An IncN plasmid (p541) from Escherichia coli carried a Citrobacter freundii-derived sequence of 4,252 bp which included an ampC-ampR region and was bound by two directly repeated IS26 elements. ampC encoded a novel cephalosporinase (CMY-13) with activity similar to that of CMY-2. AmpR was likely functional as indicated in induction experiments.
Serotype 012 Pseudomonas aeruginosa resistant to gentamicin (MIC greater than 4 mg/l) and carbenicillin (MIC greater than 128 mg/l) occur widely in Europe and are homogeneous in their phenotypic and genetic properties. It has been suggested that a single multiresistant strain of this serotype has become widespread. This study examined the resistance mechanisms present in multiresistant serotype 012 P. aeruginosa isolates from Austria, Belgium, France, Greece, Italy, Holland, West Germany and the UK. Disseminated isolates produced a PSE-1 type beta-lactamase, correlating with their resistance to the known substrates of this enzyme (carbenicillin, azlocillin and cefsulodin). These isolates also reacted with gene probes for the aminoglycoside modifying enzymes AAC(6')I and ANT(3'). The probe for AAC(6')I is known to cross-react with the gene for AAC(6')II. The fact that the organisms were resistant to netilmicin, gentamicin, sisomicin and tobramycin, but less so to amikacin, suggested that the latter enzyme was produced rather than AAC(6')I. PSE-1 beta-lactamase and the gene for AAC(6')I/AAC(6')II were absent from the International Antigenic Typing Scheme 012 reference strain, which was sensitive to beta-lactams and aminoglycosides, and also from a multiresistant serotype 012 strain isolated at a London burns unit in 1987. These organisms have been shown previously to be distinct from the disseminated multiresistant strain in their phenotypic properties. Two 012 isolates appeared to have additional resistance determinants to amikacin and isepamicin.
Staphylococcus aureus was isolated in 88 (30. 8%) of 286 adult patients suffering from various skin and soft-tissue infections examined in the outpatient department of a 650 bed tertiary-care hospital of Athens, Greece between January 2006 and December 2007. Twenty-seven (30.7%) of the S. aureus infections were caused by methicillin-resistant S. aureus (MRSA). All MRSA isolates were also resistant to tetracycline, fucidic acid and kanamycin, but were sensitive to gentamicin and tobramycin, as well as to to cotrimoxazole, chloramphenicol, quinolones, clindamycin and erythromycin. All isolates belonged to staphylococcal cassette chromosome mec elements (SCCmec) type IV, and were found to carry the lukF-PV and lukS genes coding for Panton-Valentine leukocidin (PVL). Pulsed-field gel electrophoresis (PFGE) and spa-typing revealed high genetic similarity among all MRSA isolates and with the PFGE pattern of the well-described ST80 clone that seems to be spreading through Europe. The high prevalence of MRSA among S. aureus infections in the community signify that empiric therapy in Greece, when clinically indicated, should exclude β-lactam antibiotics. Moreover, the establishment of an active screening for PVL-positive community-acquired (CA)-MRSA carriage and the adoption of a search and destroy strategy for CA-MRSA in all patients admitted with purulent skin and soft-tissue is of high priority in Greece as well as in all European countries which face high rates of CA-MRSA infection.
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