Circulation of Highly Drug-Resistant <i>Clostridium difficile</i> Ribotypes 027 and 001 in Two Tertiary-Care Hospitals in Mexico

Martínez-Meléndez, Adrián; Tijerina-Rodríguez, Laura; Morfín‐Otero, Rayo; Camacho-Ortíz, Adrián; Villarreal-Treviño, Licet; Sánchez-Alanís, Hugo; Rodríguez-Noriega, Eduardo; Baines, Simon D.; Flores-Treviño, Samantha; Maldonado-Garza, Héctor Jesús; Garza‐González, Elvira

doi:10.1089/mdr.2017.0323

Cited by 12 publications

(8 citation statements)

References 34 publications

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“…This was also true in surveillance studies undertaken in Canada from 2013 to 2015 (11) and Australia from 2013 to 2015 (12). Only a handful of isolates with decreased susceptibility to fidaxomicin have been reported as follows: one isolate in Florida, isolated in 2016 from a patient with CDI with an MIC of 16 g/ml (13), and 4 isolates in Mexico from patients with recurrent CDI with MICs of 2 g/ml (14). Interestingly, fidaxomicin is not in clinical use in Mexico.…”

Section: Discussionmentioning

confidence: 99%

U.S.-Based National Surveillance for Fidaxomicin Susceptibility of Clostridioides difficile-Associated Diarrheal Isolates from 2013 to 2016

Thorpe

McDermott

Tran

et al. 2019

Antimicrob Agents Chemother

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In 2011, we initiated a sentinel surveillance network to assess changes in Clostridioides (formerly Clostridium) difficile antimicrobial susceptibility to fidaxomicin from 6 geographically dispersed medical centers in the United States. This report summarizes data from 2013 to 2016. C. difficile isolates or toxin-positive stools from patients were referred to a central laboratory. Antimicrobial susceptibility was determined by agar dilution. CLSI, EUCAST, or FDA breakpoints were used, where applicable. Toxin gene profiles were characterized by multiplex PCR on each isolate. A random sample of approximately 40% of isolates, stratified by institution and year, was typed by restriction endonuclease analysis (REA). Among 1,889 isolates from 2013 to 2016, the fidaxomicin MIC 90 was 0.5 g/ml; all isolates were inhibited at Յ1 g/ml. There were decreases in metronidazole and vancomycin MICs over time. Clindamycin resistance remained unchanged (27.3%). An increase in imipenem resistance was observed. By 2015 to 2016, moxifloxacin resistance decreased in all centers. The proportion of BI isolates decreased from 25.5% in 2011 to 2012 to 12.8% in 2015 to 2016 (P Ͻ 0.001). The BI REA group correlated with moxifloxacin resistance (BI 84% resistant versus non-BI 12.5% resistant). Fidaxomicin MICs have not changed among C. difficile isolates of U.S. origin over 5 years post licensure. There has been an overall decrease in MICs for vancomycin, metronidazole, moxifloxacin, and rifampin and an increase in isolates resistant to imipenem. Moxifloxacin resistance remained high among the BI REA group, but the proportion of BI isolates has decreased. Continued geographic variations in REA groups and antimicrobial resistance persist.

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Section: Discussionmentioning

confidence: 99%

U.S.-Based National Surveillance for Fidaxomicin Susceptibility of Clostridioides difficile-Associated Diarrheal Isolates from 2013 to 2016

Thorpe

McDermott

Tran

et al. 2019

Antimicrob Agents Chemother

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“…Although CDI is an important cause of hospital-acquired diarrhea and colitis in Latin America ( Muñoz et al, 2018 ; Guerrero-Araya et al, 2020 ), little is known about antibiotic resistance and molecular epidemiology of C. difficile in this region. In recent years, studies in Mexico have focused mainly on molecular typing of C. difficile strains, particularly on the identification of the hypervirulent strain RT027 using PCR ribotyping ( Camacho-Ortiz et al, 2015 ; Martínez-Meléndez et al, 2018 ). The aim of this study was to examine the molecular epidemiology of C. difficile strains isolated from patients at hospitals in Mexico.…”

Section: Introductionmentioning

confidence: 99%

Molecular Epidemiology and Antimicrobial Resistance of Clostridioides difficile in Hospitalized Patients From Mexico

et al. 2022

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Clostridioides difficile is a global public health problem, which is a primary cause of antibiotic-associated diarrhea in humans. The emergence of hypervirulent and antibiotic-resistant strains is associated with the increased incidence and severity of the disease. There are limited studies on genomic characterization of C. difficile in Latin America. We aimed to learn about the molecular epidemiology and antimicrobial resistance in C. difficile strains from adults and children in hospitals of México. We studied 94 C. difficile isolates from seven hospitals in Mexico City from 2014 to 2018. Whole-genome sequencing (WGS) was used to determine the genotype and examine the toxigenic profiles. Susceptibility to antibiotics was determined by E-test. Multilocus sequence typing (MLST) was used to determine allelic profiles. Results identified 20 different sequence types (ST) in the 94 isolates, mostly clade 2 and clade 1. ST1 was predominant in isolates from adult and children. Toxigenic strains comprised 87.2% of the isolates that were combinations of tcdAB and cdtAB (tcdA+/tcdB+/cdtA+/cdtB+, followed by tcdA+/tcdB+/cdtA−/cdtB−, tcdA−/tcdB+/cdtA−/ cdtB−, and tcdA−/tcdB−/cdtA+/cdtB+). Toxin profiles were more diverse in isolates from children. All 94 isolates were susceptible to metronidazole and vancomycin, whereas a considerable number of isolates were resistant to clindamycin, fluroquinolones, rifampicin, meropenem, and linezolid. Multidrug-resistant isolates (≥3 antibiotics) comprised 65% of the isolates. The correlation between resistant genotypes and phenotypes was evaluated by the kappa test. Mutations in rpoB and rpoC showed moderate concordance with resistance to rifampicin and mutations in fusA substantial concordance with fusidic acid resistance. cfrE, a gene recently described in one Mexican isolate, was present in 65% of strains linezolid resistant, all ST1 organisms. WGS is a powerful tool to genotype and characterize virulence and antibiotic susceptibility patterns.

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“…Phenotypic assays are required to validate the role of the SNPs and acquired genes in antibiotic resistance. In this context, given that C. difﬁcile exchanges DNA with intestinal Firmicutes [ 54 ], and possibly with many other members of the complex metagenome with which it coexists [ 15, 17, 56, 60, 67, 68 ], our pangenomic analyses justify further surveillance of antimicrobial resistance in this pathogen in LA and the world.…”

Section: Discussionmentioning

confidence: 99%

“…As indicated by reports from Costa Rica [ 12 ], Panama [ 13 ], Chile [ 14 ], Mexico [ 15 ], Colombia [ 16 ] and Honduras [ 17 ], the B1/NAP1/RT027/ST01 strain has been present for at least 10 years in Latin America (LA). However, since nearly all in-depth studies on the molecular epidemiology of this epidemic strain have been conducted in Europe and the USA, the origin, date of introduction, diversity and microevolution of the B1/NAP1/RT027/ST01 strain in LA remains obscure.…”

Section: Introductionmentioning

confidence: 99%

Origin, genomic diversity and microevolution of the Clostridium difficile B1/NAP1/RT027/ST01 strain in Costa Rica, Chile, Honduras and Mexico

et al. 2020

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Clostridium difficile B1/NAP1/RT027/ST01 has been responsible for outbreaks of antibiotic-associated diarrhoea in clinical settings worldwide and is associated with severe disease presentations and increased mortality rates. Two fluoroquinolone-resistant (FQR) lineages of the epidemic B1/NAP1/RT027/ST01 strain emerged in the USA in the early 1990s and disseminated trans continentally (FQR1 and FQR2). However, it is unclear when and from where they entered Latin America (LA) and whether isolates from LA exhibit unique genomic features when compared to B1/NAP1/RT027/ST01 isolates from other regions of the world. To answer the first issue we compared whole-genome sequences (WGS) of 25 clinical isolates typed as NAP1, RT027 or ST01 in Costa Rica ( n =16), Chile ( n =5), Honduras ( n =3) and Mexico ( n =1) to WGS of 129 global isolates from the same genotype using Bayesian phylogenomics. The second question was addressed through a detailed analysis of the number and type of mutations of the LA isolates and their mobile resistome. All but two B1/NAP1/RT027/ST01 isolates from LA belong to the FQR2 lineage ( n =23, 92 %), confirming its widespread distribution. As indicated by analysis of a dataset composed of 154 WGS, the B1/NAP1/RT027/ST01 strain was introduced into the four LA countries analysed between 1998 and 2005 from North America (twice) and Europe (at least four times). These events occurred soon after the emergence of the FQR lineages and more than one decade before the first report of the detection of the B1/NAP1/RT027/ST01 in LA. A total of 552 SNPs were identified across all genomes examined (3.8–4.3 Mb) in pairwise comparisons to the R20291 reference genome. Moreover, pairwise SNP distances were among the smallest distances determined in this species so far (0 to 55). Despite this high level of genomic conservation, 39 unique SNPs (7 %) in genes that play roles in the infection process (i.e. slpA ) or antibiotic resistance (i.e. rpoB , fusA ) distinguished the LA isolates. In addition, isolates from Chile, Honduras and Mexico had twice as many antibiotic resistance genes (ARGs, n =4) than related isolates from other regions. Their unique set of ARGs includes a cfr -like gene and tetM , which were found as part of putative mobile genetic elements whose sequences resemble undescribed integrative and conjugative elements. These results show multiple, independent introductions of B1/NAP1/RT027/ST01 isolates from the FQR1 and FQR2 lineages from different geographical sources into LA and a rather rapid accumulation of distinct mutations and acquired ARG by the LA isolates.

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Circulation of Highly Drug-Resistant Clostridium difficile Ribotypes 027 and 001 in Two Tertiary-Care Hospitals in Mexico

Abstract: Ribotypes 027 and 001 were the most frequent C. difficile isolates recovered in this study, and demonstrated higher MICs. Furthermore, we found four isolates with reduced susceptibility to fidaxomicin, raising a concern since this drug is currently unavailable in Mexican Hospitals.

Cited by 12 publications

References 34 publications

U.S.-Based National Surveillance for Fidaxomicin Susceptibility of Clostridioides difficile-Associated Diarrheal Isolates from 2013 to 2016

U.S.-Based National Surveillance for Fidaxomicin Susceptibility of Clostridioides difficile-Associated Diarrheal Isolates from 2013 to 2016

Molecular Epidemiology and Antimicrobial Resistance of Clostridioides difficile in Hospitalized Patients From Mexico

Origin, genomic diversity and microevolution of the Clostridium difficile B1/NAP1/RT027/ST01 strain in Costa Rica, Chile, Honduras and Mexico

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