Biomaterial-associated staphylococcal peritoneal infections in a neutropaenic mouse model

Abstract

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.

In vitro effects of zirconia and alumina particles on human blood monocyte-derived macrophages: X-ray microanalysis and flow cytometric studies

“…12,13 Reduced bactericidal activity of phagocytes has been observed following biomaterial implantation. 14,15 These phagocytosing cells have been shown to undergo an associated respiratory burst in response to a stimulus (reviewed by Rossi et al 16 ). The oxidative burst, which is characterized by the generation of reactive oxygen species (ROS) as superoxide, hydrogen peroxide, hydroxyl radicals, and singlet oxygen, has been used to test hemodialysis membrane biocompatibility in vitro.…”

Specific immune response to staphylococcal antigens during long-lasting biomaterial implantation

“…The outcome of biomaterial‐associated infections depends on microbial virulence and host defense mechanisms, properties of the biomaterial, and local growth conditions for microbes [1–4]. Microorganisms causing device‐related infections usually emanate from the patient's skin or mucosa, and both coagulase‐positive and coagulase‐negative staphylococci dominate in these infections [4].…”

“…The persistence of the bacteria on biomaterials is facilitated by biofilm formation, production of slime, and specific bacterial adhesion to the host proteins adsorbed to polymers [2, 4, 5]. A contact reaction of macrophages with non‐ingestible biomaterial produces so‐called frustrated phagocytes [1, 3–5], induces inflammation and, if long‐lasting, an unbalanced production of various cytokines causes a derangement of hematopoiesis and affects development of the immune response [6, 7].…”

Effects of Granulocyte‐Macrophage Colony Stimulating Factor (GM‐CSF) on Biomaterial‐Associated Staphylococcal Infection in Mice

“…Infections are a major complication in the usage of biomaterials for therapeutic or diagnostic purposes (6,14,26). The microorganisms implicated in intravenous or intraperitoneal device-related infections usually emanate from the patient's skin or mucosa, and both coagulasenegative and coagulase-positive staphylococci dominate in these infections (14,18,19,26). The bacterial colonization of biomaterials is facilitated by biofilm formation (slime production, specific bacterial adhesion to the host proteins adsorbed by polymers) (14,18,19,26).…”

“…Once established, biomaterial-associated infections are resistant to antibiotic therapy and to the host defense (26). A reduction in the bactericidal activity of phagocytes during biomaterial implantations has frequently been observed; a contact-reaction of phagocytes with non-ingestible biomaterial produces so called frustrated phagocytes (6,(18)(19)(20).…”