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Author Notes:

Correspondence: Jonas M. Winchell, PhD, Centers for Disease Control and Prevention, 1600 Clifton Rd. NE, MS G-03, Atlanta, GA 30333: jwinchell@cdc.gov

We thank the patients who graciously consented to participate in this study and all members of the Etiology of Pneumonia in the Community Study Team for their contributions.

Potential conflicts of interest. J. D. C. received grants from the CDC during the conduct of the study and has a patent licensed to Vanderbilt University (US patent 8 293 498 B2, October 23, 2012) and a patent pending (Provisional application for US letters patent, VBLT:171USP1).

D. J. W. received grants from the CDC during the conduct of the study.

S. R. A. received grants from the CDC during the conduct of the study and received grants from GlaxoSmithKline outside the submitted work.

K. A. received grants from the CDC during the conduct of the study and collaborated with BioFire Diagnostics, Inc.

W. H. S. received grants from the CDC during the conduct of the study; received research supplies from CareFusion; received grants from BioMerieux, Affinium Pharmaceuticals, Astute Medical, Crucell Holland BV, BRAHMS GmbH, Pfizer, Rapid Pathogen Screening, Venaxis, Cempra Pharmaceuticals, BioAegis Inc, and Sphingotec GmbH; received personal fees from BioFire Diagnostics and Venaxis, Inc. outside the submitted work; and has a patent pending (13/632,874).

E. J. A. received grants from MedImmune and nonfinancial support from Roche outside the submitted work.

J. A. M. received grants from the CDC during the conduct of the study.

A. T. P. received grants from the CDC during the conduct of the study; and travel support and consultant fee from BioFire Diagnostics outside the submitted work.

R. G. W. received grants from the CDC during the conduct of the study and received grants and personal fees from BioMerieux Inc and personal fees from Cempra Pharmaceuticals.

K. M. E. received grants from the CDC during the conduct of the study and received grants from Novartis and funding for service on a Data and Safety Monitoring Board from Novartis outside the submitted work.

All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest.

Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.

Subjects:

Research Funding:

Financial support. This work was supported by the Influenza Division in the National Center for Immunization and Respiratory Diseases at the Centers for Disease Control and Prevention (CDC) through cooperative agreements with each study site and was based on a competitive research funding opportunity.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Immunology
  • Infectious Diseases
  • Microbiology
  • community-acquired pneumonia
  • macrolide resistance
  • molecular epidemiology
  • Mycoplasma pneumonia
  • TANDEM-REPEAT ANALYSIS
  • REAL-TIME PCR
  • MACROLIDE-RESISTANT STRAINS
  • RESOLUTION MELT ANALYSIS
  • CHLAMYDIA-PNEUMONIAE
  • PEDIATRIC-PATIENTS
  • INFECTIONS
  • CHINA
  • CHILDREN
  • OUTBREAK

Molecular Detection and Characterization of Mycoplasma pneumoniae Among Patients Hospitalized With Community-Acquired Pneumonia in the United States

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Journal Title:

Open Forum Infectious Diseases

Volume:

Volume 2, Number 3

Publisher:

, Pages ofv106-ofv106

Type of Work:

Article | Final Publisher PDF

Abstract:

Background.  Mycoplasma pneumoniae is a common cause of community-acquired pneumonia (CAP). The molecular characteristics of M pneumoniae detected in patients hospitalized with CAP in the United States are poorly described. Methods.  We performed molecular characterization of M pneumoniae in nasopharyngeal/oropharyngeal swabs from children and adults hospitalized with CAP in the Centers for Disease Control and Prevention Etiology of Pneumonia in the Community (EPIC) study, including P1 typing, multilocus variable-number tandem-repeat analysis (MLVA), and macrolide susceptibility genotyping. Results.  Of 216 M pneumoniae polymerase chain reaction-positive specimens, 40 (18.5%) were obtained from adults and 176 (81.5%) from children. P1 type distribution differed between adults (64% type 1 and 36% type 2) and children (84% type 1, 13% type 2, and 3% variant) (P < .05) and among sites (P < .01). Significant differences in the proportions of MLVA types 4/5/7/2 and 3/5/6/2 were also observed by age group (P < .01) and site (P < .01). A macrolide-resistant genotype was identified in 7 (3.5%) specimens, 5 of which were from patients who had recently received macrolide therapy. No significant differences in clinical characteristics were identified among patients with various strain types or between macrolide-resistant and -sensitive M pneumoniae infections. Conclusions.  The P1 type 1 genotype and MLVA type 4/5/7/2 predominated, but there were differences between children and adults and among sites. Macrolide resistance was rare. Differences in strain types did not appear to be associated with differences in clinical outcomes. Whole genome sequencing of M pneumoniae may help identify better ways to characterize strains.

Copyright information:

Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US.

This is an Open Access work distributed under the terms of the Creative Commons Universal : Public Domain Dedication License (http://creativecommons.org/publicdomain/zero/1.0/).

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