Carbapenemase-Encoding Genes and Colistin Resistance in Gram-Negative Bacteria During the COVID-19 Pandemic in Mexico: Results from the Invifar Network

Detection of Plasmid-Mediated Resistance against Colistin in Multi-Drug-Resistant Gram-Negative Bacilli Isolated from a Tertiary Hospital

“…The low prevalence of mcr genes found in this investigation among colistin-resistant strains (2/12) suggests that in our population, resistance to this agent might be mainly driven, as suggested by Gogry et al [26], by chromosomal mutations, such as those in the genes regulating the two-component systems, PhoPQ or PmrAB, or in its negatively regulating gene, mgrB, by mcr genes different from the mcr-1 to mcr-5 genes included in this investigation or by unknown colistin resistance mechanisms. The results of the current investigation are in agreement with those found in a recent report by Garza-Ramos et al who found that the more prevalent colistin-resistant mechanism in Mexico is not driven by mcr genes but by mgrB mutations [30]. Moreover, the low prevalence of mcr genes in our population might be partially explained by the fact that colistin-resistance in Enterobacterales has been linked mainly to mgrB mutations [35], rather than to plasmid-mediated genes.…”

“…The first mcr gene ( mcr -1) was originally described in 2015 in China [ 8 ], and in Mexico, mcr -1 was first identified in 2019 in an E. coli strain isolated from a fecal sample from a child [ 31 ]. The presence of this plasmid-mediated gene in our country was recently confirmed in K. pneumoniae strains isolated from different clinical samples [ 30 ]. In the present study, only two E. coli strains, both isolated from female patients with urinary tract infections that required hospitalization, were found to carry the mcr -1 gene and both strains were able to efficiently transfer this colistin-resistant determinant to recipient strains by means of an approximately 60 kb plasmid, as demonstrated by Southern blot analysis.…”

“…The prevalence of colistin resistance in this study is in agreement with reports in different geographical areas of the world among muti-drug-resistant strains isolated from hospitalized patients [ 10 , 27 , 28 ], but higher than the 1.26% worldwide prevalence reported by Dadashi et al [ 29 ]. In Mexico, reports on the prevalence of colistin-resistant strains are scarce; however, in a recent report by the Red Temática de Investigación y Vigilancia de la Farmacorresistencia (INVIFAR network), that included clinical strains isolated from different parts of the country, the colistin resistance prevalence among K. pneumoniae strains was 17.8% [ 30 ], a rate similar to that found in the current study among isolates of this bacterial species (3/20 = 15.0%). Unlike the INVIFAR report, where no resistance to colistin was found among E. coli strains, we found that 2.5% of the E. coli strains included in the current study presented this resistance trait.…”

Comprehensive study reveals phenotypic heterogeneity in Klebsiella pneumoniae species complex isolates

“…In this study, the primary mechanism of colistin-resistant isolates was modifications in the mgrB gene, and the main carbapenemase was NDM-1. Unlike the panorama in different regions of Latin America, a recent study carried out in Mexico showed that the NDM-type carbapenemases were more frequent than KPC-type 17 . Thus, we consider that Mexico is New-Delhi metallo-β-lactamase territory.…”

Active Surveillance of Antimicrobial Resistance and Carbapenemase-Encoding Genes According to Sites of Care and Age Groups in Mexico: Results from the INVIFAR Network

“…As part of the active surveillance performed by the INVIFAR network, centers sent relevant carbapenem-resistant Gram negatives to the coordinating laboratory. In the clinical isolates received from centers, polymerase chain reaction (PCR) was performed to detect the most frequent carbapenemase-encoding genes previously reported in this population [ 15 ], that is, bla NDM-1 , bla KPC , bla VIM , bla IMP , and bla OXA-48-like [ 16 , 17 ] in E. coli and K. pneumoniae isolates; bla OXA-23 and bla OXA-24 in A. baumannii isolates [ 18 , 19 ]; and bla VIM , bla IMP , and bla GES in P. aeruginosa isolates [ 10 ].…”