中华皮肤科杂志 ›› 2004, Vol. 37 ›› Issue (8): 481-483.

• 论著 • 上一篇    下一篇

阿萨希毛孢子菌致小鼠播散性毛孢子菌病的实验和治疗研究

杨蓉娅, 王文岭, 敖俊红, 张洁, 郝震锋, 王聪敏   

  1. 北京军区总医院皮肤科 100700
  • 收稿日期:2003-08-29 出版日期:2004-08-15 发布日期:2004-08-15

Study on Disseminated Trichosporonosis Caused by Trichosporon asahii in Murine Model

YANG Rong-ya, WANG Wen-ling, AO Jun-hong, ZHANG Jie, HAO Zhen-feng, WANG Cong-min   

  1. Department of Dermatology, General Hospital of Beijing Military Command of PLA, Beijing 100700, China
  • Received:2003-08-29 Online:2004-08-15 Published:2004-08-15

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摘要： 目的 研究阿萨希毛孢子菌致小鼠播散性毛孢子菌病的感染条件及脏器播散情况。方法 于接种阿萨希毛孢子菌前3d及接种后第7天腹腔注射环磷酰胺进行免疫抑制;根据接种阿萨希毛孢子菌的途径将75只昆明鼠随机分为免疫抑制+静脉接种组(n=15)、免疫抑制+皮内接种组(n=7)、免疫抑制+胃肠灌注组(n=8)、免疫抑制+静脉接种+治疗组(n=15),对照组为非免疫抑制的健康小鼠,分别进行上述接种。治疗组给予脂质体两性霉素B及氟康唑治疗。对死亡小鼠的主要脏器进行组织真菌培养及病理检查。结果 免疫抑制+静脉接种组12只小鼠中有10只至少有1个脏器分离出阿萨希毛孢子菌;而非免疫抑制+静脉接种组14只小鼠中有2只分离出该菌。免疫抑制+皮内接种组7只小鼠中有2只仅于接种部位出现皮损,而无其他脏器感染。其余3组非静脉接种小鼠均未出现脏器感染。治疗组小鼠的死亡只数、系统感染及受累脏器数均显著低于非治疗组(P<0.01〉。感染小鼠的各脏器组织病理改变主要为急性化脓性炎症及肉芽肿性炎症,组织中可见关节孢子及菌丝。结论 阿萨希毛孢子菌为一种机会致病菌,可致免疫低下或免疫缺陷宿主的皮肤或脏器感染,但对健康宿主并非绝对不致病。主要受累脏器依次为肝、肺、肾、脾、心。脂质体两性霉素B联合氟康唑可有效抑制该菌的感染和扩散。

关键词: 毛孢子菌属, 毛孢子菌病, 动物替代试验

Abstract: Objective To investigate the pathogenic factors and the visceral involvement in murine disseminated trichosporonosis caused by Trichosporon asahii. Methods Forty-five mice were immunosuppressed with cyclophospamide 3 days hefore and 7 days after inoculation of T. asahii, and were divided into intravenously inoculated group (n=15), intradermal inoculated group (n=7), gastrointestinal infusion group (n=8), intravenously inoculated + treatment group (n=15). In the control groups the mice were not immunosuppressed, and were also divided into intravenous, intradermal, and G.I. infusion groups with the same number of mice respectively. In the treatment group the mice were given both liposomal amphotericin B and fluconazole. The main viscera of the mice were examined by mycologic culture and pathologic sections. Results In the intravenous inoculation group of immunized mice, Trichosporon asahii were isolated from at least one organ in 10/12 mice, while T. asahii were only isolated in 2/14 mice in the control group; in 2/7 mice of the intradermal group of immunosuppressed mice, skin lesion appeared at the inoculation site, but no visceral infection was observed. No visceral infection was found in the groups that T. asahii was inoculated by non-intravenous injection in both immunosuppressed and non-immunosuppressed mice. The number of mice died, the number of visceral organs involved and the incidence of systemic infection were significantly less in the treatment group than those in the non-treatment groups (P<0.01). Histopathology showed acute pyogenous inflammation and granuloma with arthrospores and mycelia in the tissues. Conclusions Trichosporon asahii is an opportunistic pathogen which can lead to the infection of the skin or viscera in immunocompromized host. However, the immnocompetent host may be infected when there are enough Trichosporon asahii present. The most susceptible viscera are liver, lung, kidney, spleen and heart. The combination treatment of the liposomal amphotericin B and the fluconazole can inhibit the infection and dissemination.

Key words: Trichosporon, Trichosporonosis, Animal testing alternative