The study identifies fusB-mediated fusidic acid resistance islands in Staphylococcus epidermidis isolates, highlighting the association of fusB with phage-related resistance islands and its role in conferring resistance to fusidic acid.

FusB-type proteins mediate resistance to fusidic acid by binding to elongation factor G (EF-G) and promoting the dissociation of stalled ribosome-EF-G-GDP complexes, thus allowing ribosomes to resume translation.

The study found that the fusB gene is the predominant determinant of fusidic acid resistance among Staphylococcus aureus clinical isolates in China.

The study identified fusB and fusC genes as the primary mediators of fusidic acid resistance in commensal staphylococci, highlighting their potential role as reservoirs for resistance genes.

The study identifies a Staphylococcus aureus clone resistant to mupirocin and fusidic acid, carrying exotoxin genes such as mupA, fusB, ermC, ermA, lukS/lukF-PV, eta, etb, and fnbA, which contribute to its pathogenicity and resistance mechanisms.

The study identified several AMR genes, including mecA, fusB, fusC, blaZ, qacA/qacC, ileS2, and ACME-arc, in nasal staphylococci from medical students, highlighting the potential for gene transfer between S. aureus and CoNS in the absence of antibiotic pressure.

The paper discusses various antimicrobial resistance genes and mutations in staphylococci of animal origin, highlighting their roles in resistance to multiple antibiotics such as macrolides, lincosamides, streptogramins, oxazolidinones, and others. Key genes include erm, msr, mph, ere, lnu, vga, cfr, optrA, dfr, fus, ileS2, blaZ, aadD, ble, fosD, fosB, czrC, and qac genes, which confer resistance to specific antibiotics and are prevalent in different staphylococcal species.

The study identified rpoB mutations and fusB/fusC genes associated with rifampin and fusidic acid resistance in Staphylococcus aureus isolates from tuberculosis patients receiving rifampin-containing regimens.

The study identifies several AMR genes in multidrug-resistant Staphylococcus capitis isolates associated with neonatal sepsis, including blaZ, fusB, aadD, qacA, and aac(6')-aph(2'). These genes confer resistance to amoxicillin, fusidic acid, aminoglycosides, chlorhexidine, and gentamicin, respectively.

The paper discusses the mechanisms of antibiotic resistance in Staphylococcus aureus, focusing on beta-lactam resistance through the blaZ and mecA genes, glycopeptide resistance via the vanA operon, and resistance to other antibiotics through various genes and mutations.

The study identified fusA mutations, fusB, and fusC as resistance determinants for fusidic acid in canine-derived staphylococci. Additionally, qacA/B and smr were found to be associated with chlorhexidine resistance.

The study identified several AMR genes in multidrug-resistant staphylococci from high-frequency touched surfaces in London, including blaZ, qacA/B, dfrC, norA, ant(4')-Ib, AAC(6')-Ie-APH(2")-Ia, fusB, msrA, ermC, mphC, tetK, mupA, cat, dfrG, lnuA, fusC, aph3-IIIa, sat4A, vgaA, and others. These genes conferred resistance to various antibiotics such as penicillin, fusidic acid, mupirocin, tetracycline, erythromycin, and chloramphenicol.

The study identified various AMR genes and mutations in MRSA strains from endotracheal tubes, including ermC, ermA, msrA, aac(6')-aph(2"), tetK, and fusB, along with quinolone resistance mutations in gyrA, gyrB, grlA, and grlB.

The study identifies that FusB-mediated resistance to fusidic acid is primarily due to changes in the conformational dynamics of domain III of EF-G, which prevents the steric block of conformational changes caused by FA binding.

The study identified various AMR genes in MRSA isolates from Kuwait hospitals, including mupA, aacA-aphD, erm(A), erm(C), tet(K), tet(M), fusC, fusB, and faR1, which conferred resistance to mupirocin, gentamicin, erythromycin, tetracycline, and fusidic acid.

The study presents a cross-resistance platform (CRP) consisting of 28 Staphylococcus aureus strains with defined resistance genotypes, designed to detect cross-resistance between established and novel antibacterial agents. The CRP includes various AMR genes and mutations that confer resistance to multiple antibiotic classes.

The paper discusses ribosome protection proteins (RPPs) as significant contributors to antibiotic resistance, particularly against tetracyclines, fusidic acid, and various other antibiotics targeting the ribosome. Key RPPs include TetM, TetO, FusB, VgaA, LsaA, MsrE, MsrA, optrA, and poxtA, which confer resistance through mechanisms involving direct interaction with the ribosome and displacement of antibiotics.

The study identifies a mupirocin-resistant, methicillin-susceptible Staphylococcus aureus clone (ST121) associated with skin and soft tissue infections in Greece, carrying resistance genes mupA, fusB, and ant(4')-Ia.

The study identified several AMR genes in commensal CoNS from healthy individuals in Germany, including mecA, tetK/L, tetM, ermA, ermC, ermB, fusB, fusC, aac(6')/aph(2"), cat194, fexB, and spc. These genes were associated with resistance to methicillin, tetracycline, erythromycin, fusidic acid, gentamicin, chloramphenicol, florfenicol, and spectinomycin.

The study identified three genetic determinants, fusA mutation (fusA), fusB, and fusC, responsible for fusidic acid resistance in methicillin-resistant Staphylococcus aureus isolates from Kuwait hospitals. The majority of isolates carried fusC, while fusA mutations were associated with high-level resistance.

The study identified fusA mutations, particularly L461K, as the primary cause of high-level fusidic acid resistance in MRSA isolates, while fusB was associated with low-level resistance. The ST5-MRSA-II-t2460 clone with fusA L461K mutation was prevalent in several Chinese regions.

The study identified fusB and fusC genes in S. epidermidis and fusB/C in M. sciuri as the primary genetic determinants of fusidic acid resistance. A V599I mutation in the fusA gene was also found in one S. epidermidis isolate, although it did not significantly increase resistance levels.

The study identified fusB and fusC genes in S. epidermidis and fusB/C in M. sciuri as the primary genetic determinants of fusidic acid resistance. A V599I mutation in the fusA gene was also found in one S. epidermidis isolate, although it did not significantly increase resistance levels.

The study characterizes various tetracycline and methicillin-resistant Staphylococcus aureus genetic lineages circulating in Spanish hospitals, identifying multiple AMR genes including blaZ, tetK, tetL, tetM, ermC, ermB, ant(4')-Ia, aac(6')-Ie-aph(2'')-Ia, mupA, and fusB.

The study identified multiple antimicrobial resistance genes in multidrug-resistant methicillin-resistant Staphylococcus epidermidis isolates, including mecA, blaZ, fusB, fosB, aadD, aac(6')-aph(2"), tet(K), dfrG, msr(A), and qacA. These genes contribute to resistance against various antibiotics such as methicillin, penicillin, fusidic acid, fosfomycin, aminoglycosides, tetracycline, trimethoprim, macrolides, and chlorhexidine.

The paper discusses the molecular mechanisms of drug resistance in Staphylococcus aureus, focusing on beta-lactam, glycopeptide, oxazolidinone, MLS-B, aminoglycoside, and other resistance mechanisms. Key genes identified include blaZ, mecA, mecC, vanA, cfr, ermA, ermC, aac(6')-Ib, aph(3')-IIIa, and aadD. Mutations in pbp2 and pbp2a were also found to contribute to resistance.

The study identified several AMR genes in methicillin-resistant staphylococci isolates from goats and their farm environments in Saudi Arabia, including mecA, blaZ, norA, lmrS, mepA, mepR, arlR, arlS, tet(38), mecR1, dfrC, fusC, fosB, fexA, tetM, msrA, mphC, fusB, APH(3′)-IIIa, tetK, and dfrG. These genes confer resistance to various antibiotics such as penicillins, fluoroquinolones, aminoglycosides, macrolides, phenicols, diaminopyrimidines, oxazolidinones, tetracyclines, and fosfomycin.

The study identifies fusB and tetK as key resistance genes contributing to the clonal spread of ST42 Staphylococcus haemolyticus strains, along with capsule-related genes.

The study identified methicillin-resistant Staphylococcus and Mammaliicoccus species in dromedary camels in Algeria, including the first detection of a SCCmec-mecC hybrid in Mammaliicoccus lentus. Key resistance genes identified include mecA, mecC, blaZ, aadD, dfrG, ermB, ermA, msrA, mphC, fosB, fusB, and tet(K).

The study identified various antimicrobial resistance genes in Staphylococcus species isolated from diabetic foot ulcers and healthy skin, highlighting the prevalence of resistance to beta-lactams, aminoglycosides, macrolides, tetracyclines, fusidic acid, trimethoprim-sulfamethoxazole, fosfomycin, kanamycin, neomycin, and quaternary ammonium compounds.

The study identifies multiple antibiotic resistance genes in coagulase-negative staphylococci (CoNS) isolated from European hakes, including blaZ, mphC, msr(A/B), lnuA, vgaA, fusB, and dfrA, which confer resistance to penicillin, macrolides/lincosamides, fusidic acid, and trimethoprim-sulfamethoxazole. These CoNS isolates also carry virulence factors such as scn and hla.

The study identified multiple antibiotic resistance genes in coagulase-negative staphylococci (CoNS) isolates from acne patients in Egypt, including blaZ, mecA, tet(K), erm(C), lnuA, vgaA, dfrC, fusB, fosBx1, norA, and vanT. These genes were found to be located on plasmids and chromosomes, indicating a multidrug-resistant profile.

The study identified specific mutations and gene acquisitions in OM-MRSA ST45 isolates that confer resistance to fluoroquinolones, fusidic acid, gentamicin, and doxycycline, highlighting their increased pathogenicity and resistance mechanisms compared to CL-MRSA ST45 isolates.

The study identifies a mupirocin-resistant variant of the European epidemic fusidic acid-resistant impetigo clone of Staphylococcus aureus, which carries the mupA gene for mupirocin resistance and the fusB gene for fusidic acid resistance.

The study identified several AMR genes in Staphylococcus pettenkoferi isolates from human and feline sources, including blaZ, mecA, ermA, tet(L), vanA, aph3-IIIa, ter(M), mupA, and fusB, which confer resistance to various antibiotics such as penicillins, methicillin, erythromycin, tetracyclines, vancomycin, gentamicin, mupirocin, and fusidic acid.

The study identifies FusB as a resistance protein that rescues protein synthesis from fusidic acid (FA) inhibition by inducing conformational changes in EF-G, leading to its dissociation from the ribosome and FA release.

AmrProfiler identifies a wide range of AMR genes and mutations across multiple bacterial species, demonstrating high accuracy and broader species coverage compared to existing tools.

The study highlights the prevalence of antimicrobial resistance in Staphylococcus spp., Escherichia coli, and Salmonella spp. isolated from food handlers, emphasizing the role of genes such as mecA, blaZ, msrA, linA, and fusB in conferring resistance to various antibiotics.

The study identified several AMR genes and mutations in Staphylococcus isolates from small- to medium-scale and large-scale dairy farms in Thailand, highlighting differences in resistance profiles between farm types.

The study identified several AMR genes in Staphylococcus saprophyticus strains isolated from humans and animals, including blaZ, mecA, ermA, ermB, tetM, fusB, and mupA, which confer resistance to various antibiotics such as beta-lactams, macrolides, tetracyclines, fusidic acid, and mupirocin.

The paper discusses three main mechanisms of fusidic acid resistance in Staphylococcus aureus: mutations in the fusA gene encoding EF-G, expression of resistance proteins like FusB, FusC, FusD, and FusF, and mutations in the rplF gene encoding ribosomal protein uL6. These mechanisms involve either direct interference with FA binding, target protection, or disruption of the FA-locked state of EF-G.