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Infection and Immunity, June 2005, p. 3251-3260, Vol. 73, No. 6
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.6.3251-3260.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Changes in Lipopolysaccharide O Antigen Distinguish Acute versus Chronic Leptospira interrogans Infections
Jarlath E. Nally,1*
Emilie Chow,1
Michael C. Fishbein,2
David R. Blanco,1 and
Michael A. Lovett1
Department of Medicine, Division of Infectious Diseases,1
Department of Pathology and Laboratory Medicine, University of California, Los Angeles, California2
Received 19 November 2004/
Returned for modification 23 December 2004/
Accepted 16 January 2005
Leptospirosis is the most geographically widespread zoonotic disease in the world. A severe pulmonary form of leptospirosis (SPFL) is being recognized with increased frequency. We have reported that human SPFL isolates of Leptospira cause acute lethal infection with prominent pulmonary hemorrhage in guinea pigs. We have found that the same SPFL strains cause asymptomatic infection and chronic renal shedding in rats, where infection is restricted to the renal tubules. To address the antigenic composition of host tissue-derived Leptospira (HTL), motile leptospires were purified from guinea pig liver by centrifugation on Percoll density gradients and compared to Percoll-purified in vitro-cultivated Leptospira (IVCL). The lipopolysaccharide O antigen (Oag) content of guinea pig liver-derived HTL was markedly reduced compared to that of IVCL, as demonstrated both by immunoblotting with a monoclonal antibody that was serovar specific for Oag and by periodate-silver staining. Confocal microscopy of HTL in guinea pig liver and kidney with the Oag-specific monoclonal antibody provided further evidence that diminution of the Oag content occurred in situ during lethal infection. In contrast, the Oag content of HTL in chronically infected rat renal tubules was indistinguishable from that of IVCL. These findings suggest that there may be regulation of Oag synthesis by Leptospira specific to the animal host infected. The hypothesis that the Oag content is related to whether lethal infection or chronic renal tubular colonization occurs remains to be tested.
* Corresponding author. Mailing address: Department of Medicine, 37-121 CHS, Division of Infectious Diseases, University of California Los Angeles, 10833 Le Conte Avenue, Los Angeles, CA 90095. Phone: (310) 825-4188. Fax: (310) 825-3632. E-mail: jnally{at}mednet.ucla.edu.
Editor: W. A. Petri, Jr.
Infection and Immunity, June 2005, p. 3251-3260, Vol. 73, No. 6
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.6.3251-3260.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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Copyright © 2005 by the American Society for Microbiology. All rights reserved.