细菌的碳青霉烯耐药性是全球公共健康面临的一个重大挑战，由碳青霉烯耐药菌（CRO）引起的临床感染通常有很高的发病率和死亡率。头孢他啶-阿维巴坦（CAZ-AVI）是一种新型头孢菌素/β-内酰胺酶抑制剂，为临床治疗CRO感染提供了一项重要选择。据报道，CAZ-AVI 能够抑制Ambler A类、C类以及部分D类酶的活性。然而，这种药物在临床使用后不久，细菌的耐药性就已经出现，并且呈上升趋势。了解细菌对CAZ-AVI 的耐药机制，对于指导开发新型治疗方法、帮助预测潜在的耐药机制至关重要。本文旨在系统总结CAZ-AVI 耐药菌株的流行病学发展过程和最近发现的CAZ-AVI 耐药机制；将重点关注β-内酰胺酶突变体的产生、β-内酰胺酶高表达、细胞表面通透性降低以及药物外排泵的过表达。短时间内多种CAZ-AVI耐药机制的产生，强调了临床合理用药的重要性以及监测CAZ-AVI 耐药性病原体的必要性。

Carbapenem resistance presents a major challenge for the global public health network, as clinical infections caused by carbapenem-resistant organisms (CRO) are frequently associated with significant morbidity and mortality. Ceftazidime–avibactam (CAZ–AVI) is a novel cephalosporin/β-lactamase inhibitor combination offering an important advance in the treatment of CRO infections. CAZ–AVI has been reported to inhibit the activities of Ambler classes A, C, and some class D enzymes. However, bacterial resistance has been emerging shortly after the introduction of this combination in clinical use, with an increasing trend. Understanding these resistance mechanisms is crucial for guiding the development of novel treatments and aiding in the prediction of underlying resistance mechanisms. This review aims to systematically summarize the epidemiology of CAZ–AVI-resistant strains and recently identified resistance mechanisms of CAZ–AVI, with a focus on the production of β-lactamase variants, the hyperexpression of β-lactamases, reduced permeability, and overexpressed efflux pumps. The various mechanisms of CAZ–AVI resistance that have emerged within a short timescale emphasize the need to optimize the use of current agents, as well as the necessity for the surveillance of CAZ–AVI-resistant pathogens.