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Clin Microbiol Infect ; 14 Suppl 1: 53-62, 2008 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-18154528

RESUMO

Acquired resistance to penicillin-beta-lactamase inhibitor combinations in Escherichia coli is due to: (i) penicillinase hyperproduction due to the presence of the bla(TEM-1) gene in small multicopy plasmids or strong promoters; (ii) overproduction of constitutive AmpC cephalosporinase; and (iii) OXA-type and inhibitor-resistant TEM (IRT) beta-lactamases. IRT enzymes emerge via mutational events from TEM-1 or TEM-2 beta-lactamases that affect substrate affinity for beta-lactamase inhibitors. They are mainly isolated in urinary infections from community patients. Prevalence is variable, depending on geographical area, detection methods and potential selection pressure. These enzymes may evolve into complex mutants (CMT enzymes), which also confer resistance to extended-spectrum cephalosporins. CTX-M enzymes with the IRT phenotype have not been detected to date. New studies of IRT enzymes, including population structure, association with virulence traits and plasmid dispersion, are needed.


Assuntos
Substituição de Aminoácidos , Inibidores Enzimáticos/farmacologia , Bactérias Gram-Negativas/enzimologia , Inibidores de beta-Lactamases , beta-Lactamases/genética , Inibidores Enzimáticos/química , Bactérias Gram-Negativas/efeitos dos fármacos , Infecções por Bactérias Gram-Negativas/microbiologia , Humanos , Infecções Urinárias/microbiologia , Resistência beta-Lactâmica , beta-Lactamases/química , beta-Lactamases/farmacologia , beta-Lactamas/farmacologia
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