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人类免疫缺陷综合征中亨氏罗卡利马氏体感染导致无血管瘤病或紫癜的炎症性疾病。通过免疫细胞化学证实并经DNA扩增确证。

Rochalimaea henselae infection in acquired immunodeficiency syndrome causing inflammatory disease without angiomatosis or peliosis. Demonstration by immunocytochemistry and corroboration by DNA amplification.

作者信息

Slater L N, Pitha J V, Herrera L, Hughson M D, Min K W, Reed J A

机构信息

Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City.

出版信息

Arch Pathol Lab Med. 1994 Jan;118(1):33-8.

PMID:7506902
Abstract

Rochalimaea henselae causes bacillary angiomatosis, bacillary peliosis, and persistent bacteremia. Difficult to cultivate, it is detectable in infected tissues by immunocytochemistry. This technique demonstrated R henselae in autopsy specimens obtained from three deceased patients who had acquired immunodeficiency syndrome, with pathologic tissue changes lacking neoangiogenic features. From the first patient, the cause of nodular collections of lymphocytes and nonepithelioid histiocytes in the liver, spleen, lymph nodes, bone marrow, and heart eluded detection until immunocytochemical identification of R henselae. In the second case, unexpected gross and microscopic necroinflammatory nodules in the liver and spleen contained Warthin-Starry-staining bacilli identified as R henselae immunocytochemically. The third patient was found to have pathologic changes in his liver and spleen comparable with those of the second case, as well as several other disseminated infections. In two cases, identification of R henselae was corroborated through sequencing polymerase chain reaction-amplified bacterial DNA recovered from tissue; in one case, DNA could not be amplified, possibly because of postmortem degradation. Application of the immunocytochemical technique thus has expanded the recognized spectrum of histopathologic findings associated with R henselae infection in acquired immunodeficiency syndrome, as well as proving to be potentially more sensitive than DNA amplification for this purpose when applied to autopsy tissues.

摘要

汉赛巴尔通体可引起杆菌性血管瘤病、杆菌性紫癜和持续性菌血症。由于其难以培养,可通过免疫细胞化学在感染组织中检测到。这项技术在从三名获得性免疫缺陷综合征死亡患者身上获取的尸检标本中发现了汉赛巴尔通体,病理组织改变缺乏新生血管形成特征。在第一名患者中,肝脏、脾脏、淋巴结、骨髓和心脏中淋巴细胞和非上皮样组织细胞的结节性聚集原因一直未被发现,直到通过免疫细胞化学鉴定出汉赛巴尔通体。在第二个病例中,肝脏和脾脏中意外出现的大体和显微镜下坏死性炎症结节含有经免疫细胞化学鉴定为汉赛巴尔通体的沃辛-斯塔里染色杆菌。第三名患者的肝脏和脾脏病理改变与第二个病例相似,还存在其他几种播散性感染。在两个病例中,通过对从组织中回收的聚合酶链反应扩增的细菌DNA进行测序,证实了汉赛巴尔通体的鉴定;在一个病例中,DNA无法扩增,可能是由于死后降解。因此,免疫细胞化学技术扩大了在获得性免疫缺陷综合征中与汉赛巴尔通体感染相关的组织病理学发现的已知范围,并且在应用于尸检组织时,事实证明在这方面可能比DNA扩增更敏感。

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