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Antimicrobial Resistance

The introduction of antimicrobials transformed human and animal health systems by revolutionizing our weaponry in the war against infectious diseases, resulting in improved survivability for both humans and their domestic animals.  However, this health triumph was immediately ebbed by the subsequent realization that bacterial populations could quickly modify themselves to resist antimicrobials, propagate these resistance traits, and even share resistance genes with other contemporary bacteria within their environment.  Such abilities have seriously compromised the usefulness of antibiotics in the war against microbes and warn of a future when antimicrobials may have very limited usefulness to control bacterial infection

Antimicrobial resistance is the ability of a microorganism to survive and multiply in the presence of an antimicrobial agent that would normally inhibit or kill this particular kind of organism.  Antimicrobial resistance is just one of the many adaptive traits that resilient bacterial subpopulations may possess or acquire, enabling them to out-compete and out-survive their microbial neighbors and overcome host strategies aimed against them.  This phenomenon is nearly as old as the discovery of antimicrobials themselves, having been described by pioneers like Ehrlich for trypanosomes8 and Fleming for staphylococci10.  What is most alarming today is the rate at which antibiotic resistance often develops and how quickly it spreads across the globe and among different species of bacteria. 

Furthermore, as a result of sequential, cumulative acquisition of resistance traits against different antibiotics, more bacterial pathogens with multiple-drug resistance are being reported worldwide. As a consequence, many bacterial organisms, including major human and animal pathogens such as Mycobacterium and Salmonella species, have become resistant to antibiotics which were previously quite efficacious

 

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Resistance to single antibiotics became prominent in organisms that encountered the first commercially produced antibiotics. The most notable example is resistance to penicillin among staphylococci, specified by an enzyme (penicillinase) that degraded the antibiotic. Over the years, continued selective pressure by different drugs has resulted in organisms bearing additional kinds of resistance mechanisms that led to multidrug resistance (MDR), novel penicillin-binding proteins (PBPs), enzymatic mechanisms of drug modification, mutated drug targets, enhanced efflux pump expression, and altered membrane permeability.  Some of the most problematic MDR organisms that are encountered currently include Pseudomonas aeruginosa, Acinetobacter baumannii, Escherichia coli and Klebsiella pneumoniae bearing extended-spectrum β-lactamases (ESBL), vancomycin-resistant enterococci (VRE), methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant MRSA, and extensively drug-resistant (XDR) Mycobacterium tuberculosis.

Alekshun MN and Levy SB. 2007. Molecular Mechanisms of Antibacterial Multidrug Resistance. Cell 128:1037-1050.

 

 

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