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CARBAPENEM-RESISTANT ACINETOBACTER BAUMANNII FROM BRAZIL: ROLE OF CARO ALLELES EXPRESSION AND BLAOXA-23 GENE
Afiliación
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Genética Molecular de Microrganismos. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Genética Molecular de Microrganismos. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Genética Molecular de Microrganismos. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Maranhão. Departamento de Medicina 1. São Luis, MA, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Genética Molecular de Microrganismos. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Genética Molecular de Microrganismos. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Genética Molecular de Microrganismos. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Maranhão. Departamento de Medicina 1. São Luis, MA, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Genética Molecular de Microrganismos. Rio de Janeiro, RJ, Brasil.
Resumen en ingles
Background: Carbapenems are the antibiotics of choice to treat infections caused by Acinetobacter baumannii, and
resistance to this class can be determined by loss of membrane permeability and enzymatic mechanisms. Here, we
analyzed the basis of carbapenem resistance in clinical A. baumannii isolates from different Brazilian regions.
Results: The analyses addressed the carbapenemase activity of OXA-23, CarO expression and alterations in its primary
structure. Susceptibility test revealed that the strains presented the COS (Colistin-Only-Sensitive) profile. PCR and
sequencing showed the presence of the chromosomally-encoded blaOXA-51 in all isolates. The majority of strains (53%)
carried the carbapenemase blaOXA-23 gene associated with ISAba1. The Hodge test indicated that these strains are
carbapenemase producers. PFGE revealed 14 genotypes among strains from Rio de Janeiro and Maranhão. The
influence of carO on imipenem resistance was evaluated considering two aspects: the composition of the primary
amino acid sequence; and the expression level of this porin. Sequencing and in silico analyses showed the occurrence
of CarOa, CarOb and undefined CarO types, and Real Time RT-PCR revealed basal and reduced carO transcription levels
among isolates.
Conclusions: We concluded that, in general, for these Brazilian isolates, the major carbapenem resistance mechanism
was due to OXA-23 carbapenemase activity and that loss of CarO porin plays a minor role in this phenotype. However,
it was possible to associate the carO alleles and their expression with imipenem resistance. Therefore, these findings
underline the complexity in addressing the role of different mechanisms in carbapenem resistance and highlight the
possible influence of CarO type in this phenotype.
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