Usual and unusual antibacterial effects of quinolones

Abstract

Recently documented antibacterial effects of quinolones are reviewed. DNA gyrase is most likely to be the primary target site for these agents. Quinolones rapidly kill susceptible bacteria; the mechanisms of the bactericidal activity, still poorly understood, probably involve new protein synthesis. Quinolones alter membrane integrity before cell death, leading to leakage of cytoplasmic constituents. In Gram-negative bacteria, quinolones act as chelating agents for outer membrane divalent cations, disorganizing the bacterial lipopolysaccharide layer and facilitating the further entry of quinolone molecules in a 'self-promoted' pathway. Quinolones inhibit plasmid replication and reduce the efficacy of plasmid conjugation. Subinhibitory concentrations of quinolones can interfere with bacterial virulence factors, such as bacterial adherence to the host cell, phagocytosis and production of enzymes implicated in virulence. Recent studies also indicate synergism of quinolones with oxacillin against mcthicillin-rcsistant staphylococci and describe improved activity of newer compounds against Gram-positive pathogens.

Ecological implications of an improved direct viable count method for aquatic bacteria

“…It has previously been reported that some marine bacteria have very long generation times (sometimes more than 1 week [6]) and are probably not detectable during a 24-h incubation period, suggesting that even the new DVC procedure underestimates the real fraction of viable cells within marine communities. Another hypothesis to explain the high differences between culturable and viable counts is the fact that quinolone antibiotics act as chelating agents on the divalent cations of the cellular wall (13), resulting in the passive entrance of nutrients into starved cells, which facilitates their recovery (27).…”

Evaluation of Antibacterial in vitro Activity of Moxifloxacin and its Effects on Pulmonary Clearance of Klebsiella pneumoniae in an Animal Experimental Model

“…The mechanism of filamentation is probably related to the induction of the SOS response caused by initial DNA-gyrase inhibition and subsequent alterations in DNA topology and synthesis. The SOS pathway causes the block of cell division and, as a consequence, formation of filamentous forms [4,5,27].…”

Relative beta-lactamase- and transpeptidase-inhibitory activities of the new quinolone WIN-57273 in Staphylococcus aureus

“…However, the sequence of lethal events and the potential importance of secondary target sites require further investigation (2). [14CJpefloxacin labeling of Staphylococcus aureus membrane proteins showed binding of the quinolone to penicillin-binding protein (PBP) 2' and 0-lactamase (7), which are suggested to have a common ancestral gene (14).…”