Charles A. Kallick

Abstract In the United States, ۲۰,۰۰۰ patients each year lose their sight from diabetic retinopathy. The cause has been attributed to a failure of control of glucose levels. Recent studies have challenged this, and have suggested that there is no evidence for a consistent glycemic threshold in various populations relating to the incidence of retinopathy. The Ehrlichia have been recently suggested as having a role in diabetes. The action of this obligate parasitic bacterium which often affects the cells involved in immunity has the potential of affecting various tissues randomly.   This includes self-reactive T or B cells which may be erroneously altered or released from the marrow because of infection of marrow precursors by an Ehrlichia. The discovery of a gene obtained by molecular methodology from a leukemia patient, has given us a tool to identify by molecular methods, the presence of this gene and assumed bacterium in the blood of patients with various syndromes that includes diabetes. Because of the inconsistent evidence of a uniform glycemic threshold in retinopathy and the failure of its control, this hypothesis raises the question of something else that might be causing this damage. The suspected bacterium in diabetes may have as a significant side effect of its infection of the immune system, specifically the site of action of damage to the small vessels of the retina which could lead to what is regularly described in retinopathy; further, and that may include damage to other vessels seen in peripheral and coronary arteries. The availability of a molecular test in whole blood specimens from diabetics suggests a survey for the gene of the bacterium described in diabetic patients and matched controls. Such an investigation could lead to other therapies directed against the bacterium's presence in the marrow if discovered, and strategies to eliminate the harmful self-reactive T or B cells, if found in diabetes.