Detection of synergistic antimicrobial resistance mechanisms in clinical isolates of Pseudomonas aeruginosa from post-operative wound infections

Author(s):  
Asad Bashir Awan ◽  
Aixin Yan ◽  
Yasra Sarwar ◽  
Peter Schierack ◽  
Aamir Ali
Author(s):  
Anusha Gopinathan ◽  
Chiranjay Mukhopadhyay ◽  
Vandana K. E.

Background: Extended spectrum beta lactamases, AmpC and Metallo-betalactamases in GNB isolates are a common occurrence in most Indian hospitals. The presence of these antimicrobial resistance mechanisms contributes to prolonged hospital stay, poor quality of life, increased morbidity and mortality among patients with these infections. The aim of the study was to analyse the antimicrobial resistance mechanisms of multidrug resistant Gram negative bacterial wound infection and their clinical epidemiology.Methods: A prospective study was conducted for one year among 100 patients of Kasturba Medical College, Manipal admitted with MDR GNB wound infections. The antibiogram and phenotypic resistance mechanisms of the bacterial isolate from these infections were identified using phenyl boronic acid and ethyl diacetate.  The empirical therapy, specific therapy and clinical outcome of the patients were also analyzed.Results: Out of 100 study patients, 152 MDR GNB isolates were obtained.  73% patients were admitted in the surgical wards. 43% patients had diabetes. Ulcers (27%) and abscess (25%) were the most common diagnosis. Escherichia coli (39%), Klebsiella pneumoniae (24%) and Pseudomonas aeruginosa (19%) were the most common isolates. Maximum number of ESBL was seen among Enteric Gram negative bacilli (36%), MBL was seen among Pseudomonas aeruginosa and Acinetobacter species (55% each), AmpC was seen among enteric GNB (10%) and Acinetobacter species (18%). Cefaperazone sulbactam, amikacin and meropenem were the most common antibiotics given as specific therapy. Clinical response was observed among 93% patients.Conclusions: The determination of the antimicrobial resistance mechanisms of GNB isolates from wound infections plays a major role in establishing an antibiotic policy for the treatment of these infections.


Heliyon ◽  
2019 ◽  
Vol 5 (7) ◽  
pp. e02021 ◽  
Author(s):  
Sagar S. Arya ◽  
Mansi M. Sharma ◽  
Ratul K. Das ◽  
James Rookes ◽  
David Cahill ◽  
...  

2020 ◽  
Vol 21 (3) ◽  
pp. 1026 ◽  
Author(s):  
Weihua Huang ◽  
Joelle El Hamouche ◽  
Guiqing Wang ◽  
Melissa Smith ◽  
Changhong Yin ◽  
...  

Multidrug-resistant (MDR) Pseudomonas aeruginosa is one of the main causes of morbidity and mortality in hospitalized patients and the leading cause of nosocomial infections. We investigated, here, two MDR P. aeruginosa clinical isolates from a hospitalized patient with differential antimicrobial resistance to ceftazidime/avibactam (CZA), ceftolozane/tazobactam (C/T), and piperacillin/tazobactam (P/T). Their assembled complete genomes revealed they belonged to ST235, a widespread MDR clone; and were isogenic with only a single nucleotide variant, causing G183D mutation in AmpC β-lactamase, responsible for a phenotypic change from susceptible to resistant to CZA and C/T. Further epigenomic profiling uncovered two conserved DNA methylation motifs targeted by two distinct putative methyltransferase-containing restriction-modification systems, respectively; more intriguingly, there was a significant difference between the paired isolates in the pattern of genomic DNA methylation and modifications. Moreover, genome-wide gene expression profiling demonstrated the inheritable genomic methylation and modification induced 14 genes being differentially regulated, of which only toxR (downregulated), a regulatory transcription factor, had its promoter region differentially methylate and modified. Since highly expressed opdQ encodes an OprD porin family protein, therefore, we proposed an epigenetic regulation of opdQ expression pertinent to the phenotypic change of P. aeruginosa from resistant to susceptible to P/T. The disclosed epigenetic mechanism controlling phenotypic antimicrobial resistance deserves further experimental investigation.


2019 ◽  
Vol 74 (7) ◽  
pp. 1825-1835 ◽  
Author(s):  
Ester del Barrio-Tofiño ◽  
Laura Zamorano ◽  
Sara Cortes-Lara ◽  
Carla López-Causapé ◽  
Irina Sánchez-Diener ◽  
...  

2019 ◽  
Vol 38 (8) ◽  
pp. 1547-1552 ◽  
Author(s):  
Annalisa De Rosa ◽  
Nico T. Mutters ◽  
Claudio M. Mastroianni ◽  
Stefan J. Kaiser ◽  
Frank Günther

2007 ◽  
Vol 56 (7) ◽  
pp. 956-963 ◽  
Author(s):  
Tanya Strateva ◽  
Vessela Ouzounova-Raykova ◽  
Boyka Markova ◽  
Albena Todorova ◽  
Yulia Marteva-Proevska ◽  
...  

A total of 203 clinical isolates of Pseudomonas aeruginosa was collected during 2001–2006 from five university hospitals in Sofia, Bulgaria, to assess the current levels of antimicrobial susceptibility and to evaluate resistance mechanisms to antipseudomonal antimicrobial agents. The antibiotic resistance rates against the following antimicrobials were: carbenicillin 93.1 %, azlocillin 91.6 %, piperacillin 86.2 %, piperacillin/tazobactam 56.8 %, ceftazidime 45.8 %, cefepime 48.9 %, cefpirome 58.2 %, aztreonam 49.8 %, imipenem 42.3 %, meropenem 45.5 %, amikacin 59.1 %, gentamicin 79.7 %, tobramycin 89.6 %, netilmicin 69.6 % and ciprofloxacin 80.3 %. A total of 101 of the studied P. aeruginosa isolates (49.8 %) were multidrug resistant. Structural genes encoding class A and class D β-lactamases showed the following frequencies: bla VEB-1 33.1 %, bla PSE-1 22.5 %, bla PER-1 0 %, bla OXA-groupI 41.3 % and bla OXA-groupII 8.8 %. IMP- and VIM-type carbapenemases were not detected. In conclusion, the studied clinical strains of P. aeruginosa were problematic nosocomial pathogens. VEB-1 extended-spectrum β-lactamases appear to have a significant presence among clinical P. aeruginosa isolates from Sofia. Carbapenem resistance was related to non-enzymic mechanisms such as a deficiency of OprD proteins and active efflux.


2016 ◽  
Vol 60 (10) ◽  
pp. 6407-6410 ◽  
Author(s):  
Gabriel Torrens ◽  
Gabriel Cabot ◽  
Alain A. Ocampo-Sosa ◽  
M. Carmen Conejo ◽  
Laura Zamorano ◽  
...  

ABSTRACTThe activity of ceftazidime-avibactam was compared with that of ceftazidime alone and meropenem against a collection of 190Pseudomonas aeruginosaclinical isolates recovered from a multicenter study of bloodstream infections. The addition of avibactam increased ceftazidime susceptibility in the complete collection of strains (64.7% to 91.1%) and particularly among subsets of isolates showing AmpC hyperproduction (10.9% to 76.1%) or multidrug resistance (MDR) profiles (27% to 77.8%). The MICs of ceftazidime-avibactam, in contrast with those of ceftazidime or meropenem, remained at ≤4 μg/ml for a panel of 16P. aeruginosaPAO1 isogenic mutants expressing multiple combinations of the most relevant β-lactam resistance mechanisms.


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