Biendo Maurice, Laurans Geneviève, Thomas Danièle, Canarelli Brigitte, Hamdad-Daoudi Farida, Rousseau Florence, Castelain Sandrine, Eb François
Laboratoire de Bactériologie et Hygiène, CHU Nord, Place Victor Pauchet, 80054 Amiens, Cedex 1, France.
Int J Antimicrob Agents. 2005 Sep;26(3):219-29. doi: 10.1016/j.ijantimicag.2005.05.003.
Antimicrobial resistance patterns of Salmonella enterica serovar Typhimurium isolates obtained during the study period were examined. The molecular epidemiology and the mechanisms of resistance to ampicillin, chloramphenicol and tetracycline were investigated. Resistance to ampicillin increased from 59% between 1996 and 1999 to 62.5% in 2000 and to 66.6% in 2001. Of 51 S. Typhimurium isolates studied, 100% were resistant to ampicillin (minimum inhibitory concentration (MIC)>256 mg/L) and sulphonamide (MIC range, 128 to >256 mg/L). Ninety-eight percent of isolates were resistant to streptomycin (MIC range, 48-256 mg/L), 92.2% to tetracycline (MIC range, 32 to >256 mg/L), 88.2% to chloramphenicol (MIC>256 mg/L), 21.5% to sulphamethoxazole/trimethoprim (MIC>32 mg/L), 5.8% to amoxicillin/clavulanic acid (MIC, 32 mg/L) and 1.9% to cefalothin (MIC, 64mg/L). Six resistance phenotypes were found (a-f), with phenotypes a (47%) and b (27.5%) being predominant. Twenty-five (49%) of 51 isolates produced a single beta-lactamase, among which 48% produced PSE-1, 44% produced TEM-1 and 8% produced OXA-1. Among 26 of the 51 isolates, 10 produced PSE-1+OXA-1, 7 produced TEM-1+PSE-1+OXA-1, 6 produced TEM-1+PSE-1, and 3 produced TEM-1+OXA-1. Forty-eight (94.1%) of the 51 isolates had the plasmid-mediated resistance gene flo(ST) to chloramphenicol and tetracycline. Combining enterobacterial repetitive intergenic consensus polymerase chain reaction (ERIC-PCR) and pulsed-field gel electrophoresis (PFGE), 16 distinct patterns were identified, among which patterns IA (35.3%) and IF (27.4%) were considered as epidemic patterns. The dendrogram obtained from S. Typhimurium pulsotypes allowed five clones (S1-S5) to be identified, with two prevalent clones comprising 47.8% (S2) and 27.3% (S4) of the isolates.
对研究期间获得的肠炎沙门氏菌鼠伤寒血清型分离株的抗菌药物耐药模式进行了检测。研究了其分子流行病学以及对氨苄西林、氯霉素和四环素的耐药机制。对氨苄西林的耐药率从1996年至1999年期间的59%上升至2000年的62.5%，并在2001年达到66.6%。在所研究的51株鼠伤寒沙门氏菌分离株中，100%对氨苄西林（最低抑菌浓度（MIC）>256mg/L）和磺胺类药物（MIC范围为128至>256mg/L）耐药。98%的分离株对链霉素（MIC范围为48 - 256mg/L）耐药，92.2%对四环素（MIC范围为32至>256mg/L）耐药，88.2%对氯霉素（MIC>256mg/L）耐药，21.5%对磺胺甲恶唑/甲氧苄啶（MIC>32mg/L）耐药，5.8%对阿莫西林/克拉维酸（MIC为32mg/L）耐药，1.9%对头孢噻吩（MIC为64mg/L）耐药。发现了六种耐药表型（a - f），其中表型a（47%）和b（27.5%）占主导。51株分离株中有25株（49%）产生单一的β-内酰胺酶，其中48%产生PSE - 1，44%产生TEM - 1，8%产生OXA - 1。在51株分离株中的26株中，10株产生PSE - 1 + OXA - 1，7株产生TEM - 1 + PSE - 1 + OXA - 1，6株产生TEM - 1 + PSE - 1，3株产生TEM - 1 + OXA - 1。51株分离株中有48株（94.1%）具有质粒介导的对氯霉素和四环素的耐药基因flo(ST)。结合肠杆菌重复基因间共有序列聚合酶链反应（ERIC - PCR）和脉冲场凝胶电泳（PFGE），鉴定出16种不同的模式，其中模式IA（35.3%）和IF（27.4%）被认为是流行模式。从鼠伤寒沙门氏菌脉冲型获得的树状图允许鉴定出五个克隆（S1 - S5），其中两个流行克隆分别占分离株的47.8%（S2）和27.3%（S4）。
