Treatment is not always available, specific, or effective. Nonetheless, some encouraging results have been reported for preventing the disease and for specifically treating the infant when the correct diagnosis is made (see Table 66-1).
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Abnormal Head Size, Shape, and Fontanels Visual Impairment and Leukocoria Petechiae/Purpura
Vertical transmission of Toxoplasma gondii occurs by trans-placental transfer of the organism from the mother to the fetus after an acute maternal infection. Fetal infection rarely can occur after reactivation of disease in an immunocompromised pregnant mother. Transmission from an acutely infected mother to her fetus occurs in about 30% to 40% of cases, but the rate varies directly with gestational age. Transmission rates and the timing of fetal infection correlate directly with placental blood flow; the risk of infection increases throughout gestation to 90% or greater near term, and the time interval between maternal and fetal infection decreases.
The severity of fetal disease varies inversely with the gestational age at which maternal infection occurs. Most infants have subclinical infection with no overt disease at birth; however, specific ophthalmologic and central nervous system (CNS) evaluations may reveal abnormalities. The classic findings of hydrocephalus, chorioretinitis, and intracerebral calcifications suggest the diagnosis of congenital toxoplasmosis. Affected infants tend to be small for gestational age, develop early-onset jaundice, have hepatosplenomegaly, and present with a generalized maculopapular rash. Seizures are common, and skull films may reveal diffuse cortical calcifications in contrast to the periventricular pattern observed with CMV. These infants are at increased risk for long-term neurologic and neurodevelopmental complications.
Serologic tests are the primary means of diagnosis. IgG-specific antibodies achieve a peak concentration 1 to 2 months after infection and remain positive indefinitely. For infants with seroconversion or a fourfold increase in IgG titers, specific IgM antibody determinations should be performed to confirm disease. Especially for congenital infections, measurement of IgA and IgE antibodies can be useful to confirm the disease. Thorough ophthalmologic, auditory, and neurologic evaluations (head computed tomography and cerebrospinal fluid [CSF] examination) are indicated.
For symptomatic and asymptomatic congenital infections, initial therapy should include pyrimethamine (supplemented with folic acid) combined with sulfadiazine. Duration of therapy is often prolonged, even up to 1 year. Optimal dosages of medications and duration of therapy should be determined in consultation with appropriate specialists.
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Abnormal Head Size, Shape, and
Toxoplasma gondii Heterophil-negative mononucleosis Hydrocephalus, abnormal spinal fluid, intracranial Exposure to cats or raw meat or calcifications, chorioretinitis, jaundice, hepatosplenomegaly, immunosuppression fever High-risk exposure at 10–24 wk gestation Many infants asymptomatic at birth
Treatment: pyrimethamine plus sulfadiazine