The murid filaria Monanema martini: a model for onchocerciasis. Part I. Description of lesions.

P N Vuong, S Wanji, L Sakka, S Klager, O Bain
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引用次数: 12

Abstract

A study of the anatomo-pathological lesions induced by Monanema martini, a filaria with skin-dwelling microfilariae, was performed using 65 Lemniscomys striatus fixed from 30 minutes to 36 months after inoculation of the infective larvae, 5 Arvicanthis niloticus and 3 Meriones unguiculatus fixed during the patent phase, and controls. Attempts at quantification of lesions in L. striatus was made. Approximately 20% of L. striatus had microfilariae in the eyeballs, and many more presented ocular lesions. The delay of the patent period seems to have more effects on the gravity of lesions than repeated inoculations. The location of the lesions and parasites presuppose that microfilariae enter the eyeball through the lymphatic capillaries of the irido-corneal angles. Cutaneous lesions were often severe: there is a parallel between the importance of lesions and the abundance of microfilariae. Larvae are responsible for damage to various structures of the lymphatic system (thrombo-lymphangitis, acute or granulomatous lymphadenitis...) into which they migrate, explaining the mechanism of elephantiasis. These rodent lesions appear similar to those observed in human onchocerciasis and lymphatic filariasis. Whatever the M. martini stage and the organ examined, major lesions belonged to the inflammatory process. Various types of inflammatory reaction (acute, subacute, or chronic inflammation, scarring sclerosis etc.) can co-exist within a single tissue area. The accidental escape of a microfilaria from a lymphatic capillary into the connective tissue (including the corneal stroma) induces an inflammatory reaction. Thus M. martini, as human Onchocerca species, causes a chronic disease, associating recent lesions to old ones.

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马提尼单丝虫:盘尾丝虫病的一种模型。第一部分:病变描述。
本研究采用65只纹状尾尾蛾(leniscomys striatus), 5只niloticus和3只爪状尾尾蛾(Meriones unguiculatus),分别在接种后30分钟至36个月固定,以及对照,对马氏单丝蛾(Monanema martini)引起的解剖病理病变进行了研究。对纹状体病损进行了定量测定。大约20%的纹状螺旋体在眼球中有微丝,更多的出现眼部病变。专利期的延迟似乎比重复接种对病变的严重性有更大的影响。病变和寄生虫的位置假定微丝虫通过虹膜-角膜角的淋巴毛细血管进入眼球。皮肤病变通常是严重的:病变的重要性与微丝虫病的丰度之间存在平行关系。幼虫对淋巴系统的各种结构(血栓性淋巴管炎、急性或肉芽肿性淋巴结炎……)造成损害,它们迁移到其中,这解释了象皮病的机制。这些啮齿动物的病变与在人类盘尾丝虫病和淋巴丝虫病中观察到的类似。无论马提尼氏杆菌的分期和检查的器官如何,主要的病变都属于炎症过程。不同类型的炎症反应(急性、亚急性或慢性炎症、瘢痕性硬化症等)可以在一个组织区域内共存。微丝从淋巴毛细血管意外逃逸到结缔组织(包括角膜基质)引起炎症反应。因此M. martini,作为人类盘尾丝虫物种,引起一种慢性疾病,将最近的病变与旧的病变联系起来。
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