Oduola A M, Phillips J H, Spicer S S, Galbraith R M
Exp Parasitol. 1986 Oct;62(2):181-93. doi: 10.1016/0014-4894(86)90022-6.
The pathological changes associated with malarial infection in pregnancy were studied in rats and mice infected with Plasmodium berghei at different stages of gestation. Histopathological and ultrastructural studies of infected placentae near term in both species revealed disruption of architecture with gross thickening and necrosis of cells in the labyrinthine zone and fibrosis of the trilaminar trophoblast separating the maternal and fetal circulations. In the mouse, the extent of histopathological alterations in infected placentae ranged from the presence of immature erythrocytes in the fetal circulation in low grade maternal infection, to the marked deposition of fibrinoid material on the trilaminar trophoblast and inflammatory masses in severely infected placentae. In the rat, histopathological aberrations in the placentae were marked by placental stroma edema, fibrosis, and cellular infiltration. Immunohistological studies of cryostat sections of placentae from infected animals showed more parasites and pigment in infected mouse placentae than in the corresponding rat organ, but in both species parasites and pigment were largely confined to the maternal blood spaces and were only occasionally found in necrotic areas of trophoblast. No clear differences were observed between infected and control placentae in terms of the amount of IgG, IgM, or IgA which were each present in various amounts. These observations and the rarity of congenital malaria in the animals indicate that the placenta constitutes a major barrier to infection of the fetus. However, the pathological aberrations in the infected placentae may impose a biochemical stress upon the fetus which may account for the low birthweight, the increased frequency of abortion, and the greatly increased maternal and fetal death rates observed in malaria.
在妊娠不同阶段感染伯氏疟原虫的大鼠和小鼠中，研究了与妊娠期疟疾感染相关的病理变化。对这两个物种接近足月时受感染胎盘的组织病理学和超微结构研究显示，胎盘结构破坏，迷路区细胞明显增厚和坏死，分隔母血和胎儿血循环的三层滋养层出现纤维化。在小鼠中，受感染胎盘的组织病理学改变程度不等，从轻度母体感染时胎儿循环中出现未成熟红细胞，到重度感染胎盘时三层滋养层上有明显的类纤维蛋白物质沉积和炎性肿块。在大鼠中，胎盘的组织病理学异常表现为胎盘间质水肿、纤维化和细胞浸润。对受感染动物胎盘冰冻切片的免疫组织学研究表明，受感染小鼠胎盘中的寄生虫和色素比相应的大鼠器官更多，但在这两个物种中，寄生虫和色素主要局限于母血间隙，仅偶尔在滋养层坏死区域发现。在受感染胎盘和对照胎盘中，IgG、IgM或IgA的含量均存在差异，但差异不明显。这些观察结果以及动物中先天性疟疾的罕见情况表明，胎盘是胎儿感染的主要屏障。然而，受感染胎盘的病理异常可能会给胎儿带来生化应激，这可能解释了疟疾中观察到的低出生体重、流产频率增加以及母婴死亡率大幅上升的现象。
