Detection of P. aeruginosa harboring blaCTX-M-2, blaGES-1 and blaGES-5,blaIMP-1 and blaSPM-1causing infections in Brazilian tertiary-care hospital
verfasst von:
Milena Polotto, Tiago Casella, Maria Gabriela de Lucca Oliveira, Fernando G Rúbio, Mauricio L Nogueira, Margarete TG de Almeida, Mara CL Nogueira
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 (blaSPM-1 or blaIMP-1) were detected in only 26.7% of isolates. Genes encoding ESBLs were detected in 23.2% of isolates. The blaCTX-M-2 was the most prevalent ESBL gene (19.6%), followed by blaGES-1 and blaGES-5 detected in one isolate each. In all isolates presenting MBL phenotype by double-disc synergy test (DDST), the blaSPM-1 or blaIMP-1 genes were detected. In addition, blaIMP-1 was also detected in three isolates which did not display any MBL phenotype. These isolates also presented the blaCTX-M-2 gene. The co-existence of blaCTX-M-2 with blaIMP-1 is presently reported for the first time, as like as co-existence of blaGES-1 with blaIMP-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 blaCTX-M-2,blaGES-1 and blaGES-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.
The online version of this article (doi:10.1186/1471-2334-12-176) contains supplementary material, which is available to authorized users.
Competing interests
The authors declare that they have no competing interests.
Authors’ contribution
MP, TC and MCLN carried out the molecular genetic studies, participated in the sequence alignment. MGL, FGR, MTGA, MLN and MCLN participated in the design of the study. MGL, MTGA and MP collected and characterize the isolates. MLN, MTGA, MCLN and FGR analyzed the results. MP, MLN and MCLN drafted the manuscript. All authors read and approved the final manuscript.
Background
Pseudomonas aeruginosa is an opportunistic pathogen responsible for a large spectrum of invasive diseases in healthcare settings, including pneumonia, urinary tract infections and bacteremia [1]. For such infections, antimicrobial therapy may become a difficult task, because Pseudomonas aeruginosa is naturally resistant to many drugs, and presents a remarkable ability to acquire further resistance mechanisms to multiple classes of antimicrobial agents, even during the course of a treatment [2]. In this context, infections by P. aeruginosa presenting acquired resistance to beta-lactam drugs are considered one of the most challenging targets for antimicrobial therapy [3], being responsible for high rates of therapeutic failure, increase in mortality, morbidity, and in overall cost of treatment [4‐6].
The Ambler’s class B beta-lactamases (metallo-beta-lactamases – MBLs) and class A extended-spectrum beta-lactamases (ESBLs) are acquired resistance determinants that present high clinical impact [7, 8]. These enzymes, usually codified by genes associated with mobile genetic elements, are matter of major concern with regard to the future of antimicrobial chemotherapy because of its remarkable dissemination capability [9].
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MBLs such as IMP, VIM, SPM, GIM and AIM represent the leading acquired mechanism of resistance to beta-lactams in P. aeruginosa. These enzymes hydrolyze the majority of beta-lactam drugs [10] and compromise clinical utility of carbapenems, the most potent agents for treating severe infections caused by multidrug resistant strains [11]. More recently, appearance of ESBLs such as TEM, SHV, CTX-M, BEL, PER, VEB, GES, PME and OXA-type beta-lactamases has become an emergent public health problem, since these enzymes confer resistance to at least all expanded spectrum cephalosporins and compromise efficiency of ceftazidime, an important antibiotic regimen for P. aeruginosa[12‐14].
For the establishment of the appropriate antimicrobial therapy and for assessment and control of the spread of drug resistant P. aeruginosa, the molecular detection and surveillance of resistance genes is becoming increasingly important [15, 16]. Despite of this, epidemiological data reporting the prevalence of MBL and ESBL producing P. aeruginosa is sparse, due to the inexistence of standardized methods for phenotypic detection of ESBL and MBL production [7, 17] and the complexity for the implementation of PCR based methods in the routine of clinical laboratories [17]. In order to overcome this difficulty, a number of commercial rapid molecular tests are being developed that identify pathogens and the presence of genetic determinants of antimicrobial resistance [18, 19]. The association of such new technologies with current classical methods may improve the ability of clinical laboratories to provide accurate and fast results that will impact on patient care.
Hence, this study was performed to investigate the carriage of genes codifying MBLs and ESBLs by P. aeruginosa isolated from patients admitted to a Brazilian 720-bed teaching tertiary care hospital. Despite the high rates of carbapenem resistance, genes for MBLs production were not observed in the majority of the isolates. Notably ESBLs codifying genes blaCTX-M-2, blaGES-1 and blaGES-5 were detected in several strains, and the coexistence of blaCTX-M-2 with blaIMP-1, and blaGES-1 with blaIMP-1 in P. aeruginosa was observed, and is presently reported for the first time. These findings underline the emergence of class A extended-spectrum beta-lactamases among P. aeruginosa.
Methods
Bacterial isolates
In this study were included a total of 56 P. aeruginosa isolates resistant to ceftazidime, imipenem and/or meropenem, nonrepetitively obtained from patients admitted to a teaching hospital in São Paulo State, Brazil, over a period between June to December 2009. Isolates were obtained from specimens originated from urinary tract, respiratory tract, bloodstream and soft tissue. Clinical specimens were collected in intensive care units, clinical and surgical wards as well as from outpatients as a standard care procedure and were stored for this work. This study was approved by the Ethical Review Board from our institution (Comitê de Ética em Pesquisa – FAMERP) under protocol # 3131/2009.
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Susceptibility testing and phenotypic detection of MBL production
Antimicrobial susceptibility to aztreonam, ceftazidime, cefepime, imipenem, meropenem, piperacillin/tazobactam, amikacin, gentamicin, ciprofloxacin, levofloxacin and polymyxin B were determined by the disk diffusion method, following Clinical and Laboratory Standards Institute recommendations [20]. Phenotypic detection of MBLs was performed by double-disc synergy test (DDST) using the 2-mercaptopropionic acid as a MBL inhibitor [17].
Genotypic detection of MBL and ESBL genes
Specific primers and protocols were used to detect and sequence blaTEMblaSHVblaCTX-MblaGESblaKPCblaIMP and blaVIM[17, 21‐24]. The detection and sequencing of blaSPM-1 was performed using primers previously described [25] and also others specifically designed for this study using DS Gene 2.0 Software (Accelrys, USA). PCR products were purified in ethanol according to previously described methodology [26] and subjected to direct sequencing with the ABI PRISM 3130 automated sequencer (Applied Biosystems, Foster City, CA). The products were aligned with Accelrys Gene 2.0 (Accelrys Software Inc. 2006). Database similarity searches were run with BLAST at the National Center for Biotechnology Information website (http://www.ncbi.nlm.nih.gov).
Molecular typing
Genetic relatedness was evaluated by pulsed-field gel electrophoresis (PFGE) using SpeI (Fermentas Life Sciences, MD, EUA) with a CHEF-DR II apparatus (Bio-Rad, Richmond, CA, EUA) as described elsewhere [27]. BioNumerics software (Applied Maths) was used for dendrogram construction and clustering, based on the band-based Dice’s similarity coefficient and using the unweighted pair group method (UPGMA) using arithmetic averages. Isolates were considered to belong to the same cluster when similarity coefficient was 90% [28]. The visual Tenover criteria were also applied [29].
Results
A total of 80.3% (45/56) of isolates were resistant to the combination piperacillin/tazobactam, 62.5% (35/56) to aztreonam, 78.6% (44/56) to ceftazidime, 96.4% (54/56) to cefepime, 96.4% (54/56) to imipenem, 75.0% (42/56) to meropenem, 51.8% (29/56) to amikacin, 82.1% (46/56) to gentamicin, 78.6% (44/56) to ciprofloxacin and 85.7% (48/56) to levofloxacin. All isolates showed sensitivity to polymyxin B (data not shown). Thirteen isolates (23.2%) presented MBL phenotype by the DDST (Table 1).
Table 1
Antimicrobial susceptibility of carbapenem resistantP. aeruginosa*
Isolate
Antimicrobials (zone diameter – mm)
DDST
blagenotype
No
Date
Unit
Infection site
CAZ
FEP
TZP
IPM
MEM
ATM
GEN
AK
CIP
LEV
R ≤ 14
R ≤ 14
R ≤ 17
R ≤ 13
R ≤ 13
R ≤ 15
R ≤ 12
R ≤ 14
R ≤ 15
R ≤ 13
S ≥ 18
S ≥ 18
S ≥ 18
S ≥ 16
S ≥ 16
S ≥ 22
S ≥ 15
S ≥ 17
S ≥ 21
S ≥ 17
Pa01
06/2009
CI
Urinary tract
6
6
6
10
8
10
6
6
6
6
N
blaCTX-M 2
Pa02
06/2009
G-ICU
Lung
18
6
6
6
6
17
6
6
6
6
N
blaIMP-1, blaCTX-M 2
Pa03
06/2009
S-ICU
Urinary tract
20
6
18
6
13
12
6
15
6
6
P
blaIMP-1
Pa04
06/2009
G-ICU
Lung
6
6
6
12
14
16
6
19
6
6
N
-
Pa05
07/2009
E-ICU
Blood
6
6
19
6
6
22
6
18
6
6
N
blaSPM-1
Pa06
07/2009
E-ICU
Lung
6
6
10
11
14
14
12
16
6
6
N
-
Pa07
07/2009
N-Dep
Lung
6
6
6
6
6
16
6
6
6
6
N
-
Pa08
07/2009
C-Dep
Urinary tract
6
6
6
6
16
8
6
6
6
6
N
-
Pa10
07/2009
Outpatient
Urinary tract
6
6
13
6
6
23
6
15
6
6
N
blaCTX-M 2
Pa11
07/2009
G-ICU
Lung
6
6
14
6
6
22
6
18
6
6
P
blaSPM-1
Pa12
08/2009
E-ICU
Lung
6
6
16
6
6
19
6
21
6
6
P
blaSPM-1
Pa14
08/2009
C-Dep
Urinary tract
6
6
6
10
15
10
6
18
6
6
N
-
Pa17
08/2009
P-ICU
Lung
17
6
16
13
17
16
6
6
6
6
N
blaCTX-M 2
Pa18
08/2009
E-ICU
Lung
6
6
6
6
6
12
6
17
6
6
P
blaSPM-1
Pa19
08/2009
P-ICU
Lung
6
6
6
6
6
14
19
23
23
10
N
-
Pa22
08/2009
SW
Skin
19
6
16
6
18
8
6
6
6
6
N
blaCTX-M 2
Pa24
08/2009
C-Dep
Urinary tract
6
6
6
6
6
6
6
18
6
6
N
-
Pa27
08/2009
G-ICU
Catheter tip
6
6
10
10
15
8
6
19
6
6
N
-
Pa28
08/2009
G-ICU
Urinary tract
6
6
6
6
6
14
6
13
6
6
P
blaSPM-1
Pa29
09/2009
C-Dep
Lung
23
6
17
6
22
12
6
6
6
6
N
-
Pa30
09/2009
P-ICU
Eyes
6
6
18
6
6
9
17
23
22
13
N
-
Pa31
09/2009
P-ICU
Abdominal
6
6
6
6
6
19
19
20
15
6
N
-
Pa32
09/2009
C-Dep
Lung
6
6
12
6
19
13
6
6
6
6
N
-
Pa33
09/2009
P-ICU
Lung
6
6
6
6
6
13
19
22
20
6
N
-
Pa34
09/2009
C-ICU
Bone
6
6
6
6
6
12
6
6
6
6
N
-
Pa35
09/2009
C-ICU
Lung
18
6
21
6
6
6
6
12
26
30
N
-
Pa36
09/2009
N-Dep
Lung
6
6
18
6
13
6
6
6
17
25
N
-
Pa37
09/2009
S-ICU
Urinary tract
6
6
14
6
6
20
6
20
6
6
P
blaSPM-1
Pa39
09/2009
G-ICU
Catheter tip
25
6
14
6
24
21
6
6
6
6
N
-
Pa40
09/2009
P-ICU
Urinary tract
6
6
19
6
6
9
14
20
31
27
N
-
Pa41
09/2009
E-ICU
Lung
20
15
6
6
18
23
6
6
6
6
N
-
Pa42
09/2009
N-ICU
Eye
6
6
25
14
16
23
6
20
30
28
N
-
Pa43
10/2009
S-ICU
Lung
6
6
6
6
14
12
6
18
6
6
N
-
Pa44
10/2009
G-ICU
Lung
17
6
20
10
11
15
16
18
23
18
N
-
Pa45
10/2009
E-ICU
Skin
21
6
15
10
11
10
6
6
6
6
N
-
Pa47
11/2009
SW
Urinary tract
6
15
10
6
6
23
6
23
6
6
P
blaSPM-1
Pa49
10/2009
N-ICU
Urinary tract
6
6
27
6
6
23
6
6
33
30
P
blaIMP-1
Pa50
10/2009
SC
Bone
6
6
6
6
12
10
6
15
6
6
N
-
Pa51
10/2009
S-ICU
Urinary tract
6
6
6
6
19
18
6
6
6
6
N
-
Pa53
10/2009
C-UTI
Lung
20
6
18
6
6
14
6
6
6
6
N
blaIMP-1, blaCTX-M 2
Pa54
10/2009
E-ICU
Urinary tract
6
6
6
6
6
17
6
16
6
6
P
blaSPM-1
Pa55
11/2009
ER
Urinary tract
6
6
6
6
6
17
6
6
6
6
N
blaCTX-M 2
Pa57
11/2009
S-ICU
Urinary tract
26
6
6
6
6
25
6
6
6
6
N
blaCTX-M 2
Pa58
11/2009
E-ICU
Urinary tract
6
6
6
6
6
21
6
18
6
6
P
blaSPM-1
Pa59
11/2009
E-ICU
Lung
6
6
22
6
6
21
14
17
20
20
P
blaIMP-1, blaGES-1
Pa60
11/2009
ER
Lung
6
6
10
12
6
8
6
6
6
6
N
blaIMP-1, blaCTX-M 2
Pa61
11/2009
N-Dep
Blood
6
6
6
6
6
10
6
6
6
6
N
blaCTX-M 2
Pa62
11/2009
E-ICU
Lung
6
6
6
13
6
11
6
6
6
6
P
blaIMP-1
Pa63
11/2009
E-ICU
Lung
6
6
15
6
6
6
6
19
6
6
N
-
Pa64
11/2009
N-Dep
Tendon
6
6
6
6
6
12
6
6
6
6
N
blaGES-5
Pa65
11/2009
S-ICU
Lung
6
6
6
6
6
11
6
6
6
6
N
-
Pa66
11/2009
C-ICU
Lung
6
6
15
6
6
14
13
20
30
25
N
-
Pa67
11/2009
ER
Urinary tract
6
6
6
6
6
15
13
6
6
6
N
-
Pa69
11/2009
E-ICU
Lung
6
6
6
19
6
6
21
6
20
6
P
blaSPM-1
Pa70
11/2009
E-ICU
Lung
6
6
6
6
11
11
12
6
6
6
N
-
Pa71
11/2009
E-ICU
Lung
6
6
6
6
6
6
6
6
6
6
N
blaCTX-M 2
CAZ , ceftazidime; FEP , cefepime; TZP ,piperacillin-tazobactam; IMP , imipenem; MEM , meropenem; ATM , aztreonam, GEN , gentamicin, AK , amikacin; CIP ,ciprofloxacin; LEV , levofloxacin; †DDDS , double disc synergy test to detect MBL production , N , negative, P , positive, ER , emergence room; E-ICU , emergence intensive care unit; G-ICU , geral intensive care unit; S-ICU , semi-intensive care unit; C-ICU , cardiology intensive care unit; P-ICU , pediatrics intensive care unit, N-ICU , neonatal intensive care unit N-Dep , neurology department; C-Dep , cardiology department; SC , surgical ward, CI , cancer institute; R , resistant; S , susceptible.
The prevalence of isolates harboring MBL genes was 30.3% (17/56). Ten (17.8%) presented the blaSPM-1 gene, and the blaIMP-1 was detected in seven isolates (12.5%). In all thirteen isolates presenting MBL phenotype by DDST, blaSPM-1 or blaIMP-1 was detected. In addition, the blaIMP-1 gene was also detected in three isolates which did not display any MBL phenotype. These isolates also presented the blaCTX-M-2 gene (Table 1). No blaVIM type was detected.
Genes encoding ESBLs were detected in 23.2% (13/56) of the isolates. The blaCTX-M-2 was detected in eleven isolates (19.6%), blaGES-1 was detected in one and blaGES-5 was detected in one isolate. Co-existence of blaCTX-M-2 with blaIMP-1 was detected in three isolates and blaGES-1 with blaIMP-1 in one isolate (Table 1). No blaTEM and blaSHV types were detected GenBank Accession Numbers are provided in Supplemental Material (Additional File 1).
The degree of relatedness among the Pseudomonas aeruginosa harboring MBL and ESBL genes was assessed by PFGE analysis (Figure 1). Eight isolates harboring blaSPM-1 were typed, and by visual inspection all were considered closely related, presenting up to three bands of difference. According to PFGE profiles these isolates were grouped within three clusters (A, B and C). Similarity between cluster A and B was of 89.1%. Clusters A and B presented 87.6% of similarity with cluster C.
Figure 1
Dendrogram of PFGE patterns presented by carbapenem resistantP. aeruginosaincluded in this study. ER, emergence room; E-ICU, emergence intensive care unit; G-ICU, geral intensive care unit; S-ICU, semi-intensive care unit; C-ICU, cardiology intensive care unit; P-ICU, pediatrics intensive care unit, N-ICU, neonatal intensive care unit N-Dep, neurology department; C-Dep, cardiology department; SC, surgical ward, CI, cancer institute.
×
The P. aeruginosa harboring blaIMP-1 were distributed among five different clusters (E to I), and isolates harboring blaCTX-M-2 in three clusters (D, E, H). Cluster E included seven isolates presenting similarity of at least 92.3%. Within this cluster, four isolates exhibited blaCTX-M-2, one exhibited blaIMP-1 and two isolates exhibited blaIMP-1 and blaCTX-M-2 simultaneously. One isolate harboring blaCTX-M-2 was placed in cluster D, four isolates harboring blaIMP-1 were placed in clusters F, G, H and I, and one isolate exhibiting blaIMP-1 and blaCTX-M-2 simultaneously was placed in cluster H. Isolates harboring blaGES-1 and blaGES-5 could not be typed.
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Discussion
The pattern of multidrug resistance presented by the P. aeruginosa included in this study was expected, since carbapenem resistant strains exhibit a broad-spectrum resistance to beta-lactams and often present resistant phenotype to additional classes of drugs. Also, acquired ESBL and MBL genes typically group with other drug resistance determinants in the variable region of multi-resistance integrons [30‐32]. Furthermore, P. aeruginosa isolated in Latin America, including Brazil, are reported as presenting the higher rates of antibiotic resistance [33]. P. aeruginosa strains resistant to polymyxins were not detected in this study. However, this result should be confirmed by a dilution method, considering that the disc diffusion technique, commonly used in clinical microbiology laboratories is reported to be an unreliable method for evaluating the susceptibility to polymyxins because these drugs diffuse poorly into agar [34].
In this study MBL genes were detected in 26.7% of isolates, indicating that despite the increasing significance of MBL production among P. aeruginosa, this was not the main mechanism of resistance to imipenem and/or meropenem. This reality was previously reported in another Brazilian hospital [35]. In fact, resistance to carbapenems in P. aeruginosa is due not only to the production of carbapenemases, but also to different mechanisms such as upregulation of multidrug efflux pumps, cell wall mutations leading to reduction in porin channels and production of different beta-lactamases [1, 11]. Expression of these mechanisms, isolated or in combination, may cause variation in rates of resistance to imipenem and meropenem, observed in this study [5]. The twelve isolates presenting MBL phenotype by the DDST harbored MBL genes (blaSPM-1 or blaIMP-1), confirming the efficacy of this method for the phenotypic detection of MBL producing strains [17, 36].
Diversity of MBL among P. aeruginosa varies by regional areas [37]. In this study the 17.5% of the carbapenem resistant isolates presented the blaSPM-1 gene, and blaIMP-1 was detected in 10.5% of the isolates. SPM-1 is in fact the most prevalent MBL in Brazil [38]. In a different way, IMP-1 producing strains have been reported in various Brazilian hospitals in diverse rates [35, 39, 40].
Molecular typing by PFGE showed a wide diversity of patterns. All isolates exhibiting blaSPM-1, a chromosomally located gene [41, 42] presented high coefficient of similarity and closely related PFGE patterns, suggesting a close genetic relationship. This is in agreement with previously described data, showing that the Brazilian SPM-1-producing P. aeruginosa are probably derived from a single clone [43]. According to the same study, even a recent genomic variety recently observed among various SPM-1-producing P.aeruginosa isolates is result of the accumulation of mutations along the time.
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Occurrence of blaIMP-1 in P. aeruginosa described in this study is likely a result of gene horizontal transferring, since isolates harboring blaIMP-1 belong to five different clusters. Dissemination of blaIMP among Gram-negative pathogens is mediated by mobile elements of DNA, explaining why the same gene might be detected in different strains. The genes for IMP enzymes are often carried as cassettes within integrons, which facilitate recombination and facilitate rapid horizontal transferring [44‐46].
The coexistence of blaIMP-1 with blaCTX-M-2 in P. aeruginosa was, at the best of our knowledge, detected for the first time. Interestingly, the three isolates presenting this combination of genes did not provide a positive result in the DDST test, and were the only blaIMP-1 carriers in which MBL phenotypic detection was unsuccessful. Since ceftazidime is poorly hydrolyzed by CTX-M-2 [31], we could not assume that inactivation of this antimicrobial, used as substrate, may have been responsible for this result. However, simultaneous production of MBLs and ESBLs by the same strain is known to promote further complexity in phenotypic detection [7, 47, 48]. This result emphasizes the importance of molecular methods for the identification of antimicrobial resistance in multidrug resistant pathogenic bacteria. In this matter, detection of resistance genes by PCR may provide clinically relevant information with positive impact in patient prognosis [18].
The detection of blaCTX-M-2blaGES-1 and blaGES-5 in this study reflects the recent emergence of ESBLs in P. aeruginosa as result of the great dissemination capability exhibited by these genes that occur mostly as part of integron structures on mobile transmissible genetic elements [49‐52]. Location of blaCTX-M-2 in P. aeruginosa is believed to be a result of their transfer from Enterobacteriaceae[51]. Recently, a high prevalence of K. pneumoniae harboring blaCTX-M-2 in the same hospital was reported [21], and this may have been the reservoir for horizontal transmission.
Regarding GES-type ESBLs, although these enzymes are not considered as primary β-lactamases in P. aeruginosa, acquisition in conditions of antimicrobial pressure may be beneficial [52]. The blaGES-1 was detected in co-existence with blaIMP-1, and blaGES-5 was detected in a strain resistant to imipenem and meropenem, but presenting no MBL phenotype. Considering that GES-5 presents enhanced hydrolyse activity against carbapenems [10], it is likely that GES-5 production contributed for the carbapenem resistance in this isolate.
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Conclusion
Production of MBLs was not the main mechanism of resistance to carbapenems among the studied strains. However, IMP-1 is disseminated among different strains of carbapenem resistant P. aeruginosa, and intra-hospital spread of SPM-1 producing strains was observed. The detection of blaCTX-M-2, blaGES-1 and blaGES-5 and the unique coexistence of blaCTX-M-2 with blaIMP-1 and blaGES-1 with blaIMP-1 exemplify the extraordinary ability presented by P. aeruginosa to acquire multiple resistance mechanisms.
Clonal dissemination of multidrug resistant P. aeruginosa within the hospital was inferred by the observation of strains presenting the identical PFGE profiles infecting different patients, and the occurrence of clonal dissemination in different ICUs and wards. This finding enhances the necessity of better observance of infection control practices, to prevent further dissemination of this challenging pathogen.
Acknowledgements
This work was supported by a FAPESP grant to MCLN. MLN is supported by FAPESP and CNPq Grants. MLN is recipient of a CNPq Fellowship. MP is a recipient of a CAPES Scholarship.
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Competing interests
The authors declare that they have no competing interests.
Authors’ contribution
MP, TC and MCLN carried out the molecular genetic studies, participated in the sequence alignment. MGL, FGR, MTGA, MLN and MCLN participated in the design of the study. MGL, MTGA and MP collected and characterize the isolates. MLN, MTGA, MCLN and FGR analyzed the results. MP, MLN and MCLN drafted the manuscript. All authors read and approved the final manuscript.
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
verfasst von
Milena Polotto Tiago Casella Maria Gabriela de Lucca Oliveira Fernando G Rúbio Mauricio L Nogueira Margarete TG de Almeida Mara CL Nogueira
Ob bei einer Notfalloperation nach Schenkelhalsfraktur eine Hemiarthroplastik oder eine totale Endoprothese (TEP) eingebaut wird, sollte nicht allein vom Alter der Patientinnen und Patienten abhängen. Auch über 90-Jährige können von der TEP profitieren.
Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.
Insektenstiche sind bei Erwachsenen die häufigsten Auslöser einer Anaphylaxie. Einen wirksamen Schutz vor schweren anaphylaktischen Reaktionen bietet die allergenspezifische Immuntherapie. Jedoch kommt sie noch viel zu selten zum Einsatz.
Beginnen ältere Männer im Pflegeheim eine Antihypertensiva-Therapie, dann ist die Frakturrate in den folgenden 30 Tagen mehr als verdoppelt. Besonders häufig stürzen Demenzkranke und Männer, die erstmals Blutdrucksenker nehmen. Dafür spricht eine Analyse unter US-Veteranen.
Update Innere Medizin
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