Very few cases of mother to infant transmission of toxoplasma in HIV 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).
Clinical features
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.
Diagnosis
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.
Treatment
Congenital Toxoplasmosis
Pyrimethamine (loading dose of 2 mg/kg/day) for 2 days and then 1 mg/kg/day for 2-6 months followed by 1 mg/kg administered three times a week
+
Sulfadiazine (50 mg/kg/dose twice daily)
+
Folinic acid (10-25 mg daily)
Recommended duration of therapy - 12 months.
HIV infected children with acquired CNS, ocular or systemic Toxoplasmosis
Pyrimethamine (2 mg/kg/day for 3 days, followed by 1 mg/kg/day)
+
Sulfadiazine (25-50 mg/kg/dose 4 times daily)
+
Folinic Acid (10-25 mg/day)
Acute therapy should be continued for 6 weeks and longer courses may be required with extensive disease or poor response.
- For an infant born to a mother with symptomatic toxoplasma during pregnancy, empiric therapy of the newborn should be given.
- Steroids may be indicated in presence of severe chorioretinitis or CNS Toxoplasmosis with mass effects. However, they should be discontinued as early as possible.
Prophylaxis
Primary Prophylaxis : TMP/SMX prophylaxis when given for PCP prophylaxis also provides prophylaxis against Toxoplasmosis. Children greater than 12 months of age who qualify for PCP prophylaxis and who receive an agent other than TMP-SMX or atovaquone should be tested for toxoplasma IgG antibodies should receive prophylaxis for Toxoplasmosis.
Drug & Dosage for of TMP-SMX for primary prophylaxis
Drugs
|
Dosage
|
TMP/SMX
|
- 150 mg of TMP m2/day PO BD on alternate day - 5 mg/kg of TMP/day PO HS daily
|
Secondary prophylaxis
Drugs
|
Dosage
|
Duration
|
A
|
Sulfadiazine + Pyrimethamine + Leucovorin
|
80-100 mg/kg/day in 2- 4 divided doses
1 mg/kg/day PO
5 mg PO alternate day
|
Life-long
|
B
|
Clindamycin + Pyrimethamine + Leucovorin
|
20-30 mg/kg/day in 4 divided dose
1 mg/kg/day PO
5 mg PO alternate day
|
Life-long
|
Secondary prophylaxis : Life-long suppression is indicted after treatment for Toxoplasmosis to prevent recurrence.