Pregnancy and Sexually Transmitted Diseases
- Pregnancy and Sexually Transmitted Diseases
- Chlamydial Infections
- Lymphogranuloma venereum
- Herpes simplex virus infection
- Human immunodeficiency virus infection
- Human papillomavirus infection
- Bacterial vaginosis
- Other Sexually Transmitted Diseases
Genital human papillomavirus infection (HPV), either symptomatic or asymptomatic, is common. Of 2597 high-risk pregnant women enrolled in the New Orleans Center of the Vaginal Infections and Prematurity Study, 28 percent were seropositive for HPV-16 capsid antibodies (Hagensee and colleagues, 1999). The most important sequelae of HPV infection are cervical, vaginal, vulvar, and anal neoplasia. Mucocutaneous external genital warts are usually caused by HPV types 6 and 11 but may also be caused by intermediate- and high-oncogenic-risk HPV (Centers for Disease Control and Prevention, 1999; Wiley and associates, 2002).
EXTERNAL GENITAL WARTS.
For unknown reasons, genital warts frequently increase in number and size during pregnancy. Accelerated viral replication by the physiological changes of pregnancy might explain the growth of perineal lesions and progression of some to cervical neoplasm (Fife and co-workers, 1999; Rando and colleagues, 1989).
High-risk HPV types are cleared more slowly during pregnancy, and clearance increases postpartum (Nobbenhuis and associates, 2002). These lesions may grow to fill the vagina or cover the perineum, making it difficult to perform vaginal delivery or episiotomy and prompting cesarean delivery (
Fig. 59-8). In women without grossly visible lesions, Snyder and co-workers (1990), but not Goldaber and colleagues (1993), found an association between papillomavirus infection and episiotomy breakdown. Because HPV infection may be subclinical and multifocal, most women with vulvar lesions also have cervical HPV infection, and vice versa (Ault, 2003; Spitzer and associates, 1989).
Figure 59-8. Extensive external genital warts in a woman near term. (From Wendel and Cunningham, 1991.)
Although there may be an incomplete response to treatment during pregnancy, these lesions commonly improve or regress rapidly following delivery. Consequently, eradication of warts during pregnancy is not always necessary. Therapy is directed toward minimizing treatment toxicity to the mother and fetus and debulking symptomatic genital warts. There are several agents employed in adults, but pregnancy limits their use. There is no definitive evidence that any one of the subsequently discussed treatments is superior to any other (Centers for Disease Control and Prevention, 2002d; Wiley and co-workers, 2002).
Trichloroacetic or bichloracetic acid, 80- to 90-percent solution, applied topically once a week, is an effective regimen for external warts. Some prefer cryotherapy or laser ablation of these lesions (Arena and colleagues, 2001). In one study, Schwartz and associates (1988) reported good results in 31 of 32 women treated with combination laser and 85-percent trichloroacetic acid therapy. Podophyllin resin, podofilox 0.5-percent solution or gel, 5-fluorouracil cream, imiquimod 5-percent cream, and interferon therapy are not recommended in pregnancy because of concerns for maternal and fetal safety (Centers for Disease Control and Prevention, 2002d).
Juvenile-onset recurrent respiratory papillomatosis is a rare, benign neoplasm of the larynx. It can cause hoarseness and respiratory distress in children and is often due to HPV types 6 or 11. In some cases, maternal genital HPV infection is associated with laryngeal papillomatosis, and studies differ in their findings of neonatal transmission rates. A Danish population-based study indicated a risk of neonatal transmission of 7 in 1000 infected women (Silverberg and co-workers, 2003). In this study, prolonged ruptured membranes was associated with a twofold increased risk, but was not associated with the method of delivery. Tseng and colleagues (1998), in a study of 301 infected women, reported a transmission rate of 40 percent for HPV 16 and 18. The rate was higher for vaginal compared with that of cesarean delivery (51 versus 27 percent). Tenti and associates (1999) reported a 30-percent neonatal transmission rate. Watts and co-workers (1998) found HPV DNA in 5 percent of samples from the oral or nasopharynx, anus, and genital areas of newborns. Surprisingly, the rates were higher in mothers without HPV detected during pregnancy (Winer and Koutsky, 2004).
Because these reports cite very few clinical infections when these children are followed, there is a question of transient HPV infection versus contamination. Smith and colleagues (2004) studied oral and genital samples from mother-newborn pairs to identify HPV DNA using PCR sequencing and found virus in only 9 of 574 (1.6 percent) newborns. The transmission rate was 3.7 percent among HPV-positive women. Importantly, they found no HPV DNA in any of the infants who returned for follow-up. In another study, Manns and associates (1999) measured the seropositive rates for HPV-16 in children at 1 to 2 years and confirmed this low rate of vertical transmission. These data support the rarity of perinatal HPV transmission. Given our limited understanding of the development of laryngeal papillomatosis and current obstetrical data, cesarean delivery cannot be recommended to reduce the risk of this disease.
Revision date: June 11, 2011
Last revised: by David A. Scott, M.D.