Pathogenic synergy: mixed intra-abdominal infections.
In this article we review our researches into the pathogenesis of mixed infections. These may conveniently be divided into in vitro and in vivo studies. In vitro we confirmed that interference with the killing of aerobes by polymorphonuclear leucocytes (PMN's) is a property of the Bacteroides strains tested and appears to depend on competition for opsonins i.e. complement factors. Further studies are in progress to define which complement factors and which bacterial structures are involved. The influence of B. fragilis on chemotaxis has also been studied. Our preliminary data suggest that B. fragilis is itself poorly chemotactic and reduces the chemoattractivity of Proteus mirabilis. This observation is surprising when we consider that abscess formation is the hall-mark of B. fragilis infections and needs clarification. In vivo we have developed a skin infection model in mice which is economical and gives reproducible and quantitative results. In this model we have demonstrated pathogenic synergy between Escherichia coli and B. fragilis. Further studies are planned to assess the role of complement and bacterial factors in this in vivo synergy.
D000818:Animals; D001419:Bacteria / Q000472:pathogenicity*; D001424:Bacterial Infections / Q000382:microbiology*; D001441:Bacteroides fragilis / Q000276:immunology / Q000472:pathogenicity; D002634:Chemotaxis, Leukocyte; D004195:Disease Models, Animal; D006801:Humans; D007410:Intestinal Diseases / Q000382:microbiology*; D051379:Mice; D009504:Neutrophils / Q000276:immunology; D009895:Opsonin Proteins / Q000276:immunology; D010587:Phagocytosis; D012874:Skin Diseases, Infectious / Q000382:microbiology; D014774:Virulence
D009895:Opsonin Proteins