ABSTRACT
Congenital respiratory viral infection is followed in the CNS of fetuses and newborns by grave dyscirculatory disturbances with glia proliferation and nervous tissue edema. The process is mainly localized in the periventricular regions of the brain ventricles. Neurologic and morphologic consequences of these damages in the CNS of fetuses and newborns need further studies.
Subject(s)
Central Nervous System Infections/congenital , Fetal Diseases/virology , Infectious Disease Transmission, Vertical , Pregnancy Complications, Infectious/virology , Respiratory Syncytial Virus Infections/congenital , Central Nervous System Infections/pathology , Central Nervous System Infections/transmission , Central Nervous System Infections/virology , Female , Fetal Diseases/pathology , Humans , Infant, Newborn , Pregnancy , Pregnancy Complications, Infectious/pathology , Respiratory Syncytial Virus Infections/pathology , Respiratory Syncytial Virus Infections/transmissionABSTRACT
Electron microscopy of the placentas affected by respiratory-syncytial virus and mycoplasmas (Mycoplasma urealyticum) revealed the most pronounced alterations in the syncytiotrophoblast structures. Destructive changes in the respiratory-syncytial infection were associated with a direct reproduction of viral particles. Two types of alterations (acute and long-lasting) reflecting two stages of the infectious process are reported in the Mycoplasma infection.
Subject(s)
Mycoplasma Infections/pathology , Placenta Diseases/pathology , Respiratory Syncytial Virus Infections/pathology , Female , Humans , Microscopy, Electron , Pregnancy , Virus Replication/physiologyABSTRACT
An investigation of 88 placentas in toxicosis of the second half of pregnancy has detected symptoms of the immune alteration detailed by means of an electron microscopic analysis and immunomorphological investigations with the help of luminescent sera against immunoglobulins A, M. G and C3 fraction of complement. The alterations found are indicative of the participation of immune mechanisms in the formation of placental insufficiency and their important role in pathogenesis of gestational toxicosis.