克氏锥虫感染小鼠模型的组织学、免疫学和寄生虫学研究

M. Villagrán-Herrera, J. Martínez-Ibarra, M. Sánchez-Moreno, H. Hernández-Montiel, R. Mercado-Curiel, N. Camacho-Calderón, J. D. Diego-Cabrera
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引用次数: 1

摘要

恰加斯病的全球蔓延是由于来自克氏锥虫病媒和非病媒传播发生率高的流行国家的个体不断迁移。该疾病存在于其不同的阶段:感染的时间特征体征和症状及其免疫系统和细胞和组织损伤的机制。第一阶段大约持续90天,通过直接方法(用吉姆萨病毒染色的血液涂片,新鲜和异种诊断)进行诊断。不确定的慢性期是无症状的,但锥乳糜虫的生长和细胞内的二元增殖继续促进细胞溶解,并允许副位点感染其他细胞,优先倾向于产生巨大综合征的器官,如心肌病、心肌炎、脑膜脑炎、巨型食道和巨型结肠。无意中,这一过程重复了好几年,导致了恰加斯病。小鼠接种可以检查体内寄生虫血症和疾病在短时间内的发展(体征、行为和倾向)、组织病理学改变和血清抗体的检测。当使用来自不同地理区域的不同克氏体菌株时,这些参数可能会有所不同;三角瘤物种由于其遗传变异而受到环境、营养、水库和生境的影响。小鼠模型ECA CD-1具有复制人类恰加斯病发现的能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Mouse Model as a Tool for Histological, Immunological and Parasitological Studies of Trypanosoma cruzi Infection
The global expansion of Chagas disease is due to the constant migration of individu- als from endemic countries with incidence of vector and nonvector transmission of Trypanosoma cruzi . The disease is present in its various stages: chronological character-istic signs and symptoms of the infection and its mechanism of immune system and cell and tissue damage. The first stage, which lasts 90 days approximately, is diagnosed by direct methods (blood smears stained with Giemsa, fresh and xenodiagnosis). The indeterminate-chronic stage is asymptomatic, but the growth and intracellular binary multiplication of the trypomastigotes continue promoting cell lysis and allowing para- sites to infect other cells, with preferential tropism to organs producing mega syndromes such as cardiomyopathy, myocarditis, meningoencephalitis, megaesophagus and mega - colon. Inadvertently, this process is repeated for several years leading to Chagas disease. The mouse inoculation allows checking the parasitemia in vivo and the development of the disease in short time (signs, behavior and tropism), histopathological alterations and detection of antibodies in serum. These parameters may vary when using different strains of T. cruzi from different geographical areas; Triatoma species due to their genetic variability are influenced by the environment, nutrition, reservoirs and habitat. The murine model ECA CD-1 has the ability to replicate human findings of Chagas disease.
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