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Infection and Immunity, August 1999, p. 4134-4142, Vol. 67, No. 8
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Comparative Analysis of Legionella pneumophila and Legionella micdadei Virulence Traits

Amrita D. Joshi, and Michele S. Swanson*

Department of Microbiology and Immunology, The University of Michigan Medical School, Ann Arbor, Michigan

Received 3 November 1998/Returned for modification 4 January 1999/Accepted 27 May 1999

While the majority of Legionnaire's disease has been attributed to Legionella pneumophila, Legionella micdadei can cause a similar infection in immunocompromised people. Consistent with its epidemiological profile, the growth of L. micdadei in cultured macrophages is less robust than that of L. pneumophila. To identify those features of the Legionella spp. which are correlated to efficient growth in macrophages, two approaches were taken. First, a phenotypic analysis compared four clinical isolates of L. micdadei to one well-characterized strain of L. pneumophila. Seven traits previously correlated with the virulence of L. pneumophila were evaluated: infection and replication in cultured macrophages, evasion of phagosome-lysosome fusion, contact-dependent cytotoxicity, sodium sensitivity, osmotic resistance, and conjugal DNA transfer. By nearly every measure, L. micdadei appeared less virulent than L. pneumophila. The surprising exception was L. micdadei 31B, which evaded lysosomes and replicated in macrophages as efficiently as L. pneumophila, despite lacking both contact-dependent cytopathicity and regulated sodium sensitivity. Second, in an attempt to identify virulence factors genetically, an L. pneumophila genomic library was screened for clones which conferred robust intracellular growth on L. micdadei. No such loci were isolated, consistent with the multiple phenotypic differences observed for the two species. Apparently, L. pneumophila and L. micdadei use distinct strategies to colonize alveolar macrophages, causing Legionnaire's disease.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, The University of Michigan Medical School, 6734 Medical Sciences Building II, Ann Arbor, MI 48109-0620. Phone: (734) 647-7295. Fax: (734) 764-3562. E-mail: mswanson{at}umich.edu.

Infection and Immunity, August 1999, p. 4134-4142, Vol. 67, No. 8
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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