Institute of Microbiology and Epizootics, Centre of Infection Medicine, Department of Veterinary Medicine, Freie Universität Berlin, 14163 Berlin, Germany.
Institute of Microbiology, University of Veterinary Medicine, A-1210 Vienna, Austria.
Microbiol Spectr. 2018 Jul;6(4). doi: 10.1128/microbiolspec.ARBA-0010-2017.
Antimicrobial resistance among staphylococci of animal origin is based on a wide variety of resistance genes. These genes mediate resistance to many classes of antimicrobial agents approved for use in animals, such as penicillins, cephalosporins, tetracyclines, macrolides, lincosamides, phenicols, aminoglycosides, aminocyclitols, pleuromutilins, and diaminopyrimidines. In addition, numerous mutations have been identified that confer resistance to specific antimicrobial agents, such as ansamycins and fluoroquinolones. The gene products of some of these resistance genes confer resistance to only specific members of a class of antimicrobial agents, whereas others confer resistance to the entire class or even to members of different classes of antimicrobial agents, including agents approved solely for human use. The resistance genes code for all three major resistance mechanisms: enzymatic inactivation, active efflux, and protection/modification/replacement of the cellular target sites of the antimicrobial agents. Mobile genetic elements, in particular plasmids and transposons, play a major role as carriers of antimicrobial resistance genes in animal staphylococci. They facilitate not only the exchange of resistance genes among members of the same and/or different staphylococcal species, but also between staphylococci and other Gram-positive bacteria. The observation that plasmids of staphylococci often harbor more than one resistance gene points toward coselection and persistence of resistance genes even without direct selective pressure by a specific antimicrobial agent. This chapter provides an overview of the resistance genes and resistance-mediating mutations known to occur in staphylococci of animal origin.
动物源葡萄球菌的抗菌药物耐药性基于广泛的耐药基因。这些基因介导了对许多类已批准用于动物的抗菌药物的耐药性，如青霉素类、头孢菌素类、四环素类、大环内酯类、林可酰胺类、苯氧酰胺类、氨基糖苷类、氨基环醇类、截短侧耳素类和二氨基嘧啶类。此外，还鉴定了许多突变，这些突变赋予了对特定抗菌药物的耐药性，如安莎霉素类和氟喹诺酮类。这些耐药基因的产物赋予了对一类抗菌药物的特定成员的耐药性，而其他基因则赋予了对整个类或甚至对不同类的抗菌药物的耐药性，包括仅批准用于人类使用的抗菌药物。耐药基因编码了所有三种主要的耐药机制：酶失活、主动外排和抗菌药物细胞靶位的保护/修饰/替换。移动遗传元件，特别是质粒和转座子，在动物葡萄球菌中作为抗菌药物耐药基因的载体起着重要作用。它们不仅促进了同一和/或不同葡萄球菌种成员之间的耐药基因交换，而且还促进了葡萄球菌和其他革兰氏阳性菌之间的耐药基因交换。观察到葡萄球菌质粒通常携带不止一个耐药基因，这表明即使没有特定抗菌药物的直接选择压力，耐药基因也会被共同选择和持续存在。本章概述了已知存在于动物源葡萄球菌中的耐药基因和介导耐药性的突变。
