The effect of selenium (Se) deficiency, produced by feeding a Se-deficient diet, on the development of central nervous system (CNS) lesions was studied in mice infected with Listeria monocytogenes, administered in dri...
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The effect of selenium (Se) deficiency, produced by feeding a Se-deficient diet, on the development of central nervous system (CNS) lesions was studied in mice infected with Listeria monocytogenes, administered in drinking water for 1 or 7 days in a daily dose of 10(9) organisms, or for 7 days in a daily dose of 10(7). Se-deficient mice differed from Se-normal controls in developing CNS lesions significantly more frequently. Moreover, regardless of Se status, mice receiving repeated doses of 10(9) organisms difficult from those receiving a single 10(9) dose in showing CNS lesions at least twice as often. The majority of animals with CNS lesions showed an inflammatory pattern of rhombencephalitis (17/24), while only two of 24 showed choroiditis-ventriculitis-meningitis;five of 24 animals showed both inflammatory patients. Listeria monocytogenes antigen was identified within the areas of inflammation by an immunoperoxidase technique. Neuritis of the trigeminal nerve was present in eight animals. The relative lack of pathological changes in the liver and spleen validates this murine model for the study of CNS listeriosis. (C) 2000 Harcourt Publishers Ltd.
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