title: Syncytiotrophoblast degradation and the pathophysiology of the malaria-infected placenta.
abstract: Malaria is associated with excessive parasitic infection of the placenta and a reduction in neonatal birthweight. This study has investigated placental cell death in women with active and past malarial infection. Term placentae, with and without malarial pathology, were obtained from women in The Gambia. Active and past malaria infections were identified in placental sections and histological examination was used to determine the number of villi, the incidence of apoptosis, syncytial degradation, fibrinoid deposition and the frequency of syncytial knots. Placentae with active malaria infection showed erythrocyte adhesion of infected cells to syncytiotrophoblast, syncytial degradation, increased syncytial knotting and, in rare cases, localized destruction of the villi. Past malarial infection was characterized by syncytiotrophoblast disruption and fibrin-type fibrinoid (FTF) deposition. Perivillous FTF deposition was consistent with increased syncytial lesions and both increased lesions and syncytial knots were associated with birthweight reductions. Active malaria infection produced no alteration in placental apoptosis. The numbers of chorionic villi remained unchanged and infiltration of inflammatory cells, although not measured directly, appeared to be non-pervasive within the infected tissue. These observations establish a direct link between malaria parasitic infection and syncytiotrophoblast damage. The placental rejection of parasite-affected syncytia may invoke structural changes to compensate for inadequate placental exchange. Syncytial destruction could have serious implications; impairing fetal growth and in some rare cases, providing a previously unrecognized pathway to congenital infection.
authors.affiliation: Maternal and Fetal Health Research Centre, University of Manchester, St Mary's Hospital, Whitworth Park, Manchester M13 0JH, UK. Ian.Crocker@man.ac.uk
authors.forename: I P
authors.initials: IP
authors.lastname: Crocker
authors.forename: O M
authors.initials: OM
authors.lastname: Tanner
authors.forename: J E
authors.initials: JE
authors.lastname: Myers
authors.forename: J N
authors.initials: JN
authors.lastname: Bulmer
authors.forename: G
authors.initials: G
authors.lastname: Walraven
authors.forename: P N
authors.initials: PN
authors.lastname: Baker
mesh_terms: D000293:Adolescent; D000328:Adult; D017209:Apoptosis; D002824:Chorionic Villi / Q000378:metabolism / Q000469:parasitology* / Q000473:pathology*; D005260:Female; D005337:Fibrin / Q000378:metabolism; D005714:Gambia; D006801:Humans; D008288:Malaria / Q000503:physiopathology*; D008423:Maternal Age; D011247:Pregnancy; D015597:Pregnancy Complications, Parasitic; D018566:Pregnancy, High-Risk; D014327:Trophoblasts / Q000378:metabolism / Q000469:parasitology* / Q000473:pathology*
chemical_list: D005337:Fibrin