Pelvic inflammatory disease. Sexually transmitted diseases treatment guidelines 2006.

Note from the National Guideline Clearinghouse and the Centers for Disease Control and Prevention: When more than one therapeutic regimen is recommended, the sequence is alphabetized unless the choices for therapy are prioritized based on efficacy, convenience, or cost. For sexually transmitted diseases (STDs) with more than one recommended regimen, almost all regimens have similar efficacy and similar rates of intolerance or toxicity unless otherwise specified.

Pelvic inflammatory disease (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 Neisseria gonorrhoeae and Chlamydia trachomatis, are implicated in many cases; however, microorganisms that comprise the vaginal flora (e.g., anaerobes, Gardnerella vaginalis, Haemophilus influenzae, enteric Gram-negative rods, and Streptococcus agalactiae) also have been associated with PID. In addition, cytomegalovirus (CMV), Mycoplasma hominis, and Ureaplasma urealyticum might be the etiologic agents in some cases of PID. All women who are diagnosed with acute PID should be tested for N. gonorrhoeae and C. trachomatis and should be screened for HIV infection.

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. 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 frequently is not readily available, and its use is not easy to justify when symptoms are mild or vague. Moreover, laparoscopy will not detect endometritis and might 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 is imprecise. Data indicate that a clinical diagnosis of symptomatic PID has a positive predictive value (PPV) for salpingitis of 65% to 90% compared with laparoscopy. The PPV of a clinical diagnosis of acute PID depends on the epidemiologic characteristics of the population, with higher PPVs among sexually active young women (particularly adolescents), among patients attending STD clinics, or in other settings where the 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 not diagnosed 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, and vaginal discharge). Because of the difficulty of diagnosis and the potential for damage to the reproductive health of women, even by apparently mild or subclinical PID, health-care providers should maintain a low threshold for the diagnosis of PID.

The optimal treatment regimen and long-term outcome of early treatment of women with asymptomatic or subclinical PID are 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. 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 other women at risk for STDs if they are experiencing pelvic or lower abdominal pain, if no cause for the illness other than PID can be identified, and if one or more of the following minimum criteria are present on pelvic examination:

cervical motion tenderness OR uterine tenderness OR adnexal tenderness.

The requirement that all three minimum criteria be present before the initiation of empiric treatment could result in insufficient sensitivity for the diagnosis of PID. The presence of signs of lower genital tract inflammation, in addition to one of the three minimum criteria, increases the specificity of diagnosis. In deciding upon the initiation of empiric treatment, clinicians should also consider the risk profile of the patient for STDs.

More elaborate diagnostic evaluation frequently 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. The following additional criteria can be used to enhance the specificity of the minimum criteria and support a diagnosis of PID:

oral temperature >101 degrees F (>38.3 degrees C)
abnormal cervical or vaginal mucopurulent discharge
presence of abundant numbers of white blood cells (WBCs) on saline microscopy of vaginal secretions
elevated erythrocyte sedimentation rate
elevated C-reactive protein, and
laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis.

The majority of women with PID have either mucopurulent cervical discharge or evidence of WBCs on a microscopic evaluation of a saline preparation of vaginal fluid. 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. A wet prep of vaginal fluid offers the ability to detect the presence of concomitant infections (e.g., bacterial vaginosis and trichomoniasis).

The most specific criteria for diagnosing PID include the following:

endometrial biopsy with histopathologic evidence of endometritis
transvaginal sonography or magnetic resonance imaging 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); and
laparoscopic abnormalities consistent with PID

A diagnostic evaluation that includes some of these more extensive studies might be warranted in some cases. Endometrial biopsy is warranted in women undergoing laparoscopy who do not have visual evidence of salpingitis, as some women with PID have endometritis alone.

Treatment

PID treatment regimens must provide empiric, broad spectrum coverage of likely pathogens. Several antimicrobial regimens have been effective in achieving clinical and microbiologic cure in randomized clinical trials with short-term follow-up. However, only a limited number of investigations have assessed and compared these regimens with regard to elimination of infection in the endometrium and fallopian tubes or determined the incidence of long-term complications (e.g., tubal infertility and ectopic pregnancy) after antimicrobial regimens.

All treatment regimens should be effective against N. gonorrhoeae and C. trachomatis because negative endocervical screening for these organisms does not rule out upper reproductive tract infection. The need to eradicate anaerobes from women who have PID has not been determined definitively. Anaerobic bacteria have been isolated from the upper reproductive tract of women who have PID, and data from in vitro studies have revealed that some anaerobes (e.g., Bacteroides fragilis) can cause tubal and epithelial destruction. In addition, BV also is present in many women who have PID. Until treatment regimens that do not adequately cover these microbes have been demonstrated to prevent long-term sequelae (e.g., infertility and ectopic pregnancy) as successfully as the regimens that are effective against these microbes, the use of regimens with anaerobic activity should be considered. Treatment should be initiated as soon as the presumptive diagnosis has been made because prevention of long-term sequelae is dependent on immediate administration of appropriate antibiotics. When selecting a treatment regimen, health-care providers should consider availability, cost, patient acceptance, and antimicrobial susceptibility.

Some specialists have recommended that all patients with PID be hospitalized so that bed rest and supervised treatment with parenteral antibiotics can be initiated. However, in women with PID of mild or moderate clinical severity, outpatient therapy can provide short- and long-term clinical outcomes similar to inpatient therapy. Limited data support the use of outpatient therapy in women with more severe clinical presentations. The decision of whether hospitalization is necessary should be based on the discretion of the health-care provider.

The following criteria for hospitalization are suggested:

surgical emergencies (e.g., 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; and
the patient has a tubo-ovarian abscess

Many practitioners have preferred to hospitalize adolescent women whose condition is diagnosed as acute PID. No evidence is available suggesting that adolescents benefit from hospitalization for treatment of PID. Younger women with mild-to-moderate acute PID have similar outcomes with either outpatient therapy or inpatient therapy. Further, clinical response to outpatient treatment is similar among younger and older women. The decision to hospitalize adolescents with acute PID should be based on the same criteria used for older women. Whether women in their later reproductive years benefit from hospitalization for treatment of PID also is unclear, although women aged >35 years who are hospitalized with PID are more likely than younger women to have a complicated clinical course.

Parenteral Treatment

For women with PID of mild or moderate severity, parenteral and oral therapy appears to have similar clinical efficacy. Many randomized trials have demonstrated the efficacy of both parenteral and oral regimens. In the majority of clinical trials, parenteral treatment for at least 48 hours has been used after the patient has demonstrated substantial clinical improvement. Clinical experience should guide decisions regarding transition to oral therapy, which usually can be initiated within 24 hours of clinical improvement. The majority of clinicians recommend at least 24 hours of direct inpatient observation for patients who have tubo-ovarian abscesses.

Recommended Parenteral Regimen A

Cefotetan 2 g intravenously (IV) every 12 hours
OR

Cefoxitin 2 g IV every 6 hours
PLUS

Doxycycline 100 mg orally or IV every 12 hours

Note: Because of the pain associated with infusion, doxycycline should be administered orally when possible, even when the patient is hospitalized. Oral and IV administration of doxycycline provide similar bioavailability.

Parenteral therapy may be discontinued 24 hours after a patient improves clinically, and oral therapy with doxycycline (100 mg twice a day) should continue to complete 14 days of therapy. When tubo-ovarian abscess is present, many health-care providers use clindamycin or metronidazole with doxycycline for continued therapy, rather than doxycycline alone, because it provides more effective anaerobic coverage.

Clinical data are limited regarding the use of other second- or third-generation cephalosporins (e.g., ceftizoxime, cefotaxime, and ceftriaxone), which also might be effective therapy for PID and may replace cefotetan or cefoxitin. However, these cephalosporins are less active than cefotetan or cefoxitin against anaerobic bacteria.

Recommended Parenteral Regimen B

Clindamycin 900 mg IV every 8 hours
PLUS

Gentamicin loading dose IV or IM (2 mg/kg of body weight), followed by a maintenance dose (1.5 mg/kg) every 8 hours. Single daily dosing may be substituted.

Although use of a single daily dose of gentamicin has not been evaluated for the treatment of PID, it is efficacious in analogous situations. Parenteral therapy can be discontinued 24 hours after a patient improves clinically; continuing oral therapy should consist of doxycycline 100 mg orally twice a day or clindamycin 450 mg orally four times a day to complete a total of 14 days of therapy. When tubo-ovarian abscess is present, many health-care providers use clindamycin for continued therapy, rather than doxycycline, because clindamycin provides more effective anaerobic coverage.

Alternative Parenteral Regimens

Limited data support the use of other parenteral regimens, but the following three regimens have been investigated in at least one clinical trial, and they have broad spectrum coverage.

Levofloxacin 500 mg IV once daily*
WITH OR WITHOUT

Metronidazole 500 mg IV every 8 hours
OR

Ofloxacin 400 mg IV every 12 hours*
WITH OR WITHOUT

Metronidazole 500 mg IV every 8 hours
OR

Ampicillin/Sulbactam 3 g IV every 6 hours
PLUS

Doxycycline 100 mg orally or IV every 12 hours

*Quinolones should not be used in persons with a history of recent foreign travel or partners' travel, infections acquired in California or Hawaii, or infections acquired in other areas with increased quinolone-resistant Neisseria gonorrhoeae (QRNG) prevalence.

IV ofloxacin has been investigated as a single agent; however, because of concerns regarding its spectrum, metronidazole may be included in the regimen. Levofloxacin is as effective as ofloxacin and may be substituted; its single daily dosing makes it advantageous from a compliance perspective. One trial demonstrated high short-term clinical cure rates with azithromycin, either alone for 1 week (at least one IV dose followed by oral therapy) or with a 12-day course of metronidazole. Ampicillin/sulbactam plus doxycycline is effective coverage against C. trachomatis, N. gonorrhoeae, and anaerobes and for patients who have tubo-ovarian abscess.

Oral Treatment

Oral therapy can be considered for women with mild-to-moderately severe acute PID, as the clinical outcomes among women treated with oral therapy are similar to those treated with parenteral therapy. The following regimens provide coverage against the frequent etiologic agents of PID. Patients who do not respond to oral therapy within 72 hours should be reevaluated to confirm the diagnosis and should be administered parenteral therapy on either an outpatient or inpatient basis.

Recommended Regimen A

Levofloxacin 500 mg orally once daily for 14 days*
OR

Ofloxacin 400 mg orally twice daily for 14 days
WITH OR WITHOUT

Metronidazole 500 mg orally twice a day for 14 days

*Quinolones should not be used in persons with a history of recent foreign travel or partners' travel, infections acquired in California or Hawaii, or infections acquired in other areas with increased QRNG prevalence.

Oral ofloxacin has been investigated as a single agent in two clinical trials, and it is effective against both N. gonorrhoeae and C. trachomatis. Despite the results of these trials, lack of anaerobic coverage with ofloxacin is a concern; the addition of metronidazole to the treatment regimen provides this coverage. Levofloxacin is as effective as ofloxacin and may be substituted. Azithromycin has been demonstrated in one randomized trial to be an effective regimen for acute PID. The addition of metronidazole should be considered, as anaerobic organisms are suspected in the etiology of the majority of PID cases. Metronidazole will also treat BV, which frequently is associated with PID.

Regimen B

Ceftriaxone 250 mg intramuscularly (IM) in a single dose
PLUS

Doxycycline 100 mg orally twice a day for 14 days
WITH or WITHOUT

Metronidazole 500 mg orally twice a day for 14 days
OR

Cefoxitin 2 g IM in a single dose and Probenecid, 1 g orally administered concurrently in a single dose
PLUS

Doxycycline 100 mg orally twice a day for 14 days
WITH or WITHOUT

Metronidazole 500 mg orally twice a day for 14 days
OR

Other parenteral third-generation cephalosporin (e.g., ceftizoxime or cefotaxime)
PLUS

Doxycycline 100 mg orally twice a day for 14 days
WITH or WITHOUT

Metronidazole 500 mg orally twice a day for 14 days

The optimal choice of a cephalosporin for Regimen B is unclear; although cefoxitin has better anaerobic coverage, ceftriaxone has better coverage against N. gonorrhoeae. Clinical trials have demonstrated that a single dose of cefoxitin is effective in obtaining short-term clinical response in women who have PID. However, the theoretical limitations in cefoxitin's coverage of anaerobes might require the addition of metronidazole to the treatment regimen). Metronidazole also will effectively treat BV, which is frequently associated with PID. No data have been published regarding the use of oral cephalosporins for the treatment of PID. Limited data suggest that the combination of oral metronidazole and doxycycline after primary parenteral therapy is safe and effective.

Alternative Oral Regimens

Although information regarding other outpatient regimens is limited, one other regimen has undergone at least one clinical trial and has broad spectrum coverage. Amoxicillin/clavulanic acid and doxycycline was effective in obtaining short-term clinical response in a single clinical trial; however, gastrointestinal symptoms might limit compliance with this regimen.

Follow-Up

Patients 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 improve within this period usually require hospitalization, additional diagnostic tests, and surgical intervention.

If no clinical improvement has occurred within 72 hours after outpatient oral or parenteral therapy (using the criteria for clinical improvement described previously), an examination should be performed. Subsequent hospitalization, parenteral therapy, and diagnostic evaluation, including the consideration of diagnostic laparoscopy for alternative diagnoses, are recommended in women without clinical improvement. Some specialists also recommend rescreening for C. trachomatis and N. gonorrhoeae 4-6 weeks after therapy is completed in women with documented infection with these pathogens. All women diagnosed with acute PID should be offered HIV testing.

Management of Sex Partners

Male sex partners of women with PID should be examined and treated if they had sexual contact with the patient during the 60 days preceding the patient's onset of symptoms. Evaluation and treatment are imperative because of the risk for reinfection of the patient 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 frequently are asymptomatic.

Sex partners should be treated empirically with regimens effective against both of these infections, regardless of the etiology of PID or pathogens isolated from the infected woman. Even in clinical settings in which only women are treated, arrangements should be made to provide care for male sex partners of women who have PID. When providing care for male sex partners is not feasible, health-care providers should ensure that sex partners are referred for appropriate treatment.

Prevention

Prevention of chlamydial infection by screening and treating high-risk women reduces the incidence of PID. Theoretically, the majority of cases of PID can be prevented by screening all women or those determined to be at high risk (based on age or other factors) by using DNA amplification on cervical specimens (in women receiving pelvic examinations) and on urine specimens (in women not undergoing examinations). Although bacterial vaginosis is associated with PID, whether the incidence of PID can be reduced by identifying and treating women with BV is unclear.

Special Considerations

Pregnancy

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

HIV Infection

Differences in the clinical manifestations of PID between HIV-infected women and HIV-negative women have not been well-delineated. In previous observational studies, HIV-infected women with PID were more likely to require surgical intervention. More comprehensive observational and controlled studies (published since the 2002 STD Treatment Guidelines) have demonstrated that HIV-infected women with PID had similar symptoms when compared with uninfected controls. They were more likely to have a tubo-ovarian abscess but responded equally well to standard parenteral and oral antibiotic regimens when compared with HIV-negative women. The microbiologic findings for HIV-positive and HIV-negative women were similar, except HIV-infected women had higher rates of concomitant M. hominis, candida, streptococcal, and HPV infections and HPV-related cytologic abnormalities. Whether the management of immunodeficient HIV-infected women with PID requires more aggressive interventions (e.g., hospitalization or parenteral antimicrobial regimens) has not been determined.

IUD

Intrauterine contraceptive devices (IUDs) are becoming a popular contraceptive choice for women. Both levonorgestrel- and copper-containing devices are marketed in the United States. The risk of PID associated with IUD use is primarily confined to the first 3 weeks after insertion and is uncommon thereafter. Given the popularity of IUDs, practitioners might encounter PID in IUD users. No evidence suggests that IUDs should be removed in women diagnosed with acute PID. However, caution should be exercised if the IUD remains in place, and close clinical follow-up is mandatory. The rate of treatment failure and recurrent PID in women continuing to use an IUD is unknown. No data exist on antibiotic selection and treatment outcomes according to type of IUD (e.g., copper or levonorgestrel).

Chairpersons: David Atkins, MD, Agency for Healthcare Research and Quality, Rockville, Maryland; Kimberly A. Workowski, MD, National Center for HIV, STD, and TB Prevention, CDC, and Emory University, Atlanta, GA

Presenters: Heidi Bauer, MD, California Sexually Transmitted Disease Control Branch, Oakland, California; Emily J. Erbelding, MD, Johns Hopkins University School of Medicine, Baltimore, Maryland; William M. Geisler, MD, Department of Medicine, University of Alabama, Birmingham, Alabama; Margaret Hammerschlag, MD, State University of New York, Downstate Medical Center, Brooklyn, New York; Peter Leone, MD, University of North Carolina School of Medicine, Chapel Hill, North Carolina; Jenne Marrazzo, MD, University of Washington, Harborview Medical Center, Seattle, Washington; Kenneth Hugh Mayer, MD, Brown University Medical School, Providence, Rhode Island; Pablo Sanchez, MD, University of Texas Southwestern Medical Center, Dallas, Texas; Bradley Stoner, MD, PhD, Washington University, St. Louis, Missouri; Anna Wald, MD, University of Washington, Harborview Medical Center, Seattle, Washington; George Wendel, MD, University of Texas Southwestern Medical School, Dallas, Texas; Karen Wendel, MD, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma; Harold C. Wiesenfeld, MD, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania

Moderators: Willard Cates, Jr., MD, Family Health International, Durham, North Carolina; King K. Holmes, MD, PhD, University of Washington, Harborview Medical Center, Seattle, Washington; David Martin, MD, Louisiana State University Medical Center, New Orleans, Louisiana

Rapporteurs: Hunter Handsfield, MD, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia, University of Washington, Seattle, Washington; William McCormack, MD, State University of New York Health Science Center, Brooklyn, New York; Anne Rompalo, MD, Johns Hopkins School of Medicine, Baltimore, Maryland

Consultants: Michael Augenbraun, MD, State University of New York Health Science Center, Brooklyn, New York; Gail Bolan, MD, California Department of Health, Oakland, California; Carolyn Deal, PhD, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland; Kenneth H. Fife, MD, PhD, Indiana University School of Medicine, Indianapolis, Indiana; J. Dennis Fortenberry, MD, Indiana University School of Medicine, Indianapolis, Indiana; Edward Hook, III, MD, Department of Medicine, University of Alabama, Birmingham, Alabama; Franklyn Judson, MD, University of Colorado Department of Medicine and Preventive Medicine, Denver, Colorado; Alice A. Kraman, PharmD; Emory Healthcare, Atlanta, Georgia; Roberta B. Ness, MD, University of Pittsburgh Department of Medicine, Pittsburgh, Pennsylvania; Paul Nyirjesy, MD, Drexel University College of Medicine, Philadelphia, Pennsylvania; Jeffrey Peipert, MD, Women and Infants Hospital, Providence, Rhode Island; Jane R. Schwebke, MD, Department of Medicine, University of Alabama, Birmingham, Alabama; Mary Ann Shafer, MD, University of California, San Francisco Department of Medicine, San Francisco, California; David Soper, MD, Medical University of South Carolina, Charleston, South Carolina; Lawrence Stanberry, MD, PhD, University of Texas Medical Branch, Galveston, Texas; Heather Watts, MD, National Institute of Child Health and Development, National Institutes of Health, Bethesda, Maryland; Jonathan M. Zenilman, MD, Johns Hopkins Bayview Medical Center, Baltimore, Maryland

Liaison Participants: Joanne Armstrong, MD, Women's Health, Aetna, Sugar Land, Texas; James R. Allen, MD, American Social Health Association, Durham, North Carolina; Margaret J. Blythe, MD, American Academy of Pediatrics, Indianapolis, Indiana; Sherry R. Crump, MD, American College of Preventive Medicine, Atlanta, GA; Carolyn D. Deal, PhD, National Institutes of Health, Bethesda, Maryland; Jordon Dimitrakov, MD, PhD, American Urological Association, Boston, Massachusetts; Mark FitzGerald, MD, British Association for Sexual Health and HIV, Southampton, United Kingdom; Edward Harrison, National Commission on Correctional Health Care, Chicago, Illinois; Edward W. Hook, III, MD, Infectious Disease Society of America, Birmingham, Alabama; Michel Janier, MD, PhD, International Union Against Sexually Transmitted Infections Europe, Paris, France; Abe Macher, MD, HIV/AIDS Bureau, Rockville, Maryland; Francis J. Ndowa, MD, World Health Organization, Geneva, Switzerland; Jeffrey F. Peipert, MD, American College of Obstetricians and Gynecologists, Providence, Rhode Island; Kees A. Rietmeijer, MD, PhD, Denver Public Health Department, Denver, Colorado; Richard Rothman, MD, American College of Emergency Physicians, Baltimore, Maryland; David Soper, MD, Infectious Diseases Society for Obstetrics and Gynecology, Charleston, South Carolina; Litjen Tan, PhD, American Medical Association, Chicago, Illinois; Bruce Trigg, MD, National Coalition for Sexually Transmitted Disease Directors, Albuquerque, New Mexico; Julia Valderrama, MD, Pan American Health Organization, Washington, DC; Tom Wong, MD, Public Health Agency of Canada, Ottawa, Ontario, Canada; Miriam Zieman, MD, Association of Reproductive Health Professionals, Atlanta, Georgia

CDC, Division of Sexually Transmitted Disease Prevention Treatment Guidelines 2006 Project. Coordinator: Kimberly A. Workowski, MD, National Center for HIV, STD, and TB Prevention, CDC, and Emory University, Atlanta, GA

Project Manager: Donald F. Dowda, ORISE, Oakridge, Tennessee; Richard Voigt, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia

Co-Moderators: Lyn Finelli, Ph.D., DSTDP; Robert Johnson, M.D., DSTDP; Lauri Markowitz, M.D., DSTDP

CDC Presenters: Joanna Buffington, MD, National Center for Infectious Diseases; Eileen Dunne, MD, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia; Matthew Hogben, PhD, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia; Emily Koumans, MD, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia; Hershel Lawson, MD, National Center for Chronic Disease Prevention and Health Promotion, Atlanta, Georgia; Catherine McLean, MD, National Center for HIV, STD, and TB Prevention, Atlanta, Georgia; Juliette Morgan, MD, National Center for Infectious Diseases, CDC, Atlanta, Georgia; Lori Newman, MD, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia; Madeline Sutton, MD, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia

CDC Consultants: Sevgi O. Aral, PhD, Stuart M. Berman, MD, John Douglas, MD, Susan J. DeLisle, Kathleen Ethier, PhD, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia; Kevin Fenton, MD, National Center for HIV, Hepatitis, Sexually Transmitted Diseases and Tuberculosis Prevention, CDC, Atlanta, Georgia; John Moran, MD, National Immunization Program, CDC, Atlanta, Georgia; Julia Schillinger, MD, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia

Support Staff: Valerie Barner, Winda Graves, Garrett Mallory, Deborah McElroy, National Center for HIV, STD, and TB Prevention, CDC, Atlanta, Georgia; Eboney Walker, NAI Personnel, Washington, DC

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