molecular panel

Antibiotic resistance profile

Also known as ABR, resistance panel

Specification

Method: qPCR — CORE-ABR molecular panel Real-time polymerase chain reaction
Add-on to: 4 molecular panels

Reporting

Reported through CORE-ABR

PACT — Pathogen Assessment & Clinical Treatment

Molecular results do not leave this laboratory as a list of organisms and genes. Every specimen on this platform is reported through CORE-ABR, which quantifies each organism detected, maps every detected resistance gene to the agents it removes, encodes intrinsic resistance per organism, and marks agents that do not apply to the specimen site rather than listing them. Targets tested and not detected are reported alongside those that were.

3 pages, one report: Assessment and therapy · Full antibiogram · Molecular detail

The antibiogram is derived from the organisms and resistance genes detected, the intrinsic biology of those organisms, and the specimen site. It is not phenotypic susceptibility testing: a detected gene predicts resistance, but the absence of a detected gene does not establish susceptibility. Full method limitations.

Resistance genes 13

Every resistance marker on the panel acts through one of five mechanisms: enzymatic destruction of the drug, replacement of its target, chemical modification of the target, protection of the target or efflux of the drug, and bypass of the targeted enzyme by a drug-insensitive copy. Each mechanism is listed with the gene channels that report it and the drug classes at stake. — Every marker on this panel acts through one of five mechanisms.

Gene	Predicts	Agents affected
`mecA / mecC`	Methicillin resistance (MRSA)	Antistaphylococcal penicillins and most cephalosporins; ceftaroline retains activity
`vanA / vanB`	Vancomycin resistance	Vancomycin and related glycopeptides
`tetB / tetM`	Tetracycline resistance	Doxycycline and minocycline; omadacycline and tigecycline were designed to evade this mechanism and retain activity
`ermB / ermC`	MLSb resistance	Macrolides, lincosamides (clindamycin), and streptogramin B
`dfrA1 / dfrA5`	Trimethoprim resistance	Trimethoprim and TMP-SMX
`sul1 / sul2`	Sulfonamide resistance	Sulfonamides
`qnrA / qnrB`	Quinolone resistance	Fluoroquinolones
`qnrS`	Quinolone resistance	Fluoroquinolones
`Class A beta-lactamase (CTX-M)`	Extended-spectrum beta-lactamase production	Penicillins and most cephalosporins
`Class A beta-lactamase (KPC / SHV)`	Carbapenemase or ESBL production	Penicillins, cephalosporins, and (KPC) carbapenems
`Class C beta-lactamase (AmpC)`	AmpC cephalosporinase production	Penicillins, cephamycins, and most cephalosporins
`Class D beta-lactamase (OXA)`	Oxacillinase production	Penicillins; some variants hydrolyze carbapenems
`Class B metallo-beta-lactamase (IMP / VIM)`	Metallo-carbapenemase production	Most beta-lactams including carbapenems; aztreonam is spared

Detection of a resistance gene predicts resistance. Absence of a detected gene does not establish susceptibility — resistance arises through mechanisms outside the target set, including efflux and porin changes. Molecular detection does not replace phenotypic susceptibility testing.

Beta-lactamases form a ladder in which each step up hydrolyses more of the beta-lactam class. From the top: metallo-beta-lactamases of Ambler class B are the broadest, followed by Ambler class A serine carbapenemases such as KPC, then OXA-48-like class D enzymes, then AmpC cephalosporinases of class C, then extended-spectrum beta-lactamases of the CTX-M family, and at the bottom narrow penicillinases. Each rung lists the drug classes lost and those spared at the enzyme level, with the panel channel that reports it. — The beta-lactamase ladder — each step up hydrolyses more of the class.