Johnson L, Wirostko E, Wirostko B
J Submicrosc Cytol. 1987 Jan;19(1):161-6.
In acute exacerbations of chronic idiopathic vitritis (CIV) non-cultivatable ultrastructurally unusual 0.5-0.7 micron cell walled coccal bacteria (B) are commonly present within phagolysosomes of 3-5% of vitreous polymorphonuclear (PMN) leukocytes. Inoculation of that CIV vitreous into mouse eyelids produces chronic mouse vitritis (CMV) with identical B within CMV PMN leukocyte phagolysosomes. This transmission electron microscopic restudy of all PMN leukocytes in those 8 CIV and 3 CMV specimens demonstrated in all 11 severe cytoskeletal lytic damage associated with pleomorphic 0.1-1.4 micron cell wall deficient B in 1-2% of the cells; both those cell wall deficient and the unusual cell walled B within the same cell in 1-3 cells per specimens; and within the cell walled B complex internal structures resembling the cell wall deficient B. The study results suggest that the morphologically diverse B may be subportions of a single unusual pathogenic B, which parasitizes, undergoes complex morphologic differentiation within, and produces profound cytoskeletal damage to host PMN leukocytes.
在慢性特发性葡萄膜炎（CIV）急性发作时，在3%-5%的玻璃体多形核（PMN）白细胞的吞噬溶酶体内通常存在不可培养的、超微结构异常的、细胞壁厚度为0.5-0.7微米的球菌（B）。将患有CIV的玻璃体接种到小鼠眼睑中会导致慢性小鼠葡萄膜炎（CMV），在CMV的PMN白细胞吞噬溶酶体内存在相同的B。对这8个CIV和3个CMV样本中的所有PMN白细胞进行的透射电子显微镜再研究表明，在所有11个样本中，1%-2%的细胞存在与多形性0.1-1.4微米细胞壁缺陷型B相关的严重细胞骨架溶解损伤；每个样本中1-3个细胞内同时存在细胞壁缺陷型B和异常细胞壁型B；在细胞壁型B复合体内部存在类似于细胞壁缺陷型B的结构。研究结果表明，形态多样的B可能是单一异常致病B的亚部分，该致病B寄生在宿主PMN白细胞内，在其中经历复杂的形态分化，并对宿主PMN白细胞造成严重的细胞骨架损伤。
