Congenital toxoplasmosis: Difference between revisions
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**However, it is possible to acquire from reactivation of latent toxoplasmosis in an HIV-infected mother |
**However, it is possible to acquire from reactivation of latent toxoplasmosis in an HIV-infected mother |
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*Risk of transplacental infection of fetus is lowest in first trimester and highest in third |
*Risk of transplacental infection of fetus is lowest in first trimester and highest in third |
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**First trimester: 10% |
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**Second trimester: 25% |
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**Third trimester: 80% |
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*See also [[toxoplasmosis in pregnancy]] |
*See also [[toxoplasmosis in pregnancy]] |
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Revision as of 12:04, 20 September 2020
Background
- Can be acquired during maternal parasitemia associated with primary infection
- However, it is possible to acquire from reactivation of latent toxoplasmosis in an HIV-infected mother
- Risk of transplacental infection of fetus is lowest in first trimester and highest in third
- First trimester: 10%
- Second trimester: 25%
- Third trimester: 80%
- See also toxoplasmosis in pregnancy
Clinical Manifestations
- At birth, 85% of infected babies are asymptomatic and only 15% are symptomatic
- Risk of infection is related to trimester of infection: 6% in first, 40% in second, and 72% in third
- Risk of signs of congenital infection is inversely related to trimester of infection: 61% in first, 25% in second, and 9% in third
- Classic triad of chorioretinitis (most common), intraparenchymal cerebral calcifications, and hydrocephalus
- Others: thrombocytopenia, hepatitis, hepatosplenomegaly, cataracts, strabismus, microphthalmia
Diagnosis
- Standard workup starts with serology, then adds PCR and other investigations if clinical suspicion is high
- Serology: in neonates, IgG serology reflects maternal status, so use IgM and IgA instead
- Molecular testing: if clinical suspicion is high, add PCR of the peripheral blood, urine, and CSF to the serology
- If clinical suspicion is high, also get ophthalmologic evaluation, hearing assessment, ultrasound or CT of the brain, and lumbar puncture
Management
- Postnatal treatment of neonates is with standard therapy for at least 12 months
- Sulfadiazine 50 mg/kg q12h
- Pyrimethamine 1 mg/kg q12h for 2 days (load), followed by 1 mg/kg for 2 to 6 months, followed by 1 mg/kg qMWF
- Folinic acid 10 mg PO thrice weekly until 1 week after pyrimethamine is stopped
- Treatment of congenital infection in older children is standard therapy until 1 to 2 weeks after resolution of signs or symptoms
- Pyrimethamine 1 mg/kg q12h (max 50 mg) for 2 days, followed by 1 mg/kg/day (max 25 mg)
- Sulfadiazine 75 mg/kg load, followed by 50 mg/kg q12h (max 4 g/day)
- Folinic acid 10-20 mg po thrice weekly
- Can add prednisone for severe chorioretinits at 1 mg/kg/day divided bid (max 40 mg/day), followed by a rapid taper
- Serial evaluations with a clinical assessment, neuroradiology, ophthalmology, and CSF analysis
- For prevention, refer to the management of toxoplasmosis in pregnancy
References
- ^ Effectiveness of prenatal treatment for congenital toxoplasmosis: a meta-analysis of individual patients' data. The Lancet. 2007;369(9556):115-122. doi:10.1016/s0140-6736(07)60072-5.