Abstract
The true nature of the lowered resistance to infection associated with diabetes mellitus is poorly understood despite a wealth of clinical and experimental information. Earlier writers1favored the view that it depended on hyperglycemia and saturation of the tissues with dextrose, since many micro-organisms, including diphtheroids, molds and cocci, had been shown to grow by preference in mediums containing sugar. More recent experiments, by Richardson,2Marble and his associates,3Pillsbury and Kulchar4and others, on the contrary, indicate that increased sugar content of blood and tissues is not significant in bringing about increased growth of bacteria in the body or in diminishing the resistance of the host. Although experimental staphylococcic cutaneous ulcers in dogs undergo rapid necrosis after large intraperitoneal injections of dextrose, this occurs only with solutions sufficiently hypertonic to have toxic effects, and these results can also be duplicated with hypertonic sodium chloride solution.4 The humoral mechanism
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