Vancomycin and linezolid resistance among multidrug-resistant Staphylococcus aureus clinical isolates and interaction with neutrophils

Abstract

BackgroundDeveloped drug resistance against vancomycin and linezolid is a huge worrisome. The aim of our study was to investigate the rate of vancomycin and linezolid resistance in multidrug-resistant (MDR) Staphylococcus aureus (S. aureus) in Baghdad, Iraq. MethodsThree-hundred S. aureus were identified from various clinical origins in Baghdad, Iraq. Methicillin-and linezolid-resistant S. aureus (MRSA and LRSA, respectively) isolates were determined by disc diffusion, agar dilution and E-test methods. Biofilm formation was assayed using microtiter tissue plate (Mtp) assay. Polymerase chain reaction (PCR) was employed to detect the mecA, vanA, B, C, cfr and adhesin genes, followed by gene sequencing. Vancomycin-resistant S. aureus (VRSA) and LRSA strains interactions with neutrophils was assessed using flow-cytometry technique. ResultsTwo-hundred (67%) isolates were MRSA. One-hundred one (50.5%) and 44 (22%) MRSA were strong and moderate-level biofilm producers, respectively. All the strong biofilm-producer MRSA carried the clfA, clfB, fnbA, fnbB, fib and eno genes. Five (1.66%) and nine (3%) of the MRSA were VRSA and LRSA, respectively which were mostly isolated from blood and tissue infections. The vanA and cfr genes were detected in two and three MRSA, respectively. Three VRSA and two LRSA strains were strong biofilm-producers and contained adhesin genes (clfA, clfB, fnbA, fnbB, eno, fib, cna and ebps, but not bbp). The neutrophils mean apoptosis rate by the VRSA and LRSA strains included 80% and 66.7%, respectively. ConclusionVirulent MRSA rate was high. In addition, MRSA, VRSA and LRSA contained adhesin genes responsible for colonization and biofilm formation. Furthermore, these strains induced the neutrophils apoptosis. The evolution of pathogenic VRSA and LRSA is a concern towards eradication of MDR-S. aureus. More detailed works will be helpful to disclose the role of bacterial components in the biofilm formation and apoptosis and control strategies.