Grinberg L M, Abramova F A, Yampolskaya O V, Walker D H, Smith J H
Department of Pathology, Tuberculosis and Pulmonary Diseases Unit, Hospital 40, Ekaterinburg, Russia.
Mod Pathol. 2001 May;14(5):482-95. doi: 10.1038/modpathol.3880337.
Forty-one cases of documented inhalational anthrax from the Sverdlovsk epidemic of 1979 traced to release of aerosols of Bacillus anthracis at a secret biologic-agent production facility were evaluated by semiquantitative histopathologic analysis of tissue concentrations of organisms, inflammation, hemorrhage, and other lesions in the mediastinum, mediastinal lymph nodes, bronchi, lungs, heart, spleen, liver, intestines, kidneys, adrenal glands, and central nervous system. These data were correlated with clinical, epidemiologic, and demographic data. The patients' courses, with a variable incubation period and short nonspecific course (4 days before hospitalization) with rapid demise (1 day of hospitalization before death), correlated with systemic bacterial infection and lesions. Bacillus anthracis were identified in all cases in which there was no antibiotic treatment or there was treatment for fewer than 21 hours. The lesions that were the most severe and apparently of longest duration were in the mediastinal lymph nodes and mediastinum. There and elsewhere, peripheral transudate surrounded fibrin-rich edema; necrosis of arteries and veins was the most likely source of large hemorrhages displacing tissue or infiltrating tissue, respectively; and apoptosis of lymphocytes was observed. Respiratory function was compromised by mediastinal expansion, large pleural effusions, and hematogenous and retrograde lymphatic vessel spread of B. anthracis to the lung with consequent pneumonia. The central nervous system and intestines manifested similar hematogenous spread, vasculitis, hemorrhages, and edema. These pathologic findings are consistent with previous experimental studies showing transport of inhaled spores to mediastinal lymph nodes, where germination and growth lead to local lesions and systemic spread, with resulting edema and cell death, owing to the effects of edema toxin and lethal toxin. The identification of the vascular lesions as a basis for the prominent hemorrhages is a novel observation for human inhalational anthrax.
对1979年斯维尔德洛夫斯克炭疽疫情中41例有记录的吸入性炭疽病例进行了评估,这些病例追溯至一家秘密生物制剂生产设施释放的炭疽芽孢杆菌气溶胶。评估方法是对纵隔、纵隔淋巴结、支气管、肺、心脏、脾脏、肝脏、肠道、肾脏、肾上腺和中枢神经系统中生物体的组织浓度、炎症、出血及其他病变进行半定量组织病理学分析。这些数据与临床、流行病学和人口统计学数据相关联。患者病程具有可变的潜伏期和短暂的非特异性病程(住院前4天),随后迅速死亡(死亡前住院1天),这与全身细菌感染及病变相关。在所有未接受抗生素治疗或治疗时间少于21小时的病例中均鉴定出炭疽芽孢杆菌。最严重且显然持续时间最长的病变位于纵隔淋巴结和纵隔。在那里及其他部位,外周漏出液围绕着富含纤维蛋白的水肿;动脉和静脉坏死分别是导致组织移位或浸润组织的大出血的最可能来源;观察到淋巴细胞凋亡。纵隔扩张、大量胸腔积液以及炭疽芽孢杆菌经血行和逆行淋巴管扩散至肺部导致肺炎,从而损害了呼吸功能。中枢神经系统和肠道表现出类似的血行扩散、血管炎、出血和水肿。这些病理发现与先前的实验研究一致,表明吸入的芽孢转运至纵隔淋巴结,在那里发芽和生长导致局部病变和全身扩散,进而由于水肿毒素和致死毒素的作用导致水肿和细胞死亡。将血管病变鉴定为显著出血的基础是人类吸入性炭疽的一项新发现。