Dubois Véronique, Arpin Corinne, Dupart Virginie, Scavelli Aline, Coulange Laure, André Catherine, Fischer Isabelle, Grobost Frédéric, Brochet Jean-Philippe, Lagrange Isabelle, Dutilh Brigitte, Jullin Jacqueline, Noury Patrick, Larribet Gilberte, Quentin Claudine
UMR 5234, CNRS, Université de Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux, France.
J Antimicrob Chemother. 2008 Aug;62(2):316-23. doi: 10.1093/jac/dkn174. Epub 2008 May 8.
The aim of this study was to assess antibiotic resistance rates and mechanisms of beta-lactam and aminoglycoside resistance among isolates of Pseudomonas aeruginosa isolated in the extra-hospital setting (community and private healthcare centres).
During a 4 month period, 226 non-repetitive strains of P. aeruginosa were collected from patients residing in private healthcare centres (73.5%) or at home (26.5%). Resistance rates were evaluated by MIC determination, and beta-lactam and aminoglycoside resistance was analysed by phenotypic tests, PCR amplification, cloning and sequencing.
Among the ticarcillin-resistant strains (38.1%), 33.7% overexpressed their chromosomal cephalosporinase, 27.9% produced acquired penicillinases (21 PSE-1, 2 OXA-21 and 1 TEM-2), 4.7% produced extended-spectrum beta-lactamases (ESBLs) (3 TEM-21 and 1 SHV-2a) and 45.3% possessed a non-enzymatic resistance (NER). Thus, 88.4% had a single mechanism of resistance, whereas 11.6% cumulated several mechanisms. No carbapenemases were detected among the 6.6% imipenem-resistant strains. With regard to aminoglycosides, 23.0% of the strains exhibited an acquired resistance to gentamicin (GEN), tobramycin (TOB), amikacin (AMK) or netilmicin (NET). Enzymatic resistance was more frequent (71.2%) than NER (34.6%). Various aminoglycoside modifying enzymes were associated with overlapping phenotypes: 36.5% strains produced AAC(6')-I with either a serine (GEN-TOB-NET) or a leucine (TOB-NET-AMK) at position 119, or both variants (GEN-TOB-NET-AMK); 21.2% expressed ANT(2'')-I (GEN-TOB), 7.7% AAC(3)-II (GEN-TOB-NET), 5.8% AAC(3)-I (GEN) and 1.9% AAC(6')-II (GEN-TOB-NET-AMK) or AACA7 (TOB-NET-AMK).
Antibiotic resistance rates in P. aeruginosa were globally similar in general practice as in French hospitals. This first analysis of resistance mechanisms showed an unexpectedly high frequency of ESBLs and an unusual distribution of aminoglycoside modifying enzymes.
本研究旨在评估在院外环境(社区和私立医疗中心)分离出的铜绿假单胞菌菌株中β-内酰胺类和氨基糖苷类抗生素的耐药率及耐药机制。
在4个月的时间里,从私立医疗中心(73.5%)或家中(26.5%)居住的患者中收集了226株非重复的铜绿假单胞菌菌株。通过测定最低抑菌浓度(MIC)评估耐药率,并通过表型试验、聚合酶链反应(PCR)扩增、克隆和测序分析β-内酰胺类和氨基糖苷类抗生素的耐药情况。
在对替卡西林耐药的菌株(38.1%)中,33.7%的菌株染色体头孢菌素酶过度表达,27.9%的菌株产生获得性青霉素酶(21株PSE-1、2株OXA-21和1株TEM-2),4.7%的菌株产生超广谱β-内酰胺酶(ESBLs)(3株TEM-21和1株SHV-2a),45.3%的菌株具有非酶促耐药性(NER)。因此,88.4%的菌株具有单一耐药机制,而11.6%的菌株累积了多种耐药机制。在6.6%对亚胺培南耐药的菌株中未检测到碳青霉烯酶。关于氨基糖苷类抗生素,23.0%的菌株对庆大霉素(GEN)、妥布霉素(TOB)、阿米卡星(AMK)或奈替米星(NET)表现出获得性耐药。酶促耐药比NER更常见(71.2%比34.6%)。各种氨基糖苷类修饰酶与重叠的表型相关:36.5%的菌株产生AAC(6')-I,在第119位有丝氨酸(GEN-TOB-NET)或亮氨酸(TOB-NET-AMK),或两种变体(GEN-TOB-NET-AMK);21.2%表达ANT(2'')-I(GEN-TOB),7.7%表达AAC(3)-II(GEN-TOB-NET),5.8%表达AAC(3)-I(GEN),1.9%表达AAC(6')-II(GEN-TOB-NET-AMK)或AACA7(TOB-NET-AMK)。
在一般医疗实践中,铜绿假单胞菌的抗生素耐药率与法国医院总体相似。对耐药机制的首次分析显示ESBLs的频率意外地高,且氨基糖苷类修饰酶的分布异常。