In order to determine whether the Tunisian PVL positive strains also carried the same PVL phage as phi7401PVL, we conducted two PCR studies to identify the regions in common with two PVL phages (phi7401PVL and phiSA2mw): a long range PCR study identifying gene linkage lukS and the tail gene that can identify HMPL-504 PVL phages of the elongated head type and another PCR study identifying the region related to lysogeny (Additional file 1: Table S1 and Figure 1a). In our experiments, all the PVL positive strains were positive in both PCR studies. Discussion Antibiotic resistance to agents other than β-lactams The majority of the HA-MRSA isolates were resistant to BYL719 order kanamycin, amikacin

and tetracycline. Although the ratio was slightly low (25~55%), these strains were also frequently resistant to tobramycin, gentamicin, erythromycin, quinolones and rifampicin. Recently, it has been reported that rifampicin resistance is related to glycopeptides resistance [25, 26]. Since the ratio of rifampicin resistant

strains was relatively high, there is a possibility that there might be glycopeptides related to low resistance strains, e.g., hetero-VISA strains. However, glycopeptide resistance is beyond selleck kinase inhibitor the focus of this study, so we did not examine the details for these findings. Similar to HA-MRSA isolates, the majority of CA-MRSA isolates were resistant to kanamycin, amikacin and tetracycline, but were susceptible to other antibiotics, except for erythromycin and ciprofloxacin. These data suggest that Tunisian CA-MRSA strains were more resistant to kanamycin, tetracycline and erythromycin than U.S. and Oceanian isolates [27]. In our study, only four CA-MRSA strains were resistant to clindamycin, thus suggesting that clindamycin can be used for the treatment of CA-MRSA infections in Tunisia. The PVL phage carried by Tunisian MRSA Thiamet G The phi7401 carried by a ST80 Tunisian MRSA was highly homologous to phiSa2mw

carried by ST1-SCCmecIVa MRSA. Only two ORFs, TUP03 and TUP16, showed a lower identity to those of phiSa2mw. Interestingly, TUP03 was identical to ORFs in phi12, phi13, and the bacteriophage in MRSA strains JH1 and JH9, and TUP16 was highly homologous to dUTPase in phiSLT and phi108PVL, with nucleotide identities of 97%. These data suggest that the components of phages were chimeric. Numerous lysogenized phages were induced from the cells of four strains, including JCSC7401 by mitomycin C induction. However, a hybridization experiment with a PVL probe showed that no plaque of the PVL phase was observed. This might have been due to the carriage of a truncated int. It seems that lysogenization of the phage occurred early to thus cause a mutation in the phage genome or that the ST80 strains might have an ability to cause a mutation in the int to keep the inserted phage genome in the chromosome in a stable form.