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The GES carbapenemase (qPCR) product is used to determine the sequence of genes encoding GES carbapenemases in DNA preparations obtained from human material.
Kit size: 100 markers
Reaction: duplex (FAM: GES-type carbapenemases, HEX: internal control)
Internal control: exogenous/endogenous
Determination: qualitative/quantitative
Kit components:
The most common mechanism of resistance of Enterobacterales to carbapenems is the production of carbapenemases, which mainly include KPC, NDM, VIM, IMP, and OXA-48-like. Most of them are encoded on plasmids. Therefore, carbapenem resistance genes spread easily through horizontal gene transfer. Another less common mechanism of carbapenem resistance is the combination of extended-spectrum beta-lactamase (ESBL) or AmpC expression and porin loss or overexpression of efflux pumps. Carbapenem-resistant Enterobacterales (CRE) resulting from the first mechanism are referred to as carbapenemase-producing CRE (CP-CRE). Carbapenem-resistant Enterobacterales resulting from the second mechanism are referred to as non-carbapenemase-producing CRE (non-CP-CRE).
GES carbapenemases belong to a broader group of enzymes known as class A β-lactamases. GES carbapenemase was first described in France in 1998 in a Klebsiella pneumoniae isolate producing GES-1, an extended-spectrum β-lactamase that confers resistance to penicillin and cephalosporins. The genes encoding GES are transferred between genera and species through horizontal transfer. They are now increasingly reported in Gram-negative bacilli, including Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacterales. GES β-lactamases confer resistance to β-lactams, but not all variants exhibit carbapenemase activity. Although GES β-lactamases are relatively rare, GES-producing microorganisms have emerged in many geographical areas, causing outbreaks of hospital-acquired infections.
