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胸膜肺炎放線桿菌第一血清型之質體與其抗藥性之研究

Studies on Plasmid-mediated Drug Resistance of Actinobacillus Pleuropneumoniae Serotype 1

摘要


自胸膜肺炎放線桿茵第一血清型(Actinobacillus pleuropneumoniae, Serotype 1, 簡稱AP-1)可分離並純化出一質體(plasmid, pC30),該質體pC30為5Kb並攜帶有抗氯黴素之基因,其氯黴素之最低抑菌濃度(MIC)為170μg/mL,pC30可轉殖至E. coli HB 101且呈現抗氯黴素之特性,因此,具有可轉殖性(Transferable)。無論AP-1或轉殖後的E. coli HB 101均能被檢出有CAT(chloramphenicol acetyltransferase)之存在,此為菌體抗氯黴素之機制。另者,本試驗結果分離到AP-1抗Flumequme之菌株,其Flumequine之最低抑菌濃度(MIC)為100μg/mL,其抗藥性與質體無關,試驗結果獲知抗Flumequine的菌株其質體被翦除後仍具有抗Flumequine之特性,因此,抗Flumequine的基因應存在於細菌之菌體染色體中而並非在質體。

並列摘要


A plasmid, pC30 which was associated with resistance to chloramphenicol, was isolated from Actinobacillus pleuropneumoniae type 1 (AP-1). The plasmid, pC30, was 5kb in size and could be transferrable to E. coli HB101 which was originally sensitive to chloramphenicol before transformation with this plasmid, pC30. However, the minimum inhibitory concentration (MIC) was 170 μg/mL for cholramphenicol. Both AP-1 and transformant E. coli HB101 had CAT (chloramphenicol acetyltransferase) when tested with ELISA-CAT assay. Thus, it was concluded that resistance to chloramphenicol is mediated by the plasmid pC30, in Actinobacillus pleuropneumoniae type 1. Moreover, three isolates of AP-1 were isolated and were resistant to flumequine. The MIC was 100 μg/mL for flumequine. It revealed that no plasmid showed evidence of the resistance to flumequine when plasmid curing technique was employed for the test of drug sensitivity. The gene of resistance to flumequine in Actinobacillus pleuropneumoniae serotype 1 should exist in genomic DNA rather than in plasmid.

被引用紀錄


楊忠祥(2008)。桃園北區豬隻內寄生蟲相之調查研究〔碩士論文,國立臺灣大學〕。華藝線上圖書館。https://doi.org/10.6342/NTU.2008.02376

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