Patrick N A Harris1,2, Nouri L Ben Zakour3, Leah W Roberts3, Alexander M Wailan1,4, Hosam M Zowawi1,5,6, Paul A Tambyah7,8, David C Lye7,9,10, Roland Jureen11, Tau H Lee9,10, Mo Yin8, Ezlyn Izharuddin9, David Looke12,13, Naomi Runnegar12,13, Benjamin Rogers14,15, Hasan Bhally16, Amy Crowe17, Mark A Schembri3, Scott A Beatson3, David L Paterson1,18. 1. University of Queensland, UQ Centre for Clinical Research, Royal Brisbane & Women's Hospital, Queensland, Australia. 2. Microbiology Department, Central Laboratory, Pathology Queensland, Royal Brisbane & Women's Hospital, Queensland, Australia. 3. School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Queensland, Australia. 4. Infection Genomics, Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK. 5. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia. 6. WHO Collaborating Centre for Infection Prevention and Control, and GCC Centre for Infection Control, Riyadh, Saudi Arabia. 7. Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. 8. Division of Infectious Diseases, Department of Medicine, National University Hospital, Singapore. 9. Communicable Disease Centre, Institute of Infectious Diseases and Epidemiology, Tan Tock Seng Hospital, Singapore. 10. Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore. 11. Department of Laboratory Medicine, Division of Microbiology, National University Hospital, Singapore. 12. Infection Management Services, Princess Alexandra Hospital, Brisbane, Queensland, Australia. 13. The University of Queensland, School of Medicine, Brisbane, Queensland, Australia. 14. Centre for Inflammatory Disease, Monash University, Clayton, Victoria, Australia. 15. Monash Infectious Diseases, Monash Health, Clayton, Victoria, Australia. 16. Department of Medicine, North Shore Hospital, Milford, Auckland, New Zealand. 17. Department of Infectious Diseases, St Vincent's Hospital, Melbourne, Australia. 18. Wesley Medical Research, Wesley Hospital, Toowong, Queensland, Australia.
Abstract
Objectives: To characterize MDR Escherichia coli from bloodstream infections (BSIs) in Australia, New Zealand and Singapore. Methods: We collected third-generation cephalosporin-resistant (3GC-R) E. coli from blood cultures in patients enrolled in a randomized controlled trial from February 2014 to August 2015. WGS was used to characterize antibiotic resistance genes, MLST, plasmids and phylogenetic relationships. Antibiotic susceptibility was determined using disc diffusion and Etest. Results: A total of 70 3GC-R E. coli were included, of which the majority were ST131 (61.4%). BSI was most frequently from a urinary source (69.6%), community associated (62.9%) and in older patients (median age 71 years). The median Pitt score was 1 and ICU admission was infrequent (3.1%). ST131 possessed more acquired resistance genes than non-ST131 (P = 0.003). Clade C1/C2 ST131 predominated (30.2% and 53.5% of ST131, respectively) and these were all ciprofloxacin resistant. All clade A ST131 (n = 6) were community associated. The predominant ESBL types were blaCTX-M (80.0%) and were strongly associated with ST131 (95% carried blaCTX-M), with the majority blaCTX-M-15. Clade C1 was associated with blaCTX-M-14 and blaCTX-M-27, whereas blaCTX-M-15 predominated in clade C2. Plasmid-mediated AmpC genes (mainly blaCMY-2) were frequent (17.1%) but were more common in non-ST131 (P < 0.001) isolates from Singapore and Brisbane. Two strains carried both blaCMY-2 and blaCTX-M. The majority of plasmid replicon types were IncF. Conclusions: In a prospective collection of 3GC-R E. coli causing BSI, community-associated Clade C1/C2 ST131 predominate in association with blaCTX-M ESBLs, although a significant proportion of non-ST131 strains carried blaCMY-2.
Objectives: To characterize MDR Escherichia coli from bloodstream infections (BSIs) in Australia, New Zealand and Singapore. Methods: We collected third-generation cephalosporin-resistant (3GC-R) E. coli from blood cultures in patients enrolled in a randomized controlled trial from February 2014 to August 2015. WGS was used to characterize antibiotic resistance genes, MLST, plasmids and phylogenetic relationships. Antibiotic susceptibility was determined using disc diffusion and Etest. Results: A total of 70 3GC-R E. coli were included, of which the majority were ST131 (61.4%). BSI was most frequently from a urinary source (69.6%), community associated (62.9%) and in older patients (median age 71 years). The median Pitt score was 1 and ICU admission was infrequent (3.1%). ST131 possessed more acquired resistance genes than non-ST131 (P = 0.003). Clade C1/C2 ST131 predominated (30.2% and 53.5% of ST131, respectively) and these were all ciprofloxacin resistant. All clade A ST131 (n = 6) were community associated. The predominant ESBL types were blaCTX-M (80.0%) and were strongly associated with ST131 (95% carried blaCTX-M), with the majority blaCTX-M-15. Clade C1 was associated with blaCTX-M-14 and blaCTX-M-27, whereas blaCTX-M-15 predominated in clade C2. Plasmid-mediated AmpC genes (mainly blaCMY-2) were frequent (17.1%) but were more common in non-ST131 (P < 0.001) isolates from Singapore and Brisbane. Two strains carried both blaCMY-2 and blaCTX-M. The majority of plasmid replicon types were IncF. Conclusions: In a prospective collection of 3GC-R E. coli causing BSI, community-associated Clade C1/C2 ST131 predominate in association with blaCTX-M ESBLs, although a significant proportion of non-ST131 strains carried blaCMY-2.
Authors: Joost Hordijk; Aldert L Zomer; Luis Ricardo Castellanos; Linda van der Graaf-van Bloois; Pilar Donado-Godoy; Dik J Mevius; Jaap A Wagenaar Journal: Antimicrob Agents Chemother Date: 2019-06-24 Impact factor: 5.191
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