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Infection and Immunity, March 2003, p. 1574-1579, Vol. 71, No. 3
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.3.1574-1579.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Harold M. McClure,3 Richard B. Raybourne,4 Kristina M. Williams,4 Uma S. Babu,4 Glenn O. Ware,5 J. Roger Broderson,6 and Michael P. Doyle2
Department of Environmental Health Science,1 Experimental Statistics,5 Office of the Vice President for Research, University of Georgia, Athens, Georgia 30602,6 Center for Food Safety, University of Georgia, Griffin, Georgia 30223,2 Yerkes Regional Primate Research Center, Emory University, Atlanta, Georgia 30322,3 U.S. Food and Drug Administration, Laurel, Maryland 207084
Received 5 August 2002/ Returned for modification 12 September 2002/ Accepted 23 November 2002
Listeria monocytogenes, isolated from outbreaks in either human or nonhuman primate populations, was administered orally at doses ranging from 106 to 1010 CFU. Four of 10 treated animals delivered stillborn infants. L. monocytogenes was isolated from fetal tissue, and the pathology was consistent with L. monocytogenes infection as the cause of pregnancy loss. For all pregnancies resulting in stillbirths, L. monocytogenes was isolated from maternal feces, indicating that L. monocytogenes had survived and had probably colonized the gastrointestinal tract. Antibodies and antigen-specific lymphocyte proliferation against Listeria increased in animals that had stillbirths.
Present address: U.S. Food and Drug Administration, College Park, MD 20740.
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