Tobias L, Cordes D O, Schurig G G
Department of Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg.
Vet Pathol. 1993 Mar;30(2):119-29. doi: 10.1177/030098589303000204.
Fifty-five pregnant BALB/c mice received various doses of Brucella abortus virulent strain 2308 intraperitoneally on day 9 of gestation, and uteri and spleens were examined at 3, 5, 7, and 9 days post-inoculation to study the pathogenesis of infection. A dose of 10(5.7) B. abortus organisms produced a severe, necrosuppurative placentitis. Bacteria multiplied preferentially within the placenta and were identified within the rough endoplasmic reticulum of trophoblast giant cells and within the visceral yolk sac endoderm. Abortions did not occur, but infarction of the labyrinth region of severely affected placentas occasionally resulted in fetal death. The severity of infection in the spleens of nonpregnant mice receiving the same challenge dose was not significantly different from that in the spleens of challenged pregnant mice. These results suggest that the sensitivity of the pregnant mouse to placental brucellosis is not due to a generalized immunosuppression but rather may involve a combination of local suppression of the immune response and a susceptible cell population suitable for Brucella colonization and replication. Experimental murine brucellosis resembles ruminant brucellosis and provides a model to study the intracellular replication of B. abortus in trophoblasts.
55只怀孕的BALB/c小鼠在妊娠第9天经腹腔注射不同剂量的流产布鲁氏菌强毒株2308，并在接种后3、5、7和9天检查子宫和脾脏，以研究感染的发病机制。10(5.7)个流产布鲁氏菌生物体的剂量导致了严重的坏死性化脓性胎盘炎。细菌优先在胎盘中繁殖，并在滋养层巨细胞的粗面内质网和内脏卵黄囊内胚层中被发现。未发生流产，但严重受影响胎盘的迷路区梗死偶尔导致胎儿死亡。接受相同攻击剂量的未怀孕小鼠脾脏中的感染严重程度与受攻击的怀孕小鼠脾脏中的感染严重程度无显著差异。这些结果表明，怀孕小鼠对胎盘布鲁氏菌病的敏感性不是由于全身性免疫抑制，而是可能涉及局部免疫反应抑制和适合布鲁氏菌定植和复制的易感细胞群的组合。实验性小鼠布鲁氏菌病类似于反刍动物布鲁氏菌病，并提供了一个研究流产布鲁氏菌在滋养层细胞内复制的模型。
