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Resistance of Acinetobacter spp. to Antimicrobials — Overview of Clinical Resistance Patterns and Therapeutic Problems
Published in E. Bergogne-Bénézin, M.L. Joly-Guillou, K.J. Towner, Acinetobacter, 2020
Figure 7.7 shows killing curves of A. baumannii obtained in the presence of four fluoroquinolones (Joly-Guillou and Bergogne-Bérézin, 1992). Sparfloxacin showed significantly better bactericidal activity than temafloxacin, while ciprofloxacin and pefloxacin were bacteriostatic only. The strains used in this study were more resistant than those found in some other studies (Table 7.16), but a recent study in Spain of 32 isolates (Garcia-Rodriguez et al., 1994) found similar MIC90 values of >16 mg/L for all fluoroquinolones tested. Possible mechanisms of resistance to fluoroquinolones are discussed in Chapter 8.
Discontinued Fluoroquinolones
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Temafloxacin was a newer generation fluoroquinolone with a broad range of activity against Gram-positive, as well as Gram-negative, pathogens and some anaerobes, with good activity against S. pneumoniae, S. aureus, Legionella spp., and Mycoplasma spp. (Hardy et al., 1987; Gorzynski et al., 1989; Bryan et al., 1990; Bille and Glauser, 1991; Finegold et al., 1991; Jacobs, 1991; King et al., 1991; Pankey, 1991; Segreti et al., 1989; Segreti, 1991; Swanson et al., 1991; Glatt et al., 1992). Clinical studies demonstrated rates of efficacy in the treatment of lower respiratory tract infections of 90–100%, of skin and soft tissue infections, > 90%, of urinary tract infections, > 95%, of prostatitis, > 84%, and excellent activity against gonococcal and nongonococcal (other than syphilis) sexually transmitted diseases (Davies et al., 1990; Cox and Childs, 1991; Cox, 1991; Davey, 1991; Iravani, 1991a; Iravani, 1991b; Kosmidis, 1991; Mogabgab, 1991; Naber et al., 1991; Pankey, 1991; Parish and Jungkind, 1991; Carbon et al., 1992; Lindsay et al., 1992). Initially reported toxicities and drug interactions were similar to those generally associated with other fluoroquinolones, such as ciprofloxacin (Norrby and Pernet, 1991; Pankey, 1991; Ruff et al., 1991; Granneman et al., 1992; Mahr et al., 1992; Millar et al., 1992; Sorgel et al., 1992). Temafloxacin was approved by the Food and Drug Administration (FDA) for use in the treatment of lower respiratory tract infections, urinary tract infections, and skin and soft tissue infections.
Ameliorative effects of Moringa oleifera leaf extract on levofloxacin-induced hepatic toxicity in rats
Published in Drug and Chemical Toxicology, 2020
Ayman Samir Farid, Ahmed Medhat Hegazy
The pathophysiology of fluoroquinolone hepatotoxicity is not well understood. There is a higher rate of liver damage in patients receiving molecules that generate reactive intermediates (temafloxacin and trovafloxacin), and this mechanism may be applicable to other fluoroquinolones (Blum et al.1994, Chen et al.2000, Sun et al.2008). In the present study, there were significant increases in ALT, AST and GGT levels, which indicates liver damage in the Levofloxacin-treated group. The elevation in ALT was almost two times that of the value in the control groups, especially in week 2 after administration of Levofloxacin. Similarly, the elevations in ALT and GGT were more than two times the levels of the control groups after the first and second weeks of receiving Levofloxacin (Table 1). Elevated serum levels of ALT and AST may be due to hepatocellular inflammation, which leads to an increase in the permeability of the cell membrane resulting in the release of transaminases in the blood stream (Kaneko et al.2008). A similar increase in ALT, AST and GGT values by Levofloxacin has been reported in humans (Figueira-Coelho et al. 2010, Karim et al.2001). Increases in GGT are associated with all forms of primary and secondary hepatobiliary disorders. Cholestasis due to intrahepatic or extrahepatic biliary obstruction causes higher serum levels of GGT (Clark and Kruse 1990). There were significant decreases in ALT, AST, and GGT levels with Levofloxacin and M. oleifera cotreatment, and this observation might be due to hepatoprotective activity. The reversal of elevated serum intracellular enzyme levels by M. oleifera extract may be attributed to a hepatoprotective property of M. oleifera leaf extract. Previous research reported that the hepatoprotective effect was due to the presence of a well-recognized flavonoid (quercetin and kaempferol) (Hamza 2010, Pari and Karthikesan 2007). These results concurred with the improvement in histopathological features of the livers of M. oleifera leaf extract-treated rats when compared with the livers of Levofloxacin-treated rats. These findings coincided with Awodele et al. (2012) and Sharifudin et al. (2013) who found that the M. oleifera leaf extract moderately reduced hepatocyte necrosis, indicating the reduction of hepatocellular damage.