Bacterial resistance is the capacity of bacteria to withstand the effects of antibiotics or biocides that are intended to kill or control them. There are three fundamental mechanisms of antimicrobial resistance; (1) enzymatic degradation of antibacterial drugs that inactivate the drug, (2) alteration of target bacterial proteins so the drug no longer recognizes it, and (3) changes in membrane permeability to antibiotics leading to a decreased intracellular concentration of antibiotics.
Since the first introduction of penicillin in the 1920’s, there have been numerous new antimicrobials produced in response to increasing resistance of bacteria. The outcome however has always been the same; organisms evolve and find ways to resist these antimicrobials.
Resistance among gram negative bacilli is becoming increasingly common and plays an important role in laboratory work. Enterobacteriaciae can exhibit all three types of resistance mechanisms. The most commonly seen worldwide is beta-lactam resistance, which involves enzymatic degradation of antibacterial drugs. This is carried out by beta lactamases, which are enzymes that inactivate beta-lactam antibiotics by hydrolysis. There are two schemes used to classify beta-lactamases, the Ambler and the Bush-Jacoby-Medeiros. Within these schemes, there are three categories of beta-lactam resistance, that being carbapenemase resistant enterobacteriacae (CPE), AmpC resistance and extended spectrum beta lactamases (ESBL’S). There are numerous steps in the laboratory to identify these resistance genes, involving specialised susceptibility testing, Etests, PCR and rapid screening tests. These are critical to properly guide antibiotic therapy for patients, implement appropriate isolation measures, and follow any emerging resistance patterns around the globe.