BEFORE 1923, patients with insulin-dependent diabetes mellitus lived with hyperglycemia, dehydration, and semistarvation for several months before they contracted a minor infection and died. It thus became a clinical axiom that diabetics had decreased resistance to infection.¹This concept has been perpetuated by the observation that diabetic ketoacidosis is precipitated by acute infection and by the fact that infections of the feet and of the urinary tract are more common and more difficult to treat in diabetic patients.²Consequently, many physicians believe that diabetics represent a high-risk group that should be protected by improved sanitation, meticulous hygiene, increased immunization, and prophylactic antibiotics. The currently available data indicate that all four of these measures are unnecessary. Pathophysiology In the presence of hyperglycemia, there is decreased phagocytosis by granulocytes.³⁻⁶In the presence of ketosis, there is decreased mobility of granulocytes.⁶⁻⁸These two host deficiencies are corrected readily by
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James M. Moss (1980) studied this question.
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