Acquired aminoglycoside resistance in pseudomonas aeruginosa from a cystic fibrosis patient

Hanks-Thomson, Kirstin R., Kidd, Timothy J., Wainwright, Claire E., Ramsey, Kay A., Steen, Jason A., Bell, Scott C., Zakour, Nouri L. Ben and Beatson, Scott A. (2012). Acquired aminoglycoside resistance in pseudomonas aeruginosa from a cystic fibrosis patient. In: Australian Society for Microbiology Annual Scientific Meeting (ASM2012), Brisbane, Australia, (). 1-4 July 2012.

Author Hanks-Thomson, Kirstin R.
Kidd, Timothy J.
Wainwright, Claire E.
Ramsey, Kay A.
Steen, Jason A.
Bell, Scott C.
Zakour, Nouri L. Ben
Beatson, Scott A.
Title of paper Acquired aminoglycoside resistance in pseudomonas aeruginosa from a cystic fibrosis patient
Conference name Australian Society for Microbiology Annual Scientific Meeting (ASM2012)
Conference location Brisbane, Australia
Conference dates 1-4 July 2012
Publication Year 2012
Sub-type Oral presentation
Language eng
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status Non-UQ
Additional Notes Pseudomonas aeruginosa (PA) is an opportunistic pathogen of a wide variety of host organisms, including humans. In the lungs of cystic fibrosis (CF) patients PA infections can persist for many years, during which time the bacteria adapts to the host. Acquired antibiotic resistance is a key feature in the development of chronic PA infection in CF. In this study we investigated acquired antibiotic resistance in PA in an Australian CF patient. We sequenced the genome of an isolate of PA (Bris34) from the lower airways of a paediatric CF patient, who was persistently infected for over two years with PA with a consistent enterobacterial repetitive intergenic consensus-PCR (ERIC-PCR) genotype. This clone is phylogenetically distinct from most previously sequenced isolates from CF patients, indicating that PA from a variety of genetic backgrounds can cause persistent infections in CF patients. Analysis of the genome revealed the presence of a large (88 Kb) plasmid, which has a backbone resembling an IncP-9 incompatibility group plasmid. Bris34 was resistant to several antibiotics to which earlier isolates of the same genotype from the same patient were susceptible. The arrival of the plasmid - as determined by PCR on other isolates from the same patient - coincides with the development of gentamycin and tobramycin resistance, potentially attributable to an aminoglycoside N(3')-acetyltransferase encoded by the plasmid. These results indicate that plasmid encoded genes for antibiotic modifying enzymes are one potential cause of acquired antibiotic resistance during persistent Pseudomonas aeruginosa infection in the CF lung.

Document type: Conference Paper
Collection: School of Chemistry and Molecular Biosciences
 
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Created: Sun, 25 Nov 2012, 18:02:31 EST by Kirstin Hanks on behalf of School of Chemistry & Molecular Biosciences