Serum-Associated Antibiotic Tolerance in Pediatric Clinical Isolates of Pseudomonas aeruginosa.


Journal

Journal of the Pediatric Infectious Diseases Society
ISSN: 2048-7207
Titre abrégé: J Pediatric Infect Dis Soc
Pays: England
ID NLM: 101586049

Informations de publication

Date de publication:
31 Dec 2020
Historique:
received: 25 06 2019
accepted: 05 12 2019
pubmed: 31 12 2019
medline: 19 8 2021
entrez: 31 12 2019
Statut: ppublish

Résumé

When grown in human serum, laboratory isolates of Pseudomonas aeruginosa exhibit tolerance to antibiotics at inhibitory concentrations. This phenomenon, known as serum-associated antibiotic tolerance (SAT), could lead to clinical treatment failure of pseudomonal infections. Our purpose in this study was to determine the prevalence and clinical impact of SAT in Pseudomonas isolates in hospitalized children. The SAT phenotype was assessed in patients aged <18 years admitted with respiratory or blood cultures positive for P. aeruginosa. The SAT phenotype was a priori defined as a ≥2-log increase in colony-forming units when grown in human serum compared with Luria-Bertani medium in the presence of minocycline or tobramycin. SAT was detected in 29 (64%) patients. Fourteen patients each (34%) had cystic fibrosis (CF) and tracheostomies. Patient demographics and comorbidities did not differ by SAT status. Among CF patients, SAT was associated with longer duration of intravenous antibiotics (10 days vs 5 days; P < .01). This study establishes that SAT exists in P. aeruginosa from human serum and may be a novel factor that contributes to differences in clinical outcomes. Future research should investigate the mechanisms that contribute to SAT in order to identify novel targets for adjunctive antimicrobial therapies.

Sections du résumé

BACKGROUND BACKGROUND
When grown in human serum, laboratory isolates of Pseudomonas aeruginosa exhibit tolerance to antibiotics at inhibitory concentrations. This phenomenon, known as serum-associated antibiotic tolerance (SAT), could lead to clinical treatment failure of pseudomonal infections. Our purpose in this study was to determine the prevalence and clinical impact of SAT in Pseudomonas isolates in hospitalized children.
METHODS METHODS
The SAT phenotype was assessed in patients aged <18 years admitted with respiratory or blood cultures positive for P. aeruginosa. The SAT phenotype was a priori defined as a ≥2-log increase in colony-forming units when grown in human serum compared with Luria-Bertani medium in the presence of minocycline or tobramycin.
RESULTS RESULTS
SAT was detected in 29 (64%) patients. Fourteen patients each (34%) had cystic fibrosis (CF) and tracheostomies. Patient demographics and comorbidities did not differ by SAT status. Among CF patients, SAT was associated with longer duration of intravenous antibiotics (10 days vs 5 days; P < .01).
CONCLUSIONS CONCLUSIONS
This study establishes that SAT exists in P. aeruginosa from human serum and may be a novel factor that contributes to differences in clinical outcomes. Future research should investigate the mechanisms that contribute to SAT in order to identify novel targets for adjunctive antimicrobial therapies.

Identifiants

pubmed: 31886511
pii: 5690156
doi: 10.1093/jpids/piz094
pmc: PMC7974018
doi:

Substances chimiques

Anti-Bacterial Agents 0
Tobramycin VZ8RRZ51VK

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

671-679

Subventions

Organisme : NIDCR NIH HHS
ID : T90 DE021985
Pays : United States

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press on behalf of The Journal of the Pediatric Infectious Diseases Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Auteurs

John M Morrison (JM)

Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Medicine, Division of Hospital Medicine, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA.

Michaelle Chojnacki (M)

Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York, USA.

Jeffrey J Fadrowski (JJ)

Department of Pediatrics, Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Colleen Bauza (C)

Department of Health Informatics, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA.

Paul M Dunman (PM)

Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York, USA.

Robert A Dudas (RA)

Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Medicine, Division of Hospital Medicine, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA.

Neil A Goldenberg (NA)

Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, and All Children's Research Institute, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA.

David M Berman (DM)

Department of Medicine, Division of Infectious Diseases, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA.

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