Published in:
01-12-2016 | Editorial
In 2035, will all bacteria be multiresistant? Yes
Authors:
George Dimopoulos, Marin H. Kollef, Jon Cohen
Published in:
Intensive Care Medicine
|
Issue 12/2016
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Excerpt
The “golden era” of antibiotics started with the discovery of penicillin, streptomycin, chloramphenicol, and tetracycline [
1]. However, their introduction into medical practice was associated with rapid appearance of resistance: 50 % of hospital
Staphylococcus aureus isolates were resistant within 7 years of penicillin’s first use [
1]. During the following years a huge number of newer antibiotics have been released but simultaneously more and more pathogenic bacteria developed resistance to nearly all antibiotic classes through intrinsic or acquired resistance mechanisms; this has created a global public health problem that affects all parts of the world (in 2004, more than 70 % of pathogenic bacteria were resistant to at least one of the currently used antibiotics) [
2,
3]. Bacterial resistance mechanisms to antibiotics include their inactivation via hydrolysis, alteration or bypassing the drug target, preventing access of the drug to the target sites making the cells unrecognizable to the antibiotic, and active efflux out of the cell via membrane-bound efflux transporters. These resistance mechanisms primarily occur as a result of mutations of endogenous genes and/or lateral gene transfer of resistance genes from other pathogens [
4]. Studies on genomics and metagenomics recently reported that diverse natural ecosystems (human gut, soil, etc.), the so-called resistomes, contain genes able to confer resistance to antimicrobials, in addition to some pathogens being considered as disseminated multicellular organisms having interactions mediated by complex cell–cell signaling [
5]. These interactions lead to the formation of complex matrices of polysaccharide/extracellular DNA and biofilm development, especially in the ICU setting where many devices are used. The biofilm promotes cellular resistance due to a high mutation rate (up to 100 times higher than planktonic cells) leading to faster development of antibiotic-resistant mutants while the various pathogens within biofilm facilitate horizontal gene transfer and acquisition and spread of resistance determinants [
6]. From all the above it appears that bacteria are involved in a continuous effort to “find” new pathways and to develop newer and newer mechanisms of resistance in order to overcome antibiotics usage. …