Other STDs

Chancroid

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; since 2000, the annual number of reported cases has been less than 100, and since 2011, the annual number of reported cases has been less than 20. In 2018, only three cases of chancroid were reported in the United States (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

See text for description.

Human Papillomavirus

Human papillomavirus (HPV) is a 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 civilian, non-institutionalized adults aged 18–59 years in the United States during 2013–2014.10 Among sexually active non-Hispanic Whites and non-Hispanic Blacks, prevalence was significantly higher in males.11 Persistent infection with some HPV types can cause cancer and genital warts.12 HPV types 16 and 18 account for approximately 66% of cervical cancers in the United States,13 and approximately 25% of low-grade and 50% of high-grade cervical intraepithelial lesions, or dysplasia.14,15 HPV types 6 and 11 are responsible for approximately 90% of genital warts.16, 17

Quadrivalent HPV vaccine, which targets HPV types 6, 11, 16, and 18, was licensed in the United States in mid-2006 for females18 and in late 2009 for males.19  Although a bivalent vaccine was also licensed for females,20 almost all HPV vaccine administered in the United States through late 2014 was quadrivalent.21 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.22 All HPV vaccines have been recommended for routine use in United States females aged 11–12 years, with catch-up vaccination through age 26.18, 22 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;22-24 in June 2019, this age limit was extended to 26 years.25 Vaccination through age 26 has been recommended since late 2011 for gay, bisexual, and other men who have sex with men (MSM) and persons who are immunocompromised (including those infected with HIV).22-24  In October 2018, the FDA extended licensing approval of the 9-valent vaccine for women and men aged 27–45 years,26 and in June 2019 the CDC’s Advisory Committee on Immunization Practices (ACIP) recommended that unvaccinated adults aged 27–45 years discuss receiving the HPV vaccine with their health care providers.25

HPV vaccine uptake in the United States remains lower than the Healthy People 2020 goal of 80% coverage.27 A national survey conducted in 2018 found that 70% of girls aged 13–17 years had received at least one dose of the HPV vaccine, and 54% had received all doses in the series28 based on recommendations published in late 2016.24 Among boys, 66% of those aged 13–17 years received at least one dose and 49% received all recommended doses.28

A recent meta-analysis that included data from over 60 million individuals from 14 high-income countries, including the United States, showed a substantial impact of HPV vaccination on: genital HPV infections among adolescent girls and young women; high-grade cervical lesions among young women; and anogenital warts among adolescent boys and girls, and among young men and women.29 Although HPV infection is not a nationally notifiable condition in the United States, cervicovaginal prevalence of any quadrivalent HPV vaccine type has been estimated for civilian, non-institutionalized females aged 14–34 years using data from the National Health and Nutrition Examination Survey (NHANES; see Section A2.4 in the Appendix).30 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 were 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.31

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.32 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).33 Prevalence among adolescent females aged 15–19 years declined non-significantly during 2006–2008, and then significantly decreased through 2014 (APC=-14.1). Among women aged 20–24 years, anogenital 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 anogenital 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.34 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.33 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 males23 and vaccination coverage in adult males through 2014 was extremely low.35 Also, the most likely sexual partners for men in this age group were females of a similar age or younger;36, 37 therefore, the observed declines in anogenital wart prevalence among young men are consistent with herd protection from vaccination among females.

A study conducted in 27 clinics participating in the STD Surveillance Network (SSuN; see Section A2.2 in the Appendix) observed significant declines in prevalence of anogenital warts during 2010–2016 among women and men who have sex with women only (MSW) aged less than 40 years, and among MSM of all ages.38 Although some of the observed declines may be due to HPV vaccination, changes over time in the population of STD clinic patients or clinical practices, such as a decrease in physical examinations resulting in fewer anogenital warts diagnoses, may partially account for these findings.

See text for description.

See text for description.

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, 39 Although most infections are subclinical,40 clinical manifestations are characterized by recurrent, painful genital and/or anal lesions.41 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;40, 42 however, the prevalence of genital HSV-1 infections appears to be increasing among young adults.43, 44

Genital HSV infection is not a nationally notifiable condition. Most persons with genital HSV infection have not received a diagnosis.45 The overall percentage of the HSV-2 seropositive NHANES population 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).45

NHANES data indicate the seroprevalence of HSV-2 in the civilian, non-institutionalized United States population has decreased from 1999–2000 to 2015–2016; age-adjusted seroprevalence declined from 18.0% in 1999–2000 to 12.1% in 2015–2016 (Figure 53).46 Although these declines were observed among all race/Hispanic ethnicity groups, HSV-2 seroprevalence was highest among non-Hispanic Blacks throughout the entire time period.

A recent analysis of NHANES data showed that among men who reported having been diagnosed with genital HSV, 25.2% were HSV-1 positive and HSV-2 negative during 1999–2010; this percentage did not change significantly during 2011–2016.47 In contrast, the percentage of diagnosed women who were HSV-1 positive and HSV-2 negative significantly increased from 16.5% during 1999–2010 to 31.6% during 2011–2016, while HSV-2 seropositivity in women decreased significantly, from 77.6% to 63.3%. These findings indicate the percentage of genital HSV infections associated with HSV-1 has increased among women in the United States since 2010.

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.42 HSV-2 seroprevalence in this age group was much lower, less than 2% in both time periods.42 Other studies have found that genital HSV-1 infections are increasing among young adults.43, 44 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.42, 48 Increasingly common oral sex behavior among adolescents and young adults also has been suggested as a contributing factor.42, 49 The absence of HSV-1 antibodies also increases the likelihood of developing symptomatic disease from newly-acquired (i.e., primary) genital HSV-2 infection.50 Young women may therefore be increasingly likely to first acquire HSV-1 infection genitally, or acquire a primary genital HSV-2 infection, during their child-bearing years,48, 51 and first-episode primary genital HSV infection during pregnancy increases the risk of neonatal HSV transmission.48, 52 Another 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 2007–2014,53 raising 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.

See text for description.

Trichomonas vaginalis

Trichomonas vaginalis is a common sexually transmitted protozoal infection associated with adverse health outcomes such as preterm birth and symptomatic vaginitis.7, 54-55 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. NHANES data during 2013–2016 indicated prevalence of T. vaginalis in urine specimens obtained from participants aged 14–59 years was 0.5% among males and 2.1% among females; highest prevalences were observed among non-Hispanic Black males (3.4%) and females (9.6%).56 An analysis of NHANES data during 2001–2004 from cervicovaginal swab specimens also found higher T. vaginalis prevalence among non-Hispanic Black females.57

See text for description.

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