016 474 AAC → AAT –         498 GCG → GCT –         502 GTA → GTG –         518 ACA → ACG – ST5- MRSA-I (5) C (1)/t045 (1) Cape Town, RSA ≥ 256 481 CAT → TAT H481Y         498 GCG → GCT –         630 AAT → AAC –         658 GGT → GGA – ST612- MRSA-IV (8) AR-13324 supplier D (2), E (5), sporadic isolates (2)/t064 (3), t1443 (5), t1257 (1) Cape Town, RSA ≥ 256 481 CAT → AAT H481N         498 GCG → GCT –         512 CGT → CGC –         527 ATT → ATG I527M ST612- MRSA-IV (8) ND6 (2)/t064

(2) RSA (N83; N84) ≥ 256 481 CAT → AAT H481N         498 GCG → GCT –         512 CGT → CGC –         527 ATT → ATG I527M ST612- MRSA-IV (8) ND (1)/t064 (1) Australia (04-17052) ≥ 256 481 CAT → AAT H481N         498 GCG → GCT –         512 CGT → CGC –         527 ATT → ATG I527M ST612- MRSA-IV (8) ND (1)/t7571 (1) Australia (09-15534) ≥ 256 481 CAT → AAT H481N         498

GCG → GCT –         512 CGT → CGC –         527 ATT→ATG I527M         579 AAA→AGA K579R 1 Clonal types are indicated using the current international nomenclature (sequence type (ST) – antimicrobial phenotype – staphylococcal cassette chromosome mec (SCCmec) type) 2 PFGE, pulsed-field gel electrophoresis 3 As determined by E-test 4 S. aureus co-ordinates 5 RSA, Republic of South Africa 6 ND, not determined In addition to the mutations associated with amino acid substitutions in RpoB, silent single nucleotide polymorphisms (SNPs) were detected in the rpoB sequences of all 16 isolates (Table 2). Based on a comparison with the corresponding sequence eFT508 supplier of the rifampicin-susceptible S. aureus strain RN4220, all isolates shared a common SNP at amino acid 498 (GCG → GCT), as shown in Table 2. Otherwise between one and three additional SNPs particular to each clonal type were identified. Of note is the conserved SNP at amino acid 512 (CGT → CGC), which was detected in Adenylyl cyclase all 13 ST612-MRSA-IV isolates (Table 2). Discussion A number

of factors drive the emergence and spread of antibiotic resistance, including antibiotic usage, infection control Capmatinib order practices and the organism’s genetics [1]. Previous studies carried out in South Africa have reported large proportions of rifampicin-resistant MRSA isolates [2–5], and this study is no exception with the prevalence of rifampicin-resistance among MRSA isolates ranging from 39.7% to 46.4% (Figure 1). It is likely that the frequent use of rifampicin to treat tuberculosis in South Africa has driven the high prevalence of rifampicin-resistance among local MRSA. Support for this suggestion comes from the work of Sekiguchi et al. [14] who reported a significantly higher prevalence of rifampicin-resistant MRSA in tuberculosis wards compared to non-tuberculosis wards in two hospitals in Japan. A previous study showed that ST612-MRSA-IV was the dominant clone circulating in public hospitals in Cape Town. The 44 isolates corresponding to this clonal type were uniformly resistant to rifampicin.