Toxoplasmosis: Perinatal Parasitic Infection

Women's Health & Education Center's Contribution

Many parasitic infections are associated with significant maternal and fetal consequences if acquired during pregnancy. In general, perinatal infections have more severe fetal consequences when they occur early in gestation, because first-trimester infections may disrupt organogenesis. Second and third trimester infections can cause neurologic impairment or growth disturbances.

The purpose of this document is to describe the mode of transmission, the maternal and fetal effects, and to offer guidelines for counseling and management during pregnancy.

Epidemiology:

Toxoplasmosis is caused by the intracellular parasite Toxoplasma gondii. T gondii exists in several forms: a trophozoite, which is the invasive form, and a cyst or an oocyst, which are latent forms. Human infection is acquired by consuming cysts in undercooked meat of infected animals, by insect contamination of food, by contact with oocysts from the feces of infected cats (the only definitive hosts), or by contact with infected material of insects in soil (1). Infection with T gondii usually is asymptomatic, although after an incubation of 5-18 days, some non-specific symptoms may occur.

Symptoms and diagnosis:

Most often, toxoplasmosis presents as asymptomatic cervical lymphadenopathy, with symptoms occurring in only 10-20% of adult cases. Other symptoms include fever, malaise, night sweats, myalgias, and hepatosplenomegaly. Parasitemia can occur after infection, which in pregnant women can seed the placenta and cause subsequent fetal infection. Congenital transmission of T gondii depends on the time of acquisition of maternal infection. The later in gestation that the infection occurs, the more likely transmission is to occur. The rate of vertical transmission increases from 10% to 15% in the first trimester, to 25% in second trimester, and to more than 60% in third trimester (2).

Isolation of T gondii from blood or body fluids establishes that the infection is acute; however serologic testing for the detection of specific antibody to T gondii is the primary method of diagnosis. After an acute infection, IgM antibodies appear early and reach maximum levels in 1 month. IgG antibodies appear after IgM antibodies, are detectable within a few weeks after infection, and confer immunity. High titers of both IgG and IgM may persist for years. In the immunocompetent adult, the clinical course is benign and self-limiting. IgG and IgM testing should be used for the initial evaluation of patients suspected to have toxoplasmosis. Testing of serial specimens 3 weeks apart in parallel gives the most accurate assessment if the initial test results are equivocal. In cases in which clinical suspicion is high, specimens should be saved for repeat testing at the reference laboratory, because of the wide variation between laboratories.

Effect on Fetus and Newborn:

The severity of infection depends on gestational age at the time of transmission. The earlier the fetus is infected, the more severe the disease. Most infected infants do not have clinical signs of infection at birth, but 55-85% will develop sequelae, including chorioretinitis - leading to severe impairment of vision. Other clinical manifestations are hearing loss or mental retardation. Rash, hepatosplenomegaly, ascites, fever, periventricular calcifications, ventriculomegaly, and seizures are also seen in the newborns and infants infected by toxoplasmosis (3).

Perinatal Assessment and Monitoring:

Ultrasonography can demonstrate severe congenital toxoplasmosis; suggestive findings include ventriculomegaly, intracranial calcifications, microcephaly, ascites, hepatosplenomegaly, and intrauterine growth restriction. Testing fetal blood samples after 20 weeks of gestation for the presence of specific IgM is the most sensitive test in diagnosing congenital toxoplasmosis. Using fetal blood for antibody testing or mouse inoculation, amniotic fluid for PCR, or fetal ultrasonography to detect ventriculomegaly, 77-93% of infected infants can be identified prenatally, although no single test is very sensitive (4). Successful identification of T gondii intrauterine infection with PCR testing of amniotic fluid allows for earlier testing than fetal blood sampling, with high sensitivity, although false-positive and false-negative findings do occur.

Treatment:

Treatment of the pregnant woman with acute toxoplasmosis reduces but does not eliminate the risk of congenital infection (5). Identification of acute maternal infection necessitates immediate institution of treatment until results of fetal testing are known. Spiramycin, which concentrates in the placenta, may reduce the risk of fetal transmission by 60%, but as a single agent, it does not treat established fetal infection. If fetal infection is established; pyrimethamine, sulfadiazine, and leucovorin (folinic acid) are added to the regimen because they more effectively eradicate parasites in the placenta and in the fetus than spiramycin alone. With treatment, even early fetal infection with toxoplasmosis can result in successful pregnancy outcomes.

Spiramycin - 1.0 g, po every 8 hourly.
Pyrimethamine - 50-100 mg, po twice a day on 1st day, then 25 mg once a day.
Sulfadiazine - 1-1.5 g, po every 6 hourly
Leucovorin (folinic acid) - 10 mg or more/day.