Genetic Diversity of Mycobacterium tuberculosis from Guadalajara, Mexico and Identification of a Rare Multidrug Resistant Beijing Genotype

Abstract

Determining the genetic diversity of M. tuberculosis strains allows identification of the distinct Mycobacterium tuberculosis genotypes responsible for tuberculosis in different regions. Several studies have reported the genetic diversity of M. tuberculosis strains in Mexico, but little information is available from the state of Jalisco. Therefore, the aim of this study was to determine the genetic diversity of Mycobacterium tuberculosis clinical isolates from Western Mexico. Sixty-eight M. tuberculosis isolates were tested for susceptibility to first-line drugs using manual Mycobacteria Growth Indicator Tube method and genotyped using spoligotyping and IS6110-restriction fragment length polymorphism (RFLP) pattern analyses. Forty-seven (69.1%) isolates were grouped into 10 clusters and 21 isolates displayed single patterns by spoligotyping. Three of the 21 single patterns corresponded to orphan patterns in the SITVITWEB database, and 1 new type that contained 2 isolates was created. The most prevalent lineages were T (38.2%), Haarlem (17.7%), LAM (17.7%), X (7.4%), S (5.9%), EAI (1.5%) and Beijing (1.5%). Six (12.8%) of the clustered isolates were MDR, and type 406 of the Beijing family was among the MDR isolates. Seventeen (26.2%) isolates were grouped into 8 clusters and 48 isolates displayed single patterns by IS6110-RFLP. Combination of IS6110-RFLP and spoligotyping reduced the clustering rate to 20.0%. The results show that T, Haarlem, and LAM are predominant lineages among clinical isolates of M. tuberculosis in Guadalajara, Mexico. Clustering rates indicated low transmission of MDR strains. We detected a rare Beijing genotype, SIT406, which was a highly resistant strain. This is the first report of this Beijing genotype in Latin America.

Resistance of Mycobacterium tuberculosis strains to Rifampicin: A systematic review and meta-analysis

“…And they were identified as the causative agents of tuberculosis in the world. For each families of MTB resistance to rifampicin, the prevalence was analyzed for the selected studies as follows: Beijing nineteen studies [14, 15, 16, 17, 18, 19, 20, 21, 22, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31], LAM ten studies [15, 17, 23, 25, 28, 29, 32, 33, 34, 35], T ten studies [3, 15, 16, 17, 23, 27, 28, 32, 34, 35], EAI eight studies [18, 22, 25, 27, 28, 29, 33, 36], Ural four studies [15, 17, 30, 34] Haarlem five studies [15, 23, 25, 28, 34], CAS four studies [15, 29, 30, 35] and MANU two studies [16, 29]. The proportion of rifampicin resistance varies by the type of regions and strains.…”

“…Eigteen studies reported rifampicin resistance Beijing family. Of these studies, nine were conducted in Western Pacific Region, reported 1309 (97.68%) resistance Beijing family [2, 16, 20, 21, 22, 28, 29, 30, 31], three studies were conducted in South-East Asia Region, reported 15 (1.11%) resistance Beijing family [15, 19, 25], two studies were conducted in European Region and identified 14 (1.04%) resistance Beijing family [17, 24] and two studies were conducted in Region of American but only two resistance Beijing family [18, 23]. One study which was conducted in African Region [29] and one study conducted in Eastern-Mediterranean Region did not report a rifampicin resistance Beijing family [30].…”

Tuberculosis Genetic Epidemiology: A Latin American Perspective

“…Despite this, whole-genome sequencing has revealed substantial genetic diversity between strains, leading to an improved phylogenetic SNP-based strain classification [28]. Studies in Peru [25,29,30], Argentina [31], Mexico [32,33], and Brazil [34,35,36,37] have all examined the genetic diversity of MTB in Latin America and have established that the predominant strains have evolved from the Euro-American lineage 4. This domination of lineage 4 in South America, alongside its worldwide distribution, supports the hypothesis that it was introduced and dispersed by European colonialists in the mid-sixteenth to nineteenth centuries, as discussed above [38,39,40,41].…”

Type-2 diabetes alters the basal phenotype of human macrophages and diminishes their capacity to respond, internalise, and control Mycobacterium tuberculosis

“…Little information is available on the molecular epidemiology in Mexico of Mycobacterium species. However, the published data report a variety of lineages that are prevalent in the surveyed regions ( Lopez-Rocha et al 2013 , Vera-Cabrera et al 2014 , Flores-Treviño et al 2015 , Zenteno-Cuevas et al 2015 ). While it is clear that T2D constitutes a risk for the development of TB, the immunological abnormalities that contribute to this event and the influence of the virulence of Mtb strains are less clear.…”