PubMedCrossRef 33 Savioz A, Jeenes DJ, Kocher HP, Haas D: Compar

MK-4827 PubMedCrossRef 33. Savioz A, Jeenes DJ, Kocher HP, Haas D: Comparison of proC and other housekeeping genes of Pseudomonas aeruginosa with their counterparts in Escherichia coli . Gene 1990, 86:107–111.PubMedCrossRef 34. Essar DW, Eberly L, Hadero A, Crawford IP: Identification and characterization of genes for a second

anthranilate synthase in Pseudomonas aeruginosa : interchangeability of the two anthranilate synthases and evolutionary implications. J Bacteriol 1990, 172:884–900.PubMedCentralPubMed 35. Mahajan-Miklos S, Tan MW, Rahme LG, Ausubel FM: Molecular mechanisms of bacterial virulence elucidated using a Pseudomonas aeruginosa – Caenorhabditis elegans pathogenesis model. Cell 1999, 96:47–56.PubMedCrossRef Authors’ contributions RR, CB-5083 nmr DV, FV, and GB conceived and designed the experiments. RR, RM, and FV performed the experiments. RR, DV, and GB analyzed the data. DV and GB wrote the paper. buy Repotrectinib All authors read and approved the final manuscript.”
“Background The species of the Mycobacterium tuberculosis complex (MTC) show a 99.9% of similarity in their nucleotide sequence and their 16SrRNA do not differ between members, only M. canetti does [1]. Despite this identity in their genomes, a large number of long sequence

polymorphisms (LSPs), a variation in repetitive elements in the genome, and single nucleotide polymorphisms (SNPs) have been detected [2, 3]. It is the diversity of such polymorphisms, which is taken for phylogenetic studies with clinical isolates. In 1997, Sreevatsan et al. based on the presence of two SNPs in gyrA 95(AGC→ACC) and katG 463(CGC→CTG), classified all MTC isolates into three principal genetic groups or PGGs [4]. Afterwards, Brudey et al. based on the “Direct Repeat” locus (DR) diversity detected by Spoligotyping, classified thousands of MTC clinical strains isolated worldwide in different lineages or families [5]. These families were named according with their main geographical

origin; Latin American-Mediterranean family (LAM) isolates, which are the cause of 15% of the new TB (tuberculosis) cases detected each year worldwide, are highly prevalent in Latin America and the Mediterranean Terminal deoxynucleotidyl transferase area [6, 7]. Within this family a sub-lineage has been characterized by a genomic deletion known as RDRio, which was firstly detected in Brazil, but it was widely spread throughout the world [8, 9]. Haarlem family is ubiquitous throughout the world and accounts for 25% of the isolates extracted in Europe, Central America and the Caribbean [10]. The T family is an “ill defined” family that was characterized by default. It includes over 600 shared international types (SITs) and it has been divided into 5 subgroups, from T1 to T5 [5, 7]. Beijing family has become significant due to several multidrug-resistant (MDR) outbreaks identified [11]. S family was identified predominantly in patients of Italian origin [7]. “X” family was described to be highly prevalent in North America (21.5%) and Central America (11.

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