Department of Biology, Emory University, Atlanta, GA 30322.
Emory Antibiotic Resistance Center, Atlanta, GA 30322.
Proc Natl Acad Sci U S A. 2024 Apr 16;121(16):e2318600121. doi: 10.1073/pnas.2318600121. Epub 2024 Apr 8.
Antibiotics are considered one of the most important contributions to clinical medicine in the last century. Due to the use and overuse of these drugs, there have been increasing frequencies of infections with resistant pathogens. One form of resistance, heteroresistance, is particularly problematic; pathogens appear sensitive to a drug by common susceptibility tests. However, upon exposure to the antibiotic, resistance rapidly ascends, and treatment fails. To quantitatively explore the processes contributing to the emergence and ascent of resistance during treatment and the waning of resistance following cessation of treatment, we develop two distinct mathematical and computer-simulation models of heteroresistance. In our analysis of the properties of these models, we consider the factors that determine the response to antibiotic-mediated selection. In one model, heteroresistance is progressive, with each resistant state sequentially generating a higher resistance level. In the other model, heteroresistance is non-progressive, with a susceptible population directly generating populations with different resistance levels. The conditions where resistance will ascend in the progressive model are narrower than those of the non-progressive model. The rates of reversion from the resistant to the sensitive states are critically dependent on the transition rates and the fitness cost of resistance. Our results demonstrate that the standard test used to identify heteroresistance is insufficient. The predictions of our models are consistent with empirical results. Our results demand a reevaluation of the definition and criteria employed to identify heteroresistance. We recommend that the definition of heteroresistance should include a consideration of the rate of return to susceptibility.
抗生素被认为是上个世纪临床医学最重要的贡献之一。由于这些药物的使用和滥用,具有耐药性的病原体感染的频率不断增加。一种耐药形式,即异质性耐药,尤其成问题;病原体通过常见的药敏试验似乎对药物敏感。然而,一旦接触抗生素,耐药性迅速上升,治疗失败。为了定量探索治疗过程中导致耐药性出现和上升以及治疗停止后耐药性减弱的过程,我们开发了两种不同的异质性耐药的数学和计算机模拟模型。在分析这些模型的特性时,我们考虑了决定抗生素介导选择反应的因素。在一个模型中,异质性耐药是渐进的,每个耐药状态依次产生更高的耐药水平。在另一个模型中,异质性耐药是非渐进的,易感人群直接产生具有不同耐药水平的人群。在渐进模型中,耐药性上升的条件比非渐进模型更窄。从耐药状态到敏感状态的回复率取决于转变率和耐药的适应成本。我们的结果表明,用于识别异质性耐药的标准测试是不够的。我们的模型预测与经验结果一致。我们的结果要求重新评估用于识别异质性耐药的定义和标准。我们建议,异质性耐药的定义应包括对恢复敏感性的速率的考虑。