Baumgärtner W, Bachmann S
Institut für Veterinär-Pathologie, Justus-Liebig-Universität, Giessen, Germany.
Infect Immun. 1992 Dec;60(12):5232-41. doi: 10.1128/iai.60.12.5232-5241.1992.
The fetoplacental units and the postgravid uterus of BALB/cJ (H-2d) mice inoculated intraperitoneally with Coxiella burnetii (Nine Mile isolate, phase I) on day 6 of pregnancy were examined histologically and immunocytochemically at 1 to 160 days postinoculation. Clinically, abortions, stillbirths, and perinatal deaths were observed. Histological lesions in the placenta were characterized by severe necrosis of the decidua basalis and the labyrinth, fibrinoid degeneration of decidual vessels, and microthrombosis. Pyometra and endometritis at the sites of previous placental attachment, characterized by ulceration, central necrosis, and moderate cellular infiltration consisting of neutrophils and macrophages, were observed postpartum. Pups sacrificed at the age of 9 days exhibited interstitial pneumonia with few granulomas and granulomatous hepatitis and splenitis. Immunocytochemically, antigen-bearing cells were first detected in the decidua 9 days postconception, and single immunopositive cells were detected in the fetal placenta 4 days later. Thereafter, until abortion or parturition, abundant accumulation of C. burnetii antigen was observed in the maternal and fetal compartments of the placenta. Up to 28 days postinoculation, many immunopositive cells were demonstrated at the sites of previous placental attachment, whereas the adjacent endometrium contained only a few antigen-positive cells. C. burnetii antigen was demonstrated in decidual cells, trophoblasts, and macrophages and extracellularly within the sinuses of the labyrinth and in the uterine lumen but not in granulated metrial gland cells. Fetuses in utero and aborted, stillborn, or perinatally dying offspring were immunocytochemically negative for C. burnetii antigen; however, pups killed 9 days after birth showed lesion-associated positive immunoreaction in the lung, liver, and spleen. The present study shows that infection with C. burnetii during pregnancy results in uncontrolled growth of the organism in the murine uteroplacental unit and that associated lesions are characterized by necrosis of placental tissues, fibrinoid degeneration of decidual vessels, and microthrombosis.
在妊娠第6天经腹腔接种伯纳特立克次体（九里分离株，I相）的BALB/cJ（H-2d）小鼠，在接种后1至160天对其胎盘胎儿单位和妊娠后子宫进行了组织学和免疫细胞化学检查。临床上，观察到流产、死产和围产期死亡。胎盘的组织学病变特征为基底蜕膜和迷路严重坏死、蜕膜血管的纤维素样变性以及微血栓形成。产后观察到先前胎盘附着部位的子宫积脓和子宫内膜炎，其特征为溃疡、中央坏死以及由中性粒细胞和巨噬细胞组成的中度细胞浸润。在出生9天时处死的幼崽表现出间质性肺炎，伴有少量肉芽肿以及肉芽肿性肝炎和脾炎。免疫细胞化学检测显示，在受孕后9天首次在蜕膜中检测到含抗原细胞，4天后在胎儿胎盘中检测到单个免疫阳性细胞。此后，直至流产或分娩，在胎盘的母体和胎儿部分均观察到大量伯纳特立克次体抗原的积聚。接种后长达28天，在先前胎盘附着部位可见许多免疫阳性细胞，而相邻的子宫内膜仅含有少量抗原阳性细胞。伯纳特立克次体抗原在蜕膜细胞、滋养层细胞和巨噬细胞中以及在迷路窦内和子宫腔内的细胞外被检测到，但在颗粒状子宫腺细胞中未检测到。子宫内的胎儿以及流产、死产或围产期死亡的后代经免疫细胞化学检测对伯纳特立克次体抗原呈阴性；然而，出生9天后处死的幼崽在肺、肝和脾中显示出与病变相关的阳性免疫反应。本研究表明，孕期感染伯纳特立克次体导致该病原体在小鼠子宫胎盘单位中不受控制地生长，并且相关病变的特征为胎盘组织坏死、蜕膜血管的纤维素样变性以及微血栓形成。
