Deficient phagocytosis secondary to breakdown of opsonic factors in infected exudates

Abscess formation or development of a purulent exudate within a closed cavity (empyema) remains an unpredictable complication of pyogenic infections. The mechanisms leading to abscess formation are largely unknown. Once established abscess or empyema are characterized by the presence of a large number of viable bacteria, despite the ingress and the persistence of a large population of polymorphonuclear leukocytes (PMNLs). Here again, we do not have adequate data to explain this biological paradox: How can bacteria persist in a surrounding rich in phagocytic cells ? Obviously, one or several of the mechanisms controlling attachment, ingestion or killing of microorganisms must be deficient in such a situation. Biophysical factors such as low pH and/or low pO2, as measured occasionally in inflammatory exudates, have been reported to play an inhibitory role on phagocytosis (1,2). This does not seem to be constantly the case since unpublished observations from our laboratory on experimental abscesses in the guinea pig have shown biochemical+biophysical parameters compatible with normal PMNL function (3).