Zhan Li, Zhang Jiaqi, Zhao Boyu, Li Xintian, Zhang Xiqing, Hu Renge, Elken Emad Mohammed, Kong Lingcong, Gao Yunhang
College of Animal Science and Technology, Jilin Agricultural University, Changchun, China.
Marine College, Shandong University, Weihai, China.
Front Vet Sci. 2021 Nov 10;8:765495. doi: 10.3389/fvets.2021.765495. eCollection 2021.
is one of the primary pathogens of bovine respiratory disease (BRD), and causes huge losses in the cattle industry. The Pm3 strain was a natural isolate, which is a strong form of pathogen and is sensitive to fluoroquinolones antibiotics. A high fluoroquinolone resistant strain, Pm64 (MIC = 64 μg/mL), was formed after continuous induction with subinhibitory concentration (1/2 MIC) of enrofloxacin, with the enhanced growth characteristics and large attenuation of pathogenicity in mice. This study reports the whole genome sequence and the transcription profile by RNA-Seq of strain Pm3/Pm64. The results showed an ineffective difference between the two strains at the genome level. However, 32 genes could be recognized in the gene islands (GIs) of Pm64, in which 24 genes were added and 8 genes were lost. Those genes are involved in DNA binding, trehalose metabolism, material transportation, capsule synthesis, prophage, amino acid metabolism, and other functions. In Pm3 strain, 558 up-regulated and 568 down-regulated genes were found compared to Pm64 strain, from which 20 virulence factor-related differentially expressed genes (DEGs) were screened. Mainly differentially transcribed genes were associated with capsular polysaccharide (CPS), lipopolysaccharide (LPS), lipooligosaccharide (LOS). Iron utilization, and biofilm composition. We speculated that the main mechanism of virulence attenuation after the formation of resistance of Pm64 comes from the change of the expression profile of these genes. This report elucidated the toxicity targets of serogroup A which provide fundamental information toward the understanding of the pathogenic mechanism and to decreasing antimicrobial drugs resistance.
是牛呼吸道疾病(BRD)的主要病原体之一,给养牛业造成巨大损失。Pm3菌株是一种天然分离株,是一种强致病性菌株,对氟喹诺酮类抗生素敏感。用亚抑菌浓度(1/2 MIC)的恩诺沙星连续诱导后,形成了高氟喹诺酮耐药菌株Pm64(MIC = 64 μg/mL),其生长特性增强,对小鼠的致病性大幅减弱。本研究报告了菌株Pm3/Pm64的全基因组序列和通过RNA-Seq得到的转录谱。结果表明,这两个菌株在基因组水平上差异不显著。然而,在Pm64的基因岛(GIs)中可识别出32个基因,其中新增24个基因,缺失8个基因。这些基因参与DNA结合、海藻糖代谢、物质运输、荚膜合成、原噬菌体、氨基酸代谢等功能。与Pm64菌株相比,在Pm3菌株中发现558个上调基因和568个下调基因,从中筛选出20个与毒力因子相关的差异表达基因(DEGs)。主要差异转录基因与荚膜多糖(CPS)、脂多糖(LPS)、脂寡糖(LOS)、铁利用和生物膜组成有关。我们推测Pm64耐药形成后毒力减弱的主要机制来自这些基因表达谱的变化。本报告阐明了A血清群的毒性靶点,为理解致病机制和降低抗菌药物耐药性提供了基础信息。