Syphilis

The incidence of syphilis increased in the United States through the 1980s peaked in 1990, and then subsequently declined (Centers for Disease Control and Prevention, 2003a). The rate of syphilis in the United States in 2002 was 2.4 cases per 100,000 persons, and the rate among neonates was even lower at 1.1 cases per 100,000 population. The Centers for Disease Control and Prevention created a National Syphilis Elimination Plan with a goal of fewer than 1000 cases of primary and secondary syphilis in the country by 2005 (Mitka, 2000).

Increased rates of maternal syphilis have been linked to substance abuse, especially crack cocaine, and to inadequate prenatal care (Lago, 2004; Minkoff, 1990; Warner, 2001, and all their colleagues). Klass and associates (1994), in a study of prenatal syphilis at the Boston City Hospital during four decades, concluded that the continued prevalence of syphilis at delivery was associated with substance abuse, HIV infection, lack of prenatal care, treatment failures, and reinfection.

Antepartum syphilis can profoundly affect pregnancy outcome by causing preterm labor, fetal death, and neonatal infection by transplacental or perinatal infection (Genc and Ledger, 2000; Watson-Jones and co-workers, 2002). Fortunately, of the many congenital infections, syphilis is the most readily prevented and the most susceptible to therapy.

FETAL AND NEONATAL INFECTIONS.

In the past, syphilis accounted for nearly a third of stillbirths. Today it plays a smaller but persistent role in fetal death, especially before 30 weeks (Goldenberg and Thompson, 2003; Gust and associates, 2002). Spirochetes readily cross the placenta and can result in congenital infection. Because of fetal immunocompetence prior to about 18 weeks, the fetus generally does not manifest the immunological inflammatory response characteristic of clinical disease before this time (Silverstein, 1962). Once fetal syphilis develops, there appears to be a continuum of involvement (Fig. 59-1). Hepatic involvement is followed by anemia and thrombocytopenia and then ascites and hydrops (Hollier and colleagues, 2001).

The frequency of congenital syphilis varies with both the stage and duration of maternal infection. McFarlin and associates (1994) reported that high serological titers and unknown duration of infection were major predictors of congenital syphilis. Thus, the highest incidence is in neonates born to mothers with early syphilis — primary, secondary, and early latent — and the lowest incidence with late latent disease of greater than 1-year duration (Fiumara and colleagues, 1952; Golden and co-workers, 2003). Importantly, any stage of infectious maternal syphilis may result in fetal infection.

Figure 59-1. Hypothesized continuum of fetal syphilis infection. (VDRL = Venereal Disease Research Laboratory.)