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Levofloxacin, a recently introduced third-generation fluoroquinolone, is the L-isomer ofloxacin and possesses excellent activity against Gram-positive, Gram-negative and anaerobic bacteria (North et al., 1998). Compared with other fluoroquinolones (FQs), it also has more pronounced bactericidal activity against organisms such as Pseudomonas, Enterobacteriaceae and Klebsiella spp.(Klesel et al., 1995). Several species of staphylococci, streptococci including Streptococcus pneumoniae, bacteroides, clostridium, haemophilus, moraxella, legionella, mycoplasma and chlamydia are susceptible to levofloxacin (Langtry & Lamb, 1998). The bactericidal effect of levofloxacin is achieved through reversible binding to DNA gyrase and subsequent inhibition of bacterial DNA replication and transcription (Fu et al., 1992). Levofloxacin distributes well to target body tissues and fluids in the respiratory tract, skin, urine and prostrate, and its uptake by cells makes it suitable for use against intracellular pathogens. However, it penetrates poorly into the central nervous system (Langtry & Lamb, 1998). FQs act by a concentration-dependent killing mechanism, whereby the optimal effect is attained by the administration of high doses over a short period of time (Drusano et al., 1993). This concentration-dependent killing profile is associated with a relatively prolonged postantibiotic effect (Aliabadi & Lees, 2001). The drug undergoes a limited metabolism in rats and human (Langtry & Lamb, 1998) and is primarily excreted by kidney mainly as active drug. Inactive metabolites (N-oxide and demethyl metabolites) represent< 5% of the total dose (Hurst et al., 2002). The …