Abstract: Congenital toxoplasmosis is a rare but severe infection caused by transplacental transmission of Toxoplasma gondii from mother to fetus. This case report describes a neonate with clinical manifestations suggestive of congenital toxoplasmosis, diagnostic challenges, and management strategies. Early recognition and timely intervention are essential to mitigate long-term complications.
Introduction: Congenital toxoplasmosis results from maternal infection with Toxoplasma gondii during pregnancy. The severity of fetal involvement depends on gestational age at infection, with early infections often leading to severe complications, including chorioretinitis, hydrocephalus, intracranial calcifications, and neurodevelopmental impairment. This report highlights a case of a neonate diagnosed with congenital toxoplasmosis based on clinical, serological, and radiological findings.
Case Presentation: A male neonate was born at 38 weeks of gestation to a 28-year-old primigravida woman with no significant antenatal complications. The mother had no known history of toxoplasmosis, but routine antenatal screening was not performed. The neonate had a birth weight of 2800 grams and an Apgar score of 8 and 9 at one and five minutes, respectively.
At birth, the baby presented with hepatosplenomegaly, mild jaundice, and hypotonia. On further evaluation, cranial ultrasound revealed periventricular calcifications and mild ventriculomegaly. Fundoscopic examination identified chorioretinitis. A TORCH (Toxoplasmosis, Other [syphilis], Rubella, Cytomegalovirus, and Herpes simplex) panel was performed, revealing elevated Toxoplasma gondii IgM and IgG titers in both the neonate and mother.
Polymerase chain reaction (PCR) analysis of cerebrospinal fluid (CSF) confirmed the presence of T. gondii DNA, supporting the diagnosis of congenital toxoplasmosis.
Management and Outcome: The neonate was initiated on a combination therapy of pyrimethamine, sulfadiazine, and leucovorin for one year. Corticosteroids were administered due to significant chorioretinitis with vitreous inflammation. Regular follow-up assessments, including neuroimaging and ophthalmologic evaluations, were scheduled. By six months, the infant demonstrated improved neurological function, with resolution of hepatosplenomegaly, though mild developmental delay persisted.
Discussion: Congenital toxoplasmosis poses diagnostic challenges, especially in asymptomatic or mildly symptomatic cases. A combination of serological testing, imaging, and molecular assays enhances diagnostic accuracy. Early treatment significantly improves outcomes, reducing the risk of long-term sequelae such as vision loss, hydrocephalus, and intellectual disabilities.
Prevention strategies, including maternal education on avoiding undercooked meat, unwashed vegetables, and cat litter exposure, are crucial in reducing the incidence of congenital toxoplasmosis. Routine prenatal screening in endemic regions may facilitate early detection and intervention.
Conclusion: Congenital toxoplasmosis remains a significant yet preventable cause of neonatal morbidity. A high index of suspicion, prompt diagnostic workup, and timely initiation of treatment are key to optimizing patient outcomes. This case underscores the importance of prenatal screening and awareness programs in mitigating the disease burden.
References:
- Montoya JG, Remington JS. “Management of Toxoplasma gondii Infection During Pregnancy.” Clin Infect Dis. 2008;47(4):554-566.
- Peyron F, Wallon M, Kieffer F, Garweg J. “Toxoplasmosis in Pregnancy and Early Childhood: New Aspects of an Old Disease.” Clin Microbiol Rev. 2016;29(1):1-44.
- Dunn D, Wallon M, Peyron F, Petersen E, Peckham C, Gilbert R. “Mother-to-child transmission of toxoplasmosis: risk estimates for clinical counseling.” Lancet. 1999;353(9167):1829-1833.
