论文部分内容阅读
将ｐ Ｒ Ｓ Ｔ９８ 导入不含质粒且对抗菌药物敏感的大肠杆菌、伤寒杆菌，并用十二烷基硫酸钠（ Ｓ Ｄ Ｓ） 消除耐药菌株的ｐ Ｒ Ｓ Ｔ９８ ，计算接合子及 Ｒ 质粒消除前后菌株在人、兔及豚鼠的不同浓度、不同成份血清中的存活率。ｐ Ｒ Ｓ Ｔ９８ 介导其宿主菌对血清杀菌的抗性，但在不同宿主菌中抵抗力不同；补体经典途径及旁路途径均参与血清杀菌过程。ｐ Ｒ Ｓ Ｔ９ ８ 具有多效性，其广泛的宿主性在介导细菌多重耐药的同时，还赋予细菌抵抗血清的杀菌作用，使病原菌致病性增强。
PR S T98 was introduced into plasmid-free and antibacterial drug-resistant Escherichia coli and Salmonella typhi, and pR S T98 of the drug-resistant strain was eliminated with sodium dodecyl sulfate (S D S), and the zygotes and R plasmids were eliminated Survival rate of the strains in different concentrations and in different sera of human, rabbit and guinea pig. pR S T98 mediates the resistance of its host bacterium to bactericidal activity, but it has different resistance in different host bacterium. Both the classical complement pathway and the alternative pathway are involved in the process of bactericidal activity. pR S T9 8 is pleiotropic, its extensive host resistance mediates bacterial multidrug resistance and at the same time it confers bacterial bactericidal activity against sera and enhances the pathogenicity of pathogens.