Quantitative pathology of inhalational anthrax I: Quantitative microscopic findings
Quantitative pathology of inhalational anthrax I: Quantitative microscopic findings
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DOI：
10.1038/modpathol.3880337
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发表时间：
2001-05-01
期刊：
影响因子：
7.5
通讯作者：
Smith, JH
中科院分区：
文献类型：
--
作者：
Grinberg, LM;Abramova, FA;Smith, JH
通过对纵隔、纵隔淋巴结、支气管、肺、心、脾、肝、肠、肾、肾上腺和中枢神经系统的组织浓度、炎症、出血和其他病变的半定量组织病理学分析，对1979年斯维尔德洛夫斯克疫情中记录的41例吸入性炭疽病例进行了评估。这些数据与临床、流行病学和人口统计数据相关。患者病程长短不一，病程短（住院前4天），死亡快（死亡前1天），与全身性细菌感染和病变相关。在没有抗生素治疗或治疗时间少于21小时的所有病例中均发现炭疽芽胞杆菌。纵隔淋巴结和纵隔的病变最严重，持续时间最长。此处及其他部位，外周渗出液包围富含纤维蛋白的水肿；动脉坏死和静脉坏死是大出血最可能的来源，它们分别取代组织或浸润组织；观察淋巴细胞凋亡情况。呼吸功能受到纵隔扩张、大量胸膜积液、炭疽杆菌向肺的血行和逆行淋巴管扩散并随之发生肺炎的损害，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，这些病理结果与先前的实验研究一致，表明吸入的孢子转运到纵隔淋巴结。由于水肿毒素和致死毒素的作用，发芽和生长导致局部病变和全身扩散，导致水肿和细胞死亡。血管病变的识别作为突出出血的基础是一个新的观察人类吸入性炭疽。
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. Bacilllus 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.