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The safety of levofloxacin was compared to that of non-fluoroquinolone alternatives used for respiratory tract infections. Results from five randomised controlled trials revealed that the incidence of any adverse events possibly associated with levofloxacin ranged from 5.8% to 22.7%, whereas that of comparators (ceftriaxone, cefuroxime axetil, clarithromycin and amoxicillin–clavulanic acid) ranged from 8.5% to 39.3%. The rate of adverse drug reactions (ADRs) was lower for levofloxacin in all trials. The most common adverse events for all agents tended to be gastrointestinal in nature. Levofloxacin was associated with a mild effect on the normal microflora, reaching a maximum at four days of therapy, with complete recovery being achieved by seven days post-therapy. No colonisation with resistant strains was observed during the period of levofloxacin therapy. Amoxicillin–clavulanic acid administration selected for resistant strains of Enterobacteriaceae, and ampicillin administration was associated with both resistant strains of Enterobacteriacae as well as Candida spp. Ceftriaxone selected resistant strains of Clostridium difficile and Candida spp. Thus, microflora effects favoured levofloxacin over all of the agents tested, including macrolides and tetracyclines. These results confirm that the ecological impact of levofloxacin is markedly less than that associated with non-fluoroquinolone comparators.

Throughout the antibiotic era, the emergence of drug-resistant bacteria has paralleled the development of new antimicrobial agents. As a result of selection pressures and invasive techniques that prolong the lives of seriously ill hospital patients, gram-negative bacilli have become the dominant causes of nosocomial infection. These microorganisms produce a diversity of antibiotic-inactivating enzymes. Moreover, the cell envelope of gram-negative bacteria provides a series of barriers that keep antibiotics from reaching their targets. Resistance factors can be transmitted among bacteria of different genera and species, thus conferring multidrug resistance. These problems continue to challenge scientists to better understand resistance mechanisms and to develop new compounds to circumvent them.

Between February 1992 and February 1993, 12 patients were seen who were infected or colonized with methicillin-resistant strains of Staphylococcus aureus. The strains had decreased susceptibility to teicoplanin (MICs, 8–16 µg/mL). Field inversion gel electrophoresis showed the strains belonged to three related clones (A1, A2, and A3). The patients were thought to have acquired the strains nosocomially. Consistent with results of laboratory studies of teicoplanin-resistant S. aureus, all but 1 strain expressed a 35-kDa membrane protein, and 9 strains expressed increased levels of penicillin-binding protein 2 complex. Six strains were isolated from patients treated with glycopeptides. These data suggest that nosocomial transmission of S. aureus with decreased teicoplanin susceptibility may occur during glycopeptide use and that such strains develop resistance by a mechanism associated with the appearance of a 35-kDa membrane protein. Surveillance is necessary to monitor for the potential selection of resistant clones that may be capable of dissemination.

Many disease-causing organisms have the complex mechanisms which can make them resistant to destruction by antibiotics. Since the use of antibiotics has become widespread, the number of bacteria resistant to it have increased as well.

The minimal antibiotic concentration (MAC) refers to the lowest concentration of drug that results in a detectable effect on bacteria (e.g., inhibition of growth, change in morphology, and delay in recovery to normal growth in drug-free medium). Strains of Escherichia coli and of Staphylococcus aureus were subjected to a range of subminimal inhibitory concentrations of four drugs-ampicillin, gentamicin, rosaramicin, and tetracycline. Inhibition curves (percentage of normal growth vs. concentration of drug) were related to the period of recovery before resumption of normal growth, which was chosen to express an MAC value. In both E. coli and S. aureus, the longest delay in recovery of normal growth was observed with rosaramicin. Ampicillin resulted in a delay in recovery only with S. aureus.