These results suggest that the co-integrates were stable and not resolved;

furthermore, these co-integrates maintained their architecture after a second round of conjugation. Acquisition of the CMY region by pX1 IncX plasmids Selleckchem Barasertib have been less studied that IncA/C plasmids, but their record extends through the pre-antibiotic era [30]. Recent studies have focused on IncX because of their find more implication in biofilm formation and drug-resistance in Enterobacteriaceae[13, 15, 31]. In Salmonella, IncX plasmids have been related to co-integrates with serotype-specific virulence plasmids. pOG669 is a Typhimurium virulence plasmid co-integrated with an IncX conjugative plasmid carrying ampicillin and kanamycin resistance, which has been used in compatibility experiments among Typhimurium strains [32, 33]. pOU1115 is a Dublin virulence plasmid that co-integrated with an IncX plasmid similar to pOU1114 [34]. In serovar Enteritidis, phage-type conversion has been demonstrated by the acquisition of IncX plasmids, such as pOG670 and pSE34 [35, 36]. All IncX plasmids studied

so far exhibit a type IV secretion system as part of their plasmid backbone [35, 36]; this feature enables horizontal transfer of these plasmids between host cells. The ability to induce MM-102 concentration biofilm formation and the expression of conjugative type IV secretion systems could have a synergistic effect that ultimately could be related to the pathogenic potential of a bacterium [37]. YU39 pX1 was negative for the amplification of the biofilm-formation operon mrk (data not shown) characteristic of pX1 plasmids pMAS2027, Protein kinase N1 pOLA52 and pLN126_33 [19]. However, the laboratory cultures of YU39 and its pX1 transformants and transconjugant exhibited a biofilm-formation-like

halo, which could be the result of other fimbrial or outer membrane proteins carried by this plasmid. YU39 was originally isolated from an eight year old boy in Yucatán with a systemic infection that presented severe thrombocytopenia and active bleeding [4]. The contribution of pX1 to the pathogenic potential of YU39 will be addressed in further experimental research. This is the first study to report the acquisition of an ESC-resistance gene by an IncX1 plasmid. The genetic contexts of bla CMY-2 genes have been addressed over the last decade [20, 38–42]. The core CMY region is composed of a transposon-like element consisting of a specific ISEcp1-bla CMY-2-blc-sugE structure. The genetic context of this structure varies in different plasmids, particularly for those genes downstream of sugE[20, 39, 41]. ISEcp1 codes for the transposase (tnpA) that mobilizes the CMY region by the one-end transposition mechanism, which only requires the action of one IS [43].