Trueperella pyogenes (T. pyogenes) is a well-known opportunistic pathogen of many animal species. It can cause a variety of suppurative infections. The objective of this research was to get insight into the gene context and the location of the antimicrobial resistance determinants in the two multi-resistant T. pyogenes isolates TP3 and TP4. Comparative analysis of key factors leading to antimicrobial resistance was performed. Both isolates were resistant to erythromycin, azithromycin and tetracycline, and susceptible to ciprofloxacin, enrofloxacin, cefazolin and florfenicol. In addition, TP4 was resistant to amikacin and gentamicin. Whole-genome analyses revealed that both TP3 and TP4 contained two different genomic islands (TP3-GI1, TP3-GI5, TP4-GI5 and TP4-GI8) involved in multi-drug resistance. There is a common region in TP3-GI1 and TP4-GI5, containing the tetracycline resistance gene tet(W) and a series of genes involved in type IV secretion systems. Several genes located on TP3-GI5 and TP4-GI8 are highly homologous. Tetracycline-resistance gene tet(33) was potentially acquired by horizontal gene transfer via IS6100 located on 57,936 bp TP3-GI5. The macrolide resistance gene erm(X) was located near the end of the TP3-GI5. The sequence analysis of TP4-GI8 showed that two copies of erm(X) and two IS1634 elements located in the same orientation may have formed a composite transposon. GI-type T4SS, transposons and multiple resistance genes located on GIs play a key role in multiple drug resistance of TP3 and TP4.

中文翻译：

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基因岛IV型分泌系统和基因岛中的转座子参与化脓性疟原虫的抗药性。

化脓性疟原虫（T. pyogenes）是许多动物的著名的机会病原体。它可以引起多种化脓性感染。这项研究的目的是深入了解两个多耐药性化脓性支原体分离株TP3和TP4的基因背景和抗药性决定因素的位置。进行了导致抗菌素耐药性的关键因素的比较分析。两种分离物均对红霉素，阿奇霉素和四环素具有抗性，并对环丙沙星，恩诺沙星，头孢唑林和氟苯尼考敏感。另外，TP4对阿米卡星和庆大霉素具有抗性。全基因组分析显示，TP3和TP4都包含两个涉及多药耐药性的不同基因组岛（TP3-GI1，TP3-GI5，TP4-GI5和TP4-GI8）。TP3-GI1和TP4-GI5中有一个公共区域，包含四环素抗性基因tet（W）和一系列与IV型分泌系统有关的基因。位于TP3-GI5和TP4-GI8上的几个基因高度同源。四环素抗性基因tet（33）可能是通过位于57,936 bp TP3-GI5上的IS6100通过水平基因转移获得的。大环内酯类抗性基因erm（X）位于TP3-GI5末端附近。TP4-GI8的序列分析表明，erm（X）和位于相同方向的两个IS1634元素的两个副本可能已经形成了一个复合转座子。GI型T4SS，转座子和位于GI上的多重耐药基因在TP3和TP4多重耐药中起关键作用。四环素抗性基因tet（33）可能是通过位于57,936 bp TP3-GI5上的IS6100通过水平基因转移获得的。大环内酯类抗性基因erm（X）位于TP3-GI5末端附近。TP4-GI8的序列分析表明，erm（X）和位于相同方向的两个IS1634元素的两个副本可能已经形成了一个复合转座子。GI型T4SS，转座子和位于GI上的多重耐药基因在TP3和TP4多重耐药中起关键作用。四环素抗性基因tet（33）可能是通过位于57,936 bp TP3-GI5上的IS6100通过水平基因转移获得的。大环内酯类抗性基因erm（X）位于TP3-GI5末端附近。TP4-GI8的序列分析表明，erm（X）和位于相同方向的两个IS1634元素的两个副本可能已经形成了一个复合转座子。GI型T4SS，转座子和位于GI上的多重耐药基因在TP3和TP4多重耐药中起关键作用。TP4-GI8的序列分析表明，erm（X）和位于相同方向的两个IS1634元素的两个副本可能已经形成了一个复合转座子。GI型T4SS，转座子和位于GI上的多重耐药基因在TP3和TP4多重耐药中起关键作用。TP4-GI8的序列分析表明，erm（X）和位于相同方向的两个IS1634元素的两个副本可能已经形成了一个复合转座子。GI型T4SS，转座子和位于GI上的多重耐药基因在TP3和TP4多重耐药中起关键作用。