This Article Full Text Full Text (PDF) Other Versions of this Article: IAI.00085-07v1 75/5/2580    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fux, B. Articles by Sibley, L. D. Search for Related Content PubMed PubMed Citation Articles by Fux, B. Articles by Sibley, L. D.

 Previous Article  |  Next Article 

Infection and Immunity, May 2007, p. 2580-2590, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.00085-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Toxoplasma gondii Strains Defective in Oral Transmission Are Also Defective in Developmental Stage Differentiation

Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110,¹ Department of Microbiology, University of Tennessee, Knoxville, Tennessee 37996²

Received 15 January 2007/ Returned for modification 20 February 2007/ Accepted 27 February 2007

Toxoplasma gondii undergoes differentiation from rapidly growing tachyzoites to slowly growing bradyzoites during its life cycle in the intermediate host, and conversion can be induced in vitro by stress. Representative strains of the three clonal lineages showed equal capacity to differentiate into bradyzoites in vitro, as evidenced by induction of bradyzoite antigen 1, staining with Dolichos biflorus lectin (DBL), pepsin resistance, and oral infectivity in mice. We also examined several recently described exotic strains of T. gondii, which are genetically diverse and have a different ancestry from the clonal lineages. The exotic strain COUG was essentially like the clonal lineages and showed a high capacity to induce bradyzoites in vitro and in vivo, consistent with its ability to be efficiently transmitted by the oral route. In contrast, exotic strains MAS and FOU, which are defective in oral transmission, showed a decreased potential to develop into bradyzoites in vitro. This defect was evident from reduced staining with DBL and the cyst antigen CST1, failure to down-regulate tachyzoite antigens, such as tachyzoite surface antigens 1 and 2A, and decreased resistance to pepsin treatment. Despite normal in vitro differentiation, the exotic strains CAST and GPHT also showed decreased oral transmission, due to formation of smaller cysts and a lower tissue burden during chronic infection, traits also shared by MAS and FOU. Collectively, these findings reveal that the limited oral transmission in some strains of T. gondii is due to inefficient differentiation to the bradyzoite form, leading to defects in the formation of tissue cysts.

Published ahead of print on 5 March 2007.

Editor: W. A. Petri, Jr.

This article has been cited by other articles:

• Brossier, F., Starnes, G. L., Beatty, W. L., Sibley, L. D. (2008). Microneme Rhomboid Protease TgROM1 Is Required for Efficient Intracellular Growth of Toxoplasma gondii. Eukaryot Cell 7: 664-674 [Abstract] [Full Text]  
• Khan, A., Fux, B., Su, C., Dubey, J. P., Darde, M. L., Ajioka, J. W., Rosenthal, B. M., Sibley, L. D. (2007). Recent transcontinental sweep of Toxoplasma gondii driven by a single monomorphic chromosome. Proc. Natl. Acad. Sci. USA 104: 14872-14877 [Abstract] [Full Text]