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Detection of P. aeruginosa harboring bla CTX-M-2, bla GES-1 and bla GES-5, bla IMP-1 and bla SPM-1causing infections in Brazilian tertiary-care hospital
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Abstract
Background
Nosocomial infections caused by
Pseudomonas aeruginosa
presenting resistance to beta-lactam drugs are one of the most challenging targets for antimicrobial therapy, leading to substantial increase in mortality rates in hospitals worldwide. In this context,
P. aeruginosa
harboring acquired mechanisms of resistance, such as production of metallo-beta-lactamase (MBLs) and extended-spectrum beta-lactamases (ESBLs) have the highest clinical impact. Hence, this study was designed to investigate the presence of genes codifying for MBLs and ESBLs among carbapenem resistant
P. aeruginosa
isolated in a Brazilian 720-bed teaching tertiary care hospital.
Methods
Fifty-six carbapenem-resistant
P. aeruginosa
strains were evaluated for the presence of MBL and ESBL genes. Strains presenting MBL and/or ESBL genes were submitted to pulsed-field gel electrophoresis for genetic similarity evaluation.
Results
Despite the carbapenem resistance, genes for MBLs (
bla
SPM-1
or
bla
IMP-1
) were detected in only 26.7% of isolates. Genes encoding ESBLs were detected in 23.2% of isolates. The
bla
CTX-M-2
was the most prevalent ESBL gene (19.6%), followed by
bla
GES-1
and
bla
GES-5
detected in one isolate each. In all isolates presenting MBL phenotype by double-disc synergy test (DDST), the
bla
SPM-1
or
bla
IMP-1
genes were detected. In addition,
bla
IMP-1
was also detected in three isolates which did not display any MBL phenotype. These isolates also presented the
bla
CTX-M-2
gene. The co-existence of
bla
CTX-M-2
with
bla
IMP-1
is presently reported for the first time, as like as co-existence of
bla
GES-1
with
bla
IMP-1
.
Conclusions
In this study MBLs production was not the major mechanism of resistance to carbapenems, suggesting the occurrence of multidrug efflux pumps, reduction in porin channels and production of other beta-lactamases. The detection of
bla
CTX-M-2,
bla
GES-1
and
bla
GES-5
reflects the recent emergence of ESBLs among antimicrobial resistant
P. aeruginosa
and the extraordinary ability presented by this pathogen to acquire multiple resistance mechanisms. These findings raise the concern about the future of antimicrobial therapy and the capability of clinical laboratories to detect resistant strains, since simultaneous production of MBLs and ESBLs is known to promote further complexity in phenotypic detection. Occurrence of intra-hospital clonal dissemination enhances the necessity of better observance of infection control practices.
Springer Science and Business Media LLC
Title: Detection of P. aeruginosa harboring bla
CTX-M-2, bla
GES-1 and bla
GES-5,
bla
IMP-1 and bla
SPM-1causing infections in Brazilian tertiary-care hospital
Description:
Abstract
Background
Nosocomial infections caused by
Pseudomonas aeruginosa
presenting resistance to beta-lactam drugs are one of the most challenging targets for antimicrobial therapy, leading to substantial increase in mortality rates in hospitals worldwide.
In this context,
P.
aeruginosa
harboring acquired mechanisms of resistance, such as production of metallo-beta-lactamase (MBLs) and extended-spectrum beta-lactamases (ESBLs) have the highest clinical impact.
Hence, this study was designed to investigate the presence of genes codifying for MBLs and ESBLs among carbapenem resistant
P.
aeruginosa
isolated in a Brazilian 720-bed teaching tertiary care hospital.
Methods
Fifty-six carbapenem-resistant
P.
aeruginosa
strains were evaluated for the presence of MBL and ESBL genes.
Strains presenting MBL and/or ESBL genes were submitted to pulsed-field gel electrophoresis for genetic similarity evaluation.
Results
Despite the carbapenem resistance, genes for MBLs (
bla
SPM-1
or
bla
IMP-1
) were detected in only 26.
7% of isolates.
Genes encoding ESBLs were detected in 23.
2% of isolates.
The
bla
CTX-M-2
was the most prevalent ESBL gene (19.
6%), followed by
bla
GES-1
and
bla
GES-5
detected in one isolate each.
In all isolates presenting MBL phenotype by double-disc synergy test (DDST), the
bla
SPM-1
or
bla
IMP-1
genes were detected.
In addition,
bla
IMP-1
was also detected in three isolates which did not display any MBL phenotype.
These isolates also presented the
bla
CTX-M-2
gene.
The co-existence of
bla
CTX-M-2
with
bla
IMP-1
is presently reported for the first time, as like as co-existence of
bla
GES-1
with
bla
IMP-1
.
Conclusions
In this study MBLs production was not the major mechanism of resistance to carbapenems, suggesting the occurrence of multidrug efflux pumps, reduction in porin channels and production of other beta-lactamases.
The detection of
bla
CTX-M-2,
bla
GES-1
and
bla
GES-5
reflects the recent emergence of ESBLs among antimicrobial resistant
P.
aeruginosa
and the extraordinary ability presented by this pathogen to acquire multiple resistance mechanisms.
These findings raise the concern about the future of antimicrobial therapy and the capability of clinical laboratories to detect resistant strains, since simultaneous production of MBLs and ESBLs is known to promote further complexity in phenotypic detection.
Occurrence of intra-hospital clonal dissemination enhances the necessity of better observance of infection control practices.
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