1. Wstęp. 2. Oporność na antybiotyki β-laktamowe. 2.1. Enzymy CHDL. 2.2. Enzymy MBL. 2.3. Karbapenemazy należące do klasy A wg Amblera. 2.4. Nabyte enzymy ESβL hamowane przez inhibitory β-laktamaz. 2.5. Enzymy AmpC. 3. Oporność na antybiotyki inne niż β-laktamy. 3.1. Oporność na chinolony i fluorochinolony. 3.2. Oporność na aminoglikozydy. 3.3. Oporność na kolistynę. 4. Aktywne usuwanie antybiotyków z komórki bakteryjnej przy udziale pomp błonowych – mechanizm efflux. 4.1. System pomp RND. 4.2. Inne systemy pomp błonowych. 5. Kanały błonowe – pory. 6. Biofilm i zjawisko quorum sensing. 7. Podsumowanie

Abstract: Acinetobacter baumannii has become one of the most dangerous Gram-negative bacterial species, causing numerous infections over the last 20 years. A. baumannii is responsible for nosocomial ventilator-associated pneumonia (VAP), urinary tract infections, meningitidis and bacteremia. Its remarkable ability to acquire resistance determinants against multiple antibiotics of different classes and to tolerate harsh environments resulted in the dissemination of multi-drug-resistant (MDR) strains. Diverse mechanisms of resistance limit therapeutic options and make the infections difficult to treat. The described resistance mechanisms include: production of β-lactamases, i.e. enzymes modifying structure of antibiotics, activity of efflux pumps, loss of membrane porins and formation of biofilm.

1. Introduction. 2. Resistance to β-lactams. 2.1. CHDLs. 2.2. MBLs. 2.3. Ambler class A carbapenemases. 2.4. Acquired ESβLs inhibited by clavulanic acid. 2.5. AmpC enzymes. 3. Resistance to antibiotics other than β-lactams. 3.1. Resistance to quinolones and fluoroquinolones. 3.2. Resistance to aminoglycosides. 3.3. Resistance to colistin. 4. Efflux systems. 4.1. RND efflux system. 4.2. Other efflux systems. 5. Outer membrane porins. 6. Biofilm and quorum sensing process. 7. Summary