Abstract
The spread of mupirocin-resistant Staphylococcus aureus strains in hospitals and communities is a universal challenge. Limited data is available on the genetic features of high-level mupirocin resistant- (HLMUPR-) S. aureus isolates in Tehran. In the present research, we investigated 48 high-level mupirocin resistance S. aureus by antimicrobial activity, virulence analysis, biofilm formation, multilocus sequence typing (MLST), and staphylocoagulase (SC) typing. All the HLMUPR strains were positive for mupA gene. The frequency of multidrug resistance was 97.9%. Twenty-one (43.8%) were toxinogenic with 14 producing pvl (29.2%), 5 tst (10.4%), and two eta (4.2%). Among the HLMUPR isolates, biofilm production was detected in 45 (89.6%) isolates with complete dominance clfB, clfA genes, and a noticeably high frequency fnbA (95.8%), followed by fnbB (93.8%), eno and icaD (each 83.3%), sdrC (81.3%), ebps (79.2%), icaA (75%), sdrD (66.7%), fib (60.4%), sdrE (50%), cna (41.7%), and bap (4.2%). Coagulase typing distinguished isolates into four genotypic patterns including III (50%), II (27.1%), and type IVa (22.9%). A total of three clonal complexes (CCs) and 4 sequence types (STs) including CC/ST22 as the most prevalent (52.1%), CC8/ST239 (20.8%), CC/ST8 (16.7%), and CC/ST5 (10.4%) were identified in current work. According to our analysis, nonbiofilm producer isolates belonged to CC8/ST239 (6.3%) and CC/ST8 (4.2%). Fusidic acid-resistant isolates belonged to CC/ST45 (n = 3) and CC8/ST239 (n = 1). Observations highlighted the circulation of the CC/ST22 HLMUPR S. aureus strains with strong biofilm-production ability in our hospitals, indicating the possibility of transmission of this type between community and hospital.
Highlights
As the most frequent pathogen, Staphylococcus aureus causes various diseases ranging from skin and soft tissue infections (SSTIs) to bacteremia, endocarditis, and osteomyelitis in hospitals and communities
Resistance to mupirocin has been described in two categories: (i) high level that occurs via plasmid-borne gene mupA and or the newly described mupB gene, coding for an alternate isoleucyl-tRNA synthetase (IleS), and (ii) low level, which results from point mutations in the chromosomal encoding isoleucyl-tRNA synthetase gene
Since extensive studies have not been performed in connection with HLMUPR S. aureus infection and the high importance of its timely diagnosis and treatment, it has become urgently needed to figure out the antibacterial activity, carriage of virulence determinants, biofilm-forming ability, and specific genes that may be involved in biofilm formation and molecular types in HLMUPR strains isolated from various clinical samples
Summary
As the most frequent pathogen, Staphylococcus aureus causes various diseases ranging from skin and soft tissue infections (SSTIs) to bacteremia, endocarditis, and osteomyelitis in hospitals and communities. Data worldwide indicate that lack of proper and timely identification, distribution of molecular types, and managing of highlevel mupirocin resistance S. aureus infections (HLMUPR) could lead to decolonization failure, increase in carriage rate, and subsequently wide range of staphylococcal infections [10, 11]. Diagnosis of HLMUPR in S. aureus clinical isolates is a great challenge due to the distribution of different types related to the type of infection, their antimicrobial profile, and biofilm formability [10]. Since extensive studies have not been performed in connection with HLMUPR S. aureus infection and the high importance of its timely diagnosis and treatment, it has become urgently needed to figure out the antibacterial activity, carriage of virulence determinants, biofilm-forming ability, and specific genes that may be involved in biofilm formation and molecular types in HLMUPR strains isolated from various clinical samples. Coagulase (coa) typing and multilocus sequence typing (MLST) were applied to determine the molecular types of the HLMUPR strains
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