17 - Neurological sequelae of congenital perinatal infection

Summary

Introduction

Maternal infections, contracted during pregnancy, may be without fetal consequence or they may have serious adverse effects on the fetus. These adverse effects may include fetal death, stillbirth, intrauterine growth retardation, or congenital infection. Congenitally infected neonates may be symptomatic or asymptomatic at birth. Those who are symptomatic at birth generally have significant long-term sequelae. Those who are asymptomatic at birth may never manifest evidence of damage or they may develop clinically evident sequelae later in life. The overwhelming morbidity attributable to congenital infections is borne by this latter group.

The following chapter will discuss the neurologic consequences of congenital infections. The specific infectious agents that will be discussed are often referred to as the TORCH agents; T represents the parasite Toxoplasma gondii; O represents other agents such as varicella-zoster virus (VZV), human immunodeficiency virus (HIV), and Treponema pallidum (syphilis); R represents rubella virus; C represents cytomegalovirus (CMV); and H represents herpes simplex virus (HSV). With the exception of HSV, the major clinical impact of these agents results from exposure in utero. Morbidity and mortality attributable to neonatal HSV infection usually result from infection contracted at delivery.

Toxoplasmosis

The etiologic agent of toxoplasmosis, Toxoplasma gondii, was first demonstrated in the brain of a newborn infant with encephalomyelitis in 1939. The incidence of congenital toxoplasmosis in the USA is estimated to range from 1:1000 to 1:10,000 live births. Among immunocompetent women, transmission to the fetus is limited almost solely to those who contract primary infection during gestation.