Other Sexually Transmitted Diseases

Chancroid

Reported cases of chancroid declined steadily between 1987 and 2001. Since then, the number of reported cases has fluctuated (Figure 46, Table 1). In 2013, a total of 10 cases of chancroid were reported in the United States. Only 4 states reported one or more cases of chancroid in 2013 (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

Human papillomavirus (HPV) is the most common sexually transmitted infection.³Over 40 distinct types can infect the genital tract;⁴ about 90% of infections are asymptomatic and resolve spontaneously within 2 years.⁵ However, persistent infection with some HPV types can cause cancer and other benign diseases. Of the 13 HPV types designated as human carcinogens, types 16 and 18 account for 70% of cervical cancers worldwide.^6,7Among non-carcinogenic types, types, HPV 6 and 11 are responsible for 90% of genital warts.^8,9

A quadrivalent HPV vaccine that targets HPV 6, 11, 16 and 18 has been licensed in the United States for use in females aged 9–26 years since June 2006,¹⁰ and in males aged 9–26 years since October 2009.¹¹ In October 2009, a bivalent HPV vaccine against HPV 16 and 18 was licensed for use in females aged 10–25 years.¹² Routine vaccination with either vaccine is recommended for females aged 11 or 12 years, and through age 26 years for those not previously vaccinated.¹²The quadrivalent vaccine is recommended for routine use in males aged 11 or 12 years and through age 21 years for those not previously vaccinated.¹³

HPV vaccine uptake in the U.S. remains lower than the Healthy People 2020 goal of 80% coverage.¹⁴ In 2013, a national survey found that 57% of girls aged 13–17 years had received at least 1 dose of the HPV vaccine series, but only 38% had received all 3 doses in the series.¹⁵ Vaccine uptake is much lower among boys.¹⁵

National population-based data were obtained from the National Health and Nutrition Examination Survey (NHANES) 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% CI: 40.3–44.7) among females aged 14–59 years.¹⁶ Prevalence varied significantly by age, peaking in young women 20–24 years of age (Figure 47). 

Despite low vaccine coverage in the U.S., 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 prevaccine 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 48). Among other age groups, vaccine-type HPV prevalence did not differ significantly between the 2 time periods.¹⁷

Data from the National Disease and Therapeutic Index (NDTI) suggest that cases of genital warts (Figure 49, 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.  Prevalence of genital warts in a large U.S. cohort of individuals with private health insurance significantly declined in 2007 through 2010 among girls aged 15–19 years. ¹⁸ 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 50).¹⁸ 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. 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.¹⁹

For data reported in Figures 51 and 52, enhanced behavioral and demographic information on patients who presented for care in 2013 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. Gay, bisexual, and other men who have sex with men (collectively referred to as MSM) and men who have sex with women only (MSW) were defined by self-report or by sex of reported sex partners. For more detailed information about SSuN methodology, see the Appendix.  Between 2010 and 2013, 57,974 (4.6%) patients aged 12–82 years in the SSuN clinics were diagnosed with genital warts; among those patients, 17.0% were women, 20.5% were MSM and 62.5% were MSW.  In 2013, the prevalence of diagnosed genital warts among MSM was 3.0 times that of women and the prevalence among MSW was 4.0 times that of women, with similar male:female ratios for all years (Figure 51). MSW had a higher prevalence of genital warts compared to MSM across all years; during this time period, prevalence among MSW increased (6.8% to 7.4%), while prevalence among MSM decreased (6.3% to 5.5%). The proportion of women diagnosed with genital warts decreased slightly over time, from 1.9% in 2010 to 1.6% in 2013 (Figure 51). The prevalence of genital warts in 2013 is presented separately for MSM, MSW, and women by SSuN site in Figure 52. Among women the median prevalence of genital warts was 1.4% (range 0.4 to 2.7) across all sites, compared to 3.8% (range 1.2 to 5.8) for MSM and 5.0% (range 1.9 to 8.5) 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. Data on initial visits to physicians’ offices for this condition are available from NDTI (Figure 53, Table 45).

National trend data on the gender-specific seroprevalence of HSV-2 among those aged 14–49 years from 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%.²⁰ 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). These data, along with data from NHANES survey years 1976–1980,²¹ 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).²⁰ However, an overall increase in the number of visits for genital herpes over time, as suggested by NDTI data, may indicate increased recognition of infection.

Neonatal HSV Infections, although relatively rare, cause significant morbidity and mortality.  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 2006.²² 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).

Trichomoniasis

Trend data for this infection are limited to estimates of initial physician office visits from the NDTI (Figure 55, Table 45). 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).²³

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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):1795–8.

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

4  Bouvard V, Baan R, Straif K, Grosse Y, Secretan B, El Ghissassi F, et al. A review of human carcinogens — part B: biological agents. Lancet Oncol. 2009;10:321–2.

5  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.

6 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.

7 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.

8 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.

9 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.

10 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.

11 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.

12 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.

13 Centers for Disease Control and Prevention. Recommendations on the use of quadrivalent human papillomavirus vaccine in males — Advisory Committee on Immunization Practices (ACIP), 2011. MMWR Morb Mortal Wkly Rep. 2011;60(50):1705–8.

14 HealthyPeople.gov. 2020 Topics & Objectives. Immunization and Infectious Diseases. Objectives. IID-11.4. Increase the vaccination coverage level of 3 doses of human papillomavirus (HPV) vaccine for females by age 13 to 15 years. https://www.healthypeople.gov/2020/topics-objectives/topic/immunization-and-infectious-diseases/objectives, Accessed August 26, 2015.

15 Stokley S, Jeyarajah J, Yankey D, Cano M, Gee J, Roark J, et al. Human papillomavirus vaccination coverage among adolescents, 2007–2013, and postlicensure vaccine safety monitoring, 2006–2014 — United States. MMWR Morb Mortal Wkly Rep. 2014;63(29):620–4.

16 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.

17 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.

18 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.

19 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.

20 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.

21 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.

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

23 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.

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