No abstract

Granulocytes of patients with diabetes mellitus have an impaired capability to engulf bacteria, but it is not clear whether subsequent intracellular killing, which has separate energy sources, is also defective. We separately assayed engulfment and intracellular killing of Staphylococcus aureus 502a by granulocytes of 17 diabetic patients with fasting hyperglycemia to better characterize the phagocytic defect. Diabetic granulocytes engulfed a smaller proportion than controls of a 106 inoculum of bacteria after 20 minutes of incubation in vitro (56.8 ± 9.4 per cent versus 72.4 ± 3.6 per cent, mean ± S.E. of 10 patients and paired controls, p < 0.05), but after 60 minutes of incubation this defect had disappeared. Intracellular killing of staphylococci by granulocytes from seven diabetics (68.6 ± 8.9 per cent of a 106 inoculum) was less (p < 0.01) than that of paired controls (80.3 ± 4.5 per cent) after two hours of incubation. Seven patients were retested during a period of improved diabetes' control; intracellular killing of staphylococci by granulocytes of six of the seven increased considerably and either exceeded the paired control value or approached it to within 75 per cent. These data suggest that a primary defect exists in intracellular killing of staphylococci by granulocytes from poorly controlled diabetics in addition to that previously shown in engulfment. This bactericidal activity becomes more efficient when the diabetes is brought under better control.

No abstract

An animal model of Legionella pneumophila pneumonia was developed to study aerosol infection, pathogenesis, and pulmonary host defense mechanisms. Guinea pigs were exposed in an inhalation facility that limited the aerosol of L pneumophila to the snout. Bronchoalveolar lavage was used to sample airspace cells, secretions, and bacteria during developing infection in 79 exposed animals and 13 uninfected controls. An influx of polymorphonuclear neutrophils followed exponential bacterial growth during the initial three days of infection and coincided with limitation of the increase in bacteria recovered. A macrophage influx occurred at three to five days. Bacteria were eliminated from the lung by 11 days after exposure. Albumin in lavage fluid peaked at two days. Most viable L pneumophila organisms were associated with alveolar macrophages, whereas most of the bacteria associated with polymorphonuclear neutrophils were nonviable. Recruited, and possibly immune, defenses appear to be required for successful resolution of legionella pneumonia.