A Fusidic Acid-Resistant Epidemic Strain of
 Staphylococcus aureus
 Carries the
 fusB
 Determinant, whereas
 fusA
 Mutations Are Prevalent in Other Resistant Isolates

O’Neill, Alex J.; Larsen, Anders Rhod; Henriksen, Anne Santerre; Chopra, Ian

doi:10.1128/aac.48.9.3594-3597.2004

Cited by 73 publications

(97 citation statements)

References 13 publications

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“…This clonal S. aureus strain is characterized as spa type 171 or single-locus variants t408, t659, t874, and t875. The presence of the agrIV allele, eta (and in a large proportion etb), and fusB is highly indicative of the aforementioned clone (8,9,14). The last report of the aforementioned clone was from Norway in 2014, showing evidence of extinction from 2012 (15).…”

Section: Discussionmentioning

confidence: 98%

“…Beginning around 2000, impetigo caused by fusidic acid-resistant MSSA was observed in countries of northern Europe. The bacteria were found to represent a clone, namely, EEFIC (ST123, CC121), which has been observed in the United Kingdom, Ireland, France, and Scandinavian countries (8,9). This clonal S. aureus strain is characterized as spa type 171 or single-locus variants t408, t659, t874, and t875.…”

Section: Discussionmentioning

confidence: 99%

“…This clone is characterized by concurrent resistance to kanamycin, fusidic acid, and tetracycline. Secondarily, resistance to FA and a predilection for impetigo among S. aureus strains are linked to the so-called epidemic European fusidic acid-resistant impetigo clone (EEFIC) in numerous northern European countries (8,9). Molecular typing of this clone showed that it belonged to ST123 (clonal complex 121 [CC121]) (9).…”

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confidence: 99%

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Emergence of a Staphylococcus aureus Clone Resistant to Mupirocin and Fusidic Acid Carrying Exotoxin Genes and Causing Mainly Skin Infections

et al. 2017

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Skin and soft tissue infections (SSTIs) caused by mupirocin-resistant Staphylococcus aureus strains have recently increased in number in our settings. We sought to evaluate the characteristics of these cases over a 43-month period. Data for all community-acquired staphylococcal infections caused by mupirocin-resistant strains were retrospectively reviewed. Genes encoding products producing high-level resistance (HLR) to mupirocin (mupA), fusidic acid resistance (fusB), resistance to macrolides and lincosamides (ermC and ermA), Panton-Valentine leukocidin (PVL) (lukS/lukF-PV), exfoliative toxins (eta and etb), and fibronectin binding protein A (fnbA) were investigated by PCRs in 102 selected preserved strains. Genotyping was performed by SCCmec and agr typing, whereas clonality was determined by pulsedfield gel electrophoresis (PFGE) and multilocus sequence typing (MLST). A total of 437 cases among 2,137 staphylococcal infections were recorded in 2013 to 2016; they were all SSTIs with the exception of 1 case of primary bacteremia. Impetigo was the predominant clinical entity (371 cases [84.9%]), followed by staphylococcal scalded skin syndrome (21 cases [4.8%]), and there were no abscesses. The number of infections detected annually increased during the study years. All except 3 isolates were methicillin susceptible. The rates of HLR to mupirocin and constitutive resistance to clindamycin were 99% and 20.1%, respectively. Among the 102 tested strains, 100 (98%) were mupA positive and 97 (95%) were fusB positive, 26/27 clindamycin-resistant strains (96.3%) were ermA positive, 83 strains (81.4%) were lukS/lukF positive, 95 (93%) carried both eta and etb genes, and 99 (97%) were fnbA positive. Genotyping of methicillin-sensitive S. aureus (MSSA) strains revealed that 96/99 (96.7%) belonged to one main pulsotype, pulsotype 1, classified as sequence type 121 (ST121). The emergence of a single MSSA clone (ST121) causing impetigo was documented. Resistance to topical antimicrobials and a rich toxinogenic profile confer to this clone adaptability for spread in the community.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Emergence of a Staphylococcus aureus Clone Resistant to Mupirocin and Fusidic Acid Carrying Exotoxin Genes and Causing Mainly Skin Infections

et al. 2017

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“…PCR confirmation of the presence of the fusidic acid resistance gene, fusB, was determined as previously described (35).…”

Section: Methodsmentioning

confidence: 99%

Epidemiology of European Community-Associated Methicillin-Resistant Staphylococcus aureus Clonal Complex 80 Type IV Strains Isolated in Denmark from 1993 to 2004

et al. 2008

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In Europe, community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) infections have been caused predominantly by isolates belonging to the "European CA-MRSA" clone (sequence type 80, staphylococcal cassette chromosome mec type IV). In this study, the epidemiology of European CA-MRSA was investigated on a nationwide scale, covering the period from 1993 to 2004. Denmark has been a low-prevalence country regarding MRSA since the mid-1970s but has experienced an increase in the number of new MRSA cases in recent years. Our results show that European CA-MRSA contributed to this increase. The isolates primarily caused skin and soft tissue infections (SSTIs) in patients outside hospitals, and transmission between household members was the predominant mode of spread. Although some of the isolates were found in hospitalized patients, nosocomial transmission seemed likely in only one instance, pointing to endogenous infections as an important factor. Compared to the CA-MRSA clone most common in the United States (USA300), the European CA-MRSA clone seems less well adapted to persist in hospital environments. Patients with a recent history of travel or family relation to the Mediterranean or Middle East were highly overrepresented. The epidemiological data indicated that the European CA-MRSA isolates were introduced into Denmark on multiple occasions, paralleled by an increasing level of genetic diversity of the isolates found during the study period. European CA-MRSA has previously been described as a rather uniform clone. However, we found pronounced, diverse pulsed-field gel electrophoresis subtypes, staphylococcal protein A gene (spa) types, and susceptibility patterns.

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“…The most prevalent mechanism of resistance involves horizontal acquisition of the fusB-type FA resistance determinants (9, 10), a group named after the first discovered member, fusB (11,12). At least two representatives of this group (fusB and fusC) are found in S. aureus (13), and studies to investigate the mechanism of fusB-type FA resistance have to date focused on fusB.…”

mentioning

confidence: 99%

Ribosome clearance by FusB-type proteins mediates resistance to the antibiotic fusidic acid

Cox

Thompson

Jenkins

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Resistance to the antibiotic fusidic acid (FA) in the human pathogen Staphylococcus aureus usually results from expression of FusBtype proteins (FusB or FusC). These proteins bind to elongation factor G (EF-G), the target of FA, and rescue translation from FAmediated inhibition by an unknown mechanism. Here we show that the FusB family are two-domain metalloproteins, the C-terminal domain of which contains a four-cysteine zinc finger with a unique structural fold. This domain mediates a high-affinity interaction with the C-terminal domains of EF-G. By binding to EF-G on the ribosome, FusB-type proteins promote the dissociation of stalled ribosome·EF-G·GDP complexes that form in the presence of FA, thereby allowing the ribosomes to resume translation. Ribosome clearance by these proteins represents a highly unusual antibiotic resistance mechanism, which appears to be fine-tuned by the relative abundance of FusB-type protein, ribosomes, and EF-G.antibacterial | protein synthesis | translocation | structure

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A Fusidic Acid-Resistant Epidemic Strain of Staphylococcus aureus Carries the fusB Determinant, whereas fusA Mutations Are Prevalent in Other Resistant Isolates

Cited by 73 publications

References 13 publications

Emergence of a Staphylococcus aureus Clone Resistant to Mupirocin and Fusidic Acid Carrying Exotoxin Genes and Causing Mainly Skin Infections

Emergence of a Staphylococcus aureus Clone Resistant to Mupirocin and Fusidic Acid Carrying Exotoxin Genes and Causing Mainly Skin Infections

Epidemiology of European Community-Associated Methicillin-Resistant Staphylococcus aureus Clonal Complex 80 Type IV Strains Isolated in Denmark from 1993 to 2004

Ribosome clearance by FusB-type proteins mediates resistance to the antibiotic fusidic acid

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