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Clinical and laboratory studies into the pathogenesis of malacoplakia.

机译:临床和实验室研究探讨了疟疾的发病机理。

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摘要

Three cases of malacoplakia are described. Electron microscopic studies revealed intact bacteria or bacteria in varying states of degradation within phagolysosomes of the malacoplakic macrophages. Michaelis-Gutmann bodies arise within the phagolysosomes. These findings suggest that the bacteria incorporated within the phagolysosomes persist as dense amorphous aggregates which later become encrusted with calcium phosphate crystals to form the laminated Michaelis-Gutmann bodies. Possible explanations for the unusual macrophage response in malacoplakia are: (1) infection with an unusual strain of bacteria, (2) an immunological abnormality affecting intracellular killing of organisms, and (3) an abnormality affecting intracellular digestion of organisms. In considering each of the possibilities, we have been unable to detect any unusual strain of infecting organisms in association with malacoplakia, and in vitro studies have revealed normal T lymphocyte response to mitogen and normal monocyte bactericidal capacity. According to the history, each patient had reason to have a compromised immune status; in only one, however, was this demonstrated.
机译:描述了三例疟疾。电子显微镜研究揭示了完整的细菌或在畸形巨噬细胞的吞噬溶酶体内降解程度不同的细菌。 Michaelis-Gutmann体出现在吞噬体中。这些发现表明,吞噬溶酶体中掺入的细菌以致密的无定形聚集体的形式持续存在,随后被磷酸钙晶体包裹,形成层压的Michaelis-Gutmann体。疟疾引起的巨噬细胞异常反应的可能解释是:(1)感染了一种异常细菌,(2)影响机体细胞杀灭的免疫学异常,以及(3)影响机体细胞消化的异常。在考虑每种可能性时,我们无法检测到与疟疾相关的任何异常感染生物,并且体外研究显示正常的T淋巴细胞对促细胞分裂原的反应和正常的单核细胞杀菌能力。根据病史,每位患者都有理由免疫力低下。然而,只有一个证明了这一点。

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