Braenderburg found in Spain [29]. The size change in type 1 plasmids may be due to presence of multiple IS26 elements that may be involved in plasmid rearrangement (Figure 3). Although conjugation capability of type 2 plasmids was higher than that MAPK inhibitor of type 1 plasmids, we only identified coexistence of type 1 and 2 plasmids in three S. Braenderup isolates, which differed in isolation day and PFGE pattern (Table 3). Isolate 13 with type 1f and 2a plasmids was collected in July of 2004 from Taipei. Isolate 32 with type 1d and 2a plasmids and isolate 36 with 1c and 2b plasmids were collected in March and May of 2005, respectively, from Taichung (Table 3). Only one isolate 44 with a type 1d plasmid was collected

before those three isolates, in June of 2004 from Taichung. These results suggest FGFR inhibitor possibly that isolate 32 with A6 genotype and R6 resistance pattern may be derived from isolate 44 with a type 1 plasmid, A4 genotype and R6 resistance pattern by introduction of a type 2 plasmid. Interestingly, type 2 plasmids are IncI1 plasmids, carrying the tnpA-bla CMY-2-blc-sugE structure

Ro 61-8048 manufacturer (Table 3). AmpC β-lactamases are broadly distributed among the Enteribacteriaceae, and plasmid-mediated AmpC β-lactamases include ACC, ACT, CFE, CMY, DHA, FOX, LAT, MIR, and MOX [30]. At least three transposase associated genetic structures for bla CMY include ISEcp1-bla CMY-2-blc-sugE, ISCR1-bla CMY-9-yqgF-yqgE and IS26-frdC-frdD-ampR-bla CMY-13 -blc-sugE-IS26 [30]. Recently, bla CMY has been shown to be broadly spread in Salmonella worldwide [29, 31, 32] and to be present in S. Braenderup [33]. In Taiwan, since we reported the tnpA-bla CMY-2-blc-sugE structure in S. Choleraesuis in 2004 [34], this transposon-like element has been found in other Salmonella serovars

and Enterobacteriaceae [32]. In the present study, we first reported that S. Braenderup harbors tnpA-bla CMY-2-blc-sugE on a type 2 plasmid. Comparing Phosphoribosylglycinamide formyltransferase this plasmid with the 138-kb plasmid pSC138 (accession no. NC_006856) of S. Choleraesuis, both are IncI1 plasmids with the tnpA-bla CMY-2-blc-sugE structure. However, type 2 plasmids were conjugative and much smaller in size due to lack of a 60-kb DNA region with multiple integrons and transposons, which carry MDR genes [35–37]. Conclusions Over 95% cases of human salmonellosis surveyed in this study were caused by 5 Salmonella serogroups: B, C1, C2, D1, and E1. As two prevalent serogroup C1 serovars, S. Braenderup and S. Bareiley differed in patients’ age groups and XbaI-PFGE patterns. Both serovars were clonally disseminated and drug-susceptible. However, in S. Braenderup, cluster A MDR isolates were derived from susceptible isolates by sequential introduction of two distinct R plasmids. Type 1 plasmids carry bla TEM, F1A/F1B replicons, insertion sequence IS26, and a class 1 integron with a gene cluster comprised of dfrA12-orfF-aadA2-qacEΔ1-sulI.