Toxin profile of fecal Clostridium perfringens strains isolated from children with autism spectrum disorders

• Published in: Anaerobe Vol. 51; pp. 73 - 77
• Main Authors: Góra, Bartłomiej, Gofron, Zygmunt, Grosiak, Magdalena, Aptekorz, Małgorzata, Kazek, Beata, Kocelak, Piotr, Radosz-Komoniewska, Halina, Chudek, Jerzy, Martirosian, Gayane
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.06.2018
• Subjects: autism; Autism spectrum disorders (ASD); Beta2 toxin gene; children; Clostridium perfringens; diet; digestive system diseases; enterotoxins; feces; genes; intestinal microorganisms; pathophysiology; patients; Beta2 toxin gene; Autism spectrum disorders (ASD); Clostridium perfringens
• ISSN: 1075-9964; 1095-8274; 1095-8274
• DOI: 10.1016/j.anaerobe.2018.03.005

Infectious factors are taken into consideration in pathophysiology of autism spectrum disorders (ASD). ASD patients often suffer from gastrointestinal disorders. The intestinal microbiota of autistic patients significantly differs from that in healthy individuals. The aim of the study was to compare the profile of toxins produced by C. perfringens strains isolated from feces of children with ASD, with healthy individuals and obese subjects. This study included 111 strains of C. perfringens: 49 isolates from 29 children with ASD, 30 - from 17 healthy individuals and 32 - from 24 young obese subjects. Alpha, beta, beta2, epsilon, iota and enterotoxin genes were detected using appropriate PCRs. The alpha toxin gene (cpa) was present in all 111 examined strains (100%). The beta2 gene (cpb2) was detected in 45/49 strains (91.8%) isolated from children with ASD, 17/30 (56.7%) isolates from healthy subjects, and 12 of 32 (37.5%) isolates from obese subjects. C. perfringens strains with cpb2 gene were detected in 27/29 ASD patients (93.1%), 10/17 healthy subjects (58.8%) and 11/24 (45.8%) obese subjects. Beta2 toxin encoding cpb2 gene was significantly more common in strains isolated from ASD patients, with no significant difference between control subjects regardless of diet. Further research to explain observed phenomena and pathomechanism of beta2 toxin is required. •ASD patients possess beta2 toxin gene-positive C.perfringens strains significantly more often than healthy and obese subjects.•There were no changes in prevalence of such strains in healthy normal weight and obese subjects (unaffected by diet).•Further studies are required to explain beta2 toxin activity and possible neurotoxic mechanism.