Gibson D W, Connor D H, Brown H L, Fuglsang H, Anderson J, Duke B O, Buck A A
Am J Trop Med Hyg. 1976 Jan;25(1):74-87. doi: 10.4269/ajtmh.1976.25.74.
Specimens of skin from four Cameroon patients with severe onchocercal dermatitis, before and after treatment with diethylcarbamazine (DEC), were studied by light and electron microscopy. Microfilariae of Onchocerca volvulus have ultrastructural features resembling those of microfilariae of other genera. Between the surface layer of the cuticle and the trilaminate membrane, there is an electrolucent zone which is much wider in degenerating microfilariae than in intact microfilariae. Widening of the zone may result from DEC-induced release of component(s) of the cuticle, possibly collagen or mucopolysaccharide. Between the cuticle and dermal collagen there are granular deposits which might be immune complexes involving the collagenous component of cuticle. Others have shown that DEC does not kill microfilariae in vitro. Treatment with DEC presumably "unmasks" microfilariae in the skin so that they are recognized as foreign bodies and are destroyed by the host's defenses. Histiocytes and eosinophils are seen in close proximity to degenerating microfilariae. Enzymes from histiocytes and eosinophils might readily penetrate the cuticle altered by DEC treatment, and digest various components within the microfilariae. Alternatively, the widening of the electrolucent zone might result directly from the action of leucocytic or histiocytic enzymes, after the microfilaria has been killed by other mechanisms.
对喀麦隆4例患有严重盘尾丝虫性皮炎患者在使用乙胺嗪(DEC)治疗前后的皮肤标本进行了光镜和电镜研究。旋盘尾丝虫微丝蚴具有与其他属微丝蚴相似的超微结构特征。在角质层的表层和三层膜之间,有一个电子透明区,在退化的微丝蚴中比在完整的微丝蚴中宽得多。该区域的增宽可能是由于DEC诱导角质层成分(可能是胶原蛋白或粘多糖)的释放所致。在角质层和真皮胶原之间有颗粒状沉积物,可能是涉及角质层胶原成分的免疫复合物。其他人已经表明,DEC在体外不能杀死微丝蚴。用DEC治疗大概会“暴露”皮肤中的微丝蚴,使其被识别为异物并被宿主防御系统破坏。在退化的微丝蚴附近可见组织细胞和嗜酸性粒细胞。组织细胞和嗜酸性粒细胞的酶可能很容易穿透经DEC处理而改变的角质层,并消化微丝蚴内的各种成分。或者,在微丝蚴被其他机制杀死后,电子透明区的增宽可能直接是白细胞或组织细胞酶作用的结果。