Figure 1 Southern hybridization of fusC. Detection of fusC by Southern hybridization in eight representatives of clinical Apoptosis inhibitor fusidic acid-resistant S. aureus isolates that did not harbour fusB or resistance polymorphisms in fusA. CP673451 molecular weight Lane 1: 2.5-kb PCR fusC fragment from strain 2 as the positive control. Lanes 2-6 and 8-10: strains 3, 6, 15, 18, 24, 28, 29 and 34, respectively. Lane 7: strain 23 without the fusC gene. All total DNA was EcoRI-digested. Detection of fusA gene mutations PCR amplification and complete sequencing were performed to detect fusA gene mutations

in the 34 isolates (Table 1). Five isolates possessed a mutation in H457Y, two isolates (isolates 9 and 33) exhibited a G556S mutation, and two isolates (isolates 10 and 21) harboured mutations in H457Y and G556S. In addition, isolate 31 possessed a mutation in H457Y and R659L.

Single amino acid substitutions were found in seven isolates, and two amino acid substitutions were found in the other three. This is the first time that two different amino acid substitutions, G556S and R659L, have been reported in fusA gene mutations. Furthermore, one isolate (isolate 4) was encoded with fusC and fusA gene mutation. In this study, the most common amino acid substitution H457Y did not result in a high level of fusidic acid resistance (MIC ≥ 128 μg/ml). Molecular epidemiological selleck products analysis All 34 isolates included in this study met the criteria of being health care associated. The genotype analyses and their frequencies are shown in Table 1. Only one defined

MLST type (ST239) was evident. All 34 isolates carried SCCmec type III elements. PFGE patterns of SmaI macrorestriction Temsirolimus concentration fragment analysis of these 34 isolates revealed nine distinct pulsotypes (A1-A9) that were classified into one cluster (> 80% similarity) (Figure 2). The results of PFGE patterns are summarized in Table 1. Figure 2 Sma I PFGE patterns of the 34 clinical fusidic acid-resistant Staphylococcus aureus isolates. PFGE patterns analysis of these 34 isolates revealed nine distinct pulsotypes (A1-A9) that were classified into one cluster. Discussion Previous studies of fusidic acid-resistance in clinical isolates have mostly focused on methicillin-susceptible S. aureus (MSSA) and other staphylococci [17, 20, 26]. Chen et al. recently reported that the prevalence of fusidic acid-resistance determinants was quite different between MRSA and MSSA groups [27]. In northern Taiwan collections, the fusA mutations were the major determinant (84%) followed by fusC with 16% fusidic acid-resistance in MRSA isolates [27]. In the present study based in central Taiwan, we found that the fusidic acid-resistant predominant determinant in MRSA was a high prevalence of fusC with 74% in clinical isolates. Furthermore, one isolate carried the fusB determinant on the plasmid and fusC determinant on the chromosome in a clinical fusidic acid-resistant S. aureus isolate. The FusC protein has a 45% amino acid similarity to FusB.