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Pharmacology: Moxifloxacin is an antibiotic of the fluoroquinolone class. In vitro, moxifloxacin exhibits activity against both Gram-positive and Gram-negative pathogenic bacteria. It works by interfering with topoisomerase II (DNA gyrase) and IV. Topoisomerase is an essential enzyme that plays an important role in bacterial DNA replication, transcription, and repair. Topoisomerase IV is also known to influence bacterial chromosome division. Kinetically, the bactericidal effect of moxifloxacin depends on its concentration. The Minimum Bacterial Concentration (MBC) is a range of the Minimum Inhibitory Concentration (MIC).
Interference with Culture Tests: Moxifloxacin therapy may cause false-negative culture results for Mycobacterium spp. by inhibiting mycobacterium growth.
Effect on Normal Flora in the Human Gastrointestinal Tract: A decrease in the following normal flora in the digestive tract was observed in volunteers given moxifloxacin: E. coli, Bacillus spp., Enterococci, and Klebsiella spp. decreased, as well as anaerobic bacteria Bacteroides vulgatus, Bifidobacterium, Eubacterium, and Peptostreptococcus. B. fragilis increased. These changes returned to normal within two weeks. Moxifloxacin is not indicated for the treatment of Clostridium difficile.
Prevalence of Resistance patterns can vary geographically and this depend on time for the certain species and it needs the information of resistance in local area, especially when treating severe infections.
Resistance: Resistance mechanisms of penicillins, cephalosporins, aminoglycosides, macrolides, and tetracyclines do not interfere with the antibacterial activity of moxifloxacin. Other resistance mechanisms such as permeation inhibition (a common example in Pseudomonas aeruginosa) and efflux mechanisms, however, also affect the sensitivity of bacteria to moxifloxacin. There is no cross-resistance between moxifloxacin and these compounds. Plasmid-mediated resistance has not been observed. Laboratory studies of the development of moxifloxacin resistance in gram-positive bacteria have shown that resistance develops slowly, with multiple mutations, and is mediated by modification of target sites (such as topoisomerases II and IV) and efflux mechanisms. The frequency of resistance development is low (rates of 10-7-10-10). Parallel resistance has been reported with other quinolones. However, because moxifloxacin inhibits both topoisomerases (II and IV) in Gram-positive organisms, some Gram-positive and anaerobic bacteria that are resistant to other quinolones may become susceptible to moxifloxacin.
