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Infection and Immunity, September 2005, p. 5379-5387, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5379-5387.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Gliding Motility Leads to Active Cellular Invasion by Cryptosporidium parvum Sporozoites

Dawn M. Wetzel,1,{dagger} Joann Schmidt,2 Mark S. Kuhlenschmidt,2 J. P. Dubey,3 and L. David Sibley1*

Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, Missouri 63110,1 Department of Pathobiology, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, 2001 S. Lincoln Ave., Urbana, Illinois 61801,2 Animal Parasitic Diseases Lab, BARC-East, Bldg. 1001, ANRI, Agricultural Research Service, USDA, Beltsville, Maryland 207053

Received 7 February 2005/ Returned for modification 25 March 2005/ Accepted 19 April 2005

We examined gliding motility and cell invasion by an early-branching apicomplexan, Cryptosporidium parvum, which causes diarrheal disease in humans and animals. Real-time video microscopy demonstrated that C. parvum sporozoites undergo circular and helical gliding, two of the three stereotypical movements exhibited by Toxoplasma gondii tachyzoites. C. parvum sporozoites moved more rapidly than T. gondii sporozoites, which showed the same rates of motility as tachyzoites. Motility by C. parvum sporozoites was prevented by latrunculin B and cytochalasin D, drugs that depolymerize the parasite actin cytoskeleton, and by the myosin inhibitor 2,3-butanedione monoxime. Imaging of the initial events in cell entry by Cryptosporidium revealed that invasion occurs rapidly; however, the parasite does not enter deep into the cytosol but rather remains at the cell surface in a membrane-bound compartment. Invasion did not stimulate rearrangement of the host cell cytoskeleton and was inhibited by cytochalasin D, even in host cells that were resistant to the drug. Our studies demonstrate that C. parvum relies on a conserved actin-myosin motor for motility and active penetration of its host cell, thus establishing that this is a widely conserved feature of the Apicomplexa.

* Corresponding author. Mailing address: Department of Molecular Microbiology, Campus Box 8230, Washington University School of Medicine, St. Louis, MO 63110. Phone: (314) 362-8873. Fax: (314) 362-3203. E-mail: sibley{at}borcim.wustl.edu.

Editor: W. A. Petri, Jr.

{dagger} Present address: Pediatrics Residency Program, Children’s Hospital of New York, 630 W. 168th St., New York, NY 10032.

Infection and Immunity, September 2005, p. 5379-5387, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5379-5387.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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