Finegold Sydney M, Summanen Paula H, Downes Julia, Corbett Karen, Komoriya Tomoe
Infectious Diseases Section, VA Medical Center West Los Angeles, 11301 Wilshire Blvd., Los Angeles, CA 90073, United States; Research Service, VA Medical Center West Los Angeles, 11301 Wilshire Blvd., Los Angeles, CA 90073, United States; Department of Microbiology, Immunology and Molecular Genetics, UCLA School of Medicine, 405 Hilgard Ave., Los Angeles, CA 90095, United States; Department of Medicine, UCLA School of Medicine, 405 Hilgard Ave., Los Angeles, CA 90095, United States.
Research Service, VA Medical Center West Los Angeles, 11301 Wilshire Blvd., Los Angeles, CA 90073, United States.
Anaerobe. 2017 Jun;45:133-137. doi: 10.1016/j.anaerobe.2017.02.008. Epub 2017 Feb 17.
We studied stool specimens from 33 autistic children aged 2-9 years with gastrointestinal (GI) abnormalities and 13 control children without autism and without GI symptoms. We performed quantitative comparison of all Clostridium species and Clostridium perfringens strains from the fecal microbiota by conventional, selective anaerobic culture methods. We isolated C. perfringens strains and performed PCR analysis for the main C. perfringens toxin genes, alpha, beta, beta2, epsilon, iota and C. perfringens enterotoxin gene. Our results indicate that autistic subjects with gastrointestinal disease harbor statistically significantly (p = 0.031) higher counts of C. perfringens in their gut compared to control children. Autistic subjects also harbor statistically significantly (p = 0.015) higher counts of beta2-toxin gene-producing C. perfringens in their gut compared to control children, and the incidence of beta2-toxin gene-producing C. perfringens is significantly higher in autistic subjects compared to control children (p = 0.014). Alpha toxin gene was detected in all C. perfringens strains studied. C. perfringens enterotoxin gene was detected from three autistic and one control subject. Beta, epsilon, and iota toxin genes were not detected from autistic or control subjects.
我们研究了33名年龄在2至9岁、患有胃肠道(GI)异常的自闭症儿童以及13名无自闭症且无GI症状的对照儿童的粪便样本。我们通过传统的选择性厌氧培养方法,对粪便微生物群中的所有梭菌属物种和产气荚膜梭菌菌株进行了定量比较。我们分离出产气荚膜梭菌菌株,并对主要的产气荚膜梭菌毒素基因,即α、β、β2、ε、ι以及产气荚膜梭菌肠毒素基因进行了PCR分析。我们的结果表明,与对照儿童相比,患有胃肠道疾病的自闭症受试者肠道中产气荚膜梭菌的数量在统计学上显著更高(p = 0.031)。与对照儿童相比,自闭症受试者肠道中产生β2毒素基因的产气荚膜梭菌数量在统计学上也显著更高(p = 0.015),并且自闭症受试者中产生β2毒素基因的产气荚膜梭菌的发生率比对照儿童显著更高(p = 0.014)。在所研究的所有产气荚膜梭菌菌株中均检测到了α毒素基因。从3名自闭症受试者和1名对照受试者中检测到了产气荚膜梭菌肠毒素基因。在自闭症或对照受试者中未检测到β、ε和ι毒素基因。