地塞米松诱发家兔弓形虫病的动物模型

Animal model of toxoplasmosis induced by desanmethasone in rabbits

目的建立弓形虫感染免疫抑制的动物模型,探讨宿主的免疫力与感染弓形虫的关系。方法将弓形虫抗体(IgM和IgG)阴性的家兔20只随机分4组:正常对照组(A组)、免疫抑制组(B组)、接种虫体组(C组)和免疫抑制接种虫体组(D组)。A组家兔肌注生理盐水,B组肌注地塞米松,C组腹腔注射活的、纯化的弓形虫速殖子,D组除肌注地塞米松外,在注药48h后腹腔接种活的、纯化的弓形虫速殖子。观察C、D组是否感染成功,比较4组家兔的健康和发病情况,观察弓形虫抗原的分布及致病情况。结果A组未见异常。B组仅出现食量减少。C组第6天出现体毛疏松,但在整个实验中没有出现死亡现象。D组第4天出现体毛疏松,10d后出现脱毛、怠惰、厌食、体重下降,腹胀、眼内有分泌物,但停药后症状渐减轻。第2次重复给药后呼吸加快、眼底视乳头轻度充血,1只家兔肢体抽风、瘫痪、昏迷而死亡。结论成功建立弓形虫感染免疫缺损的动物模型。正常家兔感染弓形虫可转为隐性感染。免疫抑制剂对宿主感染弓形虫可起协同作用。

Objective To create an animal model of immunosuppressed rabbits infected with Toxoplasrna gondii and explore the relationship between the immunity of host and T. gondii infection. Methods Twenty rabbits whose anti-Toxoplasrna antibodies （IgM and IgG）in serum were negative were randomly divided into four groups： normal control group （A）, immunosuppressed group （B）, control group infected with T. gondii （C）, immunosuppressed group injected with T. gondii （D）. Group A was muscularly injected with normal saline, Group B was muscularly injected with desamethasone （DEX）, Group C was peritoneally infected with living tachyzoites of RH strain after purifying, Group D was peritoneally infected with living tachyzoites of T. gondii RH strain after muscularly being injected with DEX 48 hours. The infection of Toxoplasrna in Group C and Group D was investigated; the health and episode of the four groups and the distribution of To.toplasma antigen and pathogenic phenomenon were also investigated. Results Group A had no change. Group B only presented slight anorexia. Group C presented hair rarefaction at Day 6, but not dying throughout the experiment. Group D presented hair rarefaction at Day 4, and presented dehairing, activities decreasing, anorexia, body weight descending, abdomen exponding and having secretion in eyes after Day 10, but these symptoms gradually relieved after withdrawal of the drug. After the second administration, the rabbits presented respiring urgently, optic papilla hyperemia gently. A rabbit presented limbs＇ paralysing, convulsion and coma, and died. Conclusion An animal model of immunosuppressed host infected with T. gondii is built successfully, and immunosup pressed agents has the synergism with T. gondii infection.