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Infect Immun. 1975 June; 11(6): 1216-1221
Copyright © 1975 American Society for Microbiology. All Rights Reserved.

Platelet Kinetics in Canine Ehrlichiosis: Evidence for Increased Platelet Destruction as the Cause of Thrombocytopenia

Ronald D. Smith*, Miodrag Ristic, David L. Huxsoll1 and Richard A. Baylor

* Department of Veterinary Pathology and Hygiene, College of Veterinary Medicine, University of Illinois at Champaign-Urbana, Urbana, Illinois 61801
Division of Veterinary Medicine, Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington, D.C. 20012
Department of Nuclear Medicine, Carle Clinic, Urbana, Illinois 61801

ABSTRACT

A significant (P < 0.025) increase in the mean platelet diameter occurred in five Ehrlichia canis-infected dogs when platelet numbers decreased to 100,000/µl or less. Maximal incorporation of [75Se]selenomethionine into platelets of six uninfected dogs was 0.080 ± 0.019% (mean ± standard error) and occurred 5 to 6 days after dosage, whereas maximal incorporation was 0.036 ± 0.004% within 2 to 3 days after dosage in seven chronically infected dogs that had thrombocytopenia. Analysis of the [75Se]selenomethionine curves yielded a platelet lifespan of 9 days in uninfected dogs versus 4 days in chronically infected dogs. Thus, megakaryocyte maturation and/or platelet release occurred at an accelerated rate in infected dogs, whereas increased destruction of newly produced labeled platelets diminished their number of peripheral blood. [51Cr]sodium chromate-labeled platelet survival was exponential, with a half-life of approximately 1 day in two dogs at 2 to 4 days postinfection and three chronically infected dogs. Platelet survival time was 8 days and rectilinear in four uninfected dogs. Platelet recovery was 39.43 ± 2.86% in infected dogs as compared with 68.2 ± 10.72% in uninfected dogs. Whole-body scans of one dog prior to and 7 days after infection showed that labeled platelets were destroyed primarily in the spleen. It is concluded that the thrombocytopenia in E. canis-infected dogs is the result of increased platelet destruction which begins within a few days after infection.


FOOTNOTES

1 Present address: U.S. Army Medical Research Unit, Kuala Lumpur, Department of State, Washington, D.C. 20520.


Infect Immun. 1975 June; 11(6): 1216-1221
Copyright © 1975 American Society for Microbiology. All Rights Reserved.




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