Antimicrobial Interfaces - Biointerfaces: Where Material Meets Biology - page 405

virulent sub-populations is activated by both phenotypic phase adaptation of
bacteria (leading to the production of defensive biofilm structures) and local
variation in host immune responses. 11 These two events are strongly inter-
related as the intact host immune systems frequently get rid of transient
bacterial contamination except when the inoculum load surpasses a distinct
threshold. Although most of the medically used materials are inert and non-
toxic they can often cause unfavourable physiological effect termed as a
'foreign body reaction' at the site of insertion, which induces local im-
munosuppression. 60,61 Under such conditions, even low numbers of bacteria
will not be eradicated by an appropriate response from the host immune
system which then leads to a bacterial threshold that may cause an infection
to decrease dramatically. 62-65

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14.4 Biofilm Antimicrobial Surface Interfaces
The biofilm matrix which constitutes EPS, proteins and DNA can trap anti-
microbial agents by physicochemical interactions. This leads to antibacterial
agents (such as antibacterial metal ions, antibiotics, disinfectants or ger-
micides) being deactivated, delayed or stopped from penetrating into the
biofilm interior through diffusion. It was reported that formation of a dead
bacterial layer at the interface with the silver-releasing phosphate-based
glasses caused re-emergence of viable bacteria after 24 h growth of S. aur-
eus 66 suggesting the diffusion limitation of silver ions released from the
phosphate-based glasses (Figure 14.2). Many reports studied the diffusion
and interaction of antibacterial agents with that of the biofilm matrix ma-
chinery. 67-70 The uptake of antibacterial agents differs significantly with
their chemical composition, size, charge and hydrophilicity. For instance,
aminoglycosides such as gentamicin and tobramycin adhere strongly to
biofilm matrix of Pseudomonas aeruginosa made of alginate thus totally
blocking its diffusion through to the interior. 71 However, b-lactam anti-
biotics displayed a higher diffusion coe cient. 72 The phenotypic variation in
growth, metabolism and genetic mutations undergone by biofilm associated
species all add to the creation of drug resistance among such bacteria.
Bacterial cells which are part of a biofilm are known to grow at a significantly
reduced speed compared to their planktonic counterparts and possess a
decreased metabolic activity. These reduced metabolic activities contribute
to decreased sensitivity to antimicrobial compounds. 73,74 Furthermore, ele-
vated rates of exchange of genetic material and mutations inside biofilms

.

Figure 14.2 A cross-sectional view of confocal laser scanning microscopic image
showing the S. aureus biofilm on silver-doped phosphate based glasses.
Viable (green) and non-viable (blue) bacteria.