Department of Infectious Diseases, Coverdell Center for Biomedical and Health Sciences, 500 D. W. Brooks Drive, University of Georgia, Athens, GA, USA.
Graduate Program in Microbiology, University of Georgia, Athens, GA, USA.
J Antimicrob Chemother. 2018 Oct 1;73(10):2797-2805. doi: 10.1093/jac/dky264.
Why resistance to specific antibiotics emerges and spreads rapidly in some bacteria confronting these drugs but not others remains a mystery. Resistance to erythromycin in the respiratory pathogens Staphylococcus aureus and Streptococcus pneumoniae emerged rapidly and increased problematically. However, resistance is uncommon amongst the classic Bordetella species despite infections being treated with this macrolide for decades.
We examined whether the apparent progenitor of the classic Bordetella spp., Bordetella bronchiseptica, is able to rapidly generate de novo resistance to antibiotics and, if so, why such resistance might not persist and propagate.
Independent strains of B. bronchiseptica resistant to erythromycin were generated in vitro by successively passaging them in increasing subinhibitory concentrations of this macrolide. Resistant mutants obtained were evaluated for their capacity to infect mice, and for other virulence properties including adherence, cytotoxicity and induction of cytokines.
B. bronchiseptica rapidly developed stable and persistent antibiotic resistance de novo. Unlike the previously reported trade-off in fitness, multiple independent resistant mutants were not defective in their rates of growth in vitro but were consistently defective in colonizing mice and lost a variety of virulence phenotypes. These changes rendered them avirulent but phenotypically similar to the previously described growth phase associated with the ability to survive in soil, water and/or other extra-mammalian environments.
These observations raise the possibility that antibiotic resistance in some organisms results in trade-offs that are not quantifiable in routine measures of general fitness such as growth in vitro, but are pronounced in various aspects of infection in the natural host.
为什么某些细菌在接触抗生素时会迅速产生并传播对抗生素的耐药性,而其他细菌则不会,这仍然是一个谜。在呼吸道病原体金黄色葡萄球菌和肺炎链球菌中,对红霉素的耐药性迅速出现并增加,这是一个问题。然而,尽管几十年来一直在用大环内酯类药物治疗这些感染,但经典博德特氏菌属的细菌中却很少出现耐药性。
我们研究了经典博德特氏菌属的明显前体——支气管败血博德特氏菌,是否能够迅速产生对抗生素的新的耐药性,如果是这样,为什么这种耐药性不会持续存在和传播。
通过在亚抑菌浓度下连续传代,在体外独立生成了对红霉素耐药的支气管败血博德特氏菌株。获得的耐药突变体用于评估其感染小鼠的能力,以及其他毒力特性,包括粘附、细胞毒性和细胞因子诱导。
支气管败血博德特氏菌迅速产生了稳定和持久的新抗生素耐药性。与之前报道的适应性权衡不同,多个独立的耐药突变体在体外生长速度上没有缺陷,但在感染小鼠方面一直存在缺陷,并且失去了多种毒力表型。这些变化使它们失去了毒力,但表型与之前描述的与在土壤、水和/或其他非哺乳动物环境中存活能力相关的生长阶段相似。
这些观察结果提出了一种可能性,即在某些生物体中,抗生素耐药性导致的权衡在常规测量的一般适应性方面无法量化,例如体外生长,但在自然宿主的感染的各个方面都很明显。