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伊氏锥虫感染的发病机制。

Pathogenic mechanisms of Trypanosoma evansi infections.

机构信息

Department of Biochemistry, Ahmadu Bello University, Zaria 810001, Nigeria.

出版信息

Res Vet Sci. 2012 Aug;93(1):13-7. doi: 10.1016/j.rvsc.2011.08.011. Epub 2011 Sep 21.

Abstract

Insect-borne diseases exact a high public health burden and have a devastating impact on livestock and agriculture. To date, control has proved to be exceedingly difficult. One such disease that has plagued sub-Saharan Africa is caused by the protozoan African trypanosomes (Trypanosoma species) and transmitted by tsetse flies (Diptera: Glossinidae). This presentation describes Trypanosoma evansi (T. evansi) which causes the disease known as trypanosomosis (Surra) or trypanosomiasis in which several attempts have being made to unravel the clinical pathogenic mechanisms in T. evansi infections, yielding various reports which have implicated hemolysis associated to decrease in life span of erythrocytes and extensive erythrophagocytosis being among those that enjoy prominence. T. evansi generates Adenosine Triphosphate (ATP) from glucose catabolism which is required for the parasite motility and survival. Oxidation of the erythrocytes induces oxidative stress due to free radical generation. Lipid peroxidation of the erythrocytes causes membrane injury, osmotic fragility and destruction of the red blood cell (RBC) making anemia a hallmark of the pathology of T. evansi infections.

摘要

虫媒病对公共卫生造成沉重负担,对畜牧业和农业造成严重影响。迄今为止,控制工作已被证明极其困难。在撒哈拉以南非洲肆虐的一种此类疾病是由原生动物非洲锥虫(锥虫属)引起的,由采采蝇(双翅目:舌蝇科)传播。本演讲描述了引起疾病的伊氏锥虫(T. evansi),这种疾病被称为锥虫病(苏拉病)或锥虫病,人们曾多次试图揭示 T. evansi 感染中的临床发病机制,产生了各种报告,其中涉及与红细胞寿命缩短相关的溶血和广泛的红细胞吞噬作用。T. evansi 从葡萄糖分解代谢中产生三磷酸腺苷(ATP),这是寄生虫运动和生存所必需的。红细胞的氧化会因自由基的产生而引起氧化应激。红细胞的脂质过氧化会导致膜损伤、渗透脆性和红细胞破坏,使贫血成为 T. evansi 感染病理的标志。

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