Characterization of the Epidemic European Fusidic Acid-Resistant Impetigo Clone of
            <i>Staphylococcus aureus</i>

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

doi:10.1128/jcm.01984-06

Cited by 90 publications

(84 citation statements)

References 37 publications

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“…These strains commonly cause staphylococcal scalded skin syndrome and bullous impetigo (28,43), toxin-mediated staphylococcal diseases which are associated with eta or etb in 65 to 100% of the cases (10,18,26,30,60). One such CC121 clone, characterized by ST123 and spa type t171, is notorious as the "epidemic European fusidic acid-resistant impetigo clone (EEFIC)" (27-29, 42, 44, 52).…”

Section: Discussionmentioning

confidence: 99%

Association of Recurrent Furunculosis with Panton-Valentine Leukocidin and the Genetic Background of Staphylococcus aureus

et al. 2010

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Staphylococcus aureus is a major cause of skin and soft tissue infections, such as furuncles, carbuncles, and abscesses, but it also frequently colonizes the human skin and mucosa without causing clinical symptoms. Panton-Valentine leukocidin (PVL) is a pore-forming toxin that has been associated with soft tissue infections and necrotizing pneumonia. We have compared the genotypes, virulence gene repertoires, and phage patterns of 74 furunculosis isolates with those of 108 control strains from healthy nasal carriers. The large majority of furunculosis strains were methicillin sensitive. Clonal cluster (CC) 121 (CC121) and CC22 accounted for 70% of the furunculosis strains but for only 8% of the nasal isolates. The PVL-encoding genes luk-PV were detected in 85% of furunculosis strains, while their prevalence among colonizing S. aureus strains was below 1%. luk-PV genes were distributed over several lineages (CCs 5, 8, 22, 30, and 121 and sequence type 59). Even within the same lineages, luk-PV-positive phages characterized furunculosis strains, while their luk-PV-negative variants were frequent among nasal strains. The very tight epidemiological linkage between luk-PV and furunculosis, which could be separated from the genetic background of the S. aureus strain as well as from the gene makeup of the luk-PV-transducing phage, lends support to the notion of an important role for PVL in human furunculosis. These results make a case for the determination of luk-PV in recurrent soft tissue infections with methicillin-sensitive as well as methicillin-resistant S. aureus.Skin and soft tissue infections (SSTIs) are the most frequent type of disease caused by Staphylococcus aureus outside the hospital setting. SSTIs comprise a diverse range of clinical pictures, such as furuncles, carbuncles, subcutaneous abscesses, folliculitis, bullous impetigo, and staphylococcal scalded skin syndrome (23

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Section: Discussionmentioning

confidence: 99%

Association of Recurrent Furunculosis with Panton-Valentine Leukocidin and the Genetic Background of Staphylococcus aureus

et al. 2010

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“…Several studies have described that the topical use of this drug has led to an increase of resistance. [20][21][22] Some suggest that a S. aureus clone responsible for the resistance to fusidic acid is spreading, 22,23 and that this is resulting in increased resistance. An earlier study in the Netherlands from 2002 showed no resistance to fusidic acid among impetigo isolates.…”

Section: Comparison With Existing Literaturementioning

confidence: 99%

Staphylococcus aureuscarriage among GPs in the Netherlands

Rijnders

Nys²,

Driessen³

et al. 2010

Br J Gen Pract

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Observational, point-prevalence, and cross-sectional study. SettingGPs attending the annual conference of the Dutch College of General Practitioners in 2006. MethodNasal swabs were randomly taken from 395 GPs and analysed for the presence of S. aureus. Antimicrobial susceptibility was determined by a microbroth dilution method and the genotypes by spa typing, which was associated with multilocus sequence typing. ResultsOf the GPs, 129/395 (33%; 95% confidence interval [CI] = 28 to 37%) were carriers of S. aureus. No meticillin-resistant S. aureus (MRSA) was found. Resistance was observed to penicillin (71%; 95% CI = 63 to 79%), fusidic acid (7%; 95% CI = 3 to 13%), and clarithromycin (6%; 95% CI = 3 to 12%). In 72% of the isolates, an MRSA-related genotype of S. aureus was found. ConclusionThe low antibiotic resistance found among S. aureus of GPs suggests that GPs are not a reservoir of antibioticresistant S. aureus strains. The relatively high resistance to fusidic acid, which has not previously been described in the Netherlands and is mostly because of antibiotic use, suggests that patients infect GPs and not the other way round. GPs may be at risk for nasal carriage of S. aureus with an MRSA-related genotype.

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“…The fusB determinant originally was found on the plasmid pUB101 in S. aureus (26). Later, the fusB determinant also was found on a transposon-like element (27) or in a staphylococcal pathogenicity island (29).…”

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Fusidic Acid Resistance Determinants in Staphylococcus aureus Clinical Isolates

Chen¹,

Hung²,

Tseng³

et al. 2010

Antimicrob Agents Chemother

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A total of 71 fusidic acid-resistant Staphylococcus aureus (45 methicillin-resistant and 26 methicillin-susceptible) isolates were examined for the presence of resistance determinants. Among 45 fusidic acid-resistant methicillin-resistant S. aureus (MRSA), isolates, 38 (84%) had fusA mutations conferring high-level resistance to fusidic acid (the MIC was >128 g/ml for 22/38), none had fusB, and 7 (16%) had fusC. For 26 fusidic acid-resistant methicillin-susceptible S. aureus (MSSA), only 3 possessed fusA mutations, but 15 (58%) had fusB and 8 (31%) had fusC. Low-level resistance to fusidic acid (MICs < 32 g/ml) was found in most fusB-or fusC-positive isolates. For 41 isolates (38 MRSA and 3 MSSA), with fusA mutations, a total of 21 amino acid substitutions in EF-G (fusA gene) were detected, of which R76C, E444K, E444V, C473S, P478S, and M651I were identified for the first time. The nucleotide sequencing of fusB and flanking regions in an MSSA isolate revealed the structure of partial IS257-aj1-LP-fusB-aj2-aj3-IS257-partial blaZ, which is identical to the corresponding region in pUB101, and the rest of fusB-carrying MSSA isolates also show similar structures. On the basis of spa and staphylococcal cassette chromosome mec element (SCCmec) typing, two major genotypes, spa type t037-SCCmec type III (t037-III; 28/45; 62%) and t002-II (13/45; 29%), were predominant among 45 MRSA isolates. By pulsed-field gel electrophoresis analysis, 45 MRSA isolates were divided into 12 clusters, while 26 MSSA isolates were divided into 15 clusters. Taken together, the distribution of fusidic acid resistance determinants (fusA mutations, fusB, and fusC) was quite different between MRSA and MSSA groups.

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Characterization of the Epidemic European Fusidic Acid-Resistant Impetigo Clone of Staphylococcus aureus

Cited by 90 publications

References 37 publications

Association of Recurrent Furunculosis with Panton-Valentine Leukocidin and the Genetic Background of Staphylococcus aureus

Association of Recurrent Furunculosis with Panton-Valentine Leukocidin and the Genetic Background of Staphylococcus aureus

Staphylococcus aureuscarriage among GPs in the Netherlands

Fusidic Acid Resistance Determinants in Staphylococcus aureus Clinical Isolates

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