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IDDF2023-ABS-0233 The study of molecular pathogenesis of pediatric clostridiodes difficile infection

2023; Springer International Publishing; Linguagem: Inglês

10.1136/gutjnl-2023-iddf.209

2197-7704

Xiaolu Li, Rong Cao, Fangfei Xiao, Lin Ye, X. Wang, Yizhong Wang,

Nosocomial Infections in ICU

Background To evaluate the clinical characteristics and the molecular pathogenesis of C. difficile . Methods A total of 51 strains of C. difficile were collected from our hospital from 2014.10 to 2022.8. MICs for each strain against 11 antimicrobial agents were detected by the agar dilution method. Whole gene sequencing was performed on Illumina's next-generation sequencing platform for 36 C. difficile strains. Results 51 strains were isolated from 250 fecal samples. 44 strains were toxicogenic, and the detection rate of toxin A+B+ was 100%. Antimicrobial susceptibility testing showed that all isolates were sensitive to rifaximin. The resistance rates of rifampicin and vancomycin were low. All strains were resistant to ceftriaxone, ceftazidime and clindamycin, followed by erythromycin (84.31%), tetracycline, levofloxacin, metronidazole and meropenem. WGS showed that the molecular size of C. difficile was about 3.98-4.22Mb. The GC content was about 28.13-29.21%. More than 3000 CDSs were found and classified by COG functional annotation. There were 21-23 COG functional classifications, among which the genes of transcribed (K) were the maximum. KEGG annotation revealed that the metabolism genes in various pathways were the most. All isolates can be classified into 16 STs based on the MLST scheme, and ST 3 was the most common type, followed by ST 129 and ST 35 (4/36, 11.1%). Two biosynthetic gene clusters (BGCs) of secondary metabolites were annotated for each strain. 414 pathogenicity islands (PAIs) were predicted and 117 prophages were identified. 1718 CRISPR arrays, 3430 carbohydrate active enzyme genes, 14664 virility genes and 9276 antimicrobial resistance genes were found according to WGS. The macrolide and tetracycline resistance genes were found in most of these strains. Conclusions The toxins of the strains were mainly toxin A and toxin B. All isolates were sensitive to rifaximin. The resistance rates of rifampicin and vancomycin were low. All strains were resistant to ceftriaxone, ceftazidime and clindamycin. Rifaximin may be used as the primary treatment for nonrecurrent CDI in children. Biological functional genes such as energy, metabolism and transcription repair of C. difficile were abundant. The isolates were mainly ST 3 according to the MLST scheme.