Abstract

The presence of the class I integron gene is associated with the emergence of multiple drug resistance (MDR) phenotype in Pseudomonas aeruginosa (P. aeruginosa) isolates. The objectives of this research were to study the prevalence of integrase genes I (Intel I) and integrase genes II (Intel II) in clinical isolates of P. aeruginosa and its association with antibiotic resistance in these isolates. The study was a retrograde cross-sectional study that was carried out on 150 clinical isolates of P. aeruginosa isolated from patients with healthcare-associated infections. The isolates were subjected to biochemical identification and antibiotic sensitivity study by discs diffusion test. Intel I & Intel II genes were detected by polymerase chain reaction (PCR). Intel I gene was present in 48% of the isolates, and Intel II was present in 1.3% of the isolates. Intel I gene was detected at a statistically significant high rate in MDR- P. aeruginosa (76.9%, P=0.001) compared to non-MDR- P. aeruginosa (3.4%), while intel II had a statistically insignificant increase in MDR- P. aeruginosa (1.1%, P=1.00) compared to non-MDR-P. aeruginosa (1.7%). Both Intl I/Intl II genes were detected in 2.2% of MDR-P. aeruginosa isolates and were absent in non- MDR-P. aeruginosa isolates with statistically insignificant difference (P=1.00). P. aeruginosa isolates with Intel I gene had an increase in antibiotic resistance pattern to the used antibiotics discs. However, this increase had statistically significant rates only for gentamicin (63.9%, P≤0.001), meropenem (47.2%, P=0.009), trimethoprim/sulfamethoxazole (37.5%, P=0.013) and imipenem (44.4%, P=0.025). The present study highlights the high prevalence of the Intel I gene in clinical isolates of P. aeruginosa, while the Intel II gene was less prevalent in these isolates. There was a significant association between the prevalence of the Intel I gene and the MDR phenotype of P. aeruginosa and resistance to gentamicin, meropenem, trimethoprim/sulfamethoxazole, and imipenem. These findings need future evaluation in a higher number of clinical isolates of P. aeruginosa.

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