Persistence of Community-Acquired Respiratory Distress Syndrome Toxin-Producing Mycoplasma pneumoniae in Refractory Asthma

  1. Joel B. Baseman, PhD
  1. From the Department of Medicine (Drs Peters and Singh), the Department of Pediatrics (Dr Brooks), the Department of Microbiology and Immunology (Drs Kannan and J. B. Baseman and Ms Cagle), and the Department of Pathology (Dr Coalson), University of Texas Health Science Center at San Antonio, TX; Asthma and Allergy Associates of South Texas (Dr Diaz), San Antonio, TX; and the Department of Epidemiology (Dr J. G. Baseman), University of Washington School of Public Health, Seattle, WA.
  1. Correspondence to:
    Jay Peters, MD, FCCP, 7704 Merton Minter Blvd (111E), San Antonio, TX 78229; e-mail: peters{at}uthscsa.edu

Abstract

Background: The role of Mycoplasma pneumoniae (Mp) in the initiation and persistence of asthma remains elusive. Mp community-acquired respiratory distress syndrome toxin (CARDS Tx) is a unique virulence factor that induces an intense lymphocytic response and exacerbates asthma in animal models. We sought to determine the incidence of Mp infection and the presence of CARDS Tx in subjects with refractory asthma (RA).

Methods: We conducted a prospective observational study in 64 subjects with RA. Respiratory secretions (sputum, nasal lavage, and throat swab) and blood were analyzed for the presence of CARDS Tx and P1 adhesin (P1) DNA by polymerase chain reaction (PCR), and CARDS Tx by antigen capture. Serum IgM and IgG antibodies to CARDS Tx were determined by enzyme-linked immunosorbent assay (ELISA).

Results: Thirty-three of 64 subjects (52%) tested positive for Mp: 29 of 33 by CARDS Tx vs 10 of 33 by P1 assays. Ten subjects followed longitudinally for up to 633 days tested persistently positive for Mp. There were no significant differences in Mp-specific IgG responses between Mp-positive and Mp-negative groups. Eight of 10 subjects who tested persistently positive failed to mount a substantial IgG response to CARDS Tx, and up to 8 weeks of clarithromycin failed to eradicate Mp in five subjects.

Conclusions: Subjects with RA may be chronically infected with Mp. PCR for CARDS Tx appears to be the most sensitive method of identifying Mp infection. Despite the persistence of Mp in subjects with RA, some subjects failed to mount an IgG response, and macrolide therapy was insufficient to eradicate Mp.

Footnotes

  • Funding/Support: This study was supported by the National Institutes of Health [Grant U19A1070412-01] and The Kleberg Foundation to J. B. B.

  • Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).

  • Abbreviations

    CARDS Tx
    community-acquired respiratory distress syndrome toxin
    ELISA
    enzyme-linked immunosorbent assay
    Mp
    Mycoplasma pneumoniae
    P1
    P1 adhesin
    PCR
    polymerase chain reaction
    RA
    refractory asthma
    rCARDS Tx
    recombinant community-acquired respiratory distress syndrome toxin
    rP1
    recombinant P1 adhesin immunodominant carboxy domain
    • Received February 8, 2011.
    • Accepted April 13, 2011.
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    1. CHEST vol. 140 no. 2 401-407

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