How CORE-ABR grades it
No clinically relevant intrinsic resistance beyond the agents all gram-negative organisms resist (glycopeptides, oxazolidinones, daptomycin, clindamycin). Its grid is shaped mostly by detected genes — beta-lactamases, plasmid quinolone resistance and folate-pathway genes.
What the report shows for Escherichia coli
- Detected or not detected, with Ct, limit of detection and cycles above LOD — see PCR reporting.
- A short pathogen summary, including colonizer likelihood where it applies.
- A graded column on the antibiogram, and therapy options by scenario on the P.A.C.T. report.
- When not detected, it is still listed among targets tested.
Resistance genes CORE-ABR applies
When detected, each of these genes is applied to Escherichia coli only for the agents its mechanism defeats.
Class A beta-lactamase (CTX-M)Extended-spectrum beta-lactamase (ESBL) production6 organisms on panelClass A beta-lactamase (KPC / SHV)Carbapenemase (KPC) or ESBL (SHV variants) production5 organisms on panelClass C beta-lactamase (AmpC)AmpC cephalosporinase production5 organisms on panelClass D beta-lactamase (OXA)Oxacillinase production4 organisms on panelClass B metallo-beta-lactamase (IMP / VIM)Metallo-carbapenemase production5 organisms on panelqnrA / qnrBPlasmid-mediated quinolone resistance7 organisms on panelqnrSPlasmid-mediated quinolone resistance3 organisms on paneldfrA1 / dfrA5Trimethoprim resistance6 organisms on panelsul1 / sul2Sulfonamide resistance6 organisms on panel
Tagged
Decision support only. The treating clinician decides. Molecular genotype does not replace phenotypic susceptibility testing, culture, or public-health reporting. Absence of a detected resistance gene does not establish susceptibility. Organism targets vary by panel; CORE-ABR is configured to the assay each laboratory runs.