Very few cases of mother to infant transmission of toxoplasma
infected women have been reported (26-30)
. The risk for congenital infection is low among infants born to women who became infected during first trimester (range: 2-6%) but increases sharply thereafter with a risk as high as 81% for women acquiring infection during the last few weeks of pregnancy(31)
. Infection of the fetus in early gestation results in more severe involvement with milder disease with infection late in gestations.
CNS involvement with Toxoplasma gondii is uncommon in HIV
infected children. In most cases, Toxoplasma encephalitis
is considered to be due to congenital infection. Rarely it may be due to primary acquired toxoplasmosis (32-36)
Most children are asymptomatic at birth. Late sequelae such as retinitis, visual impairment and neurological impairment may be seen after several months to years. Symptoms in infants may include maculopapular rash, generalized lymphadenopathy, hepatosplenomegaly, jaundice, hematologic abnormalities, hydrocephalus
, microcephaly, intracerebral calcifications and seizures
. Acquired toxoplasmosis may lead to malaise, fever
, sore throat, myalgia, lymphadenopathy and mononucleosis - like syndrome.
Isolated ocular toxoplasmosis is rare and is usually in association with CNS infection. CNS toxoplasmosis may present as headache
, fever, changes in mental status, seizures, psychosis and focal neurological deficits.
Congenital toxoplasmosis is diagnosed by detection of Toxoplasma specific IgM, IgA or IgE in neonatal serum within the first 6 months of life or persistence of specific IgG antibody beyond 12 months of age.
A presumptive diagnosis of CNS toxoplasmosis is done with correlating clinical symptoms, presence of Toxoplasma specific IgG and presence of space occupying lesion on imaging studies of the brain especially ring-enhancing lesions in the basal ganglia and cerebral corticomedullary junction. Definitive diagnosis requires histologic or cytologic confirmation by brain biopsy