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    Editorial: Immune response to gram-negative bacteria in the lungs
    (2024)
    Agnes Jara-Collao
    ;
    POLI HARLOWE, MARIA CECILIA BERTA  
    ;
    William Bain
    ;
    Hernán F. Peñaloza
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    Excess burden of antibiotic-resistant bloodstream infections: evidence from a multicentre retrospective cohort study in Chile, 2018–2022
    (2024)
    Kasim Allel
    ;
    Anne Peters
    ;
    Hassan Haghparast-Bidgoli
    ;
    Maria Spencer-Sandino
    ;
    Jose Conejeros
    Scopus© Citations 2  4
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    Ceftazidime/avibactam resistance is associated with PER-3-producing ST309 lineage in Chilean clinical isolates of non-carbapenemase producing Pseudomonas aeruginosa
    (2024)
    Katherine D. Soto
    ;
    ALCALDE RICO, MANUEL  
    ;
    UGALDE, JUAN ANTONIO
    ;
    Jorge Olivares Pacheco
    ;
    Valeria Quiroz
    <jats:sec><jats:title>Introduction</jats:title><jats:p>Ceftazidime/avibactam (CZA) is indicated against multidrug-resistant <jats:italic>Pseudomonas aeruginosa</jats:italic>, particularly those that are carbapenem resistant. CZA resistance in <jats:italic>P. aeruginosa</jats:italic> producing PER, a class A extended-spectrum β-lactamase, has been well documented <jats:italic>in vitro</jats:italic>. However, data regarding clinical isolates are scarce. Our aim was to analyze the contribution of PER to CZA resistance in non-carbapenemase-producing <jats:italic>P. aeruginosa</jats:italic> clinical isolates that were ceftazidime and/or carbapenem non-susceptible.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Antimicrobial susceptibility was determined through agar dilution and broth microdilution, while <jats:italic>bla</jats:italic><jats:sub>PER</jats:sub> gene was screened through PCR. All PER-positive isolates and five PER-negative isolates were analyzed through Whole Genome Sequencing. The mutational resistome associated to CZA resistance was determined through sequence analysis of genes coding for PBPs 1b, 3 and 4, MexAB-OprM regulators MexZ, MexR, NalC and NalD, AmpC regulators AmpD and AmpR, and OprD porin. Loss of <jats:italic>bla</jats:italic><jats:sub>PER-3</jats:sub> gene was induced in a PER-positive isolate by successive passages at 43°C without antibiotics. </jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Twenty-six of 287 isolates studied (9.1%) were CZA-resistant. Thirteen of 26 CZA-resistant isolates (50%) carried <jats:italic>bla</jats:italic><jats:sub>PER</jats:sub>. One isolate carried <jats:italic>bla</jats:italic><jats:sub>PER</jats:sub> but was CZA-susceptible. PER-producing isolates had significantly higher MICs for CZA, amikacin, gentamicin, ceftazidime, meropenem and ciprofloxacin than non-PER-producing isolates. All PER-producing isolates were ST309 and their <jats:italic>bla</jats:italic><jats:sub>PER-3</jats:sub> gene was associated to ISCR1, an insertion sequence known to mobilize adjacent DNA. PER-negative isolates were classified as ST41, ST235 (two isolates), ST395 and ST253. PER-negative isolates carried genes for narrow-spectrum β-lactamases and the mutational resistome showed that all isolates had one major alteration in at least one of the genes analyzed. Loss of <jats:italic>bla</jats:italic><jats:sub>PER-3</jats:sub> gene restored susceptibility to CZA, ceftolozane/tazobactam and other β-lactamsin the <jats:italic>in vitro</jats:italic> evolved isolate. </jats:p></jats:sec><jats:sec><jats:title>Discussion</jats:title><jats:p>PER-3-producing ST309 <jats:italic>P. aeruginosa</jats:italic> is a successful multidrug-resistant clone with <jats:italic>bla<jats:sub>PER-3</jats:sub></jats:italic> gene implicated in resistance to CZA and other β-lactams.</jats:p></jats:sec>
    Scopus© Citations 1  4
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    Pseudomonas aeruginosa Bloodstream Infections Presenting with Septic Shock in Neutropenic Cancer Patients: Impact of Empirical Antibiotic Therapy
    (2024)
    Cristina Royo-Cebrecos
    ;
    Júlia Laporte-Amargós
    ;
    Marta Peña
    ;
    Isabel Ruiz-Camps
    ;
    Carolina Garcia-Vidal
    <jats:p>This large, multicenter, retrospective cohort study including onco-hematological neutropenic patients with Pseudomonas aeruginosa bloodstream infection (PABSI) found that among 1213 episodes, 411 (33%) presented with septic shock. The presence of solid tumors (33.3% vs. 20.2%, p &lt; 0.001), a high-risk Multinational Association for Supportive Care in Cancer (MASCC) index score (92.6% vs. 57.4%; p &lt; 0.001), pneumonia (38% vs. 19.2% p &lt; 0.001), and infection due to multidrug-resistant P. aeruginosa (MDRPA) (33.8% vs. 21.1%, p &lt; 0.001) were statistically significantly higher in patients with septic shock compared to those without. Patients with septic shock were more likely to receive inadequate empirical antibiotic therapy (IEAT) (21.7% vs. 16.2%, p = 0.020) and to present poorer outcomes, including a need for ICU admission (74% vs. 10.5%; p &lt; 0.001), mechanical ventilation (49.1% vs. 5.6%; p &lt; 0.001), and higher 7-day and 30-day case fatality rates (58.2% vs. 12%, p &lt; 0.001, and 74% vs. 23.1%, p &lt; 0.001, respectively). Risk factors for 30-day case fatality rate in patients with septic shock were orotracheal intubation, IEAT, infection due to MDRPA, and persistent PABSI. Therapy with granulocyte colony-stimulating factor and BSI from the urinary tract were associated with improved survival. Carbapenems were the most frequent IEAT in patients with septic shock, and the use of empirical combination therapy showed a tendency towards improved survival. Our findings emphasize the need for tailored management strategies in this high-risk population.</jats:p>
    Scopus© Citations 7  1
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      2Scopus© Citations 3
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      5Scopus© Citations 22
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    Scopus© Citations 13  2
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    Pseudomonas aeruginosa Bloodstream Infections in Patients with Cancer: Differences between Patients with Hematological Malignancies and Solid Tumors
    (2022)
    Cristina Royo-Cebrecos
    ;
    Julia Laporte-Amargós
    ;
    Marta Peña
    ;
    Isabel Ruiz-Camps
    ;
    Pedro Puerta-Alcalde
    <jats:p>Objectives: To assess the clinical features and outcomes of Pseudomonas aeruginosa bloodstream infection (PA BSI) in neutropenic patients with hematological malignancies (HM) and with solid tumors (ST), and identify the risk factors for 30-day mortality. Methods: We performed a large multicenter, retrospective cohort study including onco-hematological neutropenic patients with PA BSI conducted across 34 centers in 12 countries (January 2006–May 2018). Episodes occurring in hematologic patients were compared to those developing in patients with ST. Risk factors associated with 30-day mortality were investigated in both groups. Results: Of 1217 episodes of PA BSI, 917 occurred in patients with HM and 300 in patients with ST. Hematological patients had more commonly profound neutropenia (0.1 × 109 cells/mm) (67% vs. 44.6%; p &lt; 0.001), and a high risk Multinational Association for Supportive Care in Cancer (MASCC) index score (32.2% vs. 26.7%; p = 0.05). Catheter-infection (10.7% vs. 4.7%; p = 0.001), mucositis (2.4% vs. 0.7%; p = 0.042), and perianal infection (3.6% vs. 0.3%; p = 0.001) predominated as BSI sources in the hematological patients, whereas pneumonia (22.9% vs. 33.7%; p &lt; 0.001) and other abdominal sites (2.8% vs. 6.3%; p = 0.006) were more common in patients with ST. Hematological patients had more frequent BSI due to multidrug-resistant P. aeruginosa (MDRPA) (23.2% vs. 7.7%; p &lt; 0.001), and were more likely to receive inadequate initial antibiotic therapy (IEAT) (20.1% vs. 12%; p &lt; 0.001). Patients with ST presented more frequently with septic shock (45.8% vs. 30%; p &lt; 0.001), and presented worse outcomes, with increased 7-day (38% vs. 24.2%; p &lt; 0.001) and 30-day (49% vs. 37.3%; p &lt; 0.001) case-fatality rates. Risk factors for 30-day mortality in hematologic patients were high risk MASCC index score, IEAT, pneumonia, infection due to MDRPA, and septic shock. Risk factors for 30-day mortality in patients with ST were high risk MASCC index score, IEAT, persistent BSI, and septic shock. Therapy with granulocyte colony-stimulating factor was associated with survival in both groups. Conclusions: The clinical features and outcomes of PA BSI in neutropenic cancer patients showed some differences depending on the underlying malignancy. Considering these differences and the risk factors for mortality may be useful to optimize their therapeutic management. Among the risk factors associated with overall mortality, IEAT and the administration of granulocyte colony-stimulating factor were the only modifiable variables.</jats:p>
    Scopus© Citations 11  1
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    A multispecies outbreak of carbapenem-resistant bacteria harboring the blaKPC gene in a non-classical transposon element
    (2021)
    Aniela Wozniak
    ;
    Cristian Figueroa
    ;
    Francisco Moya-Flores
    ;
    Piero Guggiana
    ;
    Claudia Castillo
    <jats:title>Abstract</jats:title><jats:sec> <jats:title>Background</jats:title> <jats:p><jats:italic>Klebsiella pneumoniae</jats:italic> is the most frequent KPC-producing bacteria. The <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub> gene is frequently embedded in Tn4401 transposon, and less frequently in non-Tn4401 elements (NTE<jats:sub>KPC</jats:sub>) variants I-III. The first case of KPC in the UC-CHRISTUS Clinical Hospital was detected in <jats:italic>Pseudomonas aeruginosa</jats:italic>. Soon after this event, KPC was detected in 2 additional <jats:italic>Pseudomonas aeruginosa</jats:italic>, 3 <jats:italic>Escherichia coli</jats:italic>, 3 <jats:italic>Enterobacter cloacae</jats:italic>, 3 <jats:italic>Klebsiella pneumoniae,</jats:italic> and 1 <jats:italic>Citrobacter freundii</jats:italic>, isolated from 6 different patients. We aimed to elucidate the possible mechanisms of genetic transfer and dissemination of the <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub> gene among isolates of this multispecies outbreak. A molecular epidemiology analysis of the above mentioned clinical isolates (<jats:italic>n</jats:italic> = 13) through Multi-Locus Sequence Typing, plasmid analysis, Pulsed-Field Gel-Electrophoresis, and Whole-genome sequencing (WGS) was performed.</jats:p> </jats:sec><jats:sec> <jats:title>Results</jats:title> <jats:p>High-risk sequence types were found: <jats:italic>K. pneumoniae</jats:italic> ST11, <jats:italic>P. aeruginosa</jats:italic> ST654, and <jats:italic>E. cloacae</jats:italic> ST114. All enterobacterial isolates were not clonal except for 3 <jats:italic>E. coli</jats:italic> isolated from the same patient. WGS analysis in 6 enterobacterial isolates showed that 4 of them had <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub> embedded in a novel variant of NTE<jats:sub>KPC</jats:sub> designated NTE<jats:sub>KPC</jats:sub>-IIe. Upstream of <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub> gene there was a 570 pb truncated <jats:italic>bla</jats:italic><jats:sub>TEM-1</jats:sub> gene followed by an insertion sequence that was 84% similar to ISEc63, a 4473 bp element of the Tn3 family. Downstream the <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub> gene there was a truncated ISKpn6 gene, and the inverted repeat right sequence of Tn4401. The ISec63-like element together with the <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub> gene plus Tn4401 remnants were inserted in the Tra operon involved in conjugative transfer of the plasmid. This NTE was carried in a broad host-range IncN plasmid. <jats:italic>P. aeruginosa</jats:italic> isolates carried <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub> gene embedded in a typical Tn4401b transposon in a different plasmid, suggesting that there was no plasmid transfer between <jats:italic>Enterobacteriaceae</jats:italic> and <jats:italic>P. aeruginosa</jats:italic> as initially hypothesized.</jats:p> </jats:sec><jats:sec> <jats:title>Conclusions</jats:title> <jats:p>Most enterobacterial isolates had <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub> embedded in the same NTE<jats:sub>KPC</jats:sub>-IIe element, suggesting that this multispecies KPC outbreak was due to horizontal gene transfer rather than clonal spread. This poses a greater challenge to infection control measures often directed against containment of clonal spread.</jats:p> </jats:sec>
    Scopus© Citations 21  3
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    Molecular mechanisms leading to ceftolozane/tazobactam resistance in clinical isolates of Pseudomonas aeruginosa from five Latin American countries
    (2022)
    María F. Mojica
    ;
    Elsa De La Cadena
    ;
    Rafael Ríos
    ;
    Juan Carlos García-Betancur
    ;
    Lorena Díaz
    <jats:sec><jats:title>Objectives</jats:title><jats:p>Identify molecular mechanisms responsible for the <jats:italic>in vitro</jats:italic> non-susceptibility to ceftolozane/tazobactam (TOL) in a group of 158 clinical isolates of <jats:italic>Pseudomonas aeruginosa</jats:italic> from five Latin American countries collected before the introduction of TOL into the clinical practice.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Clinical isolates of <jats:italic>P. aeruginosa</jats:italic> (<jats:italic>n</jats:italic> = 504) were collected between January 2016 and October 2017 from 20 hospitals located in Argentina, Brazil, Chile, Colombia, and Mexico. Minimum inhibitory concentrations (MICs) to TOL were determined by standard broth microdilution and interpreted according to CLSI breakpoints. Initially, production of carbapenemases in TOL non-susceptible isolates was assessed by Rapidec® followed by qPCR to detect <jats:italic>bla</jats:italic><jats:sub>KPC</jats:sub>, <jats:italic>bla</jats:italic><jats:sub>NDM-1</jats:sub>, <jats:italic>bla</jats:italic><jats:sub>VIM</jats:sub>, and <jats:italic>bla</jats:italic><jats:sub>IMP</jats:sub>. Illumina® WGS was performed for isolates in which non-susceptibility to TOL was not mediated by carbapenemases.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>A total of 158 (31.3%) isolates were non-susceptible to TOL. In 74 (46.8%) of these isolates, non-susceptibility to TOL was explained by the production of at least one carbapenemase. WGS revealed that some isolates carried ESBLs, mutated <jats:italic>bla</jats:italic><jats:sub>PDC</jats:sub> and <jats:italic>ampD</jats:italic>, associated with decreased susceptibility to TOL.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Substitutions found in PDC and carbapenemase production were the most common presumed mechanisms of resistance to TOL detected in this study. This study shows that epidemiological surveillance is warranted to monitor the emergence of novel mechanisms of resistance to TOL that might compromise its clinical utility.</jats:p></jats:sec>
      5Scopus© Citations 14