Multicentre evaluation of the VITEK 2 Advanced Expert System for interpretive reading of antimicrobial resistance tests

• Published in: Journal of antimicrobial chemotherapy Vol. 49; no. 2; pp. 289 - 300
• Main Authors: Livermore, D. M., Struelens, M., Amorim, J., Baquero, F., Bille, J., Canton, R., Henning, S., Gatermann, S., Marchese, A., Mittermayer, H., Nonhoff, C., Oakton, K. J., Praplan, F., Ramos, H., Schito, G. C., Van Eldere, J., Verhaegen, J., Verhoef, J., Visser, M. R.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.02.2002; Oxford Publishing Limited (England)
• Subjects: Antibacterial agents; Antibiotics. Antiinfectious agents. Antiparasitic agents; Biological and medical sciences; Data Interpretation, Statistical; Drug Resistance, Multiple, Bacterial - genetics; Humans; Medical sciences; Microbial Sensitivity Tests - instrumentation; Microbial Sensitivity Tests - methods; Microbial Sensitivity Tests - statistics & numerical data; Pharmacology. Drug treatments; Europe; Enterococcus; Human; Automated equipment; Multicenter study; Instrumentation; Genotype; In vitro; Biological activity; Staphylococcus; Resistance; Streptococcaceae; Sensitivity resistance; Streptococcus; Investigation method; Bacteria; Micrococcales; Micrococcaceae; Antibacterial agent; Mechanism of action; Clinical isolate; Enterobacteriaceae
• ISSN: 0305-7453; 1460-2091; 1460-2091
• DOI: 10.1093/jac/49.2.289

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 β-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 β-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 β-lactams. Further editing may be desirable (e.g. of cephalosporin results for salmonellas inferred to have ESBLs).