Antimicrobial resistance (AR) mechanisms encoded on plasmids can affect other phenotypic traits in bacteria, including biofilm formation. These effects may be important contributors to the spread of AR and the evolutionary success of plasmids, but it is not yet clear how common such effects are for clinical plasmids/bacteria, and how they vary among different plasmids and host strains. Here, we used a combinatorial approach to test the effects of clinical AR plasmids on biofilm formation and population growth in clinical and laboratory Escherichia coli strains. In most of the 25 plasmid-bacterium combinations tested, we observed no significant change in biofilm formation upon plasmid introduction, contrary to the notion that plasmids frequently alter biofilm formation. In a few cases we detected altered biofilm formation, and these effects were specific to particular plasmid-bacterium combinations. By contrast, we found a relatively strong effect of a chromosomal streptomycin-resistance mutation (in rpsL) on biofilm formation. Further supporting weak and host-strain-dependent effects of clinical plasmids on bacterial phenotypes in the combinations we tested, we found growth costs associated with plasmid carriage (measured in the absence of antibiotics) were moderate and varied among bacterial strains. These findings suggest some key clinical resistance plasmids cause only mild phenotypic disruption to their host bacteria, which may contribute to the persistence of plasmids in the absence of antibiotics.

质粒上编码的抗菌素耐药性（AR）机制可以影响细菌的其他表型特征，包括生物膜的形成。这些效应可能是 AR 传播和质粒进化成功的重要因素，但目前尚不清楚这些效应对于临床质粒/细菌有多常见，以及它们在不同质粒和宿主菌株之间有何不同。在这里，我们使用组合方法来测试临床 AR 质粒对临床和实验室大肠杆菌菌株生物膜形成和群体生长的影响。在测试的 25 种质粒-细菌组合中的大多数中，我们观察到质粒引入后生物膜形成没有显着变化，这与质粒经常改变生物膜形成的观点相反。在少数情况下，我们检测到生物膜形成发生了改变，并且这些效应特定于特定的质粒-细菌组合。相比之下，我们发现染色体链霉素抗性突变（rpsL）对生物膜形成有相对较强的影响。进一步支持临床质粒对我们测试的组合中细菌表型的微弱和宿主菌株依赖性影响，我们发现与质粒携带相关的生长成本（在没有抗生素的情况下测量）是中等的，并且在细菌菌株之间存在差异。这些发现表明，一些关键的临床耐药质粒仅对其宿主细菌造成轻微的表型破坏，这可能有助于质粒在没有抗生素的情况下持续存在。