Biofilms

Microorganisms in colonies on surfaces form layers two to hundreds of organisms thick composed of cellular material, extracellular polysaccharides, environmental adsorbates, and debris. This surface composite is called the biofilm or slime. In nature, biofilms accumulate to significant thicknesses and may impede flow in hydraulic systems.

Most organisms within a mature microcolony are not attached to a two-dimensional surface but are fixed within the three-dimensional structure of the biofilm. Bacterial species in consortia have shown higher metabolic activities than those of free organisms, a characteristic that may be related to cross-feeding and the development of suitable microenvironments within the adherent biofilm (Paerl, 1985).

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FIG. 5ยป Surface disruption by wear, corrosion, trauma, or bacterial mechanisms frees metabolites or ions, which .ire rhcu available to bacteria (Bj within a biofilm tnicroenvironmenr. At micro/ones, metal ions required by pathogenic bacteria are not lost by diffusion and may be shielded from host protein-binding complexes, bacteria are also protected by biofilms and tttav metabolite polymer or tissue components, interactions occur between exposed receptors on bacttria or surfaces.

Many differ em species of bacteria may thrive within the biofilm, with significant interaction and even interdependent-^ between organisms (Hamilton, 1987), such as the growth and activity of anaerobic species within a biofilm that is itself located in a highly aerobic bulk environment (Gibbons and van Houte, 1975: Hamilton, 1984; Paerl, 1985). For example, the formation of dental canes involves a succession of microbes. The primary colomiing aerobic species grows on salivary glycoproteins. Facultative and anaerobic organisms than use the metabolic products of the primary colonizer and produce deleterious organic acids (Hamilton, 1987), In oil pipelines, hydrocarbon-degrading bacteria create the anaerobic conditions and produce the necessary nutrients for sulfate-reducing bacteria, which are the pnnicipal cause of anaerobic corrosion (Hamilton, 1987).

WEAR AND TEAR: SUBSTRATA AND MfCROZONES

Damage to substrata by wear, corrosion, toxins, viral effects, bacteria! mechanisms, or biosystemic chemical degradation establishes environmental conditions that microorganisms can exploit. Surfaces provide an interface for the concentration of charged particles, molecules, and nutrients, or may themselves be metabolized (Tig. 5).

The micro zone may be thought of as an environmental, metabolic microclimate at a surface created by a complex biofilm (Paerl, 1985; Stenstrom, 1985). This concept may be applied to implant surfaces on which adhesive, possibly polymicrobial, colonization creates a microclimate of favorable conditions and excludes antagonistic environmental factors.

Under normal conditions, host defense mechanisms are available to limit the nutrients necessary for bacterial propaga tion. For example, iron is an essential element in bactcria! growth and virulence (Bullen etal., 1974; Bullen, 1981). However, free ionic iron is not usually available in the extracellular matrix of the human host (Weinberg, 1974). In serum, the concentration of free iron is kept at a low level through binding by the protein transferrin (Bullen et al., 1974).

Biomateriais disrupt these mechanisms (Bullen etal., 1974) by providing a surface for bacterial adhesion, and corrosion of the biomaterial surface, which provides nutrients for bacterial propagation and growth.

Bacteria may use trace ions such as Mg2' and Cai+ to stabilize (via acidic groups) ex polysaccharides in a gel, which enhances cell-to-cell and cell-to-surface adhesion and increases resistance to antagonists (Gristma et al., 1987; Fletcher, 1980), Some synthetic polymers, such as polyurethane and methyl inethacrylate, contain ester bonds that may be bydroiyzed by staphylococci (Ludwicka et al., 1983).

The formation of slime-enclosed microcolonies allows bacteria to compete with host proteins for iron and other nutrients. Bacteria may accumulate ions such as iron by localization of metabolites and siderophores (Sriyoschati and Cox, 1986) and by sequestering them from binding by transferrin or lactoferrin. The release of free iron from the biomaterial surface may also serve to saturate rhe iron-binding proteins. The sequence of inflammation, corrosion, reduced pH, increased iron concentration, and saturation of iron-binding proteins may result in increased virulence and inhibition of macrophage function (Weinberg, 1974; Bullen et al., 1974; Lehmnger, 1982).

Biofilm development involves not only phases of attachment, growth, and polysaccharide production, but also a phase of detachment (Hamilton, 1987). Portions of the slime-enclosed microcolony may eventually be detached secondary to hemodynamic forces or trauma. Detachment may also be a normal feature of a dynamic equilibrium resulting, for example, from nutrient or oxygen depletion arising withm the film (How-

ell and Atkinson, 1976). These pathogenic inocula may then serve as a source of secondary infection and hematogenous septic emboli.

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