JAC Advance Access originally published online on May 8, 2008
Journal of Antimicrobial Chemotherapy 2008 62(2):316-323; doi:10.1093/jac/dkn174
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Original research |
β-Lactam and aminoglycoside resistance rates and mechanisms among Pseudomonas aeruginosa in French general practice (community and private healthcare centres)
1 UMR 5234, CNRS, Université de Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux, France 2 Laboratoire d'Analyses Médicales (LAM), 17 allées de Tourny, 33000 Bordeaux, France 3 LAM, av. du 11 novembre, 64100 Bayonne, France 4 LAM, 114 av. Arès, 33000 Bordeaux, France 5 LAM, Ma campagne Mas de Pierre Levée, 16000 Angoulême, France 6 LAM, 190 crs St Louis, 33300 Bordeaux, France 7 LAM, ZI Dumes, 33000 Bordeaux, France 8 LAM, 64 av. des Pyrénées, 33140 Villenave d'Ornon, France 9 LAM, 89 av. JJ Rousseau, 33160 St Médard-en-Jalles, France
Received 30 January 2008; returned 10 March 2008; revised 28 March 2008; accepted 29 March 2008
* Corresponding author. Tel: +33-5-57-57-10-75; Fax: +33-5-56-90-90-72; E-mail: veronique.dubois{at}bacterio.u-bordeaux2.fr
Objectives: The aim of this study was to assess antibiotic resistance rates and mechanisms of β-lactam and aminoglycoside resistance among isolates of Pseudomonas aeruginosa isolated in the extra-hospital setting (community and private healthcare centres).
Patients and methods: 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 β-lactam and aminoglycoside resistance was analysed by phenotypic tests, PCR amplification, cloning and sequencing.
Results: 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 β-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).
Conclusions: 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.
Keywords: cephalosporinase , penicillinase , extended-spectrum β-lactamase , aminoglycoside modifying enzymes , non-enzymatic resistance mechanism