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Other Sexually Transmitted Diseases

This web page is archived for historical purposes and is no longer being updated. Newer data is available on the STD Data and Statistics page.


Since 1987, reported cases of chancroid had declined steadily until 2001. Since then, the number of cases reported has fluctuated (Figure 51, Table 1). In 2011, a total of 8 cases of chancroid were reported in the United States. Only six states reported one or more cases of chancroid in 2011 (Table 43).

Although the overall decline in reported chancroid cases most likely reflects a decline in the incidence of this disease, these data should be interpreted with caution because Haemophilus ducreyi, the causative organism of chancroid, is difficult to culture, and as a result, this condition may be substantially underdiagnosed.1,2

Human Papillomavirus

Persistent infection with high-risk human papillomavirus (HPV) can lead to development of anogenital cancers (e.g., cervical cancer). In June 2006, a quadrivalent HPV vaccine was licensed for use in the United States in females aged 9–26 years; in October 2009, this vaccine also was licensed for use in males aged 9–26 years. The vaccine provides protection against HPV types 6, 11, 16, and 18. Types 6 and 11 are responsible for about 90% of anogenital warts, while types 16 and 18 are high-risk oncogenic types associated with anogenital cancers. In October 2009, a bivalent HPV vaccine that provides protection against types 16 and 18 was licensed for use in females aged 10–25 years.

Sentinel surveillance for cervical infection with high-risk HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, or 68 was conducted in 26 STD, family planning, and primary care clinics in 6 locations (Boston, Baltimore, New Orleans, Denver, Seattle, and Los Angeles) as part of an effort to estimate national burden of disease and guide prevention efforts, such as vaccine programs, in the United States. Testing was performed using a commercially available test for high-risk HPV DNA (Hybrid Capture 2, Qiagen).

Results during 2003–2005 documented an overall high-risk HPV prevalence of 23%. Prevalence was 27% in STD clinics, 26% in family planning clinics, and 15% in primary care clinics. Prevalence by age group was 35% in women aged 14–19 years, 29% in those aged 20–29, 13% in those aged 30–39, 11% in those aged 40–49, and 6% in those aged 50–65.3

National population-based data were obtained from NHANES to examine the prevalence of both high-risk HPV and low-risk HPV—including types 6 and 11—in the civilian, non-institutionalized female population during 2003–2006 (Figure 52). HPV detection and typing were performed using the Research Use Only Linear Array genotyping assay (Roche Diagnostics), resulting in higher HPV prevalence than previously reported for NHANES 2003–2004 data. The overall HPV prevalence of high- and low-risk types was 42.5% (95% confidence interval [CI]: 40.3–44.7) among females aged 14–59 years.4 HPV vaccine-preventable low-risk types 6 or 11 or high-risk types 16 or 18 were detected in 8.8% of female participants: HPV-6 in 2.8% (95% CI: 2.2–3.6), HPV-11 in 0.3% (95% CI: 0.2–0.7), HPV-16 in 4.7% (95% CI: 4.0–5.5), and HPV-18 in 1.9% (95% CI: 1.4–2.5).5

Data from the National Disease and Therapeutic Index (NDTI) suggest that incidence of genital warts (Figure 53, Table 44), as measured by initial visits to physicians’ offices, may be increasing. NHANES data for 1999–2004 indicated that 5.6% (95% CI: 4.9–6.4) of sexually active adults aged 18–59 years self-reported a history of a genital wart diagnosis.6

For data reported in Figure 54, enhanced behavioral and demographic information on patients who presented for care in 2011 at the 42 clinics participating in the STD Surveillance Network (SSuN) was used. Genital warts were identified by provider diagnosis or by documentation from the physical examination. Men who have sex with men (MSM) and men who have sex with women only (MSW) were defined by self-report or by sex of reported sex partners. More detailed information about SSuN methodology can be found in the STD Surveillance Network section of the Appendix, Interpreting STD Surveillance Data. The prevalence of genital warts in 2011 is presented separately for MSM, MSW, and women by SSuN site. Prevalence was lowest in women for all sites. Among women the median prevalence of genital warts was 1.7% (range 1.0% to 2.7%) across all sites compared to 5.5% (range 2.3% to 8.1%) for MSM and 5.8% (range 2.0% to 11.0%) for MSW.

Pelvic Inflammatory Disease

For data on PID, see Special Focus Profiles, STDs in Women and Infants.

Herpes Simplex Virus

Case reporting data for genital herpes simplex virus (HSV) are not available. Trend data are based on estimates of initial visits in physicians’ offices for this condition from the NDTI (Figure 55, Table 44).

National trend data on the seroprevalence of HSV-2 among those aged 14–49 years from NHANES 2005–2008 were compared with NHANES survey years 1988–1994 and 1999–2004. Seroprevalence decreased from 21.0% (95% CI: 19.1–23.1) in 1988–1994 to 17.0% (95% CI: 15.8–18.3) in 1999–2004 and 16.2% (95% CI: 14.6–17.9) in 2005–2008. These data, along with data from NHANES survey years 1976–1980, indicate that blacks had higher seroprevalence than whites for each survey period and age group (Figure 56).

Although HSV-2 seroprevalence is decreasing, most persons with HSV-2 have not received a diagnosis. During 2005–2008, the percentage of NHANES survey participants aged 20–49 years infected with HSV-2 who reported a diagnosis of genital herpes was 18.9%. An overall increase in the number of visits for genital herpes over time, as suggested by NDTI data, may indicate increased recognition of infection.


Trend data for this infection are limited to estimates of initial physician office visits from the NDTI (Figure 57, Table 44). NHANES data from 2001–2004 indicated an overall prevalence of 3.1% (95% CI: 2.3–4.3), with the highest prevalence observed among blacks (13.3%) (95% CI: 10.0–17.7).7

1 Schulte JM, Martich FA, Schmid GP. Chancroid in the United States, 1981–1990: evidence for underreporting of cases. MMWR Morb Mortal Wkly Rep. 1992;41(No. SS-3):57-61.

2 Mertz KJ, Trees D, Levine WC, Lewis JS, Litchfield B, Pettus KS, et al. Etiology of genital ulcers and prevalence of human immunodeficiency virus coinfection in 10 US cities. J Infect Dis. 1998;178:1795-8.

3 Datta SD, Koutsky L, Ratelle S, Unger ER, Shlay J, McClain T, et al. Human papillomavirus infection and cervical cytology in women screened for cervical cancer in the United States, 2003–2005. Ann Intern Med. 2008;148(7):493-500.

4 Hariri S, Unger ER, Sternberg M, Dunne EF, Swan D, Patel S, et al. Prevalence of genital human papillomavirus among females in the United States, the National Health and Nutrition Examination Survey, 2003–2006. J Infect Dis. 2011; 204(4):566-73.

5 Dunne EF, Sternberg M, Markowitz LE, McQuillan G, Swan D, Patel S, et al. Human papillomavirus (HPV) 6, 11, 16 and 18 prevalence among females in the United States-National Health and Nutrition Examination Survey, 2003–2006: opportunity to measure HPV vaccine impact? J Infect Dis. 2011;204(4):562-5.

6 Dinh TH, Sternberg M, Dunne EF, Markowitz LE. Genital warts among 18- to 59-year-olds in the United States, National Health and Nutrition Examination Survey, 1999–2004. Sex Transm Dis. 2008;35(4):357-60.

7 Sutton M, Sternberg M, Koumans EH, McQuillan G, Berman, S, Markowitz LE. The prevalence of Trichomonas vaginalis infection among reproductive-age women in the United States, 2001–2004. Clin Infect Dis. 2007;45(10):1319-26.