Bacterial Epidemiology and Antimicrobial Resistance Research Unit, Richard B. Russell Agricultural Research Center, Agricultural Research Service, U.S. Department of Agriculture, Athens, Georgia 30605-2720, USA.
Foodborne Pathog Dis. 2009 Jan-Feb;6(1):91-8. doi: 10.1089/fpd.2008.0098.
The genetic basis of macrolide resistance in Campylobacter coli (n = 17) and C. jejuni (n = 35) isolates previously subjected to in vivo selective pressure was investigated to determine if the number of copies of 23S rRNA genes with macrolide-associated mutations affects the minimum inhibitory concentration (MIC) of macrolides. Sequence data for domain V of the 23S rRNA gene revealed that two macrolide-resistant C. coli isolates had adenine-->guanine transitions at position 2059 (A2059G, Escherichia coli numbering). One of the two isolates had the A2059G transition in only two of the three gene copies. Among the macrolide-resistant C. jejuni isolates (n = 9), two different point mutations within domain V were observed. Three macrolide-resistant C. jejuni isolates had A2059G transitions. One of these three C. jejuni isolates had the A2059G transition in only two of the three gene copies. Six macrolide-resistant C. jejuni isolates had an adenine-->cytosine transversion at position 2058 (A2058C, E. coli numbering) in all three copies of the 23S rRNA gene. Campylobacter jejuni isolates with the A2058C transversion had higher erythromycin MICs (>256 microg/mL) compared to C. jejuni isolates with A2059G transitions (64-128 microg/mL). In addition, the C. jejuni and C. coli isolates with only two copies of the 23S rRNA gene having A2059G substitutions had lower macrolide MICs compared to isolates with all three copies of the gene mutated. No isolates were observed having only one copy of the 23S rRNA gene with a mutation. Sequence analysis of ribosomal proteins L4 (rplD) and L22 (rplV) indicated that ribosomal protein modifications did not contribute to macrolide resistance among the collection of Campylobacter examined.
先前经体内选择压力处理的 17 株大肠弯曲杆菌（coli）和 35 株空肠弯曲杆菌（jejuni）分离株的大环内酯类耐药的遗传基础，以确定 23S rRNA 基因与大环内酯类相关突变的基因数量是否影响大环内酯类的最低抑菌浓度（MIC）。23S rRNA 基因 V 结构域的序列数据表明，2 株大环内酯类耐药的 coli 分离株在位置 2059 有腺嘌呤（A）到鸟嘌呤（G）的转换（E.coli 编号）。这 2 个分离株中，有 1 个分离株只有 3 个基因拷贝中的 2 个有 A2059G 转换。在 9 株大环内酯类耐药的 jejuni 分离株中，观察到 V 结构域内有两个不同的点突变。3 株大环内酯类耐药的 jejuni 分离株有 A2059G 转换。其中 1 个分离株只有 3 个基因拷贝中的 2 个有 A2059G 转换。6 株大环内酯类耐药的 jejuni 分离株在 23S rRNA 基因的所有 3 个拷贝中，在位置 2058 有腺嘌呤（A）到胞嘧啶（C）的颠换（E.coli 编号）。2058 位 A 到 C 颠换的 jejuni 分离株与 2059 位 A 到 G 转换的 jejuni 分离株（64-128 微克/毫升）相比，红霉素 MIC 较高（>256 微克/毫升）。此外，23S rRNA 基因只有 2 个拷贝有 A2059G 取代的 jejuni 和 coli 分离株与所有 3 个拷贝基因都突变的分离株相比，具有较低的大环内酯类 MIC。没有分离株只观察到 23S rRNA 基因的一个拷贝发生突变。核糖体蛋白 L4（rplD）和 L22（rplV）的序列分析表明，在所研究的弯曲杆菌集合中，核糖体蛋白修饰并未导致大环内酯类耐药。
