Abstract
IbeA (invasion of brain endothelium), which is located on a genomic island termed GimA, is involved in the pathogenesis of several extraintestinal pathogenic E. coli (ExPEC) pathotypes, including newborn meningitic E. coli (NMEC) and avian pathogenic E. coli (APEC). To unravel the phylogeny of GimA and to investigate its island character, the putative insertion locus of GimA was determined via Long Range PCR and DNA-DNA hybridization in 410 E. coli isolates, including APEC, NMEC, uropathogenic (UPEC), septicemia-associated E. coli (SEPEC), and human and animal fecal isolates as well as in 72 strains of the E. coli reference (ECOR) collection. In addition to a complete GimA (∼20.3 kb) and a locus lacking GimA we found a third pattern containing a 342 bp remnant of GimA in this strain collection. The presence of GimA was almost exclusively detected in strains belonging to phylogenetic group B2. In addition, the complete GimA was significantly more frequent in APEC and NMEC strains while the GimA remnant showed a higher association with UPEC strains. A detailed analysis of the ibeA sequences revealed the phylogeny of this gene to be consistent with that obtained by Multi Locus Sequence Typing of the strains. Although common criteria for genomic islands are partially fulfilled, GimA rather seems to be an ancestral part of phylogenetic group B2, and it would therefore be more appropriate to term this genomic region GimA locus instead of genomic island. The existence of two other patterns reflects a genomic rearrangement in a reductive evolution-like manner.
Highlights
The bacterial species Escherichia coli reflects a high degree of diversity, and includes commensal, extraintestinal pathogenic E. coli (ExPEC) and intestinal pathogenic strains [1]
ExPEC, which predominantly belong to phylogenetic group B2, are currently categorized based on their original host and/or clinical background resulting in the designation of pathotypes newborn meningitis causing E. coli (NMEC), uropathogenic E. coli (UPEC), avian pathogenic E. coli (APEC), and septicemia-associated E. coli (SEPEC) [1,2,3]
The entire collection consisted of 98 APEC strains, isolated from septicemia in birds, 140 UPEC strains, implicated in urinary tract infections in humans (n = 64), cats (n = 22), and dogs (n = 54), 25 newborn meningitic E. coli (NMEC) strains, 28 SEPEC strains from cases of septicemia in humans, and 119 fecal strains from clinically healthy humans (n = 86) and animals (n = 33)
Summary
The bacterial species Escherichia coli reflects a high degree of diversity, and includes commensal, extraintestinal pathogenic E. coli (ExPEC) and intestinal pathogenic strains [1]. The development of bacterial meningitis includes several pathogenic steps, involving mucosal colonization in the gastrointestinal tract, microbial translocation of the mucous membrane and invasion of the intravascular space with subsequent intravascular survival and accompanied bacteremia. While aslA, ibeB, yijP and ompA have homologues present in non pathogenic E. coli K-12 strains [10,13,14,15], this is not the case for ibeA [11,16], which has originally been identified in archetypical NMEC strain RS218 (O18:K1:H7; ST95) through a TnphoA mutagenesis approach [12]. There has been evidence for an involvement of ibeA in the pathogenesis of systemic E. coli infections in chickens, as a knockout mutant of APEC strain BEN2908 (O2:K1:H5; ST95) was attenuated in vivo in a chicken infection model [17]
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