn infants is recommended to prevent gonococcal ophthalmia neonatorum; this procedure is required by law in most states. All the recommended prophylactic regimens in this section prevent gonococcal ophthalmia. However, the efficacy of these preparations in preventing chlamydial ophthalmia is less clear, and they do not eliminate nasopharyngeal colonization by C. trachomatis. The diagnosis and treatment of gonococcal and chlamydial infections in pregnant women is the best method for preventing neonatal gonococcal and chlamydial disease. Not all women, however, receive prenatal care; and ocular prophylaxis is warranted because it can prevent sight-threatening gonococcal ophthalmia and it is safe, easy to administer, and inexpensive.

DISEASES CHARACTERIZED BY VAGINAL DISCHARGE

Management of Patients Who Have Vaginal Infections

 

Vaginitis is usually characterized by a vaginal discharge or vulvar itching and irritation; a vaginal odor may be present. The three diseases most frequently associated with vaginal discharge are trichomoniasis (caused by T. vaginalis), BV (caused by a replacement of the normal vaginal flora by an overgrowth of anaerobic microorganisms and Gardnerella vaginalis), and candidiasis (usually caused by Candida albicans). MPC caused by C. trachomatis or N. gonorrhoeae can sometimes cause vaginal discharge. Although vulvovaginal candidiasis usually is not transmitted sexually, it is included in this section because it is often diagnosed in women being evaluated for STDs.

 

Vaginitis is diagnosed by pH and microscopic examination of fresh samples of the discharge. The pH of the vaginal secretions can be determined by narrow-range pH paper for the elevated pH typical of BV or trichomoniasis (i.e., a pH of greater than 4.5). One way to examine the discharge is to dilute a sample in one to two drops of 0.9% normal saline solution on one slide and 10% potassium hydroxide (KOH) solution on a second slide. An amine odor detected immediately after applying KOH suggests BV. A cover slip is placed on each slide, and they are examined under a microscope at low- and high-dry power. The motile T. vaginalis or the clue cells of BV usually are identified easily in the saline specimen. The yeast or pseudohyphae of Candida species are more easily identified in the KOH specimen. The presence of objective signs of vulvar inflammation in the absence of vaginal pathogens, along with a minimal amount of discharge, suggests the possibility of mechanical, chemical, allergic, or other noninfectious irritation of the vulva. Culture for T. vaginalis is more sensitive than microscopic examination. Laboratory testing fails to identify the cause of vaginitis among a substantial minority of women.

Bacterial Vaginosis

BV is a clinical syndrome resulting from replacement of the normal H2O2-producing Lactobacillus sp. in the vagina with high concentrations of anaerobic bacteria (e.g., Prevotella sp. and Mobiluncus sp.), G. vaginalis, and Mycoplasma hominis. BV is the most prevalent cause of vaginal discharge or malodor; however, half of the women whose illnesses meet the clinical criteria for BV are asymptomatic. The cause of the microbial alteration is not fully understood. Although BV is associated with having multiple sex partners, it is unclear whether BV results from acquisition of a sexually transmitted pathogen. Women who have never been sexually active are rarely affected. Treatment of the male sex partner has not been beneficial in preventing the recurrence of BV.

 

Diagnostic Considerations

 

BV can be diagnosed by the use of clinical or Gram stain criteria. Clinical criteria require three of the following symptoms or signs:

a.      A homogeneous, white, noninflammatory discharge that smoothly coats the vaginal walls;

b.      The presence of clue cells on microscopic examination;

c.      A pH of vaginal fluid greater than 4.5;

d.      A fishy odor of vaginal discharge before or after addition of 10% KOH (i.e., the whiff test).

When a Gram stain is used, determining the relative concentration of the bacterial morphotypes characteristic of the altered flora of BV is an acceptable laboratory method for diagnosing BV. Culture of G. vaginalis is not recommended as a diagnostic tool because it is not specific.

Treatment

 

The principal goal of therapy for BV is to relieve vaginal symptoms and signs of infection. All women who have symptomatic disease require treatment, regardless of pregnancy status.

 

BV during pregnancy is associated with adverse pregnancy outcomes. The results of several investigations indicate that treatment of pregnant women who have BV and who are at high risk for preterm delivery (i.e., those who previously delivered a premature infant) might reduce the risk for prematurity. Therefore, high-risk pregnant women who do not have symptoms of BV may be evaluated for treatment.

 

Although some experts recommend treatment for high-risk pregnant women who have asymptomatic BV, others believe more information is needed before such a recommendation is made. A large, randomized clinical trial is underway to assess treatment for asymptomatic BV in pregnant women; the results of this investigation should clarify the benefits of therapy for BV in women at both low and high risk for preterm delivery.

 

The bacterial flora that characterizes BV has been recovered from the endometria and salpinges of women who have PID. BV has been associated with endometritis, PID, and vaginal cuff cellulitis after invasive procedures such as endometrial biopsy, hysterectomy, hysterosalpingography, placement of an intrauterine device, cesarean section, and uterine curettage. The results of one randomized controlled trial indicated that treatment of BV with metronidazole substantially reduced postabortion PID. On the basis of these data, consideration should be given to treatment of women who have symptomatic or asymptomatic BV before surgical abortion procedures are performed. However, more information is needed before recommending whether patients who have asymptomatic BV should be treated before other invasive procedures are performed.

 

Follow-Up

 

Follow-up visits are unnecessary if symptoms resolve. Recurrence of BV is not unusual. Because treatment of BV in high-risk pregnant women who are asymptomatic might prevent adverse pregnancy outcomes, a follow-up evaluation, at 1 month after completion of treatment, should be considered to evaluate whether therapy was successful. The alternative BV treatment regimens may be used to treat recurrent disease. No long-term maintenance regimen with any therapeutic agent is recommended.

 

Management of Sex Partners

 

The results of clinical trials indicate that a woman's response to therapy and the likelihood of relapse or recurrence are not affected by treatment of her sex partner(s). Therefore, routine treatment of sex partners is not recommended.

 

Pregnancy

 

BV has been associated with adverse pregnancy outcomes (e.g., premature rupture of the membranes, preterm labor, and preterm birth), and the organisms found in increased concentration in BV also are frequently present in postpartum or postcesarean endometritis. Because treatment of BV in high-risk pregnant women (i.e., those who have previously delivered a premature infant) who are asymptomatic might reduce preterm delivery, such women may be screened, and those with BV can be treated. The screening and treatment should be conducted at the earliest part of the second trimester of pregnancy.

 

Low-risk pregnant women (i.e., women who previously have not had a premature delivery) who have symptomatic BV should be treated to relieve symptoms. Some experts prefer the use of systemic therapy for low-risk pregnant women to treat possible subclinical upper genital tract infections.

 

Lower doses of medication are recommended for pregnant women to minimize exposure to the fetus. Data are limited concerning the use of metronidazole vaginal gel during pregnancy. The use of clindamycin vaginal cream during pregnancy is not recommended, because two randomized trials indicated an increase in the number of preterm deliveries among pregnant women who were treated with this medication.

 

 

Trichomoniasis

richomoniasis is caused by the protozoan T. vaginalis. Most men who are infected with T. vaginalis do not have symptoms of infection, although a minority of men have NGU. Many women do have symptoms of infection. Of these women, T. vaginalis characteristically causes a diffuse, malodorous, yellow-green discharge with vulvar irritation; many women have fewer symptoms. Vaginal trichomoniasis might be associated with adverse pregnancy outcomes, particularly premature rupture of the membranes and preterm delivery.

Follow-Up

Follow-up is unnecessary for men and women who become asymptomatic after treatment or who are initially asymptomatic. Infections with strains of T. vaginalis that have diminished susceptibility to metronidazole can occur; however, most of these organisms respond to higher doses of metronidazole. If treatment failure occurs with either regimen, the patient should be re-treated.

 

Patients with culture-documented infection who do not respond to the regimens described in this report and in whom reinfection has been excluded should be managed in consultation with an expert; consultation is available from CDC. Evaluation of such cases should include determination of the susceptibility of T. vaginalis to metronidazole.

 

Management of Sex Partners

 

Sex partners should be treated. Patients should be instructed to avoid sex until they and their sex partners are cured. In the absence of a microbiologic test of cure, this means when therapy has been completed and patient and partner(s) are asymptomatic.

 

Vulvovaginal Candidiasis

Vulvovaginal candidiasis (VVC) is caused by C. albicans or, occasionally, by other Candida sp., Torulopsis sp., or other yeasts. An estimated 75% of women will have at least one episode of VVC, and 40%-45% will have two or more episodes. A small percentage of women (i.e., probably less than 5%) experience recurrent VVC (RVVC). Typical symptoms of VVC include pruritus and vaginal discharge. Other symptoms may include vaginal soreness, vulvar burning, dyspareunia, and external dysuria. None of these symptoms is specific for VVC.

 

Diagnostic Considerations

 

A diagnosis of Candida vaginitis is suggested clinically by pruritus and erythema in the vulvovaginal area; a white discharge may occur. The diagnosis can be made in a woman who has signs and symptoms of vaginitis, and when either a) a wet preparation or Gram stain of vaginal discharge demonstrates yeasts or pseudohyphae or b) a culture or other test yields a positive result for a yeast species. Candida vaginitis is associated with a normal vaginal pH (less than or equal to 4.5). Use of 10% KOH in wet preparations improves the visualization of yeast and mycelia by disrupting cellular material that might obscure the yeast or pseudohyphae. Identifying Candida by culture in the absence of symptoms should not lead to treatment, because approximately 10%-20% of women usually harbor Candida sp. and other yeasts in the vagina. VVC can occur concomitantly with STDs or frequently following antibacterial vaginal or systemic therapy.

 

Treatment

 

Topical formulations effectively treat VVC. The topically applied azole drugs are more effective than nystatin. Treatment with azoles results in relief of symptoms and negative cultures among 80%-90% of patients who complete therapy. Many of these creams and suppositories are oil-based and might weaken latex

condoms and diaphragms. Refer to condom product labeling for additional information.

 

Follow-Up

 

Patients should be instructed to return for follow-up visits only if symptoms persist or recur.

 

Management of Sex Partners

 

VVC usually is not acquired through sexual intercourse; treatment of sex partners is not recommended but may be considered for women who have recurrent infection. A minority of male sex partners may have balanitis, which is characterized by erythematous areas on the glans in conjunction with pruritus or irritation. These sex partners might benefit from treatment with topical antifungal agents to relieve symptoms.

PELVIC INFLAMMATORY DISEASE (PID)

PID comprises a spectrum of inflammatory disorders of the upper female genital tract, including any combination of endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis. Sexually transmitted organisms, especially N. gonorrhoeae and C. trachomatis, are implicated in most cases; however, microorganisms that can be part of the vaginal flora (e.g., anaerobes, G. vaginalis, H. influenzae, enteric Gram-negative rods, and Streptococcus agalactiae) also can cause PID. In addition, M. hominis and U. urealyticum might be etiologic agents of PID.

 

Diagnostic Considerations

 

Acute PID is difficult to diagnose because of the wide variation in the symptoms and signs. Many women with PID have subtle or mild symptoms that do not readily indicate PID. Consequently, delay in diagnosis and effective treatment probably contributes to inflammatory sequelae in the upper reproductive tract. Laparoscopy can be used to obtain a more accurate diagnosis of salpingitis and a more complete bacteriologic diagnosis. However, this diagnostic tool often is not readily available for acute cases, and its use is not easy to justify when symptoms are mild or vague. Moreover, laparoscopy will not detect endometritis and may not detect subtle inflammation of the fallopian tubes. Consequently, a diagnosis of PID usually is based on clinical findings. The clinical diagnosis of acute PID also is imprecise. Data indicate that a clinical diagnosis of symptomatic PID has a PPV for salpingitis of 65%-90% in comparison with laparoscopy. The PPV of a clinical diagnosis of acute PID differs depending on epidemiologic characteristics and the clinical setting, with higher PPV among sexually active young (especially teenaged) women and among patients attending STD clinics or from settings in which rates of gonorrhea or chlamydia are high. In all settings, however, no single historical, physical, or laboratory finding is both sensitive and specific for the diagnosis of acute PID (i.e., can be used both to detect all cases of PID and to exclude all women without PID). Combinations of diagnostic findings that improve either sensitivity (i.e., detect more women who have PID) or specificity (i.e., exclude more women who do not have PID) do so only at the expense of the other. For example, requiring two or more findings excludes more women who do not have PID but also reduces the number of women with PID who are identified.

 

Many episodes of PID go unrecognized. Although some cases are asymptomatic, others are undiagnosed because the patient or the health-care provider fails to recognize the implications of mild or nonspecific symptoms or signs (e.g., abnormal bleeding, dyspareunia, or vaginal discharge {atypical PID}). Because of the difficulty of diagnosis and the potential for damage to the reproductive health of women even by apparently mild or atypical PID, health-care providers should maintain a low threshold for the diagnosis of PID. Even so, the long-term outcome of early treatment of women with asymptomatic or atypical PID is unknown. The following recommendations for diagnosing PID are intended to help health-care providers recognize when PID should be suspected and when they need to obtain additional information to increase diagnostic certainty. These recommendations are based partially on the fact that diagnosis and management of other common causes of lower abdominal pain (e.g., ectopic pregnancy, acute appendicitis, and functional pain) are unlikely to be impaired by initiating empiric antimicrobial therapy for PID.

 

Empiric treatment of PID should be initiated in sexually active young women and others at risk for STDs if all the following minimum criteria are present and no other cause(s) for the illness can be identified:

·         Lower abdominal tenderness,

·         Adnexal tenderness, and

·         Cervical motion tenderness.

More elaborate diagnostic evaluation often is needed, because incorrect diagnosis and management might cause unnecessary morbidity. These additional criteria may be used to enhance the specificity of the minimum criteria listed previously. Additional criteria that support a diagnosis of PID include the following:

·         Oral temperature greater than 101 F (greater than 38.3 C),

·         Abnormal cervical or vaginal discharge,

·         Elevated erythrocyte sedimentation rate,

·         Elevated C-reactive protein, and

·         Laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis.

The definitive criteria for diagnosing PID, which are warranted in selected cases, include the following:

·         Histopathologic evidence of endometritis on endometrial biopsy,

·         Transvaginal sonography or other imaging techniques showing thickened fluid-filled tubes with or without free pelvic fluid or tubo-ovarian complex, and

·         Laparoscopic abnormalities consistent with PID.

Although treatment can be initiated before bacteriologic diagnosis of C. trachomatis or N. gonorrhoeae infection, such a diagnosis emphasizes the need to treat sex partners.

 

Treatment

 

PID treatment regimens must provide empiric, broad-spectrum coverage of likely pathogens. Antimicrobial coverage should include N. gonorrhoeae, C. trachomatis, anaerobes, Gram-negative facultative bacteria, and streptococci. Although several antimicrobial regimens have been effective in achieving a clinical and microbiologic cure in randomized clinical trials with short-term follow-up, few investigations have a) assessed and compared these regimens with regard to elimination of infection in the endometrium and fallopian tubes or b) determined the incidence of long-term complications (e.g., tubal infertility and ectopic pregnancy).

 

All regimens should be effective against N. gonorrhoeae and C. trachomatis, because negative endocervical screening does not preclude upper-reproductive tract infection. Although the need to eradicate anaerobes from women who have PID has not been determined definitively, the evidence suggests that this may be important. Anaerobic bacteria have been isolated from the upper-reproductive tract of women who have PID, and data from in vitro studies have revealed that anaerobes such as Bacteroides fragilis can cause tubal and epithelial destruction. In addition, BV also is diagnosed in many women who have PID. Until treatment regimens that do not adequately cover these microbes have been shown to prevent sequelae as well as the regimens that are effective against these microbes, the recommended regimens should have anaerobic coverage. Treatment should be initiated as soon as the presumptive diagnosis has been made, because prevention of long-term sequelae has been linked directly with immediate administration of appropriate antibiotics. When selecting a treatment regimen, health-care providers should consider availability, cost, patient acceptance, and antimicrobial susceptibility.

 

In the past, many experts recommended that all patients who had PID be hospitalized so that bed rest and supervised treatment with parenteral antibiotics could be initiated. However, hospitalization is no longer synonymous with parenteral therapy. No currently available data compare the efficacy of parenteral with oral therapy or inpatient with outpatient treatment settings. Until the results from ongoing trials comparing parenteral inpatient therapy with oral outpatient therapy for women who have mild PID are available, such decisions must be based on observational data and consensus opinion. The decision of whether hospitalization is necessary should be based on the discretion of the health-care provider.

 

The following criteria for HOSPITALIZATION are based on observational data and theoretical concerns:

·         Surgical emergencies such as appendicitis cannot be excluded;

·         The patient is pregnant;

·         The patient does not respond clinically to oral antimicrobial therapy;

·         The patient is unable to follow or tolerate an outpatient oral regimen;

·         The patient has severe illness, nausea and vomiting, or high fever;

·         The patient has a tubo-ovarian abscess; or

·         The patient is immunodeficient (i.e., has HIV infection with low CD4 counts, is taking immunosuppressive therapy, or has another disease).

Most clinicians favor at least 24 hours of direct inpatient observation for patients who have tubo-ovarian abscesses, after which time home parenteral therapy should be adequate.

 

There are no efficacy data comparing parenteral with oral regimens. Experts have extensive experience with both of the following regimens. Also, there are multiple randomized trials demonstrating the efficacy of each regimen. Although most trials have used parenteral treatment for at least 48 hours after the patient demonstrates substantial clinical improvement, this is an arbitrary designation. Clinical experience should guide decisions regarding transition to oral therapy, which may be accomplished within 24 hours of clinical improvement.

 

Follow-Up

 

Patients receiving oral or parenteral therapy should demonstrate substantial clinical improvement (e.g., defervescence; reduction in direct or rebound abdominal tenderness; and reduction in uterine, adnexal, and cervical motion tenderness) within 3 days after initiation of therapy. Patients who do not demonstrate improvement within this time period usually require additional diagnostic tests, surgical intervention, or both.

 

If the health-care provider prescribes outpatient oral or parenteral therapy, a follow-up examination should be performed within 72 hours, using the criteria for clinical improvement described previously. Some experts also recommend rescreening for C. trachomatis and N. gonorrhoeae 4-6 weeks after therapy is completed. If PCR or LCR is used to document a test of cure, rescreening should be delayed for 1 month after completion of therapy.

 

Management of Sex Partners

 

Sex partners of patients who have PID should be examined and treated if they had sexual contact with the patient during the 60 days preceding onset of symptoms in the patient. The evaluation and treatment are imperative because of the risk for reinfection and the strong likelihood of urethral gonococcal or chlamydial infection in the sex partner. Male partners of women who have PID caused by C. trachomatis and/or N. gonorrhoeae often are asymptomatic.

Sex partners should be treated empirically with regimens effective against both of these infections, regardless of the apparent etiology of PID or pathogens isolated from the infected woman.

 

Even in clinical settings in which only women are treated, special arrangements should be made to provide care for male sex partners of women who have PID. When this is not feasible, health-care providers should ensure that sex partners are referred for appropriate treatment.

 

Pregnancy

 

Because of the high risk for maternal morbidity, fetal wastage, and preterm delivery, pregnant women who have suspected PID should be hospitalized and treated with parenteral antibiotics.

 

 

EPIDIDYMITIS

Among sexually active men aged less than 35 years, epididymitis is most often caused by C. trachomatis or N. gonorrhoeae. Epididymitis caused by sexually transmitted E. coli infection also occurs among homosexual men who are the insertive partners during anal intercourse. Sexually transmitted epididymitis usually is accompanied by urethritis, which often is asymptomatic. Nonsexually transmitted epididymitis associated with urinary tract infections caused by Gram-negative enteric organisms occurs more frequently among men aged greater than 35 years, men who have recently undergone urinary tract instrumentation or surgery, and men who have anatomical abnormalities.

 

Although most patients can be treated on an outpatient basis, hospitalization should be considered when severe pain suggests other diagnoses (e.g., torsion, testicular infarction, and abscess) or when patients are febrile or might be noncompliant with an antimicrobial regimen.

 

Diagnostic Considerations

 

Men who have epididymitis typically have unilateral testicular pain and tenderness; hydrocele and palpable swelling of the epididymis usually are present. Testicular torsion, a surgical emergency, should be considered in all cases but is more frequent among adolescents. Torsion occurs more frequently in patients who do not have evidence of inflammation or infection. Emergency testing for torsion may be indicated when the onset of pain is sudden, pain is severe, or the test results available during the initial examination do not enable a diagnosis of urethritis or urinary tract infection to be made. If the diagnosis is questionable, an expert should be consulted immediately, because testicular viability may be compromised. The evaluation of men for epididymitis should include the following procedures:

·         A Gram-stained smear of urethral exudate or intraurethral swab specimen for diagnosis of urethritis (i.e., greater than or equal to 5 polymorphonuclear leukocytes per oil immersion field) and for presumptive diagnosis of gonococcal infection.

·         A culture of urethral exudate or intraurethral swab specimen, or nucleic acid amplification test (either on intraurethral swab or first-void urine) for N. gonorrhoeae and C. trachomatis.

·         Examination of first-void urine for leukocytes if the urethral Gram stain is negative. Culture and Gram-stained smear of uncentrifuged urine should be obtained.

·         Syphilis serology and HIV counseling and testing.

Treatment

 

Empiric therapy is indicated before culture results are available. Treatment of epididymitis caused by C. trachomatis or N. gonorrhoeae will result in a) a microbiologic cure of infection, b) improvement of the signs and symptoms, c) prevention of transmission to others, and d) a decrease in the potential complications (e.g., infertility or chronic pain).

 

Follow-Up

 

Failure to improve within 3 days requires reevaluation of both the diagnosis and therapy. Swelling and tenderness that persist after completion of antimicrobial therapy should be evaluated comprehensively. The differential diagnosis includes tumor, abscess, infarction, testicular cancer, and tuberculous or fungal epididymitis.

 

Management of Sex Partners

 

Patients who have epididymitis that is known or suspected to be caused by N. gonorrhoeae or C. trachomatis should be instructed to refer sex partners for evaluation and treatment. Sex partners of these patients should be referred if their contact with the index patient was within the 60 days preceding onset of symptoms in the patient.

 

Patients should be instructed to avoid sexual intercourse until they and their sex partners are cured. In the absence of a microbiologic test of cure, this means until therapy is completed and patient and partner(s) no longer have symptoms.

 

Edited By Julia Tortorice RN, MBA, CPHQ

 

Excerpts reprinted from the CDC publication, 1998 Guidelines for Treatment of Sexually Transmitted Diseases, January 23, 1998 / 47(RR-1);1-118, mmwrq@cdc.gov.

 

References

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2.       CDC. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1996;45(No. RR-15).

3.       CDC. Sexually transmitted diseases clinical practice guidelines, 1991. Atlanta: US Department of Health and Human Services, Public Health Service, CDC, 1991.

4.       Hatcher RA, Trussell J, Stewart F, et al. Contraceptive technology. 16th ed. New York: Irvington Publishers, 1994.

5.       CDC. Technical guidance on HIV counseling. MMWR 1993;42(No. RR-2):11-7.

6.       American Academy of Pediatrics/American College of Obstetricians and Gynecologists. Guidelines for perinatal care. 3rd ed. Elk Grove Village, IL: American Academy of Pediatrics/American College of Obstetricians and Gynecologists, 1992.

7.       U.S. Preventive Services Task Force. Guide to clinical preventive services. 2nd ed. Baltimore: Williams and Wilkins, 1996.

8.       American College of Obstetricians and Gynecologists. Gonorrhea and chlamydial infections. Washington, DC: American College of Obstetricians and Gynecologists, March 1994. (ACOG technical bulletin, no. 190).

9.       CDC. Recommendations for the prevention and management of Chlamydia trachomatis infections, 1993. MMWR 1993;42(No. RR-12).

10.   CDC. 1997 USPHS/IDSA guidelines for the prevention of opportunistic infections in persons infected with human immunodeficiency virus. MMWR 1997;46(No. RR-12).

11.   Agency for Health Care Policy and Research. Evaluation and management of early HIV infection. Rockville, MD: US Department of Health and Human Services, Public Health Service, 1994; AHCPR publication no. 94-0572. (Clinical practice guidelines, no. 7).

12.   CDC. Testing for antibodies to human immunodeficiency virus type 2 in the United States. MMWR 1992;41(No. RR-12).

13.   CDC. Purified protein derivative (PPD)-tuberculin anergy and HIV infection: guidelines for anergy testing and management of anergic persons at risk of tuberculosis. MMWR 1991;40(No. RR-5):27-33.

14.   CDC. The use of preventive therapy for tuberculous infection in the United States: recommendations of the Advisory Committee for Elimination of Tuberculosis. MMWR 1990;39(No. RR-8):9-12.

15.   CDC. Management of persons exposed to multidrug-resistant tuberculosis. MMWR 1992;41(No. RR-11):59-71.

16.   Carpenter CCJ, Fischl MA, Hammer SM, et al. Antiretroviral therapy for HIV infection in 1997: updated recommendations of the International AIDS Society -- USA Panel. JAMA 1997;277:1962-9.

17.   CDC. Recommendations for prophylaxis against Pneumocystis carinii pneumonia for adults and adolescents infected with human immunodeficiency virus: U.S. Public Health Service Task Force on Antipneumocystis Prophylaxis for Patients with Human Immunodeficiency Virus Infection. MMWR 1992;41(No. RR-4).

18.   CDC. 1995 Revised guidelines for prophylaxis against Pneumocystis carinii pneumonia for children infected with or perinatally exposed to human immunodeficiency virus. MMWR 1995;44(No. RR-4).

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Expert Consultants

Chairman: David Atkins, M.D., M.P.H., Agency for Health Care Policy and Research;

Presenters: Michael H. Augenbraun, M.D., State University of New York Health Science Center at Brooklyn, NY; Karl Beutner, M.D., Ph.D., Solano Dermatology, Vallejo, CA; Gail A. Bolan, M.D., San Francisco Department of Public Health and University of California at San Francisco; Willard Cates, Jr., M.D., M.P.H., Family Health International, Research Triangle Park, NC; Anne M. Rompalo, M.D., Johns Hopkins University, Baltimore; Pablo J. Sanchez, M.D., Southwestern Medical Center at Dallas; Bradley Stoner, M.D., Ph.D., Washington University School of Medicine, St. Louis, MO; Anna Wald, M.D., M.P.H., University of Washington, Seattle; Cheryl K. Walker, M.D., University of California at Irvine; George D. Wendel, M.D., Southwestern Medical Center at Dallas; Jonathan M. Zenilman, M.D., Johns Hopkins University, Baltimore.

Moderators: King K. Holmes, M.D., Ph.D., Center for AIDS and STDs, University of Washington, Seattle; Edward W. Hook, III, M.D., University of Alabama at Birmingham School of Medicine; A. Eugene Washington, M.D., M.Sc., University of California at San Francisco.

Rapporteurs: John M. Douglas, Jr., M.D., Denver Department of Public Health and University of Colorado Health Science Center; Margaret R. Hammerschlag, M.D., State University of New York Health Science Center; David H. Martin, M.D., Louisiana State University Medical Center, New Orleans.

Consultants: Adaora A. Adimora, M.D., M.P.H., University of North Carolina at Chapel Hill; Virginia A. Caine, M.D., Marion County Health Department, Indianapolis; Laura T. Gutman, M.D., Duke University, Durham, NC; H. Hunter Handsfield, M.D., Seattle-King County Department of Public Health and University of Washington, Seattle; Robert B. Jones, M.D., Ph.D., Indiana University, Indianapolis; Franklyn N. Judson, M.D., Denver Department of Health; William M. McCormack, M.D., State University of New York Health Science Center at Brooklyn; Daniel M. Musher, M.D., Baylor College of Medicine, Houston; Newton G. Osborne, M.D., M.P.H., Howard University Hospital, Washington, DC; Robert T. Rolfs, Jr., M.D., Utah Department of Health; Lawrence L. Sanders, Jr., M.D., Southwest Hospital and Medical Center, Atlanta; Jane R. Schwebke, M.D., University of Alabama at Birmingham School of Medicine; Jack D. Sobel, M.D., Wayne State University School of Medicine, Detroit; David E. Soper, M.D., Medical University of South Carolina, Charleston; Walter E. Stamm, M.D., University of Washington; Lawrence R. Stanberry, M.D., Ph.D., Children's Hospital, Cincinnati; Felicia H. Stewart, M.D., Kaiser Family Foundation, Menlo Park, CA; Richard L. Sweet, M.D., Magee-Women's Hospital, Pittsburgh.

Other Expert Consultants (did not attend meeting): Susan Blank, M.D., New York City Department of Health; Sharon L. Hillier, Ph.D., University of Pittsburgh; Penelope J. Hitchcock, D.V.M., M.S., National Institutes of Health; Paul N. Zenker, M.D., M.P.H., Franklin Primary Health, Mobile, AL.

Liaison Participants: Dennis J. Barbour, J.D., Association of Reproductive Health Professionals; Joan R. Cates, American Social Health Association; JoAnne Doherty, Health Canada, Ontario; Robert G. Harmon, M.D., M.P.H., United Health Care; Kate L. Heilpern, M.D., American College of Emergency Physicians; John J. Henning, Ph.D., American Medical Association; K. King Holmes, M.D., Ph.D., Infectious Diseases Society of America; John N. Krieger, M.D., American Urological Association; Marshall Kubota, M.D., American Academy of Family Practice; Noni E. MacDonald, M.D., American Academy of Pediatrics; Gary A. Richwald, M.D., M.P.H., National Coalition of STD Directors; Helen J. Sawyer, R.N., Georgia Department of Human Resources; Stanley X. Shapiro, M.D., Regional Laboratory and Infectious Disease Committee, Kaiser Permanente, Panorama City, CA; Donald Sutherland, M.D., Health Canada; Steve K. Tyring, M.D., Ph.D., American Academy of Dermatology; C. Johannes van Dam, M.D., World Health Organization; Fernando Zacarias, M.D., M.P.H., Pan American Health Organization, World Health Organization.

CDC/Division of STD Prevention (DSTDP)/STD Treatment Guidelines 1997 Project

Coordinators: Kimberly A. Workowski, M.D.; John S. Moran, M.D.; Co-Chair: Michael E. St. Louis, M.D.; Co-Moderator: Katherine M. Stone, M.D.;

Presenters: Consuelo M. Beck-Sague, M.D., National Center for Infectious Diseases (NCID); M. Riduan Joesoef, M.D., Ph.D., M.P.H.; Mary L. Kamb, M.D., M.P.H., Division of HIV/AIDS Prevention (DHAP); Jonathan E. Kaplan, M.D., NCID; H. Trent MacKay, M.D., M.P.H.; Michael M. McNeil, M.D., M.P.H., NCID; Allyn K. Nakashima, M.D., DHAP; George P. Schmid, M.D., M.Sc.;

Consultants: Sevgi O. Aral, Ph.D.; Stuart M. Berman, M.D.; Donald F. Dowda; Brian R. Edlin, M.D., DHAP; Helene D. Gayle, M.D., M.P.H., National Center for HIV, STD, and TB Prevention (NCHSTP); Robert S. Janssen, M.D., DHAP; Wanda K. Jones, Dr.P.H., Office of Women's Health; William J. Kassler, M.D., M.P.H.; Nancy C. Lee, M.D., DHAP; Beth Macke, Ph.D.; Frank J. Mahoney, M.D., NCID; Phillip I. Nieberg, M.D., M.P.H., NCHSTP; Herbert B. Peterson, M.D., National Center for Chronic Disease Prevention and Health Promotion (NCCDPHP); Martha F. Rogers, M.D., DHAP; William E. Secor, Ph.D., NCID; Dawn K. Smith, M.D., DHAP; Ronald O. Valdiserri, M.D., M.P.H., NCHSTP; Judith N. Wasserheit, M.D., M.P.H.; Lynne S. Wilcox, M.D., NCCDPHP;

Support Staff: Cynthia Ford, Contractor; Deborah McElroy; Garrett K. Mallory.