论文部分内容阅读
目的:芽囊原虫是常见的人类肠道寄生原虫,但对其致病性仍不清楚。为比较在免疫功能正常与免疫功能低下状态下,芽囊原虫不同虫株对组织的致病性。方法:我们在半数SD实验大鼠饮水中加入地塞米松(dexamethasone,DEX)建立免疫功能低下模型,然后在除对照组外的实验组大鼠经口饲喂ST1、ST3和ST7不同虫株建立芽囊原虫感染,检测各组大鼠的病理学变化。结果:有空泡型芽囊原虫侵入肠道固有层,伴有粘膜糜烂脱落和炎症细胞浸润;在相同免疫功能状态下,分离自有症状患者的芽囊原虫虫株较分离自无症状带虫者的虫株造成更严重的病理变化;在免疫功能正常大鼠中,ST1和ST3感染造成的病理变化较ST7更为严重;芽囊原虫在免疫功能低下大鼠中造成的病理变化较在免疫功能正常大鼠中的更为严重。结论:分离自有症状患者的芽囊原虫虫株在免疫功能低下时致病性增强,分离自有症状患者的ST1和ST3虫株较其他虫株毒力更强。实验结果表明芽囊原虫致病性取决于虫株毒力和宿主的免疫功能状态。
Objective: Blastocystis protozoa is a common human intestinal parasitic protozoan, but its pathogenicity remains unclear. In order to compare the pathogenicity of different strains of Blastocystis protozoa to the tissues in the condition of normal immune function and immunocompromised condition. METHODS: We established dexamethasone (DEX) in half of SD rats drinking water to establish a model of immunocompromised mice. After that, ST1, ST3 and ST7 strains were orally inoculated in the experimental group except the control group Blastocystis infection, the pathological changes of rats in each group were detected. Results: Vesicles vacuolar bursts invaded the lamina propria of the intestine with erosion and shedding of mucosa and infiltration of inflammatory cells. In the same immune function, asparaginas isolates from symptomatic patients were isolated from asymptomatic worms The worm strains caused more serious pathological changes; ST1 and ST3 infection caused by pathological changes in ST1 and ST3 more severe pathological changes in rats with immunocompromised rats; Blastocystis protozoa in immunocompromised rats caused by pathological changes in immune The function of normal rats more serious. CONCLUSIONS: The Blastocystis protozoan isolates isolated from patients with symptomatic disease have an increased pathogenicity in immunocompromised patients. ST1 and ST3 isolates from patients with symptomatic symptoms are more virulent than other strains. The experimental results show that the pathogenicity of Blastocystis depends on the virulence of the strain and the immune function of the host.