Triclosan and antibiotic resistance in Staphylococcus aureus.
Triclosan (2,4,4'-trichloro-2'-hydroxydiphenyl ether) is an antimicrobial agent used in hygiene products, plastics and kitchenware, and for treating methicillin-resistant Staphylococcus aureus (MRSA) outbreaks. S. aureus strains with low-level resistance to triclosan have emerged. It has been claimed that strains with decreased susceptibility to biocides may also be less susceptible to antibiotics. We tested the susceptibility of S. aureus clinical isolates to triclosan and several antibiotics. Triclosan MICs ranged between 0.025 and 1 mg/L. Some, but not all, strains were resistant to several antibiotics and showed low-level triclosan resistance. S. aureus mutants with enhanced resistance to triclosan (< or =1 mg/L) were isolated. In several cases this resistance was stably inherited in the absence of triclosan. These mutants were not more resistant than the parent strain to several antibiotics. Changes in triclosan MICs associated with the acquisition of a plasmid encoding mupirocin resistance were not observed, suggesting that the triclosan/mupirocin co-resistance seen in a previous study was not the result of a single resistance gene or separate genes on the same plasmid. The continuous exposure of a triclosan-sensitive S. aureus strain to sub-MIC concentrations of triclosan for 1 month did not result in decreased susceptibility to triclosan or to several antibiotics tested. Triclosan-induced potassium leakage and bactericidal effects on a triclosan-sensitive strain, a resistant strain and a strain selected for increased resistance were compared with those of non-growing organisms, exponentially growing organisms and organisms in the stationary phase. No significant differences between the strains were observed under these conditions despite their different MICs. Biocides have multiple target sites and so MICs often do not correlate with bactericidal activities. The ability of S. aureus to develop resistance to triclosan and the current view that triclosan may have a specific target in Escherichia coli, namely enoyl reductase, underline the need for more research on the mechanisms of action and resistance. (+info)
Resistance of helicobacter pylori to metronidazole, tetracycline and amoxycillin.
Resistance to metronidazole, tetracycline and amoxycillin, and beta-lactamase production were determined for 153 clinical isolates of Helicobacter pylori. Of these isolates, 77.8% were resistant to metronidazole (MIC > 8 mg/L), 58.8% to tetracycline (MIC > 16 mg/L) and 71.9% to amoxycillin (MIC > 0.5 mg/L); 39.2% were multiresistant. Resistance to metronidazole was more common in isolates from females than in those from males (P < 0.05). None of the isolates produced beta-lactamase, so the mechanism of amoxycillin resistance was not linked to production of beta-lactamase. (+info)
Enterococcal glycopeptide resistance at an Italian teaching hospital.
Two thousand one hundred and thirteen strains of enterococci isolated at Pisa General Hospital in 1998 were analysed retrospectively to determine their glycopeptide resistance. Of all the microorganisms isolated in this period, 14.7% were enterococci (1405 Enterococcus faecalis, 19 Enterococcus faecium, six Enterococcus avium and 683 Enterococcus spp.). Two hundred and thirty (10.8%) of these enterococci were resistant or demonstrated reduced susceptibility to vancomycin and/or teicoplanin. The highest rate of resistance was found in outpatient enterococcal strains isolated from the urogenital tract. The frequency of enterococcal glycopeptide resistance at Pisa Hospital is higher than that reported from other areas of Italy. (+info)
Antibiotic susceptibility and mechanisms of beta-lactam resistance in 1310 strains of pseudomonas aeruginosa: a French multicentre study (1996).
A total of 1310 consecutive strains of Pseudomonas aeruginosa were collected in 11 French hospitals in 1996. The percentages of susceptible isolates measured by the agar dilution method were: ticarcillin (53%), piperacillin (69%) (MIC 16 mg/L), ceftazidime (77%), cefepime (55%), cefpirome (40%), aztreonam (57.5%), imipenem (81.5%) (MIC 4 mg/L), amikacin (64.5%) (MIC 8 mg/L) and ciprofloxacin (58%) (MIC 1 mg/L). Resistance to beta-lactams was linked to the production of transferable beta-lactamases (30%), overproduction of cephalosporinase (29%) and to non-enzymic mechanisms (38%). (+info)
pncA mutations in clinical Mycobacterium tuberculosis isolates from Korea.
BACKGROUND: Pyrazinamide (PZA) is among the first-line drugs for the treatment of tuberculosis. In vitro, it kills semidormant mycobacteria only at low pH. The purpose of this study was to compare PZA resistance with pyrazinamidase (PZase) activity and the genotype to better understand the molecular basis of PZA resistance and to expand the profile of pncA mutations worldwide. RESULTS: Of the 28 tested strains of Mycobacterium tuberculosis, 6 were susceptible to PZA and positive for PZase activity and had no pncA mutations. Twenty-one strains were resistant to PZA and negative for PZase activity and had mutations in the pncA gene, including 15 point mutations, 5 insertions, and 2 deletions. One strain had no mutation in the pncA gene, even though it was resistant to PZA and negative for PZase activity. Three isolates had adenine to guanine point mutations in the -11 upstream region, making this the most common type of pncA mutations in this study, with at least two different RFLP patterns. CONCLUSION: These data help in the understanding of the molecular basis of PZA resistance. An adenine to guanine point mutation in the -11 upstream region was the most common type of pncA mutation in our isolates. The results of pncA mutation analyses should be carefully interpreted for epidemiologic purposes. (+info)
Sub-inhibitory concentrations of vancomycin prevent quinolone-resistance in a penicillin-resistant isolate of Streptococcus pneumoniae.
BACKGROUND: The continuous spread of penicillin-resistant pneumococci represents a permanent threat in the treatment of pneumococcal infections, especially when strains show additional resistance to quinolones. The main objective of this study was to determine a treatment modality impeding the emergence of quinolone resistance. RESULTS: Exposure of a penicillin-resistant pneumococcus to increasing concentrations of trovafloxacin or ciprofloxacin selected for mutants resistant to these drugs. In the presence of sub-inhibitory concentrations of vancomycin, development of trovafloxacin-resistance and high-level ciprofloxacin-resistance were prevented. CONCLUSIONS: Considering the risk of quinolone-resistance in pneumococci, the observation might be of clinical importance. (+info)
Characterization of mutations in the rpoB gene associated with rifampin resistance in Rhodococcus equi isolated from foals.
Treatment with a combination of erythromycin and rifampin has considerably improved survival rates of foals and immunocompromised patients suffering from severe pneumonia caused by Rhodococcus equi. Frequently, because of monotherapy, emergence of rifampin-resistant strains has been responsible for treatment failure. Using consensus oligonucleotides, we have amplified and sequenced the rifampin resistance (Rif(r))-determining regions of 12 rifampin-resistant R. equi strains isolated from three foals and of mutants selected in vitro from R. equi ATCC 3701, a rifampin-susceptible strain. The deduced amino acid sequences compared to those of four rifampin-susceptible R. equi strains showed several types of mutations. In 3 of the 10 strains isolated from one foal, His526Asn (Escherichia coli numbering) and Asp516Val mutations were associated with low-level resistance (rifampin MIC, 2 to 8 microg/ml), whereas His526Asp conferred high-level resistance (rifampin MIC, 128 microg/ml) in the 7 remaining strains. In strains from the two other foals, His526Asp and Ser531Leu mutations were found to be associated with high-level and low-level resistance, respectively. The in vitro mutants, highly resistant to rifampin, harbored His526Tyr and His526Arg substitutions. As described in other bacterial genera, His526, Ser531, and Asp516 are critical residues for rifampin resistance in R. equi, and the resistance levels are dependent on both the location and the nature of the substitution. (+info)
Improved antimicrobial interventions have benefits.
Studies have shown benefits to patients from improved interventions involving antimicrobial therapy. The purpose of the present study was to evaluate prospectively the impact of improved interventions by (i) the use of TheraTrac 2, a computer software program which electronically links susceptibility testing results immediately to the pharmacy and alerts pharmacists of potential interventions, and (ii) the education of pharmacists involving microbiologic topics. The study group had the new intervention program. The control group had interventions performed the way that they had previously been done by manually reviewing hard copies of susceptibility testing data. In a 5-month period, all inpatients whose last names began with A to K were the study group; inpatients whose last names began with L to Z were controls. Three analyses were done; one analysis (analysis A) involved only patients with interventions, one analysis (analysis B) involved all patients for whom antimicrobial testing was done and who were matched for diagnosis-related groups (DRGs), regardless of whether an intervention occurred, and one analysis (analysis C) involved these DRG-matched patients by using severity-adjusted data. In analysis A, the study group had a 4.8% decreased rate of mortality, an average of a 16.5-day decreased length of stay per patient, and $20,886 decreased variable direct costs per patient. None of these differences was statistically significant. In analysis B, the study patients had a 1.2% higher mortality rate (P = 0.741), an average of a 2.7-day decreased length of stay per patient (P = 0.035), and $2,626 decreased variable direct costs per patient (P = 0.008). In analysis C, the study patients had a 1.4% lower mortality rate, a 1.2-day decreased length of stay per patient, and $1,466 decreased variable direct costs per patient. In conclusion, the institution of this program caused substantial cost savings. (+info)