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Enterobacter cloacae is a Gram-negative, rod-shaped, facultatively anaerobic bacterium belonging to the Enterobacteriaceae family (Davin-Regli & Pagès, 2015). While it exists as a commensal in the human gastrointestinal tract, it is a significant opportunistic pathogen responsible for a wide range of nosocomial infections, including pneumonia, urinary tract infections, and bloodstream infections (Mezzatesta et al., 2012). The organism is particularly challenging in clinical settings due to its ability to develop resistance to various antibiotics, most notably through the production of chromosomal AmpC beta-lactamases and acquired carbapenemases (Annavajhala et al., 2019). Drugs used to treat E. cloacae infections generally target essential bacterial processes such as cell wall assembly or protein synthesis, but the emergence of multidrug-resistant strains has limited therapeutic options (Sanders & Sanders, 1997). Consequently, it is recognized as a major threat in healthcare environments, especially for patients in intensive care units (Paterson, 2006).
Antibiotics targeting this organism act by inhibiting cell wall synthesis (beta-lactams), inhibiting protein synthesis (aminoglycosides, tetracyclines), or inhibiting DNA replication (fluoroquinolones) (Paterson, 2006).
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