Bacterial strains acquisition

Indications for the formation of analogous species in microbial metabolism of LAS were found by Knepper and Kruse [33] during biotransformation of commercial LAS surfactant on an FBBR. However, the low concentrations of the tentative metabolites in the test liquor, which eluted under the applied reversed-phase (RP)-HPLC conditions somewhat earlier than the normal SPC, did not permit acquisition of full-scan mass spectra as was needed for unequivocal identification. Further evidence for the formation of the intermediate with a double bond in the alkanoate moiety was reported by Bird [103]. During biodegradation of Cn-LAS by a bacterial strain, a new UV adsorption band centred near 260 nm was detected, which was assumed to result from a double bond, although a definite confirmation could not be provided. 

Resistance to Tetracyclines. The tetracyclines stiU provide inexpensive and effective treatment for several microbial infections, but the emergence of acquired resistance to this class of antibiotic has limited their clinical usehilness. Studies to define the molecular basis of resistance are underway so that derivatives having improved antibacterial spectra and less susceptibiUty to bacterial resistance may be developed. Tetracyclines are antibiotics of choice for relatively few human infections encountered in daily clinical practice (104), largely as a result of the emergence of acquired tetracycline-resistance among clinically important bacteria (88,105,106). Acquired resistance occurs when resistant strains emerge from previously sensitive bacterial populations by acquisition of resistance genes which usually reside in plasmids and/or transposons (88,106,107). Furthermore, resistance deterrninants contained in transposons spread to, and become estabUshed in, diverse bacterial species (106). 

In a recent study, we found no acquisition of rifaximin resistance in 27 rifaximin-treated subjects colonized by Enterococcus [37]. The MIC50 and MIC90 for the treatment group (rifaximin at a dose of either 400 or 200 mg twice daily for 3 days) were similar (16-64 pg/ml). In two published studies, rifaximin resistance was shown to occur in the bacterial flora of individuals who received treatment with rifaximin at a dose of 800 mg/day for 5 days [9, 27]. Within 1-2 weeks after the end of rifaximin treatment, resistance rates appeared to have decreased to less than 20% of the intestinal flora. The resistant strains detected during treatment appeared to be unstable and unable to persistently colonize the intestinal tract. 

Intact-cell MALDI-TOF analysis offers several attractive features for rapid screening of bacterial collections. Analysis is performed directly on the cells after minimal sample preparation, and data acquisition is complete in only a matter of minutes. Intact biomarkers are introduced into the MALDI-TOF instrument under these conditions. Whether the observed biomarker molecules are desorbed directly from the surface of the cell wall or are extracted from the cells and co-crystallized with the matrix is currently unresolved, but MALDI spectra of intact bacteria generally contain a large number of peaks in the mass range 1-20 kDa [31]. For bacterial cells, proteins are the most often observed biomarkers. While this approach samples only a small percentage of the total proteins produced in the cells, these profiles have been reported by many groups to be suitable for taxonomic identification, down to at least the strain level. The wide availability of the MALDI-TOF instrumentation and its relative ease of use, coupled with relatively simple sample preparation procedures, have been key features in the rapid advancement of this approach. 

MECHANISMS OF BACTERIAL RESISTANCE TO PENICILLINS AND CEPHALOSPORINS A sensitive strain may acquire resistance by mutations that decrease the affinity of PBPs for the antibiotic. Because /5-lactam antibiotics inhibit many different PBPs, their affinity for several PBPs must decrease to confer resistance. Methidllin-resistant S. aureus are resistant via acquisition of an additional high-molecular-weight PBP (via a transposon) with a very low affinity for all /5-lactam antibiotics this mechanism is responsible for methicillin resistance in the coagu-lase-negative staphylococci. 

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