Introduction to Clinical Staphylococcus

What is/are Clinical Staphylococcus?

Clinical Staphylococcus - Six clinical Staphylococcus aureus strains isolated from different clinical samples. ^[1] When applied to titanium disks, the newly optimized coating was resilient to the most common sterilization procedures and it induced a 1 log reduction in biofilm cells of a clinical Staphylococcus aureus isolate (JAR060131) in vitro, without affecting the planktonic phase. ^[2] METHODS We determined minimum inhibitory concentrations (MICs) and minimum bactericidal concentrations (MBCs) for non-antibiotic drugs (amlodipine, azelastine, ebselen, and sertraline) against five clinical Staphylococcus aureus isolates and one quality control strain using microplate alamar blue assays. ^[3] In the last 10 years, the barriers preventing the uptake of foreign DNA by clinical Staphylococcus aureus isolates have been identified and powerful mutagenesis techniques such as allelic exchange are now possible in most genotypes. ^[4] Clinical Staphylococcus strains (S1, S2, S3) were obtained from a culture collection at Istanbul University, Faculty of Pharmacy, Department of Pharmaceutical Microbiology. ^[5] Seventy-two clinical Staphylococcus aureus isolates from equids were collected at the Texas A&M University Veterinary Medical Teaching Hospital between 2007 and 2017. ^[6] In this study, we compared pulsed-field gel electrophoretic (PFGE), multilocus sequence typing (MLST), Staphylococcal cassette chromosome mec (SCCmec), spa typing, and virulence gene profiles of 19 Panton–Valentine leucocidin (PVL)-positive, multidrug-, and methicillin-resistant clinical Staphylococcus aureus (MRSA) isolates obtained from a hospital intensive care unit in Pakistan. ^[7] The aim of this study was to investigate the molecular features and the antibiotic resistance profile of 98 clinical Staphylococcus aureus isolates collected during 6 months in two hospitals of Kabul, Afghanistan. ^[8] Background In recent years, clinical Staphylococcus aureus isolates have become highly resistant to antibiotics, which has raised concerns about the ability to control infections by these organisms. ^[9] Our blind testing on clinical Staphylococcus aureus infections reveals that 95. ^[10] METHODS We compared the prevalence of phenotypic trimethoprim/sulfamethoxazole resistance in 20 534 clinical Staphylococcus aureus isolates (19 096 MSSA and 1438 MRSA) of non-redundant patients at Heidelberg University Hospital over 8 years and performed WGS on trimethoprim/sulfamethoxazole-resistant MRSA. ^[11] A total of 88 clinical Staphylococcus aureus isolates were collected. ^[12] The aim of the present investigation was to characterize 50 clinical Staphylococcus isolates cultured from sick dogs. ^[13] A total of 82 non-duplicate clinical staphylococcus aureus were collected from November 2017 to April 2018 in the department of Clinical laboratory, the Third Xiangya Hospital of Central South University, China. ^[14] This study evaluated the diagnostic test accuracy of disc diffusion relative to broth-microdilution for clinical Staphylococcus pseudintermedius isolated from dogs in Australia (n = 614). ^[15] FRI was established with a clinical Staphylococcus aureus isolate. ^[16] It was also observed for some derivatives a good antibacterial activity against clinical Staphylococcus aureus resistant to methicillin (MRSA). ^[17] At a concentration of 25 ppm, the new metal complex shows biological activity against several clinical Staphylococcus aureus strains. ^[18] OBJECTIVES This study determined the prevalence of qac and smr genes in clinical Staphylococcus aureus isolates from hospital-acquired infections and their susceptibility to quaternary ammonium compounds (QACs) and antibiotics, and correlated the presence of antiseptic resistance genes with antibiotic resistance. ^[19] To investigate the association of both tsst-1 and pvl with mecA genes in clinical Staphylococcus aureus (S. ^[20] The spread of plasmid borne resistance enzymes in clinical Staphylococcus aureus isolates is rendering trimethoprim and iclaprim, both inhibitors of dihydrofolate reductase (DHFR), ineffective. ^[21] 5% of 401 clinical Staphylococcus aureus isolates, including methicillin-resistant and vancomycin-intermediate ones for a total of 95% of the 205 known multidrug-resistant isolates. ^[22] The spread of plasmid borne resistance enzymes in clinical Staphylococcus aureus isolates is rendering trimethoprim and iclaprim, both inhibitors of dihydrofolate reductase (DHFR), ineffective. ^[23] Using a transcriptomic approach, we investigated the modifications induced by fosfomycin in sessile cells of a clinical Staphylococcus aureus isolated from a device-associated infection. ^[24] In clinical Staphylococcus, only tobramycin was more active. ^[25] PURPOSE: We aimed to determine the recent pattern of antibiotic resistance and assess the vancomycin susceptibility profile of clinical Staphylococcus aureus in view of emerging reports of vancomycin creep, reduced vancomycin susceptibility (RVS), including heterogeneous vancomycin-intermediate S. ^[26]

clinical staphylococcus aureu

Six clinical Staphylococcus aureus strains isolated from different clinical samples. ^[1] When applied to titanium disks, the newly optimized coating was resilient to the most common sterilization procedures and it induced a 1 log reduction in biofilm cells of a clinical Staphylococcus aureus isolate (JAR060131) in vitro, without affecting the planktonic phase. ^[2] METHODS We determined minimum inhibitory concentrations (MICs) and minimum bactericidal concentrations (MBCs) for non-antibiotic drugs (amlodipine, azelastine, ebselen, and sertraline) against five clinical Staphylococcus aureus isolates and one quality control strain using microplate alamar blue assays. ^[3] In the last 10 years, the barriers preventing the uptake of foreign DNA by clinical Staphylococcus aureus isolates have been identified and powerful mutagenesis techniques such as allelic exchange are now possible in most genotypes. ^[4] Seventy-two clinical Staphylococcus aureus isolates from equids were collected at the Texas A&M University Veterinary Medical Teaching Hospital between 2007 and 2017. ^[5] In this study, we compared pulsed-field gel electrophoretic (PFGE), multilocus sequence typing (MLST), Staphylococcal cassette chromosome mec (SCCmec), spa typing, and virulence gene profiles of 19 Panton–Valentine leucocidin (PVL)-positive, multidrug-, and methicillin-resistant clinical Staphylococcus aureus (MRSA) isolates obtained from a hospital intensive care unit in Pakistan. ^[6] The aim of this study was to investigate the molecular features and the antibiotic resistance profile of 98 clinical Staphylococcus aureus isolates collected during 6 months in two hospitals of Kabul, Afghanistan. ^[7] Background In recent years, clinical Staphylococcus aureus isolates have become highly resistant to antibiotics, which has raised concerns about the ability to control infections by these organisms. ^[8] Our blind testing on clinical Staphylococcus aureus infections reveals that 95. ^[9] METHODS We compared the prevalence of phenotypic trimethoprim/sulfamethoxazole resistance in 20 534 clinical Staphylococcus aureus isolates (19 096 MSSA and 1438 MRSA) of non-redundant patients at Heidelberg University Hospital over 8 years and performed WGS on trimethoprim/sulfamethoxazole-resistant MRSA. ^[10] A total of 88 clinical Staphylococcus aureus isolates were collected. ^[11] A total of 82 non-duplicate clinical staphylococcus aureus were collected from November 2017 to April 2018 in the department of Clinical laboratory, the Third Xiangya Hospital of Central South University, China. ^[12] FRI was established with a clinical Staphylococcus aureus isolate. ^[13] It was also observed for some derivatives a good antibacterial activity against clinical Staphylococcus aureus resistant to methicillin (MRSA). ^[14] At a concentration of 25 ppm, the new metal complex shows biological activity against several clinical Staphylococcus aureus strains. ^[15] OBJECTIVES This study determined the prevalence of qac and smr genes in clinical Staphylococcus aureus isolates from hospital-acquired infections and their susceptibility to quaternary ammonium compounds (QACs) and antibiotics, and correlated the presence of antiseptic resistance genes with antibiotic resistance. ^[16] To investigate the association of both tsst-1 and pvl with mecA genes in clinical Staphylococcus aureus (S. ^[17] The spread of plasmid borne resistance enzymes in clinical Staphylococcus aureus isolates is rendering trimethoprim and iclaprim, both inhibitors of dihydrofolate reductase (DHFR), ineffective. ^[18] 5% of 401 clinical Staphylococcus aureus isolates, including methicillin-resistant and vancomycin-intermediate ones for a total of 95% of the 205 known multidrug-resistant isolates. ^[19] The spread of plasmid borne resistance enzymes in clinical Staphylococcus aureus isolates is rendering trimethoprim and iclaprim, both inhibitors of dihydrofolate reductase (DHFR), ineffective. ^[20] Using a transcriptomic approach, we investigated the modifications induced by fosfomycin in sessile cells of a clinical Staphylococcus aureus isolated from a device-associated infection. ^[21] PURPOSE: We aimed to determine the recent pattern of antibiotic resistance and assess the vancomycin susceptibility profile of clinical Staphylococcus aureus in view of emerging reports of vancomycin creep, reduced vancomycin susceptibility (RVS), including heterogeneous vancomycin-intermediate S. ^[22]