Applied Microbiology: Open Access
Open Access
ISSN: 2471-9315
+44 1300 500008
ISSN: 2471-9315
+44 1300 500008
Rosetta Moshirian Farahi
Alzahra University, Iran
Posters & Accepted Abstracts: Appli Micro Open Access
The major mechanism of Pseudomonas aeruginosa resistance to fluoroquinolones is the alteration of target enzymes, type II and IV topoisomerases due to mutations in the quinolone resistance-determining-regions (QRDR) of the gyrA and parC genes coding A subunits of these enzymes. 37 isolates from patients with burn wounds and 20 isolates from blood, urine and sputum specimen were selected to evaluate mutations involved in antibiotic resistance and were subsequently verified for their resistance to ciprofloxacin. QRDRs regions of gyrA and parC were amplified by Polymerase Chain Reaction (PCR) and were subsequently sequenced. 90% of isolates with MICâ�?¥8 �?¼g/ml to ciprofloxacin had a mutation in gyrA gene in which threonine at position 83 changed to isoleucine. 87.5% of isolates had mutation in parC, Serine 87 changed. 75% had Ser87Leu and 12.5% possessed Serin87Trp. Various silent mutations were also detected such as Val103Val, Ala118Ala, Ala136Ala and His132His in gyrA and Ala115Ala in parC. The data indicates that the common mutation in gyrA is Thr83Ile and in parC is Ser87Leu/Trp. No individual parC mutation was observed while mutations in gyrA and parC occurred simultaneously and appears to be the main reason of high level resistance to fluoroquinolones in patients with burn wounds and urine infection. The vast majority of P. aeruginosa isolates had mutation in parC which can play a crucial role in increased resistance of these isolates. This is the first report of parC mutations from resistant P. aeruginosa isolates from Iran, Tehran.
Email: rosa.moshirian@gmail.com