Biomedical Engineering Reference
In-Depth Information
This translates in in vivo modifi cation of the surface physical and chemical
properties of the introduced device and may explain why measures such as
hydrophilic gel and antimicrobial coating fail in preventing microbial
attachment.
Once the conditioning fi lm has been formed the next step is microorgan-
ism approach and attachment. Two theoretical models have been proposed
to explain the interaction between the microorganism, the conditioning
fi lm, and the surrounding tissue fl uid. The Derjaguin, Landau, Verwey and
Overbeck (DLVO) model is based on stability of colloidal dispersions
incorporating the effects of hydrophobicity and surface charge (Derjaguin
and Landau, 1941; Verwey et al. , 1948), while the surface free energy model
utilises the theory of thermodynamics (Absolom et al. , 1983; Busscher et al. ,
1984). The DLVO model treats microorganisms as colloidal particles
approaching a surface with attractive van der Waals forces, electrostatic
repulsion forces and solution ionic concentration controlling potential
surface adherence. From a surface thermodynamic perspective the surface
tensions of all components of the microorganism-surface-tissue fl uid
system determines adherence. Microorganism adhesion will be favoured
if the sum of interfacial energies allows the system to reach thermal
equilibrium.
Modifi cation of the surface properties of implanted devices may have an
impact on reducing bacterial adherence (Portoles et al. , 1993). The fact that
hydrophilic gel coating does not demonstrate the expected effect on reduc-
ing bacterial adhesion (Reid et al. , 1994) clearly indicates that the dynamic
interactions leading to biofi lm deposition cannot be explained entirely by
theoretical models not accounting for the biological properties of microor-
ganisms. Recent data has clearly shown that cell-cell aggregation proper-
ties held by several surface appendages such as curli and F-pilus may
amplify surface colonisation once initial adhesion is established (Beloin
et al. , 2008).
Once adherence is established biofi lms take on the three-dimensional
structural and functional characteristics of multispecies communities. In
addition to spatial localisation, surfaces appear to provide bacteria with the
protective niche in which attached organisms create a localised homeostatic
environment (Stoodley et al. , 2002). Attached cells promote excretion of
further adhesion facilitating molecules, extracellular matrix formation, as
well as undergo gene transcription modifi cations to integrate within their
new microenvironment (Donlan, 2001). From the clinical standpoint bio-
fi lms may lead to colonisation and infection. Biofi lm-related infections are
notorious for resistance to treatment with standard antimicrobials that not
infrequently necessitate surgical removal of infected prosthetic material.
Routine measures to reduce peri-procedural host bacterial load and subse-
quent biofi lm formation include prophylactic systemic antibiotics, sustained
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