Etiology, pathomorphologic changes and perinatal CNS lesions in intrauterine encephalitis in fetuses and newborns

Introduction. Among perinatal infections, the significance of intrauterine encephalitis (IUE) is determined by the high mortality rate in fetuses and newborns and the development of disabilities in subsequent periods of life, including cerebral palsy, schizophrenic, and autistic disorders. The morphological picture of IUE is characterized by significant polymorphism, which is due to both the multietiological nature of encephalitis and different types of neuron response under pathological conditions. Aim. Studying the etiology and morphological features of IUE and its outcomes. Materials and methods. The brains of 37 fetuses and newborns at a gestation period of 24–27 were examined, in which the signs of IUE were detected morphologically. Light microscopy and immunohistochemical examination were used. By immunohistochemical typing, the markers of the following pathogens were determined: herpes simplex virus types 1 and 2, cytomegalovirus, Toxoplasma gondii, Epstein-Barr virus. Results. IUE was at most a manifestation of systemic intrauterine infection – 86,48% of cases. The morphological picture in IUE was characterized by two main manifestations: productive encephalitis, including granulomatous one, and exudative and productive encephalitis, which probably reflects its etiological features. Etiology of IUE: viral (66,7%), bacterial and fungal (33,3%) pathogens predominated. IUE was complicated by hemorrhagic syndrome with the development of fatal forms: in 21,68% (8 cases) – by subependymal hemorrhages, in 16,2% (6 cases) – by intraventricular hemorrhages. Conclusion. The IUE development in fetuses and newborns is a severe form of systemic intrauterine infection associated primarily with the pathogens of the TORCH complex, the complications of which are fatal subependymal and intraventricular hemorrhages.