STDs in Women and Infants
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Public Health Impact
Women and infants bear significant long-term consequences of STDs. In addition to biological and social factors such as poverty and access to quality STD services, a woman’s inability to negotiate safer sexual practices, such as condom use, can significantly affect her sexual health and subsequently the health of her unborn baby.1,2 A woman’s relationship status with her male partner, in particular, has been identified as an important predictor of her sexual health.3 For example, a perceived shortage of available men in a community can cause women to be more accepting of their partners’ concurrent sexual relationships, and partner concurrency is a factor associated with increased risk for STDs.4 A number of studies have found significant associations between condom use and socio-demographic characteristics, including age, income, education, and acculturation.5 Because it may be the behavior of her male partner, rather than the woman’s own behavior that increases a woman’s risk for STDs, even a woman who has only one partner may be obliged to practice safer sex such as using condoms.6
Women infected with C. trachomatis or N. gonorrhoeae can develop pelvic inflammatory disease (PID), which, in turn, can lead to reproductive morbidity such as ectopic pregnancy and tubal factor infertility. An estimated 10%–20% of women with chlamydia or gonorrhea may develop PID if they do not receive adequate treatment.7,8 Among women with PID, tubal scarring can cause infertility in 8% of women, ectopic pregnancy in 9%, and chronic pelvic pain in 18%.9
About 80%–90% of chlamydial infections10 and up to 80% of gonococcal infections11 in women are asymptomatic. These infections are detected primarily through screening. Because the symptoms associated with PID can be nonspecific, up to 85% of women with PID delay seeking medical care, thereby increasing the risk for infertility and ectopic pregnancy.12 Data from two randomized controlled trials of chlamydia screening suggest that such screening programs reduce PID incidence. 13,14
HPV infections are highly prevalent in the United States, especially among young sexually active women. Although most HPV infections in women resolve within 2 years, they are a major concern because persistent infection with specific types of the virus are causally related to cervical cancer; these types also cause Papanicolaou (Pap) smear abnormalities. Other types cause genital warts, low-grade Pap smear abnormalities, and, rarely, recurrent respiratory papillomatosis in infants born to infected mothers.15
Chlamydia and gonorrhea can result in adverse outcomes of pregnancy, including neonatal ophthalmia and, in the case of chlamydia, neonatal pneumonia. Although topical prophylaxis of infants at delivery is effective for prevention of gonococcal ophthalmia neonatorum, prevention of neonatal pneumonia requires prenatal detection and treatment.
Genital infections with HSV are extremely common, can cause painful outbreaks, and can have serious consequences for pregnant women and their infants.16
When a woman has a syphilis infection during pregnancy, she can transmit the infection to the fetus in utero. Transmission can result in fetal death or an infant born with physical and mental developmental disabilities. Most cases of congenital syphilis are easily preventable if women are screened for syphilis and treated early during prenatal care.17
Chlamydial infections in women are usually asymptomatic and screening is necessary to identify most infections.18 Routine chlamydia screening of sexually-active young women has been recommended by CDC since 1993.19 Rates of reported cases among women increased steadily from the early 1990s until 2011, which likely reflect expanded screening coverage and use of more sensitive diagnostic tests (Figure 1). During 2011–2012, reported case rates among women decreased slightly (0.7%) from 643.4 cases to 638.7 cases per 100,000 females. During 2012–2013, rates decreased 2.4% to 623.1 cases per 100,000 females (Table 4).
Chlamydia rates are highest among young women, the population targeted for screening (Figure 5, Table 10). During 2012–2013, rates of reported chlamydia decreased 8.7% among females aged 15–19 years and decreased 0.3% among females aged 20–24 years. Regionally, chlamydia case rates are highest among women in the South, with a rate of 690.5 per 100,000 females in 2013 (Table 4). During 2012–2013, rates of reported chlamydia among women decreased in all regions (Table 4). Rates of reported chlamydia exceeded gonorrhea rates among women in all regions (Figures A and B, Tables 4 and 15).
Like chlamydia, gonorrhea is often asymptomatic in women. Thus, gonorrhea screening is an important strategy for the identification of gonorrhea among women. Large-scale screening programs for gonorrhea in women began in the 1970s. After an initial increase in cases detected through screening, rates of reported gonorrhea cases for both women and men declined steadily throughout the 1980s and early 1990s and then declined more gradually in the late 1990s and the 2000s (Figure 11). After reaching a 40-year low in 2009 (104.5 cases per 100,000 females), the gonorrhea rate for women increased slightly each year during 2009–2011, and plateaued at 107.9 cases per 100,000 females in 2012. In 2013, the gonorrhea rate among women decreased to 102.4 cases per 100,000 females (Figure 12, Table 15).
The gonorrhea rate among women was slightly higher than the rate among men during 2001–2012, but the rate among men surpassed the rate among women in 2013 (Figure 12, Tables 15 and 16). Gonorrhea rates are highest among young women (Figure 16, Table 21). Among young women and adolescents, rates were highest in 2013 among 19-year old females (685.6 per 100,000 females) (Table 23).
Positivity in Selected Populations
During the mid-1990s to 2011, chlamydia and gonorrhea positivity among young women screened in prenatal care clinics participating in infertility prevention activities were reported to CDC to monitor chlamydia and gonorrhea prevalence in women. As the national infertility prevention program expanded, these data became difficult to interpret as trends were influenced by changes in screening coverage, screening criteria, and test technologies, as well as demographic changes in patients attending clinics reporting data to CDC. These issues could not be addressed with the limited variables that were collected at the national level. Positivity data continue to be useful locally to inform clinic-based screening recommendations and to identify at-risk populations in need of prevention interventions, but are no longer collected to monitor national trends in chlamydia and gonorrhea.
Trends in congenital syphilis usually follow trends in primary and secondary syphilis among women, with a lag of 1–2 years (Figure 45). The rate of P&S syphilis among women declined 95.4% (from 17.3 to 0.8 cases per 100,000 females) during 1990–2004 (Figure 32). The rate of congenital syphilis declined by 92.4% (from a peak of 107.6 cases to 8.2 cases per 100,000 live births) during 1991–2005 (Table 1). Rates of both female P&S and congenital syphilis increased during 2005–2008. During 2008–2012, rates of both female P&S and congenital syphilis declined (from 1.5 to 0.9 cases per 100,000 population and from 10.5 to 8.4 cases per 100,000 live births, respectively). Rates of female P&S remained unchanged (0.9 cases) but rates of congenital syphilis increased (to 8.7 cases) during 2013 (Tables 28 and 42).
The highest rates of P&S syphilis among women and congenital syphilis were observed in the South (Figures C and D, Table 42). However, the West was the only region with increased rates of congenital syphilis in 2013, and rates of P&S syphilis among women in the West have increased each year during 2010–2013.
Although most cases of congenital syphilis occur among infants whose mothers have had some prenatal care, late or limited prenatal care has been associated with congenital syphilis. Failure of health care providers to adhere to maternal syphilis screening recommendations also contributes to the occurrence of congenital syphilis.20
Accurate estimates of PID and tubal factor infertility resulting from chlamydial and gonococcal infections are difficult to obtain, in part because definitive diagnoses of these conditions can be complex. Published data suggest overall declining rates of women diagnosed with PID in the United States in both hospital and ambulatory settings.21-23 The National Disease and Therapeutic Index (NDTI) provides estimates of initial visits to office-based, private physicians for PID. NDTI estimated that from 2003–2012 the number of visits to such physicians for PID among women aged 15–44 decreased (39.8%) from 123,000 to 88,000 visits (Figure F). Several suggestions have been put forth as factors that could influence PID rates, including increases in chlamydia and gonorrhea screening coverage, more sensitive diagnostic technologies, and availability of single-dose therapies that increase adherence to treatment.22-24 While PID is declining nationally, it still causes an enormous amount of unnecessary and expensive morbidity.
Differences in PID diagnoses or treatment by race/ethnicity have been observed in earlier research.21 Using data from the National Survey of Family Growth, the overall proportion of sexually experienced women who have been treated for PID declined from 8.6% in 1995 to 5.7% in 2002 and leveled off to 5.0% in 2006–2010 (Figure E).25 While this pattern was observed across all racial/ethnic groups, the proportion who had received PID treatment was higher among non-Hispanic blacks than those among Hispanics or non-Hispanic whites. These disparities are consistent with the marked racial disparities observed for chlamydia and gonorrhea. However, because of the subjective methods by which PID is diagnosed, racial disparity data should be interpreted with caution.
Ectopic pregnancy (EP) is a potentially life-threatening adverse pregnancy outcome that requires prompt evaluation and treatment, and an important cause of pregnancy related mortality. Past studies have found that it affects 1–2% of all pregnancies.26-27 Fallopian tube pathology is the most common etiology of EP.28 Tubal damage can result from tubal surgery, previous EP, untreated STDs and PID, in utero diethylstilbestrol exposure, and other conditions. 29–33
In the past, the National Hospital Discharge Survey, which collects information on discharged hospital inpatients in the United States, was used to estimate trends in the rate of EP. However, medical and surgical treatment of EP is currently provided in both inpatient and outpatient settings, making the task of tracking reliable estimates at the national level difficult.34 More recent attempts to estimate EP incidence use data from surveys or administrative databases of public and private insurance and managed care systems.35 Data from a large administrative claims database suggests the rate of EP increases with age among pregnancies in girls and women aged 15–44 years during the period of 2002 to 2012 (Figure G). In 2012, EP rates were highest among women aged 35–44 years. During 2002–2012, the EP rate increased slightly in certain age groups: the EP rate increased 5.7% among those aged 20–24, 11.3% among those aged 25–29 years, 4.3% among those aged 35–39 years, and 6.4% among those aged 40–44 years. Rates remained the same for women of all other age groups.
2 McCree DH, Rompalo A. Biological and behavioral risk factors associated with STDs/HIV in women: implications for behavioral interventions, In: Aral SO, Douglas JM,Lipshutz JA (editors). Behavioral Interventions for Prevention and Control of Sexually Transmitted Diseases (p. 310-324). New York, NY: Springer.
3 El-Bassel N, Gilbert L, Krishnan S, Schilling R, Gaeta T, Purpura S, et al. Partner violence and sexual HIV-Risk behaviors among women in an inner-city emergency department. Violence Vict. 1998;13(4):377-393.
4 Hogben M, Leichliter JS. Social determinants and sexually transmitted disease disparities. Sex Transm Dis. 35(12) S13 S18.
5 Manderson L, Chang T, Tye LC, Rajanayagam K. Condom use in heterosexual sex: a review of research, 1985–1994. In: Catalan J, Sherr L, Hedge B (editors). The impact of AIDS: psychological and social aspects of HIV Infection. p. 1-26. The Netherlands: Harwood Academic Publishers.
6 O’Leary A. A woman’s risk for HIV from a primary partner: balancing risk and intimacy. Annu Rev Sex Res. 2000; 11:191 234.
7 Paavonen J, Westrom L, Eschenbach. Pelvic Inflammatory Disease. In: Holmes KK, Sparling PF, Stamm WE, Piot P, Wasserheit JN, Corey L, Cohen, MS, Watts DH, (editors). Sex Transm Dis. 4th ed. New York: McGraw-Hill; 2008:1017-1050.
8 Hook EW III, Handsfield HH. Gonococcal infections in the adult. In: Holmes KK, Sparling PF, Stamm WE, Piot P, Wasserheit JN, Corey L, et al, (editors). Sex Transm Dis. 4th ed. New York: McGraw-Hill; 2008:627-45.
9 Westrom L, Joesoef R, Reynolds G, Hagdu A, Thompson SE. Pelvic inflammatory disease and fertility: a cohort study of 1,844 women with laparoscopically verified disease and 657 control women with normal laparoscopy. Sex Transm Dis. 1992;9:185-92.
10 Stamm WE. Chlamydia trachomatis infections in the adult. In: Holmes KK, Sparling PF, Stamm WE, Piot P, Wasserheit JN, Corey L, et al, (editors). Sex Transm Dis. 4th ed. New York: McGraw-Hill; 2008:575-93.
11 Marrazzo JM, Handsfield HH, Sparling PF. Neisseria gonorrhoeae In: Mandell GL, Bennett JE, Dolin R (editors). Principles and practice of Infectious Diseases, 7th ed. Philadelphia, PA: Churchill Livingstone; 2010: 2753-2770.
12 Hillis SD, Joesoef R, Marchbanks PA, Wasserheit JN, Cates W Jr, Westrom L. Delayed care of pelvic inflammatory disease as a risk factor for impaired fertility. Am J Obstet Gynecol. 1993;168:1503-9.
13 Scholes D, Stergachis A, Heidrich FE, Andrilla H, Holmes KK, Stamm WE. Prevention of pelvic inflammatory disease by screening for cervical chlamydial infection. N Engl J Med. 1996;34(21):1362-6.
14 Oakeschott, P, Kerry S, Aghaizu A, Atherton H, Hay S, et al. Randomized controlled trial of screening for Chlamydia trachomatis to prevent pelvic inflammatory disease: the POPI (prevention of pelvic infection) trial. BMJ. 2010;340:c1642.
15 Centers for Disease Control and Prevention. Prevention of genital HPV infection and sequelae: report of an external consultants’ meeting. Atlanta: U.S. Department of Health and Human Services; 1999.
16 Kimberlin DW. Herpes simplex virus infections of the newborn. Semin Perinatol. 2007;31(1):19-25.
17 Centers for Disease Control and Prevention. Guidelines for prevention and control of congenital syphilis. MMWR Morb Mortal Wkly Rep. 1988;37(No. SS-1).
18 Farley TA, Cohen DA, Elkins W. Asymptomatic sexually transmitted diseases: the case for screening. preventive medicine. 2003;36:502-9.
19 Centers for Disease Control and Prevention. Recommendations for the prevention and management of Chlamydia trachomatis infections. MMWR 1993 Aug 6;42(RR-12):1-39.
20 Centers for Disease Control and Prevention. Congenital syphilis — United States, 2003–2008. MMWR Morb Mortal Wkly Rep. 2010;59:413-17.
21 Sutton MY, Sternberg M, Zaidi A, St. Louis ME, Markowitz LE. Trends in pelvic inflammatory disease hospital discharges and ambulatory visits, United States, 1985–2001. Sex Transm Dis. 2005;32(12)778-84.
22 Bohm MK, Newman L, Satterwhite CL, et al. Pelvic inflammatory disease among privately insured women, United States, 2001–2005. Sex Transm Dis 2010;37:131–136.
23 Whiteman MK, Kuklina E, Jamieson DJ, et al. Inpatient hospitalization for gynecologic disorders in the United States. Am J Obstet Gynecol 2010;202:541 e1–6.
24 Owusu-Edusei, Kwame Jr. Bohm, Michele K. Chesson, Harrell W. Kent, Charlotte K. Chlamydia screening and pelvic inflammatory disease: Insights from exploratory time-series analyses. Am J Prev Med. 2010;38(6):652-7.
25 Leichliter JS. Chandra A. Aral SO. Correlates of self-reported pelvic inflammatory disease treatment in sexually experienced reproductive-aged women in the United States, 1995 and 2006-2010. Sex Transm Dis. 2013;40(5):413-8.
26 Ectopic pregnancy–United States, 1990–1992. MMWR Morb Mortal Wkly Rep 1995;44:46–8.
27 Van Den Eeden SK, Shan J, Bruce C, Glasser M. Ectopic pregnancy rate and treatment utilization in a large managed care organization. Obstet Gynecol 2005;105:1052–7.
28 Medical management of ectopic pregnancy. ACOG Practice Bulletin No. 94. American College of Obstetricians and Gynecologists.Obstet Gynecol 2008;111:1479–85.
29 Ankum WM, Mol BW, Van der Veen F, Bossuyt PM. Risk factors for ectopic pregnancy: a meta-analysis. Fertil Steril 1996;65:1093–9.
30 Barnhart KT, Sammel MD, Gracia CR, Chittams J, Hummel AC, Shaunik A. Risk factors for ectopic pregnancy in women with symptomatic first-trimester pregnancies. Fertil Steril 2006;86:36–43.
31 Marchbanks PA, Annegers JF, Coulam CB, Strathy JH, Kurland LT. Risk factors for ectopic pregnancy. A population-based study. JAMA 1988;259:1823–7.
32 Centers for Disease Control and Prevention. DES update home. Available at http://www.cdc.gov/DES/. Retrieved August 5, 2014.
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- Page last reviewed: December 16, 2014 (archived document)
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