Characterization of sulphonamide-resistant Escherichia coli using comparison of sul2 gene sequences and multilocus sequence typing

Abstract

The sul2 gene encodes sulphonamide resistance (Sul R ) and is commonly found in Escherichia coli from different hosts. We typed E. coli isolates by multilocus sequence typing (MLST) and compared the results to sequence variation of sul2, in order to investigate the relation to host origin of pathogenic and commensal E. coli strains and to investigate whether transfer of sul2 into different genomic lineages has happened multiple times. Sixty-eight E. coli isolated in Denmark and Norway from different hosts and years were MLST typed and sul2 PCR products were sequenced and compared. PFGE was performed in a subset of isolates. All isolates were divided into 45 different sequence types (STs), with clonal complexes CC10, CC23, CC168, CC350 and CC69 being the most frequent. The sul2 gene from the majority of E. coli strains had only two point mutations, at positions 159 and 197, leading to a synonymous and a non-synonymous change, respectively. Five strains had extra single mutations. All poultry, poultry meat, and Danish human blood isolates had the same sul2 ST and some of these strains clustered under the same MLST STs, indicating that they shared habitats. Most PFGE profiles clustered according to source, but some included different sources. Sul R E. coli from different animals, food, human faeces and infections did not cluster according to their origin, suggesting that these habitats share E. coli and sul2 gene types. However, while pig isolates on one occasion clustered with urinary tract infection isolates, poultry isolates seemed more related to isolates from bloodstream infections in humans. Presence of mainly two types of the sul2 gene in both human and animal isolates, irrespective of date and geography, and the presence of both types in the same clonal lineages, suggest horizontal transfer of sul2.

Enteroaggregative Escherichia coli O78:H10, the Cause of an Outbreak of Urinary Tract Infection

“…It also conflicts with the conventional understanding that the E. coli strains that cause diarrhea are distinct from those that cause extraintestinal disease, both phylogenetically and according to their discrete repertoires of syndrome-specific virulence genes (23). Regarding ST10 and EAEC, ST10 is known to be pathotypically heterogeneous (31), comprising EAEC, ETEC (31,50,54), ExPEC, and commensal E. coli (2,49). EAEC is a very common diarrheal pathotype, occurring in multiple lineages (31).…”

Escherichia coli ST131, an Intriguing Clonal Group

“…Finally, seven (1.5%) of the 463 E. coli isolates collected from diseased chickens in Spain between 2007 and 2009 were E. coli ST131, and two isolates produced CTX-M-9 and were susceptible to FQ (35). E. coli ST131 was also found in a pig in Denmark (198). In contrast, no ST131 isolates were identified by Wu et al among 39 clinical isolates of E. coli from cattle, sheep, chicken, and pigs (179).…”

Characterization of Escherichia coli Isolates from Hospital Inpatients or Outpatients with Urinary Tract Infection

“…The ST88 (CC23) phylogroup C clone was recently associated with the spread of different beta-lactamases in nosocomial E. coli isolates (33,34). Also, E. coli of the phylogenetic lineages A and C that belong to CC10 and CC23 frequently caused extraintestinal infections in humans, and together with CC155 isolates, they are often multiresistant (44)(45)(46). These results show that extraintestinal infections, especially in hospital patients, are frequently caused by E. coli variants with genetic backgrounds, such as phylogroups A, C, and B1, which are rather uncommon in ExPEC from communityacquired infections and which are often associated with multiple antibiotic resistances.…”