Crocker I P, Tanner O M, Myers J E, Bulmer J N, Walraven G, Baker P N
Maternal and Fetal Health Research Centre, University of Manchester, St Mary's Hospital, Whitworth Park, Manchester M13 0JH, UK.
Placenta. 2004 Apr;25(4):273-82. doi: 10.1016/j.placenta.2003.09.010.
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.
疟疾与胎盘的过度寄生虫感染以及新生儿出生体重降低有关。本研究调查了患有活动性和既往疟疾感染的女性的胎盘细胞死亡情况。从冈比亚的女性身上获取了有或无疟疾病理特征的足月胎盘。在胎盘切片中识别出活动性和既往疟疾感染，并通过组织学检查来确定绒毛数量、细胞凋亡发生率、合体滋养层降解、纤维蛋白样沉积以及合体结节的频率。患有活动性疟疾感染的胎盘表现为受感染细胞的红细胞粘附于合体滋养层、合体滋养层降解、合体结节增加，在极少数情况下，绒毛会出现局部破坏。既往疟疾感染的特征是合体滋养层破坏和纤维蛋白型纤维蛋白样（FTF）沉积。绒毛周围的FTF沉积与合体病变增加一致，病变增加和合体结节都与出生体重降低有关。活动性疟疾感染并未使胎盘细胞凋亡发生改变。绒毛膜绒毛数量保持不变，炎症细胞浸润虽然未直接测量，但在受感染组织内似乎并不普遍。这些观察结果建立了疟疾寄生虫感染与合体滋养层损伤之间的直接联系。胎盘对受寄生虫影响的合体细胞的排斥可能引发结构变化，以弥补胎盘交换不足。合体滋养层破坏可能具有严重影响；损害胎儿生长，在极少数情况下，提供一条以前未被认识的先天性感染途径。
