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炭疽芽胞经呼吸道感染能引起人和实验动物的吸入性炭疽。豚鼠气雾感染炭疽芽胞的病因学研究证明芽胞吸入正常肺泡后被肺泡巨噬细胞吞噬,运至邻近纵膈淋巴结内,然后在纵膈淋巴结,特别是肺门淋巴结的被膜下淋巴窦中,静止期芽胞发芽繁殖成链状或竹节状方头大杆菌,并在局部产生急性原发病灶。实验豚鼠和猕猴吸入性炭疽显示相类似的病变特征,呈现纵膈胶冻样水肿、纵膈淋巴结急性出血性炎症、胸腔积液、败血症脾以及多发性新鲜血栓形成。电镜下,临终期感染小白鼠的肺毛细血管、脾血窦和心耳超薄切片中均可查见变性血小板、纤维素、和血细胞凝聚的早期血液凝集的超微病变图象。这种因炭疽毒素所致的弥漫性血管内凝血是炭疽败血症在临终期继发中毒性休克而死亡的主要原因。本文报告1例顿挫型人吸入性炭疽,患者在生前曾应用大剂量抗菌素和特异抗血清治疗,尔后因不慎呛入呕吐物堵塞支气管窒息猝死。尸检病理解剖学和组织学观察仍具有吸入性炭疽的形态特征,但菌血症已得到控制。
Anthrax spores through respiratory tract infections can cause human and laboratory animals inhalation anthrax. The etiology of guinea pig aerosol infection of anthrax sprouting showed that spores inhaled normal alveoli were phagocytosed by alveolar macrophages and transported to the adjacent mediastinal lymph nodes, and then in the mediastinal lymph nodes, especially hilar lymph nodes in sub-sub-lymphatic sinus, quiescent Sprouting germination buds or sliver-shaped Stem-shaped bacteria, and in local acute primary lesions. Infectious anthrax in experimental guinea pigs and macaques showed similar lesions with mediastinal jelly-like edema, mediastinal lymph node acute hemorrhagic inflammation, pleural effusion, sepsis spleen and multiple fresh thrombosis. Under electron microscopy, the images of early blood coagulation in the blood coagulation of degenerative platelets, fibrin, and blood cells can be seen in the pulmonary capillaries, splenic sinusoids and the atrial appendages of mice with terminal-infection. This diffuse intravascular coagulation due to anthrax toxin is the leading cause of death from anthrax sepsis secondary to toxic shock at the end of life. This article reports 1 case of frustrated human inhalation anthrax. The patient was treated with large doses of antibiotics and specific antisera before his death. Then he was accidentally choked with vomit to block the sudden death of bronchial asphyxia. Autopsy pathological anatomy and histological observation still have the morphological characteristics of inhaled anthrax, but bacteremia has been controlled.