These results suggested that rifampicin-gelatin grafts are clearly valid for S epidermidis infection, whereas no efficacy was recognized against either MRSA or E coli graft infection because of early development of high minimal inhibitory concentration MRSA strains or poor susceptibility.
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Text body word count:2491 words -1- We found more Bacillus cereus isolates from blood samples in 2004 compare to the preceding years. Swab samples were collected in the particular ward from the surface of a working desk, filter unit of the air-conditioners, entrance of air inlet ducts, exit of the air outlet ducts and three-way valves of the particular ward under the consideration of iatrogenic contamination. Towels and gowns used in the ward were examined.
Undetected Bacillus Pseudo-Outbreak after Renovation WorkDens dust was noted in the filter of the air-conditioner and inlets/outlets of the air-ventilation system of the ward. Bacillus cereus was isolated from the dust, and from cleaned towels and gowns. PFGE fingerprinting differed among four patients' sample. We considered the present case as an undetected Bacillus cereus pseudo-outbreak that lasted for about one year after the renovation work of the hospital.We also considered that filters of the HVAC-system and towels and gowns were probable sources of the outbreak.
Penicillin binding protein (pbp) gene alterations of 328 clinical isolates of Streptococcus pneumoniae were examined for a correlation with their antibiotic-resistance. The frequency of penicillin G (PEN-G) resistance was determined to clarify susceptibility to several antibiotics, namely PEN-G, ampicillin, sulbactam/ampicillin, cefozopram, panipenem (PAPM), clarithromycin (CLR), azithromycin (AZM) and levofloxacin (LVX). Oligonucleotide primers for three pbp genes (pbp1a, pbp2x and pbp2b) were used to detect mutations in pbp. Of the strains, 25.9% were classified as Pen-Gs, 68.0% as Pen-Gir and 6.1% as Pen-Gr. The polymerase chain reaction product for wild-type pbp1a was found in 185 isolates, that for wild-type pbp2x was found in 66 isolates and that for wild-type pbp2b was found in 213 isolates. None of these three genes was detectable in 100 isolates while all of them were detected in 64 isolates (1aw/2xw/2bw). Of those 64 isolates with 1aw/2xw/2bw, the minimum inhibitory concentration (MIC) of PEN-G was < or =0.06 mg/l for 54 isolates and 0.12 mg/l for 10 isolates. Of the 272 strains for which the MIC of PAPM was < or =0.03 mg/l, there were 85 Pen-Gs, 184 Pen-Gir and three Pen-Gr isolates. Three strains for which the MIC of LVX was > or =4.0 mg/l included one Pen-Gs and two Pen-Gir isolates. The MICs of CLR correlated significantly with those of AZM. The MIC of CLR was > or =1 mg/l for 216 isolates, and the MIC of AZM was > or =1 mg/l for 244 of them. These data suggested that PAPM may be effective against S. pneumoniae infection, although acquisition of resistance should be considered. LVX also seemed to be effective against S. pneumoniae.
Two hundred consecutive clinical isolates of Streptococcus pneumoniae isolated in 2005 and 2006 were analysed for susceptibility to various antimicrobials, pbp gene alterations and macrolide resistance gene expression (2007 analysis) and the results were compared with previous data (2003 analysis). The average minimum inhibitory concentration (MIC) of penicillin G in isolates with 1a(m)/2x(m)/2b(m) decreased from 1.135+/-0.503 mg/L in the 2003 analysis to 0.872+/-0.540 mg/L in the 2007 analysis (P=0.0046). The prevalence of isolates with 1a(m)/2x(m)/2b(m) increased from 30.5% to 32.3%, but the difference was not statistically significant (P=0.6979). The prevalence of isolates with a clarithromycin MIC > or = 1.0mg/L increased from 65.9% to 80.0% (P=0.0005). Isolates expressing ermB increased from 46.6% to 62.6% (P=0.0004). We conclude that the decrease in penicillin resistance of S. pneumoniae does not correlate with a decrease in pbp mutations; on the contrary, the prevalence of isolates with pbp mutations increased. A decrease in penicillin resistance in S. pneumoniae with pbp mutations appears to explain the present results regarding the recovery of penicillin susceptibility. Our results suggest that the spread of mutated pbp genes among S. pneumoniae itself is not responsible for acquisition of the penicillin-resistant phenotype. Use of beta-lactams, especially oral cephalosporins, appears to be responsible for the acquisition of penicillin resistance.
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