Chancroid is caused by anogenital infection with the bacterium Haemophilus ducreyi. Clinical manifestations of chancroid include anogenital ulcers, and inguinal lymphadenopathy or buboes in up to 50% of cases.1 Reported cases of chancroid peaked in 1947 and then declined rapidly through 1957, presumably due to the increasing use of antibiotics such as sulfonamides and penicillin, which were introduced in the late 1930s and early 1940s (Figure 50, Table 1).2,3 Numerous localized outbreaks, some of which were linked to commercial sex work, were identified during 1981–1990.4,5 Chancroid has declined since 1987, and since 2000, the annual number of reported cases has been less than 100. During 2008–2017, the number of reported cases has fluctuated, ranging from 28 in 2009 to six in 2014. In 2017, a total of seven cases of chancroid were reported in the United States. Five states reported one or more cases of chancroid in 2017 (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 H. ducreyi is difficult to culture and no molecular assays have been cleared by the Food and Drug Administration (FDA) for use in the United States.6
Human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.7 Over 40 distinct HPV types can infect the genital tract;8 although most infections are asymptomatic and appear to resolve spontaneously within a few years.9 Prevalence of genital infection with any HPV type was 42.5% among United States adults aged 18–59 years during 2013–2014.10 Persistent infection with some HPV types can cause cancer and genital warts.11 HPV types 16 and 18 account for approximately 66% of cervical cancers in the United States,12 and approximately 25% of low-grade and 50% of high-grade cervical intraepithelial lesions, or dysplasia.13,14 HPV types 6 and 11 are responsible for approximately 90% of genital warts.15,16
Quadrivalent HPV vaccine, which targets HPV types 6, 11, 16, and 18,11 was licensed in the United States in mid-2006 for females17 and in late 2009 for males.18 Although a bivalent vaccine was also licensed for females,19 almost all HPV vaccine administered in the United States through late 2014 was quadrivalent.20 A 9-valent vaccine, which protects against the quadrivalent and 5 additional oncogenic HPV types (types 31, 33, 45, 52, and 58), was licensed in late 2014 for males and females.21 All HPV vaccines have been recommended for routine use in United States females aged 11–12 years, with catch-up vaccination through age 26.17,21 Since late 2011, routine use of the quadrivalent or 9-valent vaccine has been recommended for males aged 11–12, with catch-up vaccination through age 21.21-23 Vaccination through age 26 is recommended for gay, bisexual, and other men who have sex with men (collectively referred to as MSM) and persons who are immunocompromised (including those infected with HIV).21-23
HPV vaccine uptake in the United States remains lower than the Healthy People 2020 goal of 80% coverage.24 In 2016, a national survey found that 65% of girls aged 13–17 years had received at least one dose of the HPV vaccine, and 50% had received all doses in the series25 based on recommendations published in late 2016.23 HPV vaccine uptake is lower among boys; 56% of those aged 13–17 years received at least one dose, but only 38% received all recommended doses.25
HPV infection is not a nationally notifiable condition. Cervicovaginal prevalence of any quadrivalent HPV vaccine type was estimated using data for females aged 14–34 years from the National Health and Nutrition Examination Survey (NHANES; see Section A2.4 in the Appendix).26 Prevalence decreased significantly from 2003–2006 (the pre-vaccine era) to 2011–2014 in specimens from females aged 14–19 years (from 11.5% to 3.3%) and 20–24 years (from 18.5% to 7.2%); these are the age groups most likely to benefit from HPV vaccination. Among women aged 25–34 years, vaccine-type HPV prevalence did not differ significantly between the two time periods. An NHANES analysis of 2013–2014 HPV prevalence from penile swab specimens found low prevalence of quadrivalent HPV vaccine types in young males, which the authors attributed to male vaccination and/or herd protection from female vaccination.27
Health-care claims data from adolescents and adults with employer-provided private health insurance in the United States were used to examine the population effectiveness of HPV vaccination on clinical sequelae of HPV infection. Annual prevalence of high-grade histologically-detected cervical intraepithelial neoplasia grades 2 and 3 (CIN2+) during 2007–2014 was estimated using claims from 9 million females aged 15–39 years who received cervical cancer screening in a given calendar year.28 Prevalence of CIN2+ decreased significantly in females aged 15–19 and 20–24 years (Figure 51). Among those aged 15–19 years, annual percent change (APC) in CIN2+ prevalence was -19.8% during 2007–2009 and -12.1% during 2009–2014. For women aged 20–24 years, APC was -6.7% during 2007–2012, and -12.5% during 2012–2014. No decreases in CIN2+ prevalence were observed among women aged 25–39 years. The observed decreases in high-grade cervical lesions only among young women provide ecologic evidence of population effectiveness of HPV vaccination on clinical sequelae of infection among privately-insured women in the United States.
Prevalence of anogenital warts was examined using health-care claims of privately-insured females and males aged 15–39 years during 2006–2014 (Figures 52A and 52B).29 Prevalence among adolescent females aged 15–19 years declined non-significantly during 2006–2008, and then significantly decreased (APC=-14.1) through 2014. Among women aged 20–24 years, genital wart prevalence was stable during 2006–2009, but declined significantly during 2009–2014 (APC=-12.9). Prevalence among women aged 25–29 years also decreased significantly from 2009–2014 (APC=-6.0). Prevalence increased or was stable during the entire period for women aged 30–39 years. These declines in genital wart prevalence among females aged 15–29 years extend the observations of a previous study using claims from 2003 through 2010, in which decreased prevalence was found only among adolescent females aged 15–19 years.30 The observed declines in prevalence among increasingly older age groups would be expected from including more years of observation after the initiation of routine HPV vaccination for females in 2006. Among males, anogenital wart prevalence increased significantly during 2006–2009 for all age groups except those aged 15–19 years.29 From 2009 to 2014, rates decreased somewhat among male adolescents aged 15–19 years (APC=-5.4), but decreased significantly among men aged 20–24 years (APC=-6.5). Among those aged 25–29 years, prevalence declined non-significantly during 2010–2014 (APC=-1.7); prevalence increased or was stable throughout the entire period for men aged 30–39 years. The decreased prevalence observed among men aged 20–24 years is unlikely to be due to male vaccination for several reasons. Almost all men in this age group were aged 19 years or older since 2011, when HPV vaccine was first recommended for routine use in United States males22 and vaccination coverage in adult males through 2014 was extremely low.31 Also, the most likely sexual partners for men in this age group were females of a similar age or younger;32,33 therefore, the observed declines in genital wart prevalence among young men are consistent with herd protection from vaccination among females.
Pelvic Inflammatory Disease
For information 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 of sexually transmitted infections.7,34 Although most infections are subclinical,35 clinical manifestations are characterized by recurrent, painful genital and/or anal lesions.36 Most genital HSV infections in the United States are caused by HSV type 2 (HSV-2), while HSV type 1 (HSV-1) infections are typically orolabial and acquired during childhood;35,37 however, the prevalence of genital HSV-1 infections appears to be increasing among young adults.38,39
Genital HSV infection is not a nationally notifiable condition. Most persons with genital HSV infection have not received a diagnosis.40 The overall percentage of HSV-2 seropositive NHANES participants aged 14–49 years who reported never being told by a doctor or healthcare 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).40
NHANES data indicate the seroprevalence of HSV-2 in the United States has decreased from 1999–2000 to 2015–2016; age standardized seroprevalence declined from 18.0% in 1999–2000 to 2.1% in 2015–2016 (Figure 53).41 Although these declines were observed among all race and Hispanic ethnicity groups, HSV-2 seroprevalence was highest among non-Hispanic Blacks throughout the entire time period.
NHANES data also show that among adolescents aged 14–19 years, HSV-1 seroprevalence has significantly decreased by almost 23%, from 39.0% during 1999–2004 to 30.1% during 2005–2010, indicating declining orolabial infection in this age group.37 HSV-2 seroprevalence in this age group was much lower, less than 2% in both time periods.37 Other studies have found that genital HSV-1 infections are increasing among young adults.38,39 This has been attributed, in part, to the decline in orolabial HSV-1 infections, because those who lack HSV-1 antibodies at sexual debut are more susceptible to genital HSV-1 infection.37,42 Increasingly common oral sex behavior among adolescents and young adults also has been suggested as a contributing actor.37,43 The absence of HSV-1 antibodies also increases the likelihood of developing symptomatic disease from newly-acquired (i.e., primary) genital HSV-2 infection.44 Young women may therefore be increasingly likely to first acquire HSV-1 infection genitally, or acquire a primary genital HSV-2 infection, during their childbearing years,42,45 and first-episode primary genital HSV infection during pregnancy increases the risk of neonatal HSV transmission.42,46 A recent analysis of NHANES data found that among pregnant women with three or fewer lifetime sex partners, seronegativity for both HSV-1 and HSV-2 increased from 1999–2006 to 2007–2014.47 This raises the possibility that pregnant women with fewer sex partners may have increased risk of acquiring genital HSV during pregnancy and vertically transmitting HSV to their neonates.
For information on neonatal HSV infections, see Special Focus Profiles, STDs in Women and Infants.
Trichomonas vaginalis is a common sexually transmitted protozoal infection associated with adverse health outcomes such as preterm birth and symptomatic vaginitis.7,48-50 It is not a nationally notifiable condition, and trend data are limited to estimates of initial physician office visits for this condition from the National Disease and Therapeutic Index (NDTI; see Section A2.5 in the Appendix) (Figure 54, Table 44). Visits appear to be fairly stable since the 1990’s; the number of initial visits for T. vaginalis infection in 2016 was 222,000. The 2017 NDTI data were not obtained in time to include them in this report. NHANES data during 2013–2014 indicated prevalence of T. vaginalis in urine specimens obtained from adult participants aged 18–59 years was 0.5% among males and 1.8% among females; highest prevalences were observed among non-Hispanic Black males (4.2%) and females (8.9%).49 A separate analysis of NHANES data during 2013–2016 among men aged 18–59 years found higher prevalence among non-Hispanic Blacks.50 An analysis of NHANES data during 2001–2004 from cervicovaginal swab specimens also found higher T. vaginalis prevalence among non-Hispanic Black females.51
9. Insinga RP, Perez G, Wheeler CM, et al. Incident cervical HPV infections in young women: Transition probabilities for CIN and infection clearance. Cancer Epidemiol Biomarkers Prev 2011; 20(2):287–296.
10. McQuillan G, Kruszon-Moran D, Markowitz LE, et al. Prevalence of HPV in adults aged 18–69: United States, 2011–2014. NCHS Data Brief, No. 280. Hyattsville, MD: National Center for Health Statistics; 2017.
13. Clifford GM, Rana RK, Franceschi S, et al. Human papillomavirus genotype distribution in low-grade cervical lesions: Comparison by geographic region and with cervical cancer. Cancer Epidemiol Biomarkers Prev 2005; 14(5):1157–1164.
14. Porras C, Rodriguez AC, Hildesheim A, et al. Human papillomavirus types by age in cervical cancer precursors: Predominance of human papillomavirus 16 in young women. Cancer Epidemiol Biomarkers Prev 2009; 18(3):863–865.
15. Garland SM, Steben M, Sings HL, 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.
16. Gissmann L, Wolnik L, Ikenberg H, et al. 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.
17. Markowitz LE, Dunne EF, Saraiya M, et al. Quadrivalent human papillomavirus vaccine. Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep Recomm Rep 2007; 56(RR-2):1–24.
18. 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.
19. 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.
20. Stokley S, Jeyarajah J, Yankey D, 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):620–624.
21. Petrosky E, Bocchini Jr. JA, Hariri S, 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.
22. 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):1705–1708.
23. Meites E, Kempe A, Markowitz LE. Use of a 2-dose schedule for human papillomavirus vaccination — updated recommendations of the Advisory Committee on Immunization Practices. MMWR Morb Mortal Wkly Rep 2016; 65(49):1405–1408.
24. HealthyPeople.gov. Healthy People 2020 Topics & Objectives. Immunization and Infectious Diseases. Objectives IID-11.4 and IID-11.5. Available at: https://www.healthypeople.gov/2020/topics-objectives/topic/immunization-and-infectious-diseases/objectivesExternal. Accessed March 29, 2018.
25. Walker TY, Elam-Evans LD, Singleton JA, et al. National, regional, state, and selected local area vaccination coverage among adolescents aged 13–17 years — United States, 2016. MMWR Morb Mortal Wkly Rep 2017; 66(33):874–882.
26. Oliver SE, Unger ER, Lewis R, et al. Prevalence of human papillomavirus among females after vaccine introduction — National Health and Nutrition Examination Survey, United States, 2003–2014. J Infect Dis 2017; 216(5):594–603.
28. Flagg EW, Torrone EA, Weinstock H. Ecological association of human papillomavirus vaccination with cervical dysplasia prevalence in the United States, 2007–2014. Am J Public Health 2016; 106(12):2211–2218.
29. Flagg EW, Torrone EA. Declines in anogenital warts among age groups most likely to be impacted by human papillomavirus vaccination, United States, 2006–2014. Am J Public Health 2018; 108(1):112–119.
30. 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.
38. Bernstein DI, Bellamy AR, Hook EW III, et. al. Epidemiology, clinical presentation, and antibody response to primary infection with herpes simplex virus type 1 and type 2 in young women. Clin Infect Dis 2013; 56:344–351.
40. Fanfair RN, Zaidi A, Taylor LD, et al. 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):860–864.
41. McQuillan G, Kruszon-Moran D, Flagg EW, et al. Prevalence of herpes simplex virus type 1 and type 2 in persons aged 14–49: United States, 2015–2016. NCHS Data Brief, No. 304. Hyattsville, MD: National Center for Health Statistics. 2018.
43. Copen CE, Chandra A, Martinez G. Prevalence and timing of oral sex with opposite-sex partners among females and males aged 15–24 years: United States, 2007–2010. National Health Statistics Reports, No. 56. Hyattsville, MD: National Center for Health Statistics; 2012.
47. Patton ME, Bernstein K, Liu G, et al. Seroprevalence of herpes simplex virus types 1 and 2 among pregnant women and sexually active, non-pregnant women in the United States. Clin Infect Dis 2018; https://doi.org/10.1093/cid/ciy318.