Abstract
Experimental hyperglycemia and infection with L. monocytogenes, and the effects of somatotsopic hormone and cortisone, were studied. Hamsters, obese mice, and normal mice were used. The results supported the hypothesis that an upset carbohydrate metabolism initiated by stress is the trigger mechanism that makes conditions favourable for proliferation of L. monocytogenes and probably of other glucose fermenting pathogenic agents.
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Selected References
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