Proceedings of the International scientific and practical conference ―Oxford 2026: Science and Education Today‖ (May 29-31, 2026) / Publisher website: www.naukainfo.com. - Oxford, United Kingdom, 2026. - 392 p.

336 trophoblast cells during the first trimester may indicate a reduced capacity of early placental cells to recruit an immune response against intrauterine infection. Transplacental infection can lead to a wide spectrum of manifestations in the fetus and infant, including spontaneous miscarriage and stillbirth [4]. The possibility of congenital infection has also been described following reinfection of a previously seropositive pregnant woman with a different, more virulent strain of toxoplasma [5]. Congenital toxoplasmosis can also mimic congenital infections caused by agents such as herpes simplex virus, cytomegalovirus, and rubella virus [6]. Results and Discussion The classic triad of signs indicative of congenital toxoplasmosis includes chorioretinitis, hydrocephalus, and intracranial calcifications [1, 7, 8]. In contrast, a study by Almeida RR et al. found that children born to mothers infected with toxoplasma more frequently had no specific signs of infection at birth, other than low weight for their gestational age. It was considered that low birth weight may have been associated with congenital infection [6]. In premature infants with toxoplasmosis, neurological and ocular lesions may develop within the first three months of life. In contrast, full-term infants infected with T. gondii more commonly have a milder disease course, with hepatosplenomegaly and lymphadenopathy within the first two months of life. Although most children infected in utero are born without obvious signs of toxoplasmosis on routine neonatal examination, up to 80 percent develop learning or visual impairments later in life. In congenital infection, decreased visual acuity and new ocular lesions may occur throughout nearly the entire lifetime [1]. Several studies indicate a correlation between hearing impairment and congenital toxoplasmosis, which may be triggered by neurological damage. Congenital toxoplasmosis has been reported as a risk factor for hearing loss. The pathophysiology of hearing loss in congenital toxoplasmosis can be explained by a postnatal inflammatory response against parasites located in the internal auditory