Vaheesan Rajabal1, Ferdiye Taner2, Tamer Sanlidag3, Kaya Suer4, Emrah Guler4, Murat Sayan5, Steve Petrovski6. 1. Department of Physiology, Anatomy & Microbiology, La Trobe University, Bundoora 3086, Victoria, Australia. 2. Department of Physiology, Anatomy & Microbiology, La Trobe University, Bundoora 3086, Victoria, Australia; Department of Medical Microbiology and Clinical Microbiology, Faculty of Medicine, Nicosia, Cyprus. 3. DESAM Research Institute, Near East University, Nicosia, Cyprus. 4. Department of Clinical Microbiology and Infectious Diseases, Faculty of Medicine, Near East University, Nicosia, Cyprus. 5. DESAM Research Institute, Near East University, Nicosia, Cyprus; Faculty of Medicine, Clinical Laboratory, PCR Unit, Kocaeli University, Kocaeli, Turkey. 6. Department of Physiology, Anatomy & Microbiology, La Trobe University, Bundoora 3086, Victoria, Australia. Electronic address: steve.petrovski@latrobe.edu.au.
Abstract
OBJECTIVES: Antibiotic therapy is increasingly becoming difficult to treat Pseudomonas infections. Two multi-drug resistant, clinically derived Pseudomonas strains contained related transposons that are responsible for giving rise to resistance determinants. In this study we characterise these transposons. METHODS: Two clinical, multidrug resistant Pseudomonas isolates were obtained from a medical facility in Cyprus. The strains were identified as Pseudomonas putida C54 and Pseudomonas aeruginosa C69. DNA was extracted from both strains and sequenced. Transposons were identified, annotated and compared to DNA sequences in GenBank. RESULTS: Two related nested transposons, here, named Tn6608 (from P. putida C54) and Tn6609 (from P. aeruginosa C69) were characterised. The transposons are built on an ancestral Tn1403 base element (here named Tn1403A) that contains only the transposition module (tnpA and tnpR) and the associated cargo gene module (orfA, orfB, orfC and orfD) flanked by 38 bp IR. The nested transposons identified in this study have evolved via the acquisition of multiple transposons, adding multiple resistance genes to an ancestral transposon that originally lacked any resistance determinants. CONCLUSION: Transposons related to Tn6608 and Tn6609 have evolved and are globally disseminated. Of particular interest is that most of these nested transposons are located within the same site in a genomic island providing alternative avenues for dissemination.
OBJECTIVES: Antibiotic therapy is increasingly becoming difficult to treat Pseudomonasinfections. Two multi-drug resistant, clinically derived Pseudomonas strains contained related transposons that are responsible for giving rise to resistance determinants. In this study we characterise these transposons. METHODS: Two clinical, multidrug resistant Pseudomonas isolates were obtained from a medical facility in Cyprus. The strains were identified as Pseudomonas putida C54 and Pseudomonas aeruginosa C69. DNA was extracted from both strains and sequenced. Transposons were identified, annotated and compared to DNA sequences in GenBank. RESULTS: Two related nested transposons, here, named Tn6608 (from P. putida C54) and Tn6609 (from P. aeruginosa C69) were characterised. The transposons are built on an ancestral Tn1403 base element (here named Tn1403A) that contains only the transposition module (tnpA and tnpR) and the associated cargo gene module (orfA, orfB, orfC and orfD) flanked by 38 bp IR. The nested transposons identified in this study have evolved via the acquisition of multiple transposons, adding multiple resistance genes to an ancestral transposon that originally lacked any resistance determinants. CONCLUSION:Transposons related to Tn6608 and Tn6609 have evolved and are globally disseminated. Of particular interest is that most of these nested transposons are located within the same site in a genomic island providing alternative avenues for dissemination.