Biomaterial-associated staphylococcal peritoneal infections in a neutropaenic mouse model.
Adhesion of staphylococcal cells to polyethylene with end point-attached heparin was quantified by bioluminescence. Staphylococcus epidermidis 3380 and the slime-producing S. epidermidis RP12 adhered to the highest extent, and S. lugdunensis 2342 to the least extent. Preincubation of the polymer with dialysis fluid reduced adhesion of S. epidermidis 3380 and RP12 but enhanced that of S. aureus, and preadsorption of the surface with fibronectin decreased subsequent adhesion of S. epidermidis and S. haemolyticus strains. When staphylococci were grown in the presence of a biomaterial their ability to activate peritoneal cells was decreased. The bactericidal activity was impaired, whereas ingestion of opsonized coagulase-negative staphylococci (CNS) strains was unaffected. With S. epidermidis RP12 the presence of biomaterial did not influence either phagocytosis or bactericidal effect of peritoneal cells. After intra-peritoneal challenge with staphylococcal strains, the organ uptake of S. aureus Cowan 1 was increased in normal mice whereas immunosuppressed mice died. CNS strains increased mainly in the peritoneal cavity of immunosuppressed mice. The uptake of bacteria in liver and kidneys was increased with S. epidermidis 3380, S. lugdunensis 2343 and S. schleiferi 667-88. Generally, CNS strains persisted in the peritoneal cavity of both normal and immunosuppressed mice. These data indicate that host defense mechanisms, mainly polymorphonuclear neutrophils, fail to eliminate CNS infections in the peritoneum, and that initial adhesion to an implanted biomaterial may be of lesser importance in the peritoneal cavity than in e.g. catheter-associated infections. There are strain-specific virulence factors of bacteria, and slime producing strains evade the host defense mechanisms more efficiently than non-slime producing strains.
Department of Infectious Biology, University of Lodz, Poland.
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Rozalska
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Ljungh
D000327:Adsorption; D000818:Animals; D001202:Ascitic Fluid; D001422:Bacterial Adhesion / Q000187:drug effects; D003030:Coagulase / Q000032:analysis; D004198:Disease Susceptibility / Q000276:immunology; D005260:Female; D005353:Fibronectins / Q000494:pharmacology; D006493:Heparin; D016867:Immunocompromised Host; D007668:Kidney / Q000382:microbiology; D008099:Liver / Q000382:microbiology; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D009503:Neutropenia / Q000150:complications / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D010529:Peritoneal Cavity / Q000166:cytology; D010530:Peritoneal Dialysis; D010538:Peritonitis / Q000209:etiology* / Q000276:immunology; D010587:Phagocytosis; D011095:Polyethylenes; D011135:Polysaccharides, Bacterial / Q000378:metabolism; D019736:Prostheses and Implants / Q000009:adverse effects*; D013045:Species Specificity; D013203:Staphylococcal Infections / Q000209:etiology* / Q000276:immunology; D013210:Staphylococcus / Q000472:pathogenicity* / Q000502:physiology; D013211:Staphylococcus aureus / Q000502:physiology; D013212:Staphylococcus epidermidis / Q000502:physiology; D014018:Tissue Distribution
D003030:Coagulase; D005353:Fibronectins; D011095:Polyethylenes; D011135:Polysaccharides, Bacterial; D006493:Heparin