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关于南非多乳鼠感染卡氏丝状线虫时贫血和白细胞减少的发病机制

On the pathogenesis of anaemia and leukopenia in filarial (Litomosoides carinii) infection of Mastomys natalensis.

作者信息

Ziegler C, Käufer-Weiss I, Zahner H

机构信息

Institute for Veterinary Pathology, Justus Liebig University, Giessen, FRG.

出版信息

Zentralbl Veterinarmed B. 1991 Mar;38(2):123-34. doi: 10.1111/j.1439-0450.1991.tb00855.x.

DOI:10.1111/j.1439-0450.1991.tb00855.x
PMID:1853669
Abstract

Mastomys natalensis infected with the filarial parasite Litomosoides carinii show anaemia and leukopenia. Alterations start with the onset of microfilaraemia. Anaemia is temporally macrocytic (up to 80 days after infection), subsequently normocytic and hypochromic, accompanied by reticulocytosis. Increased intravascular haemolysis (i) and functional disorders of the haemopoetic system (ii) are involved in the pathogenesis. i: Circulating erythrocytes showed increased osmofragility. Hypoglycaemia demonstrated in parasitaemic animals may be one reason. ii: Histological and electron microscopical investigations of the bone marrow revealed markedly enhanced haemopoiesis in infected animals. However, a high proportion of cells was found pathologically altered already beginning in the late prepatency and increasing in the further course of infection. Thus, dyshaemopoiesis may result in the production of morphologically and functionally aberrant cells which are rapidly eliminated by the MPS which is highly activated in L. carinii infected M. natalensis.

摘要

感染丝状寄生虫卡里尼氏丝虫的南非多乳鼠会出现贫血和白细胞减少。这些变化始于微丝蚴血症的出现。贫血在初期为大细胞性(感染后长达80天),随后为正细胞性和低色素性,并伴有网织红细胞增多。发病机制涉及血管内溶血增加(i)和造血系统功能紊乱(ii)。i:循环红细胞的渗透脆性增加。患寄生虫血症的动物出现低血糖可能是原因之一。ii:对骨髓的组织学和电子显微镜研究显示,感染动物的造血明显增强。然而,早在潜伏期后期就发现高比例的细胞已发生病理改变,并在感染的进一步发展过程中增加。因此,造血异常可能导致形态和功能异常的细胞产生,这些细胞会被在感染卡里尼氏丝虫的南非多乳鼠中高度激活的单核吞噬细胞系统迅速清除。

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