Comparative genomic analysis of enterotoxigenic Escherichia coli O159 strains isolated from diarrheal patients in Korea

Abstract

Background Enterotoxigenic Escherichia coli (ETEC) is a common cause of bacterial infection that leads to diarrhea. Although some studies have proposed a potential association between the toxic profile and genetic background, association between toxin of ETEC and phylo-group has not been reported yet. The objective of this study was to examine genomic and phylogenetic characteristics of ETEC strain NCCP15731 and NCCP15733 by whole genome sequencing and comparative genomic analysis of two phylo-groups of O159 reference strains.

Results Whole genome sequencing showed that genome size of NCCP15731 strain was 4,663,459bp, containing 4435 CDS and 19 RNAs. The genome size of NCCP15733 was 4,645,336bp, containing 4369 CDS and 23 RNAs. Both NCCP15731 and NCCP15733 were classified in the phylo-group A, which is one of major E. coli phylogenetic groups. Their serotype was O159:H34. They possessed the virulence factor such as adherence systems, auto transporter systems, and flagella segments of major driving force for ETEC pathogenicity. They also harbored STh enterotoxin. Hierarchical clustering result based on the presence or absence of a total of 108 major virulence factors of 14 O159 ETEC strains showed that seven strains in phylo-group A and seven strains in phylo-group B1 were clustered each other, respectively. Colonization factors (CFs) of NCCP15731 or NCCP15733 were not detected.

Conclusions Serotype of NCCP15731 and NCCP15733, representing major types of ETEC in Korea, was O159:H34 and their MLST type was ST218. Comparison with other O159 strains revealed that NCCP15731 was specialized for transporter system and secretion system whereas NCCP15733 had unique genes related to capsular polysaccharide. Compared with E159, the most recent common ancestor, these two strains had different toxin type and virulence factors. These results will improve our understanding of ETEC O159 strains to prevent ETEC disease.