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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This web page is archived for historical purposes and is no longer being updated.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 47, Table 1). In 2009, a total of 28 cases of chancroid were reported in the United States. Only nine states reported one or more cases of chancroid in 2009 (Table 42).

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. The vaccine provides protection against HPV types 6, 11, 16, and 18. Types 6 and 11 are associated with genital 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 also was licensed.

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 by using a commercially available test for high-risk HPV DNA (Hybrid Capture 2, Digene, Gaithersburg, Maryland).

Results during 2003–2005 document 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 those aged 14–19 years, 29% in those aged 20–29 years, 13% in those aged 30–39 years, 11% in those aged 40–49 years, and 6.3% in those aged 50–65 years.3

National population-based data also were obtained from NHANES to examine the prevalence of both high-risk HPV and low-risk HPV—including types 6 and 11, which are responsible for about 90% of anogenital warts—in the civilian, noninstitutionalized female population during 2003–2004 (Figure 48). The overall HPV prevalence of high- and low-risk types was 26.8% (95% confidence interval [CI]: 23.3–30.9) among U.S. females aged 14–59 years. HPV vaccine-preventable types 6 or 11 (low-risk types) or 16 or 18 (high-risk types) were detected in 3.4% of female participants: HPV-6 in 1.3% (95% CI: 0.8–2.3), HPV-11 in 0.1% (95% CI: 0.03–0.3), HPV-16 in 1.5% (95% CI: 0.9–2.6), and HPV-18 in 0.8% (95% CI: 0.4–1.5).4

Data from the National Disease and Therapeutic Index (NDTI) suggest that incidence of genital warts (Figure 49), 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.5

For data reported in Figure 50, enhanced behavioral and demographic information on patients who presented for care in 2009 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 2009 is presented separately for MSM, MSW, and women by SSuN site. With few exceptions, prevalence was lowest in women for most sites and ranged from 1.0% to 4.0%. Prevalence was higher or similar among MSM compared with MSW in Seattle, Denver, New Orleans, Baltimore, and Philadelphia. Prevalence at these sites ranged from 3.6% to 8.0% for MSM and from 2.3% to 8.6% for MSW. Prevalence was higher in MSW compared with MSM in the remaining areas (San Francisco, Los Angeles, Chicago, and Richmond), ranging from 4.6% to 7.0% for MSW and 1.5% to 5.9% for MSM.

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 these conditions from the NDTI (Figure 51, Table 43).

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% (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 52). During 2005–2008, the percentage of NHANES survey participants aged 20–49 years who reported a diagnosis of genital herpes was 18.9%.

Although HSV-2 seroprevalence is decreasing, most persons with HSV-2 have not received a diagnosis. An increase in the number of visits for genital herpes, as suggested by NDTI data, may indicate increased recognition of infection.


Case reporting data are not available for trichomoniasis, and trend data for this infection are limited to estimates of initial physician office visits from NDTI (Figure 53, Table 43). 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).6

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 Dunne EF, Unger ER, Sternberg M, McQuillan G, Swan DC, Patel SS, et al. Prevalence of HPV infection among females in the United States. JAMA. 2007;297(8):813-9.

5 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.

6 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.