Braoudaki M, Hilton A C
Microbiology, School of Life and Health Sciences, Aston University, Aston Triangle, Birmingham, United Kingdom.
J Clin Microbiol. 2004 Jan;42(1):73-8. doi: 10.1128/JCM.42.1.73-78.2004.
The mechanisms by which bacteria resist killing by antibiotics and biocides are still poorly defined, although repeated exposure to sublethal concentrations of antibacterial agents undoubtedly contributes to their development. This study aimed both to investigate the potential of Salmonella enterica and Escherichia coli O157 for adaptive resistance to commonly used biocides and to determine any cross-resistance to antibiotics. Strains were repeatedly passaged in media containing increasing concentrations of a biocide or antibiotic until adaptive resistance was obtained. A wide panel of antimicrobial agents was then screened by using the adapted strain to determine cross-resistance, if any. Adaptive resistance was readily achieved for both S. enterica and E. coli O157. Cross-resistance in adaptively resistant S. enterica varied with the serotype; Salmonella enterica serovar Enteritidis expressed cross-resistance to chloramphenicol, whereas Salmonella enterica serovar Typhimurium expressed cross-resistance to chlorhexidine. Benzalkonium chloride-resistant Salmonella enterica serovar Virchow showed elevated resistance to chlorhexidine; however, chlorhexidine-resistant Salmonella serovar Virchow did not demonstrate reciprocal cross-resistance to benzalkonium chloride, suggesting specific rather than generic resistance mechanisms. E. coli O157 strains acquired high levels of resistance to triclosan after only two sublethal exposures and, when adapted, repeatedly demonstrated decreased susceptibilities to various antimicrobial agents, including chloramphenicol, erythromycin, imipenem, tetracycline, and trimethoprim, as well as to a number of biocides. These observations raise concern over the indiscriminate and often inappropriate use of biocides, especially triclosan, in situations where they are unnecessary, whereby they may contribute to the development of microbial resistance mechanisms.
尽管反复接触亚致死浓度的抗菌剂无疑会促使细菌产生抗药性，但其对抗生素和杀菌剂产生耐药性的机制仍不清楚。本研究旨在调查肠炎沙门氏菌和大肠杆菌O157对常用杀菌剂产生适应性耐药的可能性，并确定是否存在对抗生素的交叉耐药性。将菌株在含有浓度不断增加的杀菌剂或抗生素的培养基中反复传代培养，直至获得适应性耐药。然后使用适应性菌株对多种抗菌剂进行筛选，以确定是否存在交叉耐药性。肠炎沙门氏菌和大肠杆菌O157都很容易获得适应性耐药。适应性耐药的肠炎沙门氏菌的交叉耐药性因血清型而异；肠炎沙门氏菌肠炎血清型对氯霉素表现出交叉耐药性，而鼠伤寒沙门氏菌血清型对洗必泰表现出交叉耐药性。耐苯扎氯铵的肠炎沙门氏菌维尔乔血清型对洗必泰的耐药性增强；然而，耐洗必泰的沙门氏菌维尔乔血清型对苯扎氯铵并未表现出相互交叉耐药性，这表明耐药机制具有特异性而非普遍性。大肠杆菌O157菌株仅经过两次亚致死暴露后就对三氯生产生了高水平耐药性，并且在适应后，对包括氯霉素、红霉素、亚胺培南、四环素和甲氧苄啶在内的多种抗菌剂以及多种杀菌剂的敏感性反复降低。这些观察结果引发了人们对在不必要的情况下滥用（尤其是滥用三氯生）杀菌剂的担忧，因为这可能会促使微生物耐药机制的产生。
