Journal of Antimicrobial Chemotherapy (2002) 49, 289-300
© 2002 The British Society for Antimicrobial Chemotherapy
Multicentre evaluation of the VITEK 2 Advanced Expert System for interpretive reading of antimicrobial resistance tests
a Antibiotic Resistance Monitoring & Reference Laboratory, Central Public Health Laboratory, 61 Colindale Avenue, London NW9 5HT, UK; b Université Libre de Bruxelles, Hôpital Erasme, Route de Lennik 808, Bruxelles 1070, Belgium; c Hospital Geral Santo Antonio, Serviço Microbiologia, Largo Pr. Abel Salazar, Oporto 4099-00, Portugal; d Hospital Ramon y Cajal, Servicio de Microbiologia, Carretera De Colmenar KM 9.1, Madrid 28034, Spain; e Institut de Microbiologie, CHUV, BH 19 Sud, Rue de Bugnon 44, Lausanne 1011, Switzerland; f Institut für Med. Mikrobiologie, Westrin 28–30, 44777 Bochum 44780, Germany; g Istituto di Microbiologia, Largo R. Benzi, 10, 16132 Genoa, Italy; h Krankenhaus der Elisabethinen, Fadinger Str. 1, Linz 4010, Austria; i Laboratory of Bacteriology, University Hospital Gasthuisberg, Herestraat 49, 3000 Leuven, Belgium; j Academic Hospital, Heidelberglaan 100, Utrecht 3584 CX, The Netherlands
Interpretive reading analyses the complete resistance profiles of bacteria to multiple antibiotics and infers the resistance mechanisms present; it aids therapeutic choice and enhances surveillance data. We evaluated the Advanced Expert System (AES), which interprets MICs generated by the VITEK 2. Ten European laboratories tested 42 reference strains and 76–106 of their own strains, representing important resistance genotypes. Interpretive reading by the VITEK 2 AES achieved full agreement with genotype data for 88–89% of strains, with the correct mechanism identified as one of two possibilities for a further 5–6%. Mechanisms inferred with 90% agreement with reference data included methicillin resistance in staphylococci, glycopeptide resistance in enterococci, quinolone resistance in staphylococci and Enterobacteriaceae, AAC(6')-APH(2'')-mediated aminoglycoside resistance in Gram-positive cocci, erm-mediated macrolide resistance in pneumococci, extended-spectrum ß-lactamases (ESBLs) in Enterobacteriaceae and Pseudomonas aeruginosa, and acquired penicillinases in Enterobacteriaceae. VanA, VanB and VanC phenotypes of enterococci were distinguished reliably, and ESBL production was accurately inferred in AmpC-inducible species as well as Escherichia coli and Klebsiella spp. Mechanisms identified, but only as possibilities among several, included IRT-type ß-lactamases and individual aminoglycoside-modifying enzymes in Enterobacteriaceae. Most disagreements with reference data concerned pneumococci found to have high-level penicillin resistance by the VITEK 2 AES but previously determined, phenotypically, to have intermediate resistance. When ESBL production was inferred in E. coli and klebsiellae, the VITEK 2 AES edited susceptible results for cephalosporins (except cefoxitin) to resistant; when an acquired penicillinase was inferred in Enterobacteriaceae, piperacillin results were edited to resistant; and when staphylococci were found methicillin resistant, resistance was reported for all ß-lactams. Further editing may be desirable (e.g. of cephalosporin results for salmonellas inferred to have ESBLs).
* Corresponding author: Tel +44-20-8200-4400; Fax +44-20-8358-3292; E-mail: DLivermore{at}phls.nhs.uk
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