中国感染与化疗杂志
中國感染與化療雜誌
중국감염여화료잡지
CHINESE JOURNAL OF INFECTION AND CHEMOTHERAPY
2015年
3期
230-235
,共6页
卢曦%任志涛%李聪然%胡辛欣%聂彤颖%黄青山%陆海荣%李雪%李国庆%蒋建东%游雪甫%杨信怡
盧晞%任誌濤%李聰然%鬍辛訢%聶彤穎%黃青山%陸海榮%李雪%李國慶%蔣建東%遊雪甫%楊信怡
로희%임지도%리총연%호신흔%섭동영%황청산%륙해영%리설%리국경%장건동%유설보%양신이
重组溶葡萄球菌酶%金黄色葡萄球菌%诱导耐药%f emA B X基因%基因突变
重組溶葡萄毬菌酶%金黃色葡萄毬菌%誘導耐藥%f emA B X基因%基因突變
중조용포도구균매%금황색포도구균%유도내약%f emA B X기인%기인돌변
recombinant lysostaphin%Staphylococcus aureus%induced resistance%f emA BX gene%gene mutation
目的：探究重组溶葡萄球菌酶体外诱导金黄色葡萄球菌（金葡菌）耐药发生规律和机制。方法用3株临床分离金葡菌，体外以亚抑菌浓度重组溶葡萄球菌酶一步法诱导耐药，观察耐药株对多种抗菌药物的药敏改变情况，测序分析肽聚糖甘氨酸五肽桥联的关键合成酶编码基因 femABX。并观察其中1株耐甲氧西林金葡菌（MRSA）和1株甲氧西林敏感金葡菌（MSSA）的生长曲线、小鼠感染毒力情况。结果金葡菌耐药发生频率为10－4～10－8水平，与原代株比较，耐药株体外生长速率和小鼠体内毒力显著降低，对β内酰胺类敏感性提高2～4000倍。测序结果显示耐药株 f emA编码基因存在突变，可致终止密码子提前。结论重组溶葡萄球菌酶体外可诱导金葡菌耐药性产生，但耐药株生长繁殖力、致病力及抵抗β内酰胺类抗生素的能力显著降低。
目的：探究重組溶葡萄毬菌酶體外誘導金黃色葡萄毬菌（金葡菌）耐藥髮生規律和機製。方法用3株臨床分離金葡菌，體外以亞抑菌濃度重組溶葡萄毬菌酶一步法誘導耐藥，觀察耐藥株對多種抗菌藥物的藥敏改變情況，測序分析肽聚糖甘氨痠五肽橋聯的關鍵閤成酶編碼基因 femABX。併觀察其中1株耐甲氧西林金葡菌（MRSA）和1株甲氧西林敏感金葡菌（MSSA）的生長麯線、小鼠感染毒力情況。結果金葡菌耐藥髮生頻率為10－4～10－8水平，與原代株比較，耐藥株體外生長速率和小鼠體內毒力顯著降低，對β內酰胺類敏感性提高2～4000倍。測序結果顯示耐藥株 f emA編碼基因存在突變，可緻終止密碼子提前。結論重組溶葡萄毬菌酶體外可誘導金葡菌耐藥性產生，但耐藥株生長繁殖力、緻病力及牴抗β內酰胺類抗生素的能力顯著降低。
목적：탐구중조용포도구균매체외유도금황색포도구균（금포균）내약발생규률화궤제。방법용3주림상분리금포균，체외이아억균농도중조용포도구균매일보법유도내약，관찰내약주대다충항균약물적약민개변정황，측서분석태취당감안산오태교련적관건합성매편마기인 femABX。병관찰기중1주내갑양서림금포균（MRSA）화1주갑양서림민감금포균（MSSA）적생장곡선、소서감염독력정황。결과금포균내약발생빈솔위10－4～10－8수평，여원대주비교，내약주체외생장속솔화소서체내독력현저강저，대β내선알류민감성제고2～4000배。측서결과현시내약주 f emA편마기인존재돌변，가치종지밀마자제전。결론중조용포도구균매체외가유도금포균내약성산생，단내약주생장번식력、치병력급저항β내선알류항생소적능력현저강저。
Objective To investigate the phenotypic and genetic characteristics of the lysostaphin‐resistant Staphylococcus aureus variants induced by recombinant lysostaphin in vitro .Methods Three clinical isolates of S . aureus ,including two resistant to methicillin (MRSA ) and one susceptible to methicillin (MSSA ) were induced by treatment with sub‐MIC of recombinant lysostaphin via one‐step selection in vitro .Susceptibility of the variants to antibiotics were determined and compared with their parental strains .The full length of femABX genes was amplified by polymerase chain reaction and sequenced to identify the potential mutation sites in these genes .The growth‐curve in liquid medium and virulence in a mouse systemic infection model of both parental and variant strains were observed . Results The frequency of lysostaphin resistance in S . aureus was between 10-4 to 10-8 following induction by lysostaphin . Resistance to lysostaphin was associated with a significant decrease in growth rate in vitro and virulence in vivo ,as well as increased susceptibility toβ‐lactams evidenced by the M IC of β‐lactams against the variants as low as 1/4 000 to 1/2 of the M IC against their parental strains . Sequencing of f emA BX genes showed mutation in femA gene in both variants ,which resulted in a premature termination codon .Conclusions Resistance of S . aureus to lysostaphin may develop following induction by recombinant lysostaphin in vitro . The lysostaphin‐resistant S . aureus variants are characteristic of lower growth rate , decreased virulence ,and higher susceptibility to β‐lactams .
