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This web page is archived for historical purposes and is no longer being updated.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


Chancroid is caused by infection with the bacterium Haemophilus ducreyi. Clinical manifestations include genital ulcers and inguinal lymphadenopathy or buboes.1 Reported cases of chancroid declined steadily between 1987 and 2001. Since then, the number of reported cases has fluctuated somewhat, while still appearing to decline overall (Figure 47, Table 1). In 2014, a total of 6 cases of chancroid were reported in the United States. Only 3 states reported one or more cases of chancroid in 2014 (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 underdiagnosed.2,3

Human Papillomavirus

Human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.4 Over 40 distinct types can infect the genital tract;5 about 90% of infections are asymptomatic and resolve spontaneously within two years.6 However, persistent infection with some HPV types can cause cancer and genital warts. HPV types 16 and 18 account for approximately 70% of cervical cancers worldwide,7,8 while HPV 6 and 11 are responsible for approximately 90% of genital warts.9,10

A quadrivalent HPV vaccine that protects against HPV types 6, 11, 16 and 18 has been licensed in the United States for use in females since June 2006,11 and in males since October 2009.12 In October 2009, a bivalent HPV vaccine that protects against HPV types 16 and 18 was licensed for use in females.13 Either vaccine is recommended for routine use in females aged 11 or 12 years and in females who have not been vaccinated previously through age 26 years.11 The quadrivalent vaccine is recommended for routine use in males aged 11 or 12 years and is recommended through age 21 years for males who have not been vaccinated previously.11 Quadrivalent vaccination of gay, bisexual, and other men who have sex with men (collectively referred to as MSM) through age 26 is recommended; other males aged 22–26 years may also be vaccinated.11 Vaccination is recommended through age 26 years for immunocompromised persons (including those infected with HIV) who have not been vaccinated previously.11 In December 2014, a 9-valent vaccine that protects against the HPV types included in the quadrivalent vaccine, as well as five additional cancer causing types (HPV 31, 33, 45, 52, and 58), was licensed for use in the United States.14

HPV vaccine uptake in the United States remains lower than the Healthy People 2020 goal of 80% coverage.15 In 2014, a national survey found that 60% of girls aged 13–17 years had received at least 1 dose of the HPV vaccine, and 40% had received all 3 doses in the series.16 HPV vaccine uptake is lower among boys; 42% aged 13–17 years received at least 1 dose, but only 22% received all 3 doses.16

National population-based data were obtained from the National Health and Nutrition Examination Survey (NHANES; see Section A2.4 in the Appendix for more information) to examine the prevalence of HPV vaccine types in the civilian, non-institutionalized female population during 2003–2006. HPV detection and typing were performed on self-collected cervicovaginal swab samples using the Research Use Only Linear Array genotyping assay (Roche Diagnostics). In the pre-vaccine era (2003–2006), the overall prevalence of any HPV was 42.5% (95% Confidence Interval [CI]: 40.3–44.7) among females aged 14–59 years.17 Prevalence varied significantly by age, peaking in young women 20–24 years of age (Figure 48).

Despite low vaccine coverage in the United States, prevalence of quadrivalent HPV vaccine types 6, 11, 16, and/or 18 in cervicovaginal specimens decreased from 11.5% (95% CI: 9.2–14.4) in the pre-vaccine era (2003–2006) to 5.1% (95% CI: 3.8–6.6) in the vaccine era (2007–2010) among females aged 14–19 years, the age group most likely to benefit from HPV vaccination (Figure 49).18 Among other age groups, vaccine-type HPV prevalence did not differ significantly between the two time periods.

Data from the National Disease and Therapeutic Index (NDTI; see Section A2.5 in the Appendix for more information) suggest that cases of genital warts (Figure 50, Table 45), as measured by initial visits to physicians’ offices, may have increased during the late 1990s through 2011. Although the number of cases appears to have decreased in 2012 and 2013, compared to 2011, more years of data are needed to discern whether genital warts are declining, particularly since 2013 cases exceed those reported in 2012. The 2014 NDTI data were not obtained in time to include them in this report.

Prevalence of genital warts in a large United States cohort of individuals with private health insurance significantly declined in 2007 through 2010 among girls aged 15–19 years.19 Among women aged 20–24 years, genital wart prevalence, which had been increasing from 2003 through 2007, was stable from 2007 to 2009 and then decreased in 2010. Prevalence in women aged 25–29 increased through 2009, but decreases in genital warts were also observed for this group in 2010 (Figure 51).19 These declines are what would be expected several years after initiating routine HPV vaccination for girls aged 11 to 12 years, with catch-up vaccination through age 26 years. Although genital wart prevalence in women aged 30–34 and 35–39 years did not continue to increase between 2009 and 2010, more years of data are needed to interpret these observations, as well as the observed decline in prevalence in 2010 for men aged 20–24 years. The 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.20

For data reported in Figure 52, enhanced behavioral and demographic information on patients who presented for care in 2014 in the 6 jurisdictions that contributed data for all of 2014 to the STD Surveillance Network (SSuN) was used. See Section A2.2 in the Appendix for more information about the SSuN. Genital warts were identified by provider diagnosis or by documentation from the physical examination. MSM and men who have sex with women only (MSW) were defined by self-report or by sex of reported sex partners. The prevalence of genital warts in 2014 is presented separately for MSM, MSW, and women by SSuN jurisdiction in the figure. Among women the median prevalence of genital warts was 1.1% (range 0.8 to 2.3) across all jurisdictions, compared to 4.0% (range 2.9 to 4.7) for MSM and 4.9% (range 3.3 to 5.5) for MSW.

Pelvic Inflammatory Disease

For data on pelvic inflammatory disease, see Special Focus Profiles, STDs in Women and Infants.

Herpes Simplex Virus

Herpes simplex virus (HSV) is among the most prevalent sexually transmitted infections;4,21 although most infections are subclinical,22 clinical manifestations are characterized by recurrent, painful genital and/or anal lesions.23 Most genital herpes infections in the United States are caused by HSV-2; however genital HSV-1 infections are increasing among college students and other populations.24,25 Case reporting data for genital HSV are not available. Data on initial visits to physicians’ offices for this condition are available from the NDTI (Figure 53, Table 45), however, the 2014 NDTI data were not obtained in time to include them in this report.

National trend data on the gender-specific seroprevalence of HSV-2 among those aged 14–49 years from the NHANES were compared across survey years 1988–1994, 1999–2002, 2003–2006, and 2007–2010 (Figure 54). Overall, HSV-2 seroprevalence decreased between 1988–1994 and 2007–2010, from 21.2% to 15.5%.26 Among non-Hispanic white females, HSV-2 seroprevalence decreased from 19.5% (1988–1994) to 15.3% (2007–2010; P<0.001); HSV-2 seroprevalence remained stable among non-Hispanic black or African American (hereinafter referred to as black) females, from 52.5% (1988–1994) to 49.9% (2007–2010; P=0.1).26 These data, along with data from the NHANES survey years 1976–1980,27 indicate that blacks had higher seroprevalence than whites for each survey period and age group.

Although HSV-2 seroprevalence is decreasing, most persons with HSV-2 have not received a diagnosis. The overall percentage of HSV-2 seropositive NHANES participants who reported never being told by a doctor or health care professional that they had genital herpes did not change significantly between 1988–1994 and 2007–2010, and remained high (90.7% and 87.4%, respectively).26 However, an overall increase in the number of visits for genital herpes over time, as suggested by the NDTI data, may indicate increased use of serologic testing and increased recognition of infection.

Neonatal HSV infections, although relatively rare, cause significant morbidity and mortality.28 Most neonatal HSV infections result from vertical transmission from mother to neonate.29 An examination of inpatient records of infants aged 60 days or younger at admission using the Healthcare Cost and Utilization Project Kid’s Inpatient Database showed an overall incidence of 9.6 cases per 100,000 live births in 2006.30 Rates did not vary significantly by region or race/ethnicity; however, prevalence was significantly higher among cases for which the expected primary payer was Medicaid (15.1 per 100,000; 95% CI: 12.1–18.1) compared with private insurance or managed health care (5.4 per 100,000; 95% CI: 4.0–6.8).


Trichomonas vaginalis infection is a common sexually transmitted protozoal infection associated with adverse health outcomes such as preterm birth and symptomatic vaginitis.4,31,32 Trend data for this infection are limited to estimates of initial physician office visits from the NDTI (Figure 55, Table 45); however, the 2014 NDTI data were not obtained in time to include them in this report. The NHANES data from 2001–2004 indicated an overall trichomoniasis 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).32


1 Lewis DA. Chancroid: clinical manifestations, diagnosis, and management. Sex Transm Infect 2003;79:68-71.

2 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.

3 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):1795–8.

4 Satterwhite CL, Torrone E, Meites E, Dunne EF, Mahajan R, Banez Ocfemia MC, et al. Sexually transmitted infections among US women and men: prevalence and incidence estimates, 2008. Sex Transm Dis 2013;40(3):187–93.

5 de Villiers E-M, Fauquet C, Broker TR, Bernard H-U, zur Hausen H. Classification of papillomaviruses. Virol 2004;324:17–27.

6 Ho GYF, Bierman R, Beardsley L, Chang CJ, Burk RD. Natural history of cervicovaginal papillomavirus infection in young women. N Engl J Med 1998;338(7);423–8.

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 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):805–14.

10 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):560–3.

11 Markowitz LE, Dunne EF, Saraiya M, Chesson HW, Curtis CR, Gee J, et al. Human papillomavirus vaccination: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2014;63(RR05):1–30.

12 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):630–2.

13 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):626–9.

14 Petrosky E, Bocchini JA, Hariri S, Chesson H, Curtis CR, Saraiya M, et al. Use of 9-valent human papillomavirus (HPV) vaccine: updated HPV vaccination recommendations of the Advisory Committee on Immunization Practices. MMWR Morb Mortal Wkly Rep 2015;64(11):300–304.

15 Healthy People 2020 Topics & Objectives. Immunization and Infectious Diseases. Objective IID–11.4. Increase the vaccination coverage level of 3 doses of human papillomavirus (HPV) vaccine for females by age 13 to 15 years. Objective IID–11.5. Increase the vaccination coverage level of 3 doses of human papillomavirus (HPV) vaccine for males by age 13 to 15 years. Accessed November 12, 2015.

16 Reagan-Steiner S, Yankey D, Jeyarajah J, Elam-Evans LD, Singleton JA, Curtis CR, et al. National, regional, state, and selected local area vaccination coverage among adolescents aged 13–17 years — United States, 2014. MMWR Morb Mortal Wkly Rep 2015;64(29):784–92.

17 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.

18 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):385–93.

19 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):1428–35.

20 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.

21 Smith JS, Robinson NJ. Age-specific prevalence of infection with herpes simplex virus types 2 and 1: a global review. J Infect Dis 2002;186(Suppl 1):S3–S28.

22 Corey L, Wald A. Genital herpes. In: Holmes KK, Sparling FP, Stamm WE, et al, eds. Sexually Transmitted Diseases, 4th ed. New York, NY: McGraw-Hill; 2008:399-437.

23 Kimberlin DW, Rouse DJ. Clinical practice: genital herpes. N Engl J Med 2004;350(19):1970–7.

24 Lafferty WE, Downey L, Celum C, Wald A. Herpes simplex virus type 1 as a cause of genital herpes: impact on surveillance and prevention. J Infect Dis 2000;181(4):1454–7.

25 Roberts CM, Pfister JR, Spear SJ. Increasing proportion of herpes simplex virus type 1 as a cause of genital herpes infection in college students. Sex Transm Dis 2003;30(10):797–800.

26 Fanfair RN, Zaidi A, Taylor LD, Xu F, Gottlieb S, Markowitz L. Trends in seroprevalence of herpes simplex virus type 2 among non-Hispanic blacks and non-Hispanic whites aged 14 to 49 years — United States, 1988 to 2010. Sex Transm Dis 2013;40(11):860–4.

27 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):964–73.

28 Kimberlin DW. Herpes simplex virus infections of the newborn. Semin Perinatol 2007;31:19–25.

29 Corey L, Wald A. Maternal and neonatal herpes simplex virus infections. N Engl J Med 2009;361(14):1376–85.

30 Flagg EW, Weinstock H. Incidence of neonatal herpes simplex virus infections in the United States, 2006. Pediatrics 2011;172(1):e1–8.

31 French JI, McGregor JA, Parker R. Readily treatable reproductive tract infections and preterm birth among black women. Am J Obstet Gynecol 2006;194:1717–27.

32 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):1319–26.