Marco A J, Domingo M, Prats M, Briones V, Pumarola M, Dominguez L
Dept. de Anatomía Patológica, Facultad de Veterinaria, Universidad Autónoma de Barcelona, Spain.
J Comp Pathol. 1991 Jul;105(1):1-15. doi: 10.1016/s0021-9975(08)80057-6.
Adult female Swiss albino mice were infected intraperitoneally or subcutaneously with Listeria monocytogenes Serovar 4b or 1/2a and killed at intervals. Thymus, spleen, Peyer's patches and a variety of lymph nodes, including the jejunal (mesenteric), mediastinal, lumbar, mandibular and superficial inguinal, were examined by histopathology and by immunocytochemistry for detection of L. monocytogenes antigen. Similar results were obtained with both Serovars and by both routes of inoculation used. In the spleen, L. monocytogenes was detected, by immunoperoxidase staining, as soon as 4 h after inoculation, inside phagocytic cells located predominantly in the marginal zone of the white pulp. This was followed by inflammation, necrosis and depletion of lymphoid cells, which extended in extreme cases to the whole organ. Inflammatory lesions diminished progressively at 5 to 6 days after inoculation. In animals dying of the infection, a severe necrotizing splenitis was present. Depletion of lymphoid cells and inflammatory changes were widespread in the lymph nodes and to a lesser extent in the Peyer's patches. An extensive necrotizing lymphadenitis was the prominent lesion in severely affected nodes. Inflammatory lesions and detection of L. monocytogenes antigen started around the venules of high endothelium. A thymus depletion, not associated with the multiplication of bacteria in the organ, was also a constant feature of the infection. This study suggests that L. monocytogenes (1) is transported to the spleen and to the lymph nodes by phagocytes, entering the organs by the marginal sinus in the spleen and by the venules of high endothelium in the lymph nodes; (2) multiplies in these cells as well as in neutrophilic granulocytes (the latter rapidly migrate to the affected zones); and (3) induce a splenitis and lymphadenitis, involving predominantly T cell-dependent areas, with a necrotizing component in severe cases. From our observations it is concluded that infection of the lymphoid system is a major feature in the pathogenesis of murine listeriosis.
成年雌性瑞士白化小鼠通过腹腔内或皮下注射感染单核细胞增生李斯特菌血清型4b或1/2a，并在不同时间点处死。对胸腺、脾脏、派伊尔结以及包括空肠（肠系膜）、纵隔、腰、下颌和浅表腹股沟在内的各种淋巴结进行组织病理学和免疫细胞化学检查，以检测单核细胞增生李斯特菌抗原。两种血清型以及两种接种途径均得到了相似的结果。在脾脏中，接种后4小时，通过免疫过氧化物酶染色在主要位于白髓边缘区吞噬细胞内检测到单核细胞增生李斯特菌。随后出现炎症、坏死以及淋巴细胞耗竭，在极端情况下会扩展至整个器官。接种后5至6天炎症病变逐渐减轻。在死于感染的动物中，出现严重的坏死性脾炎。淋巴细胞耗竭和炎症变化在淋巴结中广泛存在，在派伊尔结中程度较轻。广泛的坏死性淋巴结炎是严重受累淋巴结的突出病变。炎症病变和单核细胞增生李斯特菌抗原的检测始于高内皮小静脉周围。胸腺耗竭也是感染的一个持续特征，与器官内细菌繁殖无关。本研究表明，单核细胞增生李斯特菌（1）通过吞噬细胞转运至脾脏和淋巴结，通过脾脏边缘窦和淋巴结高内皮小静脉进入器官；（2）在这些细胞以及嗜中性粒细胞（后者迅速迁移至受影响区域）中繁殖；（3）诱导脾炎和淋巴结炎，主要累及T细胞依赖区，严重时伴有坏死成分。根据我们的观察得出结论，淋巴系统感染是小鼠李斯特菌病发病机制的主要特征。
