<p>Molecular mechanisms related to colistin resistance in Enterobacteriaceae</p>

Abstract

Colistin is an effective antibiotic for treatment of most multidrug-resistant Gram-negative bacteria. It is used currently as a last-line drug for infections due to severe Gram-negative bacteria followed by an increase in resistance among Gram-negative bacteria. Colistin resistance is considered a serious problem, due to a lack of alternative antibiotics. Some bacteria, including Pseudomonas aeruginosa , Acinetobacter baumannii , Enterobacteriaceae members, such as Escherichia coli, Salmonella spp., and Klebsiella spp. have an acquired resistance against colistin. However, other bacteria, including Serratia spp., Proteus spp. and Burkholderia spp. are naturally resistant to this antibiotic. In addition, clinicians should be alert to the possibility of colistin resistance among multidrug-resistant bacteria and development through mutation or adaptation mechanisms. Rapidly emerging bacterial resistance has made it harder for us to rely completely on the discovery of new antibiotics; therefore, we need to have logical approaches to use old antibiotics, such as colistin. This review presents current knowledge about the different mechanisms of colistin resistance.

Antimicrobial resistance profile and prevalence of extended-spectrum beta-lactamases (ESBL), AmpC beta-lactamases and colistin resistance (mcr) genes in Escherichia coli from swine between 1999 and 2018

“…The existence of strains positive to a mcr gene but with a sensitive MIC value suggests that, although they do not express it, strains with a "sensitive" phenotype could contain a mcr gene and might end up expressing it. Conversely, the seven strains found phenotypically resistant to colistin and negative for the mcr genes analysed, might suggest the presence of other mcr genes such as mcr-6 and mcr-8, originally described in pigs [23,24] or other genes such as pmrA that can confer intrinsic resistance to colistin in E. coli [25] and have not been included in the study. Besides, colistin resistance could occur via chromosomal mutations, although this mechanism is often unstable [19].…”

Colistin and its role in the Era of antibiotic resistance: an extended review (2000–2019)

“…This eptB encodes a phosphoethanolamine transferase, which modifies LPS at the outer 3-deoxy-D-mannooctulosonic acid (Kdo) residue with phosphoethanolamine. The addition of a pEtN moiety to the Kdo residue of LPS decreases the net negative charge of molecules and reduces the electrostatic repulsion between neighbouring LPS molecules, thus leading to polymyxin resistance [61].…”

Cohorting KPC+ Klebsiella pneumoniae (KPC-Kp)–positive patients: A genomic exposé of cross-colonization hazards in a long-term acute-care hospital (LTACH)

“…For example, colistin/polymyxin E is a last-resort drug used to treat severe multidrug-resistant gramnegative infections, such as those due to KPC-Kp. [28][29][30][31] In our study, a single patient plausibly acquired a secondary isolate with predicted colistin resistance that was linked within 25 SNVs of another LTACH patient's isolate (Supplementary Table 1 online). Because colonization is a major risk factor for KPC-Kp infection [32][33][34] and because infections are thought to arise primarily from the patient's colonizing strain, 35 the acquisition of a colistin-resistant isolate could limit efficacious treatment options and in turn increase mortality risk.…”