Riralateenbhensaithsnehe PTOarhe aionnaaiaie tT RADIATION INJURY: Ffs PATHOGENESIS AND THREADY AT exposed in the Los Mamas rector accidents and one exposed in the Yueoslav accident died despite Vigorous antibietic therapy. bois possible that pnproved results would be obtained with a schedule of aduilnistration designed to avoid the development of resistant bacteria ‘Coulter and Millers. Of significance tn this regard ia the recent report (Hammond «fala showing that mice exposed to neutron radiation are protected from death by antibiotics during the first 10 days, hut not in the Tt- to 80-day period when most nice die following gamma or x-radiation. This would indicate that under some conditions, at Jeast, infection alone does not account for the mortality observed. Thus, there is no doubt that infection contributes greatly to the discase process, and mortality following exposure to total body radiation, However, it is equally clear that acute radiation illness is not an infeetious disease in the usual sense; rather infection is a compheation of a scrious debilitating underlying disease which specifically interferes with defense mechanisms against bacterial invasion. Death may occur in some individuals whether infection is present or not, at high dose levels. Thus antibiotics cannot be expected to be curative as with primarily infectious discases, and dramatic cures cannot be expected from this type of therapy. However, as with any debilitating disease, antibiotics definitely will prevent death in a certain number who might otherwise die -prevent death until regeneration and restoration of functions allows normal defense mechanisms to again protect the exposed individual. 9.5.7.1 Mechanisms of inercascd susceptibility to infection. Nearly all known body defenses against bacterial invasion have been reportedly impaired by large doses of total body radiation. Thus the skin and mucous membranes may show small eroded areas, frequently secondary to hemorrhage, that provide portals of entry for bacteria. It has been shown that the number of bacteria able to cross the intestinal barrier does not increase following irradiation; however, those that cross are able to multiply and produce a fatal bacteremia in the host whore defenses in general are lowered (Gordon ef al.). The leukopenia and impaired antibody pruduction contribute greatly to the increased susceptibility to infection, and a failure to adequately clear the blood stream of bacteria indicates functional impairment of the phagocytic cells. Radiation mortality correlates well with the degree of granulocytic leukopenia (Smith c al.). Antibody production is seriously impaired (Stoner). 9.6 Résumé of Acute Radiation Effects To recapitulate and summarize, it is apparent that diffuse celhilar injury of different degrees is sustained by all tissues at the time of exposure to radiation. The exact mechanism by which this injury is produced remains JU128 77