In the present study, we found that only one of the IncA/C plasmids tested was able to conjugate, albeit at very low frequencies (10-7 to10-9). The only distinctive feature

of this YUHS 05-78, 150 kb CMY+ plasmid is its lack of the mer region. It has been suggested that the inability of Salmonella CMY+ plasmids to conjugate is due to the insertion of the CMY island into the tra operon on the plasmid backbone [22]. However, the conjugative plasmid YUHS 05-78 has the CMY island inserted Tariquidar clinical trial in between traA and traC, and this is also true for almost all the other CMY+ plasmids. We think that the reduced conjugative ability of the IncA/C plasmids in Salmonella might be due to AZD6738 solubility dmso chromosomally encoded factors, such as the thickness of the cell envelope, rather than to plasmid-encoded features, or it may depend on the presence of additional helper plasmids, as previously suggested [5, 8]. The predominant lack of conjugation ability of our IncA/C plasmids agrees with the clonal dissemination trend detected BIBW2992 cost between chromosomal backgrounds and plasmid patterns, as revealed by Xba I and Pst I digests (Figure 2), respectively. This study provides evidence

of frequent rearrangements shaping the genetic composition of the IncA/C plasmids harboured by ST213 strains. It is possible that the IncA/C plasmids circulating in Typhimurium were acquired from other Salmonella serotypes or other enteric bacteria such as E. coli. The higher plasmid diversity and conjugation frequencies of E. coli in comparison with Salmonella led Daniels et al. [25] to speculate that insertions and deletions that occur during promiscuous plasmid sharing among E. coli isolates occasionally result in plasmids that are successful in Salmonella. It is possible that this is the scenario in Mexico, where resistance to ceftriaxone was detected in E. coli several years prior to that in Salmonella (M. Zaidi, unpublished data). Evolutionary origin of the two IncA/C types The combined results of the PCR screening and the nucleotide sequence analysis suggest that

the IncA/C plasmids from types I and II have a recent common origin and are evolving by the insertion/deletion of DNA stretches rather than Anacetrapib by point mutations, in agreement with the conclusions derived from other studies [5, 6, 8, 10]. For example, in this study, insertion of the IP-1 integron (dfrA12, orfF and aadA2) and deletion of the R-8 segment were observed in most of the CMY+ plasmids. The PCR markers and plasmid sizes of the IncA/C CMY+ reference plasmids of E. coli AR060302 [6] and Newport SN11 [22] corresponded with those of our Typhimurium IncA/C CMY+ plasmids. However, their Pst I restriction profiles were related to type II plasmids, which included most of our Typhimurium IncA/C CMY- plasmids (Figure 2).