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Applied and Environmental Microbiology, December 2009, p. 7488-7500, Vol. 75, No. 23
0099-2240/09/$08.00+0 doi:10.1128/AEM.01829-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Biosciences and Biotechnology Division, Lawrence Livermore National Laboratory, Livermore, California 94550,1 Department of Microbiology and Immunology, Stanford University Medical School, Stanford, California 94305,2 Department of Microbiology and Molecular Biology, Brigham Young University, Provo, Utah 846023
Received 29 July 2009/ Accepted 29 September 2009
Francisella tularensis, the causative agent of the zoonotic disease tularemia, has recently gained increased attention due to the emergence of tularemia in geographical areas where the disease has been previously unknown and to the organism's potential as a bioterrorism agent. Although F. tularensis has an extremely broad host range, the bacterial reservoir in nature has not been conclusively identified. In this study, the ability of virulent F. tularensis strains to survive and replicate in the amoeba Acanthamoeba castellanii was explored. We observe that A. castellanii trophozoites rapidly encyst in response to F. tularensis infection and that this rapid encystment phenotype is caused by factor(s) secreted by amoebae and/or F. tularensis into the coculture medium. Further, our results indicate that in contrast to the live vaccine strain LVS, virulent strains of F. tularensis can survive in A. castellanii cysts for at least 3 weeks postinfection and that the induction of rapid amoeba encystment is essential for survival. In addition, our data indicate that pathogenic F. tularensis strains block lysosomal fusion in A. castellanii. Taken together, these data suggest that interactions between F. tularensis strains and amoebae may play a role in the environmental persistence of F. tularensis.
Published ahead of print on 9 October 2009.
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