Yuoh G, Hove M G, Wen J, Haque A K
Department of Pathology, University of Texas Medical Branch, Galveston, 77555-0743, USA.
Mod Pathol. 1996 May;9(5):476-83.
Malakoplakia is an unusual inflammatory reaction to a variety of infections, characterized by the accumulation of macrophages containing the target-like calcospherites, the Michaelis-Gutmann body (MGB). We report three patients with acquired immunodeficiency syndrome with pulmonary malakoplakia associated with Rhodococcus equi infection; two patients were diagnosed at autopsy and one by examination of a transbronchial biopsy specimen. All three patients had pulmonary bacterial cultures and light and electron microscopic examination. The patients were 33-, 41-, and 43-year old men, human immunodeficiency virus-positive for 2, 6, 8 years, respectively. The two patients diagnosed at autopsy had cavitary lesions, and the patient diagnosed by biopsy specimen had nodular lesions on chest radiographs. Histologically, the lungs had well-circumscribed areas of infiltration with benign macrophages with granular cytoplasm, scattered MGBs, and numerous gram-positive coccobacilli. Electron microscopic examination showed intracellular coccobacilli, from 990 X 702 to 972 X 648 nm in diameter, with thick, homogenous cell walls, trilaminar cytoplasmic membranes, and dense cytoplasm with from one to five vacuoles. Electron microscopic studies showed that the bacteria within the pulmonary macrophages had thicker cell walls, less prominent nucleoid areas, and more vacuoles than the bacteria in cultures from the sputum and blood. The mature MGB ultrastructurally had a concentric, trilaminate structure with central mineralized core and was without recognizable bacterial forms. Early MGBs, however, consisted of a circular, electron-dense core containing bacteria, ultrastructurally similar to the R. equi seen in the culture. Pulmonary malakoplakia in patients with the acquired immunodeficiency syndrome might thus represent an acquired macrophage dysfunction of the intracellular digestion of phagocytized bacteria. The bacteria within the macrophages, however, seemed to have thicker cell walls compared with those in culture, and thus might be protected from enzyme digestion. It seems that MGBs are formed around the undigested bacteria as an alternative pathway for bacterial destruction, because R. equi was identified within the cores of early MGBs but not the mature or late stage MGBs.
软斑病是对多种感染的一种罕见炎症反应，其特征是含有靶样钙球（即迈克尔is-古特曼小体，MGB）的巨噬细胞聚集。我们报告了3例获得性免疫缺陷综合征患者，其肺部软斑病与马红球菌感染相关；2例患者在尸检时确诊，1例通过经支气管活检标本检查确诊。所有3例患者均进行了肺部细菌培养以及光镜和电镜检查。患者为33岁、41岁和43岁男性，分别感染人类免疫缺陷病毒2年、6年和8年。尸检确诊的2例患者有空洞性病变，经活检标本确诊的患者胸部X线片上有结节性病变。组织学上，肺部有界限清楚的浸润区域，有细胞质颗粒状的良性巨噬细胞、散在的MGB以及大量革兰氏阳性球菌。电镜检查显示细胞内球菌，直径为990×702至972×648纳米，有厚的、均匀的细胞壁、三层细胞质膜以及有1至5个空泡的致密细胞质。电镜研究表明，肺部巨噬细胞内的细菌细胞壁比痰液和血液培养物中的细菌更厚，类核区域不那么明显，空泡更多。成熟的MGB超微结构有同心的、三层结构，中央有矿化核心，且没有可识别的细菌形态。然而，早期MGB由含有细菌的圆形、电子致密核心组成，超微结构类似于培养物中所见的马红球菌。因此，获得性免疫缺陷综合征患者的肺部软斑病可能代表了吞噬细菌的细胞内消化的获得性巨噬细胞功能障碍。然而，巨噬细胞内的细菌与培养物中的细菌相比，细胞壁似乎更厚，因此可能受到酶消化的保护。似乎MGB是在未消化的细菌周围形成的，作为细菌破坏的替代途径，因为在早期MGB的核心内发现了马红球菌，但在成熟或晚期MGB中未发现。
