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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This web page is archived for historical purposes and is no longer being updated.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.


Reported cases of chancroid declined steadily between 1987 and 2001. Since then, the number of reported cases has fluctuated (Figure 44, Table 1). In 2012, a total of 15 cases of chancroid were reported in the United States. Only eight states reported one or more cases of chancroid in 2012 (Table 44).

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; as a result, this condition may be substantially underdiagnosed.1,2

Human Papillomavirus

In June 2006, a quadrivalent HPV vaccine was licensed for use in the United States in females aged 9–26 years;3 in October 2009, this vaccine also was licensed for use in males aged 9–26 years.4 This vaccine provides protection against HPV types 6, 11, 16, and 18. HPV 6 and 11 are responsible for about 90% of anogenital warts,5,6 while HPV 16 and 18 are high-risk oncogenic types that cause approximately 70% of cervical cancers worldwide.7,8 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.9

HPV vaccine uptake in the US is relatively low. In 2012, a national survey found that 54% of girls aged 13-17 years had received at least 1 dose of the HPV vaccine series, but only 33% had received all 3 doses in the series.10 Vaccine uptake is very low among boys.11

Sentinel surveillance for cervical infection with highrisk HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, or 68 was conducted from 2003 through 2005 in 26 STD, family planning, and primary care clinics in 6 locations (Boston, Baltimore, New Orleans, Denver, Seattle, and Los Angeles). Testing was performed using a commercially available test for highrisk HPV DNA (Hybrid Capture 2, Qiagen). Overall prevalence of high-risk HPV was 23% (95% confidence interval [CI]: 22-24). Age- and city-adjusted prevalence was 26% (95% CI: 24-29) in STD clinics, 24% (95% CI: 22-26) in family planning clinics, and 17% (95% CI: 16-20) in primary care clinics. Prevalence by age group was 35% (95% CI: 32-38) in women aged 14–19 years, 29% (95% CI: 28-30) in those aged 20–29, 13% (95% CI: 12-15) in those aged 30–39, 11% (95% CI: 9-13) in those aged 40–49, and 6% (95% CI: 4-8) in those aged 50–65.12

National population-based data were obtained from NHANES to examine the prevalence of both high-risk HPV and low-risk HPV in the civilian, non-institutionalized female population during 2003–2006 (Figure 45). 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 prevalence of high- and low-risk HPV was 42.5% (95% CI: 40.3–44.7) among females aged 14–59 years.13 HPV vaccine-preventable low-risk types 6 or 11 or highrisk 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).14 Prevalence of quadrivalent vaccine-type HPV decreased from 11.5% (95% CI: 9.2-14.4) in 2003-2006 to 5.1% (95% CI: 3.8-6.6) in 2007-2010 among females aged 14-19 years, the age group most likely to be affected by introduction of the HPV vaccine, despite low vaccine uptake.15

Data from the National Disease and Therapeutic Index (NDTI) suggest that cases of genital warts (Figure 46, Table 45), as measured by initial visits to physicians’ offices, may have increased during the late 1990s through 2011; although cases appear to have decreased in 2012, more years of data are needed to discern whether genital warts are declining. Prevalence of genital warts in a large US cohort of individuals with private health insurance significantly declined in 2007 to 2010 among girls aged 15-19.16 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.17

For data reported in Figure 47, enhanced behavioral and demographic information on patients who presented for care in 2012 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 2012 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 1.6% (range 0.5 to 2.3) across all sites compared to 4.8% (range 2.5 to 7.4) for MSM and 6.0% (range 1.9 to 9.5) for MSW.

Pelvic Inflammatory Disease

For data on pelvic inflammatory disease, 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 to physicians’ offices for this condition from the NDTI (Figure 48, Table 45).

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 1988–199418 to 17.0% (95% CI: 15.8–18.3) in 1999–200418 and 16.2% (95% CI: 14.6–17.9) in 2005–2008.19 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 49).

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%.19 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 50, Table 45). 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).20

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(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(6):1795-1798.

3 Markowitz LE, Dunne EF, Saraiya M, Lawson HW, Chesson H, Unger ER. Quadrivalent human papillomavirus vaccine. Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep. 2007;56(RR02):1-24.

4 Centers for Disease Control and Prevention. FDA licensure of quadrivalent human papillomavirus vaccine (HPV4, Gardasil) for use in males and guidance from the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep. 2010;59(20):630-632.

5 Garland SM, Steben M, Sings HL, James M, Lu S, Railkar R, et al. Natural history of genital warts: analysis of the placebo arm of 2 randomized phase III trials of a quadrivalent human papillomavirus (types 6, 11, 16, and 18) vaccine. J Infect Dis. 2009;199(6):805-814.

6 Gissmann L, Wolnik L, Ikenberg H, Koldovsky U, Schnurch HG, zur Hausen H. Human papillomavirus types 6 and 11 DNA sequences in genital and laryngeal papillomas and in some cervical cancers. Proc Natl Acad Sci USA. 1983;80(2):560-563.

7 Clifford GM, Smith JS, Plummer M, Munoz N, Franceschi S. Human papillomavirus types in invasive cervical cancer worldwide: a meta-analysis. Br J Cancer. 2003;88(1):63-73.

8 Bosch FX, Manos MM, Munoz N, Sherman M, Jansen AM, Peto J, et al. Prevalence of human papillomavirus in cervical cancer: a worldwide perspective. J Natl Cancer Inst. 1995;87(11):796-802.

9 Centers for Disease Control and Prevention. FDA licensure of bivalent human papillomavirus vaccine (HPV2, Cervarix) for use in females and updated HPV vaccination recommendations from the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep. 2010;59(20):626-629.

10 Centers for Disease Control and Prevention. Human papillomavirus vaccination coverage among adolescent girls, 2007–2012, and postlicensure vaccine safety monitoring, 2006–2013 - United States. MMWR Morb Mortal Wkly Rep. 2013;62(29):591-595.

11 Centers for Disease Control and Prevention. National and state vaccination coverage among adolescents aged 13–17 years - United States, 2011. MMWR Morb Mortal Wkly Rep. 2012;61(34):671-677.

12 Datta SD, Koutsky LA, 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.

13 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):566-573.

14 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):562-565.

15 Markowitz LE, Hariri S, Lin C, Dunne EF, Steinau M, McQuillan G, et al. Reduction in human papillomavirus (HPV) prevalence among young women following HPV vaccine introduction in the United States, National Health and Nutrition Examination Surveys, 2003–2010. J Infect Dis. 2013;208(3):385-393.

16 Flagg EW, Schwartz R, Weinstock H. Prevalence of anogenital warts among participants in private health plans in the United States, 2003–2010: potential impact of human papillomavirus vaccination. Am J Public Health. 2013;103(8):1428-1435.

17 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):357-360.

18 Xu F, Sternberg MR, Kottiri BJ, McQuillan GM, Lee FK, Nahmias AJ, et al. Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA. 2006;296(8):964- 973.

19 Centers for Disease Control and Prevention. Seroprevalence of herpes simplex virus type 2 among persons aged 14 49 years - United States, 2005–2008. MMWR Morb Mortal Wkly Rep. 2010;59(15):456-459.

20 Sutton M, Sternberg M, Koumans EH, McQuillan G, Berman S, Markowitz L. The prevalence of Trichomonas vaginalis infection among reproductive-age women in the United States, 2001–2004. Clin Infect Dis. 2007;45(10):1319-1326.