Acinetobacter Antibiotic Resistance
Approximately 50% of all
A. baumannii infections are multi-drug resistant in the United States. A. baumannii has several resistance mechanisms, including
β-lactamases, aminoglycoside-modifying enzymes, efflux pumps, permeability defects, and modifications of target sites. Resistance to carbapenems has been increasing gradually, mediated through the production of carbapenemases or metallo-β -lactamases, and soon will no longer be a reliable treatment for
A. baumannii. Compounding the problem, carbepenem-resistant A. baumannii are often resistant to all other commonly used antibiotics, leaving few treatment options. Fluoroquinolone resistance is also high in clinical A. baumannii isolates, due to target site mutations in the genes encoding DNA gyrase and topoisomerase IV, as well as enhanced efflux mechanisms.