Laboratorio Regional de Santo Andre, Instituto Adolfo Lutz, Santo Andre, SP, Brazil.
Department of Microbiology, Escola Paulista de Medicina, Universidade Federal de Sao Paulo, Immunology, Parasitology, Sao Paulo, SP, Brazil.
Braz J Microbiol. 2024 Jun;55(2):1297-1304. doi: 10.1007/s42770-024-01269-2. Epub 2024 Feb 24.
Although it has been hypothesized that the acquisition of plasmids-especially those bearing virulence factors and antimicrobial resistance genes-increases the energetic burden and reduces the fitness of a bacterium in general, some results have challenged this view, showing little or no effect on fitness after plasmid acquisition, which may lead to change in the view that there are evolutionary barriers for a wide spread of such plasmids among bacteria. Here, to evaluate the fitness impact of plasmid-encoded antibiotic resistance and virulence genes, plasmids from O26:H11, O111:H8, and O118:H16 Shiga toxin-producing Escherichia coli (STEC) human and bovine isolates were transferred to the non-virulent E. coli HS and K-12 MG1655 strains. Sequencing and PCR were used to characterize plasmids, and to identify the presence of antimicrobial resistance and/or virulence genes. The fitness impact of plasmids encoding virulence and antimicrobial resistance upon bacterial hosts was determined by pairwise growth competition. Plasmid profile analysis showed that STEC strains carried one or more high and low molecular weight plasmids belonging to the B/O, F, I, K, P, Q, and/or X incompatibility groups encoding virulence genes (SPATE-encoding genes) and/or antimicrobial resistance genes (aadA1, strAB, tetA, and/or tetB). Competition experiments demonstrated that the biological cost of carriage of these plasmids by the commensal E. coli strain HS or the laboratory strain E. coli K-12 MG1655 was low or non-existent, ranging from - 4.7 to 5.2% per generation. This suggests that there are few biological barriers-or, alternatively, it suggests that there are biological barriers that we were not able to measure in this competition model-against the spread of plasmid encoding virulence and resistance genes from STEC to other, less pathogenic E. coli strains. Thus, our results, in opposition to a common view, suggest that the acquisition of plasmids does not significantly affect the bacteria fitness and, therefore, the theorized plasmid burden would not be a significant barrier for plasmid spread.
虽然有人假设质粒的获得——特别是那些携带毒力因子和抗微生物药物耐药基因的质粒——会增加细菌的能量负担并降低其适应性，但有些结果对这一观点提出了挑战，表明质粒获得后对适应性几乎没有影响，这可能会改变这样一种观点，即这些质粒在细菌中的广泛传播存在进化障碍。在这里，为了评估质粒编码的抗生素耐药性和毒力基因对适应性的影响，将来自 O26:H11、O111:H8 和 O118:H16 产志贺毒素大肠杆菌（STEC）人源和牛源分离株的质粒转移到非致病性大肠杆菌 HS 和 K-12 MG1655 菌株中。使用测序和 PCR 来对质粒进行特征分析，并鉴定抗微生物药物耐药性和/或毒力基因的存在。通过成对生长竞争来确定编码毒力和抗微生物药物耐药性的质粒对细菌宿主的适应性影响。质粒图谱分析表明，STEC 菌株携带一个或多个属于 B/O、F、I、K、P、Q 和/或 X 不相容群的高和低分子量质粒，这些质粒编码毒力基因（SPATE 编码基因）和/或抗微生物药物耐药性基因（aadA1、strAB、tetA 和/或 tetB）。竞争实验表明，这些质粒由共生大肠杆菌菌株 HS 或实验室大肠杆菌菌株 K-12 MG1655 携带的生物学成本较低或不存在，每代的范围为-4.7%至 5.2%。这表明，在 STEC 向其他致病性较低的大肠杆菌菌株传播编码毒力和耐药性基因方面，几乎没有生物学障碍——或者，相反，我们在这种竞争模型中无法测量到生物学障碍——因此，我们的结果与普遍观点相反，表明质粒的获得不会显著影响细菌的适应性，因此，理论上的质粒负担不会成为质粒传播的显著障碍。
