Abstract
Pseudomonas aeruginosa is a nosocomial pathogen notable for its high antibiotic resistance and virulence, particularly in immune compromised patients. Understanding its genetic diversity is critical for improving treatment strategies and infection control in healthcare settings. This study aims to evaluate the genetic diversity of P. aeruginosa isolates from clinical samples using Inter Simple Sequence Repeat (ISSR) primers. One hundred clinical isolates of P. aeruginosa were collected from various sample types, including blood, urine, sputum, and wound swabs. ISSR-PCR was employed using 19 different primers to amplify genomic regions, and the resulting banding patterns were analyzed. The resulting genetic profiles were analyzed to assess similarities and differences among the isolates using phylogenetic trees, genetic similarity and Principal Component Analysis (PCA) generated with NTSYSpc software. The study examined 100 P. aeruginosa isolates, focusing on 18 multidrug-resistant (MDR) strains for genetic diversity analysis. A total of 95 polymorphic bands indicated substantial diversity, with genetic similarity coefficients ranging from 0.45 to 0.90. The UPGMA dendrogram revealed clear genetic clusters, and 83% of isolates showed resistance to antibiotics such as Cefoperazone, Meropenem, and Imipenem. Phylogenetic and PCA analyses confirmed this variability, highlighting multiple lineages in the hospital. ISSR markers varied in their genetic distinctions, with ISSR 7 showing the highest diversity. These findings emphasize the pathogen's adaptability and inform targeted treatments and infection control strategies. The study demonstrates considerable genetic diversity among P. aeruginosa isolates, emphasizing the pathogen's adaptability and the need for continuous molecular surveillance. ISSR markers proved to be a useful tool for assessing genetic variation. Future research should incorporate larger sample sizes and advanced molecular techniques to better understand the genetic dynamics and resistance mechanisms of P. aeruginosa in clinical environments.