Abstract
BackgroundSome Staphylococcus aureus strains produce Panton-Valentine leukocidin (PVL), a bi-component pore-forming toxin, which causes leukocyte lysis and tissue necrosis. Currently, there is very limited information on the molecular epidemiology of PVL-encoding S. aureus strains in Iran. This study aimed to determine the molecular epidemiology and genetic background of PVL-positive S. aureus clinical strains isolated from Iranian patients.MethodsA total of 28 PVL-positive S. aureus strains were detected from 600 S. aureus isolates between February 2015 and March 2018 from different hospitals in Tehran, Iran. Antimicrobial susceptibility testing was performed according to the Clinical and Laboratory Standards Institute (CLSI) guidelines. Molecular genotyping was performed using SCCmec and accessory gene regulator (agr) typing, PVL haplotyping, multilocus sequence typing (MLST), and pulsed-field gel electrophoresis (PFGE).ResultsThe highest antibiotic resistance rate was found to be against erythromycin (57.1%), followed by ciprofloxacin (42.8%) and clindamycin (35.7%). Moreover, 19 (67.9%) out of 28 S. aureus isolates were identified as MRSA, including CA-MRSA (14/19, 73.7%) and HA-MRSA (5/19, 26.3%). SCCmec type IVa was detected as the predominant type (10/19, 52.6%), followed by type III (5/19, 26.3%) and type V (4/19, 21.1%). The agr type I was identified as the most common type (14/28, 50%), and H and R haplotype groups were observed at frequencies of 67.9 and 32.1%, respectively. Among H variants, the predominant variant was H2 (78/9%). The isolates encompassed 21 different sequence types (STs), including 16 new STs (ST5147 to ST5162). Based on eBURST analysis, the isolates were clustered into five CCs, including CC30, CC22, CC1, CC8, and CC5 (ST5160), and nine singletons. PFGE typing showed that 24 isolates were clustered into A (4 pulsotypes), B (9 pulsotypes), and C (11 pulsotypes) clusters.ConclusionsA high prevalence of PVL-positive CA-MRSA strains was detected in Iran. The majority of PVL-positive isolates were of H (mostly H2) variant, while R variant was harbored by 100% of PVL-positive MRSA strains. Also, CC8, CC22, and CC30 were identified as the dominant clones among PVL-encoding S. aureus strains. This study promotes a better understanding of the molecular epidemiology and evolution of PVL-positive S. aureus strains in Iran.
Highlights
Some Staphylococcus aureus strains produce Panton-Valentine leukocidin (PVL), a bi-component poreforming toxin, which causes leukocyte lysis and tissue necrosis
The present study aimed to obtain a more complete description about the molecular epidemiology and genetic background of PVL-positive S. aureus clinical strains isolated from Iranian patients using a combination of molecular typing techniques, including staphylococcal cassette chromosomemec (SCCmec) and accessory gene regulator typing, PVL haplotyping, multilocus sequence typing (MLST) analysis, and pulsed-field gel electrophoresis (PFGE)
Of 28 PVL-positive S. aureus isolates, 19 (67.9%) isolates were MRSA, including community-associated MRSA (CA-MRSA) (14/19, 73.7%) and hospitalacquired MRSA (HA-MRSA) (5/19, 26.3%)
Summary
Some Staphylococcus aureus strains produce Panton-Valentine leukocidin (PVL), a bi-component poreforming toxin, which causes leukocyte lysis and tissue necrosis. This study aimed to determine the molecular epidemiology and genetic background of PVL-positive S. aureus clinical strains isolated from Iranian patients. Panton-Valentine Leukocidin (PVL) is a two-component toxin produced by some S. aureus strains in varying amounts [5, 6]. The majority of isolates that cause skin and soft tissue infections (SSTI) and severe necrotizing pneumonia are PVLpositive [7]. This preforming toxin is encoded by a 1.9kb lukSF-PV locus consisting of two contiguous, but cotranscribed lukF and lukS genes [8]. PVL causes apoptosis in neutrophils through the activation of caspase-3 and -9; the participation of TLR2 (toll like receptor 2) in causing inflammation by PVL in the lung has been reported [4]
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