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The IMI carbapenemase (qPCR) product is used to determine the sequence of genes encoding IMI carbapenemases in DNA preparations obtained from human material.
Kit size: 100 markers
Reaction: duplex (FAM: IMI group 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).
IMI carbapenemases (β-lactamases that hydrolyze imipenem, imipenemases) together with NMC-A carbapenemases (“non-metallo” carbapenemases A) belong to the IMI/NMCA subgroup of class A carbapenemases (β-lactamases). The first Enterobacter cloacae isolate producing IMI-1 was collected in 1984 in the USA. The imipenem-resistant phenotype preceded the clinical use of imipenem, as this drug was first approved for clinical use in the United States in 1985. This suggests that the clinical use of imipenem was not responsible for the evolution of class A carbapenemases. These enzymes were likely present in bacteria long before the widespread use of imipenem in the treatment of bacterial infections.
