人类血液中的新型细菌结构。2细菌变异作为特发性血尿的病因。

G J Domingue, J U Schlegel
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引用次数: 0

摘要

在特发性血尿患者的特殊培养基中发现了新的细菌结构。这些结构在体外从96%的研究患者中迅速转化为革兰氏阳性球菌(链球菌和葡萄球菌样)球菌和丝状细菌。常规血液培养结果为阴性。尽管在正常对照血液标本(尽管数量较少)中显示出结构(致密体),但在体外转化为经典细菌的很少(7%)。红霉素治疗似乎与血尿的消失有关,并且不能在体外迅速从变异恢复到经典细菌。这表明,从口腔或其他部位进入的细菌持续轰击血液可能导致变异细菌寄生的发展。为了在有害宿主的影响下生存,生物体可能转化为持久的渗透性稳定的变异细菌形式(致密体)。疾病状态的发展可能受到宿主体内某些存在或正在发生的异常(免疫、生理和/或生化)的制约。此外,在向变异形式过渡和适应体内生活的过程中,生物体本身可能发生的变化(遗传?)可能不允许某些宿主环境适应这些新形式,这可能导致病因长期不明的肾脏疾病的发病作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Novel bacterial structures in human blood. II. Bacterial variants as etiologic agents in idiopathic hematuria.

Novel bacterial structures have been demonstrated in lysed blood filtrates placed in special culture media from patients with idiopathic hematuria. These structures converted rapidly to gram-positive coccal (streptococcal and staphylococcal-like) coccobacillary and filamentous, bacterial forms in vitro from 96 per cent of the patients studied. Blood cultured conventionally yielded negative findings. Although structures (dense bodies) were demonstrated in normal control blood specimens (albeit in lesser numbers) few converted to classical bacteria in vitro (7 per cent). Erythromycin therapy appeared to correlate with disappearance of hematuria and inability to revert rapidly the variant froms to classical bacteria in vitro. It is suggested that continual bombardment of the blood by bacteria entering from the mouth or other sites may lead to the development of variant bacterial parasitism. In an effort to survive the deleterious host effects the organisms may convert to persisting osmotically stable variant bacterial forms (dense bodies). Development of a disease state may be conditioned by some existing or developing abnormality in the host (immunologic, physiologic and/or biochemical). Furthermore, changes (genetic?) that might take place in the organisms per se during their transition to variant forms and adaptation to life in vivo may not allow certain host environments to adapt to these new forms, possibly leading to a pathogenetic role in renal diseases whose etiologies have long been enigmas.

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