Human infection is acquired by eating raw or undercooked meat infected with tissue cysts or by contact with oocysts from cat feces in contaminated litter, soil, or water. Prior infection is conirmed by serological testing, and its prevalence depends on geographic locale and parasite genotype. In the United States, seroprevalence in persons aged 10 to 19 years is 5 to 30 per cent, and this can exceed 60 percent in those older than 50 (Kim, 2015). Thus, a significant segment of pregnant women in this country are susceptible to infection. The incidence of prenatal infection resulting in birth of a newborn with con genital toxoplasmosis varies from 0.8 per 10,000 live births in the United States to 10 per 10,000 in France (Cook, 2000).
Between 400 and 4000 cases of congenital toxoplasmosis are diagnosed annually in the United States Oones, 2014).
Most acute maternal infections are subclinical and are detected only by prenatal or newborn serological screening. In some cases, maternal symptoms may include fatigue, fever, headache, muscle pain, and sometimes a maculopapular rash and posterior cervical lymphadenopathy. In immunocompetent adults, initial infection confers immunity, and prep regnancy infection nearly eliminates any risk of vertical transmission. Infection in immu nocompromised women, however, may be severe, and reactiva tion may cause encephalitis, retinochoroiditis, or mass lesions.
Maternal infection is associated with a fourfold increased pre term delivery rate before 37 weeks (Freeman, 2005).
The incidence and severity of fetal toxoplasmosis depend on gestational age at the time of maternal infection. Risks for fetal infection rise with gestational age. A metaanalysis estimated the risk to be 15 percent at 13 weeks, 44 percent at 26 weeks, and 71 percent at 36 weeks (SYROCOT Study Group, 2007). Conversely, the severity of fetal infection is much greater in early pregnancy, and these fetuses are much more likely to have clinical findings of infection (American College of Obstetricians and Gynecologists, 2017).
Importantly, most infected fetuses are born without obvious stigmata of toxoplasmosis. Clinically afected neonates usually have generalized disease expressed as low birthweight, hepatosplenomegaly, jaundice, and anemia. Some primarily have neurological disease with intracranial calciications and with hydrocephaly or microcephaly (Dhombres, 2017). Many eventually develop chorioretinitis and exhibit learning disabilities. This classic triad-chorioretinitis, intracranial calcifications, and hydrocephalus-is often accompanied by convulsions. Infected neonates with clinical signs are at risk for long-term complications (Abdoli, 2014; Wallon, 2014).
With IgG antibody conirmed before pregnancy, there is no risk for a congenitally infected fetus. he American College of Obstetricians and Gynecologists (2017) does not recommend prenatal screening for toxoplasmosis in areas of low prevalence, including the United States. Screening should be performed in immunocompromised pregnant women, including those with HIV infection. In areas of high toxoplasmosis prevalence-for example, France and Austria-routine screening has resulted in diminished congenital disease (Kim, 2015; Wallon, 2013).