Other Sexually Transmitted Diseases

Chancroid

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 (Figure 45, Table 1). Since then, the number of reported cases has fluctuated somewhat, while still appearing to decline overall. In 2015, a total of 11 cases of chancroid were reported in the United States. Seven states reported one or more cases of chancroid in 2015 (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 Haemophilus ducreyi is difficult to culture; as a result, this condition may be substantially 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 types 6 and 11 are responsible for approximately 90% of genital warts.^9,10

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

HPV vaccine uptake in the United States remains lower than the Healthy People 2020 goal of 80% coverage.¹⁵ In 2015, a national survey found that 63% of girls aged 13–17 years had received at least 1 dose of the HPV vaccine, and 42% had received all 3 doses in the series.¹⁶ HPV vaccine uptake is lower among boys; 50% aged 13–17 years received at least 1 dose, but only 28% received all 3 doses.¹⁶

HPV infection is not a nationally reportable condition. Cervicovaginal prevalence of quadrivalent HPV vaccine types 6, 11, 16, and/or 18 was estimated using data for females aged 14-34 years from the National Health and Nutrition Examination Survey (NHANES; see Section A2.4 in Appendix A). Prevalence decreased significantly from the pre-vaccine era (2003–2006) to the early post-vaccine era (2009–2012) in specimens from females aged 14–19 and 20–24 years, the age groups most likely to benefit from HPV vaccination (Figure 46).¹⁷ Among those aged 25–34 years, vaccine-type HPV prevalence did not differ significantly between the two time periods, and no differences were observed in the prevalence of non- quadrivalent HPV vaccine types by time period for any age group. In a population-based study of female residents of four geographic catchment areas (Alameda County, California; New Haven County, Connecticut; Monroe County, New York; Washington and Multnomah Counties, Oregon), incidence of high-grade cervical intraepithelial neoplasia in 18–20 year olds, based on laboratory reports and medical record review, decreased during 2008–2012. However, cervical cancer screening, which was estimated using age-group-specific screening rates derived from a variety of data sources in three catchment areas, also declined in this age group during the same period.¹⁸ The larger observed decrease in cervical neoplasia, relative to the estimated decline in screening, suggests that HPV vaccination may be impacting the true burden of cervical neoplasia in young women.

Data from the National Disease and Therapeutic Index (NDTI; see Section A2.5 in Appendix A) suggest that cases of genital warts, as measured by initial visits to physicians’ offices, may have increased during the late 1990s through 2014 (Figure 47, Table 44). Although the number of visits appears to have decreased in 2012 and 2013, visits in 2014 (465,000) slightly exceeded those in 2011; more years of data are needed to better elucidate recent trends in initial genital wart visits from these data. The 2015 NDTI data were not obtained in time to include them in this report. NHANES data for 1999–2004 indicated that 5.6% of sexually active adults aged 18–59 years self-reported a history of a genital wart diagnosis.¹⁹

Prevalence of genital warts during 2003–2010 was examined using health-care claims records from a large United States cohort of individuals with employer provided private health insurance (Figure 48).²⁰ Prevalence among females aged 15–19 years was stable during 2003–2007, but then significantly declined during 2007–2010. Among females aged 20–24 years, genital wart prevalence significantly increased during 2003–2007, then was stable during 2007–2010; although prevalence in this age group appeared to decrease during 2009–2010, more years of data are needed to interpret this observation. Prevalence in females aged 25–39 years significantly increased throughout the time period, but among those aged 25–29 years a potential inflection in trend was observed in 2009, for which additional years of data are needed to appropriately assess. Genital wart prevalence significantly increased in males of all age groups during 2003–2010, although for those aged 20–24 years a potential inflection
in trend again was observed in 2009.

For data reported in Figure 49, enhanced behavioral and demographic information on patients who presented for care in 2015 in 7 jurisdictions of the STD Surveillance Network (SSuN) was used (See Section A2.2 in Appendix A). Only jurisdictions that contributed data for all of 2015 were included in the figure. 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 2015 is presented separately for MSM, MSW, and women by SSuN jurisdiction in the figure. Among women, the median prevalence of genital warts was 0.9% (range 0.7 to 2.2) across all sites, compared to 3.3% (range 1.9 to 4.6) for MSM and 4.3% (range 1.7 to 8.1) for MSW.

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.^4,21 Although most infections are subclinical,²² clinical manifestations are characterized by recurrent, painful genital and/or anal lesions.²³ 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.^22,24

HSV infection is not a nationally reportable condition. Data on initial visits to physicians’ offices for genital HSV infection are available from the NDTI; however the 2015 NDTI data were not obtained in time to include them in this report (Figure 50, Table 44). Visits have generally increased over time; the maximum number of initial visits (371,000) occurred in 2006, while 299,000 visits took place in 2014.

Most persons with genital HSV infection have not received a diagnosis. The overall percentage of HSV-2 seropositive NHANES participants aged 14–49 years 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).²⁵ However, an overall increase in the number of physician visits for genital HSV infection over time, as suggested by the NDTI data, may indicate increased recognition of infection.

NHANES data on the gender- and race/ethnicity-specific seroprevalence of HSV-2 among those aged 14–49 years were compared across survey years 1988–1994, 1999–2002, 2003–2006, and 2007–2010 (Figure 51). Overall, HSV-2 seroprevalence decreased between 1988–1994 and 2007–2010, from 21.2% to 15.5%.25 Among non-Hispanic White females, HSV-2 seroprevalence significantly decreased from 19.5% in 1988–1994 to 15.3% in 2007–2010; HSV-2 seroprevalence remained stable among non-Hispanic Black females, from 52.5% in 1988–1994 to 49.9% in 2007–2010. Similar race/ethnicity differences were observed for males. These data, along with data from NHANES survey years 1976–1980,²⁶ indicate that non-Hispanic Blacks had higher overall seroprevalence than non-Hispanic Whites in each survey period.

NHANES data also show that among adolescents aged 14–19 years HSV-1 seroprevalence has significantly decreased by almost 23%, from 39.0% in 1999–2004 to 30.1% in 2005–2010, indicating declining orolabial infection in this age group.²⁴ HSV-2 seroprevalence in this age group was much lower, less than 2% in both time periods.²⁴ Other studies have found that genital HSV-1 infections are increasing among young adults.^27,28 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;^24,29 increasingly common oral sex behavior among adolescents and young adults also has been suggested as a contributing factor.^24,30 The absence of HSV-1 antibodies also increases the likelihood of developing symptomatic disease from newly-acquired (i.e., primary) genital HSV-2 infection.³¹ 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,^29,32 and first-episode primary HSV infection during pregnancy increases the risk of neonatal HSV transmission ^29,33

For information on neonatal HSV infections, see Special Focus Profiles, STDs in Women and Infants.

Trichomonas vaginalis

Trichomonas vaginalis is a common sexually transmitted protozoal infection associated with adverse health outcomes such as preterm birth and symptomatic vaginitis.^4,34,35 It is not a nationally reportable condition, and trend data are limited to estimates of initial physician office visits from the NDTI (Figure 52, Table 44). Visits appear to be fairly stable since the 1990’s; the number of initial visits for Trichomonas vaginalis infection in 2014 was 155,000. The 2015 NDTI data were not obtained in time to include them in this report. NHANES data from 2001–2004 indicated an overall Trichomonas vaginalis infection prevalence of 3.1%, with the highest prevalence of 13.3% observed among non-Hispanic Blacks.³⁵

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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, 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, 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, et al. Classification of papillomaviruses. Virol 2004;324:17–27.

6 Ho GYF, Bierman R, Beardsley L, et al. 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, et al. 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, 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, 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, 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):560–3.

11 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 2007;56(RR02):1–24.

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, 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):300–4.

15 HealthyPeople.gov. Healthy People 2020 Topics & Objectives. Immunization and Infectious Diseases. Objectives IID-11.4 and IID-11.5. https://www.healthypeople.gov/2020/topics-objectives/topic/immunization-and-infectious-diseases/objectives Accessed July 20, 2016.

16 Reagan-Steiner S, Yankey D, Jeyarajah J, et al. National, regional, state, and selected local area vaccination coverage among adolescents aged 13–17 years — United States, 2015. MMWR Morb Mortal Wkly Rep 2016; 65(33):850-8.

17 Markowitz LE, Gui L, Hariri S, et al. Prevalence of HPV after introduction of the vaccination program in the United States. Pediatrics 2016;137(3):e20151968.

18 Hariri S, Johnson ML, Bennett NM, et al. Population-based trends in high grade cervical lesions in the early human papillomavirus vaccine era in the United States. Cancer 2015;121:2775–81.

19 Dinh T-H, Sternberg M, Dunne EF, et al. 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 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.

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):S3–28.

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. Genital herpes. N Engl J Med 2004;350(19): 1970–7.

24 Bradley H, Markowitz LE, Gibson T, et al. Seroprevalence of herpes simplex virus types 1 and 2 — United States, 1999–2010. J Infect Dis 2014;209(3):325–33.

25 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):860–4.

26 Xu F, Sternberg MR, Kottiri BJ, et al. Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA 2006;296(8):964–73.

27 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;56:344–51.

28 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.

29 Kimberlin DW. The scarlet H. J Infect Dis 2014;209(3):315–7.

30 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.

31 Langenberg AGM, Corey L, Ashley RL, et al. A prospective study of new infections with herpes simplex virus type 1 and type 2. N Engl J Med 1999;341:1432–8.

32 Sampath A, Maduro G, Schillinger JA. Infant deaths due to herpes simplex virus, congenital syphilis, and HIV in New York City. Pediatrics 2016;137(4):e20152387.

33 Brown ZA, Wald A, Morrow RA, et al. Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant. JAMA 2003;289(2):203–9.

34 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.

35 Sutton M, Sternberg M, Koumans EH, et al. 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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