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Infection and Immunity, April 1999, p. 1593-1598, Vol. 67, No. 4
0019-9567/99/$04.00+0

Antigen-Specific B-Cell Unresponsiveness Induced by Chronic Mycobacterium avium subsp. paratuberculosis Infection of Cattle

W. R. Waters,1,* J. R. Stabel,2 R. E. Sacco,3 J. A. Harp,4 B. A. Pesch,4 and M. J. Wannemuehler1

Veterinary Medical Research Institute, Iowa State University, Ames, Iowa 50011,1 and Zoonotic Diseases Research Unit,2 Avian and Swine Respiratory Disease Unit,3 and Metabolic Diseases and Immunology Research Unit,4 National Animal Disease Center, Agricultural Research Service, U.S. Department of Agriculture, Ames, Iowa 50010-0070

Received 30 July 1998/Returned for modification 5 November 1998/Accepted 5 January 1999

Mycobacterium avium subsp. paratuberculosis infection of cattle results in a chronic granulomatous enteritis. Clinical disease (i.e., cachexia, diarrhea, and high fecal bacterial counts) is preceded by a lengthy subclinical stage of disease. The immunologic mechanisms associated with the progression of infected cattle from subclinical to clinical disease are unclear. In this study, a cell proliferation assay was used in combination with flow cytometry to compare peripheral blood lymphocyte responses of cattle with subclinical paratuberculosis to responses of cattle with clinical paratuberculosis. B cells from cattle with subclinical disease proliferated vigorously upon stimulation with M. avium subsp. paratuberculosis antigen, with up to 12.4% of the total B cells responding. However, B cells from cattle with clinical disease did not proliferate upon antigen stimulation despite good proliferation in response to concanavalin A stimulation. In addition, these animals had high percentages of peripheral blood B cells. B cells from noninfected animals did not proliferate upon M. avium subsp. paratuberculosis antigen stimulation. Thus, it appears that B-cell proliferation is a sensitive indicator of subclinical Johne's disease. Furthermore, the immunologic mechanisms responsible for the antigen-specific unresponsiveness of peripheral blood B cells may be significant in the eventual progression from subclinical to clinical Johne's disease in cattle.

* Corresponding author. Mailing address: Veterinary Medical Research Institute, Iowa State University, 1802 Elwood Dr., Ames, IA 50011. Phone: (515) 294-6842. Fax: (515) 294-1401. E-mail: wwaters{at}iastate.edu.

Infection and Immunity, April 1999, p. 1593-1598, Vol. 67, No. 4
0019-9567/99/$04.00+0


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