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Pseudomonas aeruginosa is a major cause of nosocomial infections and exhibits high levels of intrinsic and acquired resistance to antibiotics, especially carbapenems, which are often used as a last-resort treatment [1]. (Poole, 2004). The increasing prevalence of carbapenem-resistant P. aeruginosa (CRPA) poses a serious threat to public health and limits therapeutic options (Rodríguez-Baños et al., 2008). Resistance mechanisms such as production of carbapenemases, efflux pump overexpression, porin loss, and mutations are critical factors in resistance (Bonomo & Szabo, 2006). Understanding the genetic basis of these mechanisms is essential for developing effective infection control strategies and therapeutic approaches (Camenisch et al., 2019). Necessity and significance of the research subject Carbapenem-resistant P. aeruginosa poses a significant challenge to public health globally, with especially high concerns in low- and middle-income countries, including Iraq, due to inadequate infection control practices, overuse of antibiotics, and limited surveillance systems. According to recent studies, P. aeruginosa infections have been linked to high morbidity and mortality rates in both hospital and community settings (Klein et al., 2019). Furthermore, the situation is exacerbated by the growing spread of carbapenem-resistant strains, which significantly limits available therapeutic options (Liu et al., 2020). Understanding the genetic basis of carbapenem resistance in P. aeruginosa is crucial for: • Developing targeted molecular diagnostics for rapid detection of resistance profiles. • Identifying key resistance genes and their transmission mechanisms, which could help in monitoring the spread of resistant strains. • Informing infection control policies and antimicrobial stewardship programs in healthcare settings. • Developing novel therapeutic strategies or alternative treatments to overcome resistance. This research is necessary to address the growing crisis of anti