الفهرس 
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Abstract
Background: Campylobacter spp. are the major cause of enteritis in humans and more than 90% of the reported Campylobacter infections are caused by Campylobacter jejuni. When antibiotic therapy is required, fluoroquinolones like ciprofloxacin (CIP) are generally recommended. However the incidence of ciprofloxacin-resistant Campylobacter is increasing globally. A major mechanism implicated is a single nucleotide change (C to T) in codon 86 of the quinolone resistance determining region (QRDR) of the gyrA gene. Other mechanisms of resistance have also been reported.
Methods: Campylobacter spp (n=118) were selected from a collection of Egyptian isolates spanning 1998 to 2005 to be tested by Mismatch Amplification Mutation Assay (MAMA) PCR. GZgyrA4 and CampyMAMAgyrA1 primers were used to identify the presence of the gyrA gene of C. jejuni, and primers CampyMAMAgyrA1 and CampyMAMAgyrA5 were used to detect the C to T mutation in the gene. The minimum inhibitory concentration (MIC) of nalidixic acid (NA) and (CIP) was measured for each isolate using E-test strips. DNA sequencing was performed on a partial fragment of the gyrA gene from 14 isolates to confirm the PCR results. Pulsed Field Gel Electrophoresis (PFGE) was performed using SmaI restriction enzyme to determine whether the mutation in codon 86 was related to a particular genotype or it could exist in chromosomally distinguishable strains.
Results: C. jejuni gyrA gene was detected in 100 of the Campylobacter spp. studied. The other 18 isolates were determined to be C. coli and unexpectedly 10 of them were amplified using the primers specific for C. jejuni. MAMA-PCR detected a change in 89 C. jejuni resistant isolates with MIC values, NA ranging from 8 - >256μg/ml and CIP 4 - >32μg/ml.