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Infection and Immunity, December 2007, p. 5769-5776, Vol. 75, No. 12
0019-9567/07/$08.00+0     doi:10.1128/IAI.00802-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Coinfection with Antigenically and Genetically Distinct Virulent Strains of Babesia bovis Is Maintained through All Phases of the Parasite Life Cycle{triangledown}

Shawn J. Berens,* Kelly A. Brayton, and Terry F. McElwain

Program in Vector-Borne Diseases, Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington 99164-7040

Received 11 June 2007/ Returned for modification 26 July 2007/ Accepted 30 August 2007

Antigenic polymorphism is a defining characteristic of the Babesia bovis variable merozoite surface antigen (VMSA) family. Sequence analysis strongly suggests that recombination between virulent strains contributes to VMSA diversity. While meiosis during the aneuploid stage of the parasite's life cycle in the tick vector Rhipicephalus (Boophilus) microplus is the most probable source of interstrain recombination, there is no definitive evidence that coinfection of the mammalian host or R. microplus ticks with more than one virulent strain occurs. Using allele-specific real-time quantitative PCR, we tested the hypotheses that cattle could support coinfection of two antigenically variant virulent tick-transmissible strains of B. bovis and that R. microplus ticks could acquire and transmit these two divergent strains. The results indicate that both calves and ticks can support virulent B. bovis coinfection through all phases of the hemoparasite's life cycle. Neither strain dominated in either the mammalian or invertebrate host, and larval tick progeny, which could be coinfected individually, were also able to transmit both strains, resulting in virulent babesiosis in recipients. While coinfection of the tick vector provides the context in which allelic antigenic diversity can be generated, recombination of VMSA genes could not be confirmed, suggesting that VMSA allelic changes are slow to accumulate.

* Corresponding author. Mailing address: Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA 99164-7040. Phone: (509) 335-6346. Fax: (509) 335-8529. E-mail: sberens{at}vetmed.wsu.edu

{triangledown} Published ahead of print on 24 September 2007.

Editor: W. A. Petri, Jr.

Infection and Immunity, December 2007, p. 5769-5776, Vol. 75, No. 12
0019-9567/07/$08.00+0     doi:10.1128/IAI.00802-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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