SINCE THE 1940s, gonorrhea has been one of the most frequently reported communicable diseases in the United States.1 Gonorrhea rates declined in the late 1940s and 1950s after the advent of penicillin therapy and during a period of relative social stability. However, rates began to increase in the late 1950s and increased markedly from 1966 to 1975, a period when sexual behavior patterns were changing dramatically.2,3 In response to the rising incidence, public health agencies and health care providers initiated gonorrhea control efforts based on widespread screening of asymptomatic women using newly developed selective culture media. Increased numbers of cases from 1972 to 1975 and falling rates since 1975 have been attributed in part to these efforts, which led to treatment of asymptomatic infected persons and their sexual partners, interrupting transmission of the infection.2,4
Despite these successes, gonorrhea rates in the United States remain the highest of any industrialized country.5 High gonorrhea rates adversely affect the nation's health through two mechanisms. First, gonorrhea is a major cause of pelvic inflammatory disease and subsequent infertility and ectopic pregnancy.6 Second, recent data suggest gonorrhea may facilitate human immunodeficiency virus (HIV) transmission.7,8
To describe the current epidemiology of gonorrhea, we examined trends in the demographic and geographic distribution of reported gonorrhea in the United States from 1981 through 1995.
We analyzed gonorrhea surveillance data reported to the Centers for Disease Control and Prevention (CDC) from 1981 through 1996. Each quarter, the 50 states, the District of Columbia, and 63 large (population more than 200,000 in 1980) cities reported aggregate cases by gender and source of report (private or public). Definitions of public sources varied by reporting area from sexually transmitted disease (STD) clinics to all publicly funded clinics. Each year, the 50 states, the District of Columbia, and six major cities reported aggregate cases by age group, gender, race/ethnicity, and source of report. Quarterly reports identified more cases than annual reports except in 1992 and 1993; the numbers of cases reported in the two data sources were within 2% of each other except in 1981 (6.4%), 1983 (19.6%), and 1984 (16.6%). Quarterly reports were used for analyses not involving age or race/ethnicity because of the large number of cases missing from annual reports 1981 through 1985.
Race/ethnicity categories were white (not of Hispanic origin), black (not of Hispanic origin), Hispanic, Asian/Pacific Islander, and American Indian/Alaska Native. Race/ethnicity data were incomplete for some states, especially during the early 1980s. For race/ethnicity analyses, cases with unknown race were excluded and states reporting race/ethnicity for less than 50% of cases in any year were excluded for that year.* The proportion of annual cases excluded from race/ethnicity analyses ranged from 16.3% in 1992 to 25.6% in 1984. For age analyses, cases with unreported age or incompatible age categories and states reporting age for less than 50% of cases in any year were excluded for that year.† The proportion of annual cases excluded from age analyses ranged from 2.0% in 1982 to 9.9% in 1993. Exclusion, rather than prorating according to the race/ethnicity, distribution in cases with complete data was used because the pattern of missing data in some years and states with many incomplete reports suggested a bias in the race/ethnicities reported. Exclusion was similarly chosen for handling missing age data.‡
Annual incidence rates (cases/100,000 persons) were calculated using published Bureau of the Census population estimates and intercensus estimates as previously described.1 When data from states that did not adequately report age or race were excluded, the state population estimates were also excluded from the denominator of rate calculations. Gender-, age-, and state-specific rates were not calculated for Hispanics, Asian/Pacific Islanders, and Native American/Alaskan Natives because of small numbers of cases and intermittent reporting of these racial/ethnic categories.
Geographic analyses were performed by state and region.‡
The annual number of reported gonorrhea cases in the United States decreased 67.1%, from 990,864 cases in 1981 to 325,883 cases in 1996. Gonorrhea incidence declined 71.3% during the period, from 431.5 to 124.0 cases per 100,000 population. This rate declined gradually from 1981 to 1984, with average annual rate decreases of 4.9%, increased 2.5% from 1984 to 1985, then decreased again through 1996 with average annual rate decreases of 9.6%.
Men comprised 51% of gonorrhea cases and women comprised 49% of cases in 1996. Whites accounted for 15% of cases in 1996, blacks for 79%, Hispanics for 5%, Asian/Pacific Islanders for 0.4%, and Native Americans for 0.7%. The South reported 54% of all cases in 1996; adolescents aged 15 to 19 years accounted for 31% of 1996 cases.
Trends in gonorrhea rates varied by race, gender, and age group (Figure 1). Rates in white men and women were consistently lower than rates in black men and women. Rates in white men declined rapidly to low levels (14.8 cases/100,000 in 1996), whereas rates in white women declined more slowly and were higher than rates in white men after 1986 (23.7 cases/100,000 in 1996). Among whites, 20- to 24-year-old men consistently had higher rates (51.0 cases/100,000 in 1996) than men of any other age group. In contrast, 15- to 19-year-old white women had higher rates (160.6 cases/100,000 in 1996) than white women of any other age group after 1984.
In 1981, the gonorrhea rate among blacks was 11 times higher than the rate among whites (1,894.3 versus 164.3 cases/100,000); by 1996, the rate among blacks had fallen but not as dramatically as among whites, causing the black-to-white incidence ratio to increase to 35 (684.4 versus 19.4 cases/100,000). Black men had rates higher than any other race or gender group throughout the period, with little decline before 1990 (811.0 cases/100,000 in 1996); rates in black women were somewhat lower (570.8 cases/100,000 in 1996) and generally paralleled those in black men (Figure 1). As with whites, 20- to 24-year-old black men had higher rates (3,160.8 cases/100,000 in 1996) than any other age group, and 15- to 19-year-old black women had higher rates (2,888.4 cases/100,000 in 1996) than any other age group after 1984. Rates among black and white 15 to 19 year olds decreased by 47.5% and 76.4%, respectively, from 1981 to 1996, whereas rates among blacks and whites aged 20 to 24 years decreased by 61.3% and 88.1%, respectively.
Gonorrhea rates in 10 to 14 year olds of all races increased from 43.9 cases/100,000 in 1981 to 66.3 cases/100,000 in 1986 and then decreased to 32.0 cases/100,000 in 1996. Rates in 10 to 14 year olds peaked among white boys in 1981 (4.8 cases/100,000), white girls in 1986 (30.7 cases/100,000), black boys in 1989 (182.8 cases/100,000), and black girls in 1989 (490.6 cases/100,000).
Gonorrhea rates decreased steadily among Native Americans (71.4 cases/100,000 in 1996) and Hispanics (60.2 cases/100,000 in 1996), whereas Asians had very low rates throughout the period (13.0 cases/100,000 in 1996) (Figure 2).
Gonorrhea rates decreased in all states but remained highest in the South throughout the period (Figure 3). Among whites, rates were highest in the West and South and lowest in the Northeast in 1981, but by 1996 all regional rates were low (range, 10.1 cases/100,000 in the Northeast to 27.3 cases/100,000 in the South). Among blacks, rates were highest in the West and South during the first half of the period and in the Midwest and South during the second half of the period. Rates among blacks in 1996 were consistently high but with substantial regional differences: 812.3 cases/100,000 in the Midwest and 707.6 cases/100,000 in the South compared with 543.8 cases/100,000 in the Northeast and 357.3 cases/100,000 in the West.
Gonorrhea rates in the 63 large cities for which separate rates are available beginning in 1984 paralleled trends in the rest of the country, with decreases of 69.4% and 63.2% for these cities and remaining areas, respectively, from 1984 to 1996. However, not all cities experienced dramatic decreases in gonorrhea, and rates remained higher than 0.5% (500/100,000) in 12 cities in 1996 (Table 1).
Source of Report
An increasing proportion of reports came from private sources during this period (24.1% in 1981 to 48.1% in 1996). Among whites, cases from private sources comprised 28.1% of cases in 1981 and 53.0% of cases in 1996. There was substantial regional variation. In 1996, 81.0% of cases among whites in the Northeast were from private sources, 66.2% in the Midwest, 55.4% in the West, and 42.7% in the South. More cases among white women were from private sources (57.5% in 1996; regional range, 45.4-87.7%) than among white men (45.6% in 1996; regional range, 37.9-69.1%).
Trends were similar, although at lower levels, among blacks, with 17.0% of cases in 1981 and 35.2% in 1996 from private sources. In 1996, 61.5% of cases among blacks in the Northeast were reported by private sources, 42.7% in the West, 40.7% in the Midwest, and 30.4% in the South. Only 23.5% of cases in black males (regional range, 20.3-43.3%) and 50.2% of cases in black females (regional range, 43.8-81.8%) were from private sources in 1996.
The proportion of cases reported by private sources was similar in adolescents (aged 15 to 19 years) compared with older persons during the entire period (data not shown).
Ratio of Cases in Men to Cases in Women
The male-to-female ratio of gonorrhea cases in the United States decreased from 1.5 in 1981 to 1.0 in 1996. Among whites, the male-to-female ratio decreased from 1.5 to 0.6, whereas among blacks the ratio changed only from 1.5 to 1.3 during the same period. Male-to-female ratios were highest in the West in all years (1996: 1.2 among whites, 1.4 among blacks) compared with other regions (1996: 0.4-0.6 among whites, 1.1-1.3 among blacks).
From 1981 through 1996, gonorrhea rates declined in all states and among all age and race groups. This decline may in part reflect the continued impact of screening programs begun in the early 1970s2,4 and the continued availability of effective single-dose therapy. Screening programs identify asymptomatic infections-especially among women-that are important in the persistence of gonorrhea in the community.9,10 Effective single-dose therapy has long been a main-stay of gonorrhea control because it avoids problems with treatment adherence.3 Changes in sexual behavior in response to the HIV epidemic may also be partly responsible for these trends. Reports of increased condom use and reduced risky sexual practices among men who have sex with men11,12 accompanied decreases in rectal gonorrhea in the mid-1980s in several cities.13–15 The decline in gonorrhea among men and the decreased male-to-female case ratio among whites seen in our data may be related to these behavioral changes in men who have sex with men. Recent data suggest, however, that gonorrhea may again be increasing among this group.16
Evidence for sexual behavior change among heterosexuals in response to the threat of HIV is more limited,17 but increasing condom use, especially among those using hormonal methods of contraception, has been documented in several studies in the 1990s.18,19 Another factor that may have contributed to the overall decline in gonorrhea rates is a shift in the age structure of the U.S. population; the proportion of the population that fell into the highest risk age groups (15-19 years and 20-24 years) decreased steadily from 18.5% in 1981 to 13.6% in 1996 (data not shown).
Decreasing gonorrhea rates in the 1980s and 1990s were accompanied by reported increases in other sexually transmitted diseases. Two syphilis epidemics during this period led to the highest rates of this disease since 1949; the first was among gay and bisexual men from the late 1970s to the early 1980s, and the second, which peaked in 1990, involved primarily blacks and was associated with crack cocaine use.20 Gonorrhea rates continued to decline, although slowly, in the same population groups that experienced rapid increases in syphilis in the late 1980s; possible explanations for this divergence of trends include differences in the sexual behaviors associated with efficient transmission of these diseases, health care-seeking behavior among infected persons, the widespread screening for asymptomatic infection among women,21,22 and dramatic differences in the endemic levels of these diseases. Reported chlamydial infection also increased in the 1980s; however, trends in chlamydial infection during that time reflect increasing recognition of the disease and availability of diagnostic tests.1
Gonorrhea rates have historically been higher in the South than in other parts of the United States. Despite rate decreases in all regions, regional differences in gonorrhea rates persisted throughout this 15-year period. Populations of southern states are marked by high prevalences of several characteristics associated with high STD rates: poverty, income inequality, low social status of women, low educational attainment, and limited accessibility and utilization of health care services.23
The South also has a greater proportion of minorities than other regions of the United States. Although overall gonorrhea rates declined throughout the 1980s, decreases in rates among blacks were substantial only after 1990, and rates remained much higher than among whites. Reporting bias may partially account for higher rates in blacks. Public sources, which identified two-thirds or more cases each year in blacks but only one-quarter to one-half of cases in whites, report more completely than private sources.24–26 Adjusting for these differences in reporting rates would nonetheless leave large, and increasing, racial disparities in gonorrhea morbidity.
Reasons for these racial disparities in gonorrhea and other STDs have been explored in recent reviews.27,28 The relationship between STD rates and race is complicated by several factors for which race may be a proxy; these factors include socioeconomic class, neighborhood, sexual partner choices, and sexual practices.27–30 Health services availability is affected by socioeconomic class and neighborhood, and health services utilization may differ by race.3,27,28 In addition, two population-level factors that may increase the incidence of certain STDs-youthful age composition and ratio of women to men greater than one-are seen to a greater extent among blacks and other minorities than among white Americans.31
Data on differences in sexual behaviors between whites and blacks are limited. A recent national survey showed that although blacks were more likely to have had more than one sexual partner in the last year, they were also more likely to have used condoms at the last sexual contact and more likely to have changed sexual behaviors in response to the acquired immunodeficiency syndrome epidemic.32 In that survey, black race was an independent risk marker for STD, after controlling for numbers of partners and other sexual behaviors.33 Smaller studies of women attending STD and family planning clinics showed that black women had sexual behaviors less risky than those of white women yet had equal or higher STD rates.29,30 In summary, intertwining social and economic factors, along with geographic clustering and sexual partner choices along both socioeconomic and racial lines, may help explain persistent racial differentials in STD rates despite similarities in other measures of risk.23
Gonorrhea rates among black and white adolescent women declined less than rates in any other demographic group from 1981 through 1996. Adolescents are more susceptible than adults to certain STDs for both physiologic and behavioral reasons and may also have a higher risk of developing complications of gonorrhea such as pelvic inflammatory disease.34 Continued high gonorrhea rates among adolescents are consistent with increased proportions of teenagers engaging in premarital sex,35 low rates of condom use, inadequate knowledge about STD prevention,34 and delays in seeking treatment for STDs because of fear of parental notification.36
Aral et al37 suggested that the denominator for rates of STDs in adolescents should be the number of adolescents who are sexually experienced, because this would more accurately reflect the disease risk faced by adolescents engaging in sex. For example, only 53% of high school students in 1995 had ever had sex35; dividing reported gonorrhea in 15 to 19 year olds by the number of sexually experienced adolescents yields a rate among those at risk twice as high as the rate calculated using standard population denominators (1,024.0 versus 542.7 cases/100,000).
The relative increase in cases reported from private sources could be explained in several ways. First, diagnosis and reporting of gonorrhea in private settings may have improved. Nonculture tests, that often allow testing for Chlamydia trachomatis and Neisseria gonorrheae with a single specimen, have simplified the diagnosis of gonorrhea and are increasingly used in the private sector; many central laboratories that process such tests report positive results directly to public health authorities (CDC, unpublished data), so reporting rates are high. Campaigns to increase awareness of reporting responsibilities and to facilitate reporting by private physicians (CDC, unpublished data) may also have increased reporting rates for private settings. Second, persons at risk for gonorrhea may be increasingly using private health services for STD care. As managed care organizations have extended their reach to poor and minority populations-traditional users of public clinics-through contracts with Medicaid programs,38 limited funds have left many public clinics with poorly maintained facilities, inadequately trained staff, outdated laboratory equipment, and limited hours of service.39,40
Interpretation of the trend in the male-to-female case ratio is complex. A high ratio may reflect failure to detect asymptomatic disease in women, underreporting of disease in women more than in men, large numbers of men infected by small numbers of women (such as commercial sex workers), or disease in men who have sex with men. A quantitative assessment of this issue in the mid-1980s suggested that one-half of gonorrhea cases in women were unreported or undetected; the actual case ratio in the United States was estimated at 0.8, much lower than the reported ratio of 1.4.41 Because women with gonorrhea are much more likely to be asymptomatic than men with gonorrhea, screening asymptomatic at-risk persons identifies more infected women than men.3,9 Thus, effective screening programs2,4 and behavioral changes leading to fewer STDs in men who have sex with men11,12 may partly explain the reduction in case ratio seen among whites during this time. The more stable case ratio in blacks may indicate that screening programs have failed to reach asymptomatic infected black women or may reflect different sexual mixing patterns.
Case ratio measurements may be biased by two main factors. First, underreporting in private settings, where whites and black women are diagnosed in higher proportions than black men, could artificially raise the male-to-female case ratio among blacks. Second, different diagnostic practices for men and women seen in private settings, whereby women receive specific testing resulting in a laboratory report and men may be treated empirically or diagnosed with the aid of a Gram stain, may artificially lower the case ratio among whites.42
The gonorrhea data presented here are part of surveillance data gathered by CDC to follow long-term trends in STD morbidity. These data are limited in several ways. First, data collection systems vary from state to state; thus, data are not directly comparable among states. In particular, definitions of public and private are not consistent across states. Second, these data are subject to reporting bias, which leads to underrepresentation of cases from private sources as previously discussed. Third, assessments of race-specific trends are limited by incomplete race data, especially before 1986. Finally, the data for races other than white or black are problematic; sporadic reporting by these categories in the 1980s make trends difficult to interpret.
Recent trends in gonorrhea raise several issues for public health programs aiming to better control morbidity due to gonorrhea and its sequelae. The overall decline in gonorrhea rates most likely reflects the impact of widespread screening and treatment initiated in the 1970s and continuing today, along with changes in the population age structure and barrier contraceptive use. This decline may be reassuring but should not lead to complacency. Gonorrhea rates in the United States remain much higher than rates in other industrialized nations, and much of the overall decline in U.S. rates is due to lower rates among whites and persons over age 20. Gonorrhea remains a serious public health problem among minorities and among adolescents of all races. In its recent report on STDs, the Institute of Medicine recommended a focus on adolescents and underserved populations. Specifically, the Institute of Medicine report recommended unique approaches to the education and provision of prevention services to adolescents and disenfranchised groups who may not otherwise access health services. Coordination with other social and health-related services should ensure that effective STD services reach these especially vulnerable populations.43 Further research should define interventions that will allow these populations to benefit from the same reduction in disease that has already occurred for most Americans.
Note: Sexually Transmitted Disease Surveillance, 1996, summarizes reported cases of all sexually transmitted diseases. It is published by the Division of STD Prevention, Centers for Disease Control and Prevention, and is available on the Worldwide Web through the CDC homepage at http://www.cdc.gov.
1. Division of STD Prevention. Sexually Transmitted Disease Surveillance, 1996. U.S. Department of Health and Human Services, Public Health Service. Atlanta: Centers for Disease Control and Prevention, September 1997.
2. Zaidi AA, Aral SO, Reynolds GH, Blount JH, Jones OG, Fichtner RR. Gonorrhea in the United States: 1967-1979. Sex Transm Dis 1983; 10:72-76.
3. Barnes RC, Holmes KK. Epidemiology of gonorrhea: current perspectives. Epidemiol Rev 1984; 6:1-30.
4. Schnell D, Zaidi A, Reynolds G. A time series analysis of gonorrhea surveillance data. Stat Med 1989; 8:343-352.
5. Piot P, Islam MQ. Sexually transmitted diseases in the 1990s: global epidemiology and challenges for control. Sex Transm Dis 1994; 21:S7-S13.
6. McCormack WM. Pelvic inflammatory disease. N Engl J Med 1994; 330:115-119.
7. Laga M, Manoka A, Kivuvu M, et al. Non-ulcerative sexually transmitted diseases as risk factors for HIV-1 transmission in women: results from a cohort study. AIDS 1993; 7:93-102.
8. Cohen MS, Hoffman IF, Royce RA, et al. Reduction of concentration of HIV-1 in semen after treatment of urethritis: implications for prevention of sexual transmission of HIV-1. Lancet 1997; 349:1868-1873.
9. Handsfield HH, Lipman TO, Narnisch JP, Tronca E, Holmes KK. Asymptomatic gonorrhea in men: diagnosis, natural course, prevalence and significance. N Engl J Med 1974; 290:117-123.
10. Pedersen AHB, Harrah WD. Followup of male and female contacts of patients with gonorrhea. Public Health Rep 1970; 85:997-1000.
11. Martin JL, Garcia MA, Beatrice ST. Sexual behavior changes and HIV antibody in a cohort of New York City gay men. Am J Public Health 1989; 79:501-503.
12. McKusick L, Coates TJ, Morin SF, Pollack L, Hoff C. Longitudinal predictors of reductions in unprotected anal intercourse among gay men in San Francisco: the AIDS behavioral research project. Am J Public Health 1990; 80:978-983.
13. Centers for Disease Control. Declining rates of rectal and pharyngeal gonorrhea among males-New York City. MMWR 1984; 33:295-297.
14. Handsfield HH. Decreasing incidence of gonorrhea in homosexually active men: minimal effect on risk of AIDS. West J Med 1985; 143:469-470.
15. Judson FN. Fear of AIDS and gonorrhea rates in homosexual men. Lancet 1983; 2:159-160.
16. Centers for Disease Control and Prevention. Gonorrhea among men who have sex with men-selected sexually transmitted diseases clinics, 1993-1996. MMWR 1997; 46:889-892.
17. Choi K-H, Catania JA. Changes in multiple sexual partnerships, HIV testing, and condom use among U.S. heterosexuals 18 to 49 years of age, 1990 and 1992. Am J Public Health 1996; 86:554-556.
18. Moran JS, Janes HR, Peterman TA, Stone KA. Increase in condom sales following AIDS education and publicity, United States. Am J Public Health 1990; 80:607-608.
19. Cates W. Contraception, unintended pregnancies, and sexually transmitted diseases: why isn't a simple solution possible? Am J Epidemiol 1996; 143:311-318.
20. Rolfs RT, Nakashima AK. Epidemiology of primary and secondary syphilis in the United States, 1981 through 1989. JAMA 1990; 264:1432-1437.
21. Gershman KA, Rolfs RT. Diverging gonorrhea syphilis trends in the 1980s: are they real? Am J Public Health 1991; 81:1263-1267.
22. Hamers FF, Peterman TA, Zaidi AA, Ransom RL, Wroten JE, Witte JJ. Syphilis and gonorrhea in Miami: similar clustering, different trends. Am J Public Health 1995; 85:1104-1108.
23. Aral SO. The social context of syphilis persistence in the southeastern United States. Sex Transm Dis 1996; 23:9-15.
24. Eisenberg MS, Wiesner PJ. Reporting and treating gonorrhea: results of a statewide survey in Alaska. J Am Vener Dis Assoc 1976; 3:79-83.
25. Rothenberg R, Bross DC, Vernon TM. Reporting of gonorrhea by private physicians: a behavioral study. Am J Public Health 1980; 70:983-986.
26. Smucker DR, Thomas JC. Evidence of thorough reporting of sexually transmitted diseases in a southern rural county. Sex Transm Dis 1995; 22:149-154.
27. Moran JS, Aral SO, Jenkins WC, Peterman TA, Alexander ER. The impact of sexually transmitted diseases on minority populations. Public Health Rep 1989; 104:560-565.
28. Toomey KE, Moran JS, Rafferty MP, Beckett GA. Epidemiological considerations of sexually transmitted diseases in underserved populations. Infect Dis Clin North Am 1993; 7:739-752.
29. Aral SO, Soskolne V, Joesoef RM, O'Reilly KR. Sex partner recruitment as risk factor for STD: clustering of risky modes. Sex Transm Dis 1991; 18:10-17.
30. Wasser SC, Aral SO, Reed DS, Bowen GS. Assessing behavioral risk for HIV infection in family-planning and STD clinics: similarities and differences. Sex Transm Dis 1989; 16:178-183.
31. Aral SO, Wasserheit JN. Interactions among HIV, other sexually transmitted diseases, socioeconomic status, and poverty in women. In: O'Leary A, Jemmott LS, eds. Women at Risk: Issues in the Primary Prevention of AIDS. New York: Plenum Press, 1995:13-40.
32. Laumann EO, Gagnon JH, Michael RT, Michaels S. The Social Organization of Sexuality: Sexual Practices in the United States. Chicago: University of Chicago Press, 1994:217, 429.
33. Laumann EO, Gagnon JH, Michael RT, Michaels S. The Social Organization of Sexuality: Sexual Practices in the United States. Chicago: University of Chicago Press, 1994:391.
34. Cates W Jr, Rauh JL. Adolescents and sexually transmitted diseases-an expanding problem. J Adolesc Health Care 1985; 6:257-261.
35. Centers for Disease Control and Prevention. Youth risk behavior surveillance-United States, 1995. MMWR 1996; 45(No. SS-4).
36. O'Reilly KR, Aral SO. Adolescence and sexual behavior: trends and implications for STD. J Adolesc Health Care 1985; 6:262-270.
37. Aral SO, Schaffer JE, Mosher WD, Cates W Jr. Gonorrhea rates: what denominator is most appropriate? Am J Public Health 1988; 78:702-703.
38. Centers for Disease Control and Prevention. Prevention and managed care: opportunities for managed care organizations, purchasers of health care, and public health agencies. MMWR 1995; 44(No. RR-14):1-12.
39. Hart G, Adler MW, Stapinski A, Mroczkowski TF, Wiesner PJ. Evaluation of sexually transmitted diseases control programs in industrialized countries. In: Holmes KK, Mardh P-A, Sparling PF, et al., eds. Sexually Transmitted Diseases. New York: McGraw-Hill, 1990:1031-1040.
40. Judson FN. Clinical facilities for sexually transmitted disease control. In: Holmes KK, Mardh P-A, Sparling PF, et al., eds. Sexually Transmitted Diseases. New York: McGraw-Hill, 1990:1047-1056.
41. Potterat JJ, Dukes RL, Rothenberg RB. Disease transmission by heterosexual men with gonorrhea: an empiric estimate. Sex Transm Dis 1987; 14:107-110.
42. Rice RJ, Roberts PL, Handsfield HH, Holmes KK. Sociodemographic distribution of gonorrhea incidence: implications for prevention and behavioral research. Am J Public Health 1991; 81:1252-1258.
43. Eng TR, Butler WT, eds. The Hidden Epidemic: Confronting Sexually Transmitted Diseases. Institute of Medicine. Washington, DC: National Academy Press, 1997.
*States and years excluded from race/ethnicity analyses were Georgia in 1983 and 1993-1995; Connecticut 1984-1986; Florida in 1981 and 1983-1985; Illinois 1981-1984; Idaho in 1983; Indiana 1983-1984; Kentucky 1986-1991; Maryland 1982-1983 and 1989-1991; Massachusetts in 1983; Michigan 1984-1985; Nebraska 1982-1986; New Jersey 1982-1985, 1990, and 1995-1996; New York 1981-1996; Tennessee in 1984; Virginia 1982-1985; Wisconsin 1982-1985; and the District of Columbia in 1984.
†States and years excluded from age analyses were Georgia in 1983, 1985, and 1988-1994; Idaho in 1983; Indiana in 1983; Maryland 1982-1983; Massachusetts in 1983 and 1990; New York 1983-1984; Tennessee in 1984; and District of Columbia in 1984.
‡Four geographic regions were defined by the Bureau of Census: West (Alaska, Arizona, California, Colorado, Hawaii, Idaho, Montana, Nevada, New Mexico, Oregon, Utah, Washington, and Wyoming); Midwest (Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, Ohio, South Dakota, and Wisconsin); Northeast (Connecticut, Maine, Massachusetts, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island, and Vermont); and South (Alabama, Arkansas, Delaware, District of Columbia, Florida, Georgia, Kentucky, Louisiana, Maryland, Mississippi, North Carolina, Oklahoma, South Carolina, Tennessee, Texas, Virginia, and West Virginia).