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Mechanisms of Antibiotic Resistance in Acinetobacter spp. — Genetics of Resistance
Published in E. Bergogne-Bénézin, M.L. Joly-Guillou, K.J. Towner, Acinetobacter, 2020
Chloramphenicol is often disregarded by clinical microbiologists as the drug is considered to be too toxic for routine use. However, its use in the past has ensured that a surfeit of chloramphenicol resistance genes exist, and these now provide the opportunity to examine the epidemiology of resistance genes without the continuous interference of new selective pressures.
Chloramphenicol and Thiamphenicol
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
Chloramphenicol-resistant S. pyogenes strains are common in Japan (Nakae et al., 1977), but they appear to be very rare elsewhere (Bourbeau and Campos, 1982; Szczypa et al., 2006; Imohl and van der Linden, 2015; Nitzan et al., 2015). Chloramphenicol-resistant S. pneumoniae is still generally rare, accounting for less than 5% of isolates in surveillance studies from Brazil, Canada, Greece, Italy, and Portugal (Zhanel et al., 2003; Castanheira et al., 2006; Dias et al., 2006; Maraki and Papadakis, 2014; Montagnani et al., 2006), although resistance is becoming more common and may be as high as 40% in some areas (Manning et al., 2011; Korona-Glowniak and Malm, 2012). Chloramphenicol resistance is more common among penicillin-resistant pneumococci (Gosbell et al., 2006), and sporadic outbreaks of infections caused by chloramphenicol-resistant pneumococci are well described. For example, in a study from Columbia between 1994 and 1996, 88% of 43 pneumococcal isolates in infected children were resistant (Tamayo et al., 1999).
Chloramphenicol
Published in Thomas T. Yoshikawa, Shobita Rajagopalan, Antibiotic Therapy for Geriatric Patients, 2005
Chloramphenicol resistance is mediated by a bacterial enzyme, acetyltransfer-ase. This enzyme acetylates the antibiotic to an inactive diacetyl derivative (7). Chloramphenicol-resistant Salmonella typhi (typhoid fever) and Shigella dysentery strains have been reported in Vietnam and India (8,9). The drug is widely used in humans and animals (dairy farms) and thus may contribute to the development of bacterial resistance to chloramphenicol (9,10). Unrestricted use of chloramphenicol in developing countries may result in a resistance pattern similar to that observed with tetracyclines.
Combined exposure to non-antibiotic pharmaceutics and antibiotics in the gut synergistically promote the development of multi-drug-resistance in Escherichia coli
Published in Gut Microbes, 2022
Danyang Shi, Han Hao, Zilin Wei, Dong Yang, Jing Yin, Haibei Li, Zhengshan Chen, Zhongwei Yang, Tianjiao Chen, Shuqing Zhou, Haiyan Wu, Junwen Li, Min Jin
The results showed that chloramphenicol resistance occurred in E. coli exposed solely to chloramphenicol (Figure 1(a)). Furthermore, they presented a dose-response pattern, and the mutation frequency declined sharply with the decrease in chloramphenicol exposure levels from 16 to 0.5 mg/L (p < .01). At the exposure level of 16 mg/L chloramphenicol for five days, the mutation frequencies of chloramphenicol resistance increased by at least 7.0 × 107-fold to 0.41 (Table S1), compared with the spontaneous mutation frequency of chloramphenicol, which was less than 5.9 × 10−9 (no spontaneous chloramphenicol-resistant mutants were observed on the plates containing 16 mg/L chloramphenicol). However, when the chloramphenicol dose was lowered to 1 mg/L, the mutation frequencies dramatically decreased to 2.6 × 10−6 over the same period. Furthermore, the bacterial mutation frequency of chloramphenicol also showed a time-dependent pattern. While no increase in the mutation frequency was found on day 1 in case of 4 mg/L chloramphenicol, the mutation frequency of chloramphenicol increased to 1.3 × 10–4 on day 3 (clones named C4-3d) and to 3.4 × 10−3 on day 5. Evidently, the higher the exposure concentration, the faster was the increase in the mutation frequency over time. The resistant E. coli began to grow on chloramphenicol selecting-plates on day 1, day 3, and day 5 for for 8 mg/L, 4 mg/L, and 1 mg/L chloramphenicol exposure, respectively. No significant increase in the mutation frequency occurred even if E. coli was exposed to 6 μg/L chloramphenicol for 50 days.