This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Kozak, N. A.
Right arrow Articles by Fields, B. S.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kozak, N. A.
Right arrow Articles by Fields, B. S.

 Previous Article  |  Next Article 

Journal of Clinical Microbiology, August 2009, p. 2525-2535, Vol. 47, No. 8
0095-1137/09/$08.00+0     doi:10.1128/JCM.02410-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Distribution of lag-1 Alleles and Sequence-Based Types among Legionella pneumophila Serogroup 1 Clinical and Environmental Isolates in the United States{triangledown}

Natalia A. Kozak,1* Robert F. Benson,1 Ellen Brown,1 Nicole T. Alexander,1 Thomas H. Taylor Jr.,1 Brian G. Shelton,2 and Barry S. Fields1

Division of Bacterial Diseases, National Center for Immunization and Respiratory Diseases, Coordinating Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333,1 PathCon Laboratories, Norcross, Georgia 300922

Received 16 December 2008/ Returned for modification 12 February 2009/ Accepted 18 June 2009

Approximately 84% of legionellosis cases are due to Legionella pneumophila serogroup 1. Moreover, a majority of L. pneumophila serogroup 1 clinical isolates react positively with monoclonal antibody 2 (MAb2) of the international standard panel. Over 94% of the legionellosis outbreaks investigated by the Centers for Disease Control and Prevention are due to this subset of L. pneumophila serogroup 1. To date, there is no complete explanation for the enhanced ability of these strains to cause disease. To better characterize these organisms, we subtyped 100 clinical L. pneumophila serogroup 1 isolates and 50 environmental L. pneumophila serogroup 1 isolates from the United States by (i) reactivity with MAb2, (ii) presence of a lag-1 gene required for the MAb2 epitope, and (iii) sequence-based typing analysis. Our results showed that the MAb2 epitope and lag-1 gene are overrepresented in clinical L. pneumophila serogroup 1 isolates. MAb2 recognized 75% of clinical isolates but only 6% of environmental isolates. Similarly, 75% of clinical isolates but only 8% of environmental isolates harbored lag-1. We identified three distinct lag-1 alleles, referred to as Philadelphia, Arizona, and Lens alleles, among 79 isolates carrying this gene. The Arizona allele is described for the first time in this study. We identified 59 different sequence types (STs), and 34 STs (58%) were unique to the United States. Our results support the hypothesis that a select group of STs may have an enhanced ability to cause legionellosis. Combining sequence typing and lag-1 analysis shows that STs tend to associate with a single lag-1 allele type, suggesting a hierarchy of virulence genotypes. Further analysis of ST and lag-1 profiles may identify genotypes of L. pneumophila serogroup 1 that warrant immediate intervention.

* Corresponding author. Mailing address: Centers for Disease Control and Prevention, 1600 Clifton Rd. NE, Mail Stop G03, Atlanta, GA 30033. Phone: (404) 639-2305. Fax: (404) 639-2070. E-mail: htv2{at}cdc.gov

{triangledown} Published ahead of print on 24 June 2009.

Journal of Clinical Microbiology, August 2009, p. 2525-2535, Vol. 47, No. 8
0095-1137/09/$08.00+0     doi:10.1128/JCM.02410-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»