Ciprofloxacin, a quinolone with good intracellular penetration may possibly be used for treatment of melioidosis caused by Burkholderia pseudomallei, but problems with resistance may be encountered. Amino acid substitutions in gyrA/gyrB have given rise to fluoroquinolone resistance in various microorganisms. Using published primers for gyrA and gyrB, PCR was performed on 11 isolates of B. pseudomallei with varying degrees of sensitivity to ciprofloxacin, followed by DNA sequencing to detect possible mutations. Results showed an absence of any point mutation in either gene. Local isolates have yet to develop full resistance to ciprofloxacin and probably other mechanisms of resistance may have been involved in the decreased sensitivity to ciprofloxacin.
The objective of this study was to investigate the antimicrobial resistance patterns of 47 clinical isolates of Aeromonas aquariorum and to identify the presence of plasmids and the relevant antibiotic resistance genes (ARGs). Antibiotic susceptibilities were determined by the standard disc diffusion method. The presence of plasmids and ARGs was detected by gel electrophoresis and monoplex PCR. Resistance to amoxicillin/clavulanic acid (98%), amoxicillin (91%), gentamicin (13%), trimethoprim/sulfamethoxazole (11%) and kanamycin (6%) was observed, whilst no ciprofloxacin- or amikacin-resistant strains were detected. All isolates harboured plasmids with sizes ranging from ca. 2 kb to 10 kb. PCR revealed that A. aquariorum carried three β-lactam resistance genes (bla(TEM), bla(MOX) and bla(PSE)) and two sulphonamide resistance genes (sul1 and sul2). This study provides further understanding of the phenotypic and genotypic characteristics of multiresistant A. aquariorum clinical isolates.
The objectives of this study were to determine the antibiotypes, SCCmec subtypes, PVL carriage, and genetic diversity of MRSA strains from a tertiary hospital. Sixtysix MRSA strains were selected randomly (2003, 2004, and 2007) and tested for the Panton-Valentine leukocidin gene, mecA gene, and SCCmec type via a PCR. The antibiograms were determined using a standard disc diffusion method, and the genetic diversity of the isolates was determined by PFGE. Thirty-four antibiograms were obtained, with 55% of the 66 strains exhibiting resistance to more than 4 antimicrobials. All the isolates remained susceptible to vancomycin, and low resistance rates were noted for fusidic acid (11%), rifampicin (11%), and clindamycin acid (19%). The MRSA isolates that were multisensitive (n=12) were SCCmec type IV, whereas the rest (multiresistant) were SCCmec type III. Only two isolates (SCCmec type IV) tested positive for PVL, whereas all the isolates were mecA-positive. The PFGE was very discriminative and subtyped the 66 isolates into 55 pulsotypes (F=0.31-1.0). The multisensitive isolates were distinctly different from the multidrug-resistant MRSA. In conclusion, no vancomycin-resistant isolate was observed. The Malaysian MDR MRSA isolates were mostly SCCmec type III and negative for PVL. These strains were genetically distinct from the SCCmec type IV strains, which were sensitive to SXT, tetracycline, and erythromycin. Only two strains were SCCmec IV and PVL-positive. The infections in the hospital concerned were probably caused by multiple subtypes of MRSA.