Antimicrobial Interfaces - Biointerfaces: Where Material Meets Biology - page 404

cells into the bulk liquid phase. 13 As a result of the dispersion of biofilm, cell
clusters become hollow in the centre 13,48 appearing as doughnut-shaped
structures under the microscope. 49 A substantial quantity of information is
available regarding the regulation of biofilm adherence and maturation, yet,
biofilm dispersion remains a relatively less well studied feature of biofilm
development. 50 A hypothesis on the mechanisms leading to biofilm dis-
persion suggests that signalling molecules reaching a threshold concen-
tration triggers the release of enzymes that cause cell cluster dismantling. 47
Another hypothesis suggests that dispersion is a response to two different
environmental factors, accumulation of a metabolic product and depletion
of a metabolic substrate. 51
It has been assumed that quorum sensing is responsible for the dis-
solution of the biofilm matrix. Once an excreted metabolite (e.g., a furanone)
reaches a threshold concentration the release of bacterial cells into the bulk
liquid is triggered. 52 It has also been proven that acyl-homoserine lactones
are responsible for maintaining bacterial cells in a dispersed state both in
Rhodobacter sphaeroides and Pseudomonas aureofaciens. 53,54 Moreover, in
P. aeruginosa, the chemotaxis regulator BdIA has been hypothesised to be
involved in the regulation of biofilm dispersion and cell adhesiveness by
acting as a sensor protein in c-di-GMP signalling. 55

d n 3 r 4 n g | 9

14.3 Biofilm Infection
Antimicrobial interfaces can be best studied at an interface which involves
development of biofilms on implant surfaces. The most frequently cultured
microorganisms that are generally linked to implant surfaces include
Staphylococcus spp., Streptococcus spp., Enteroccoccus spp. followed by Gram-
negative bacilli (which include Pseudomonas spp. and Enterobacter spp.) and
anaerobes (Propionibacterium spp.). 56 Apart from bacterial infections, a
growing proportion of infections associated with indwelling devices, mainly
the ones engaged with the urinary tract and the bloodstream, are fungal in
origin, primarily C. albicans. 57,58 Bacterial colonisation of implants used in
surgery does not automatically point towards infection; however, the growth
of virulent bacteria typically points to infection. Low virulence bacteria,
which are usually part of commensal flora of skin, might either become
harmless contaminants or potent pathogens. In many cases, the objective of
infection control is attained with the help of both surgical intervention and
antibiotic therapy.
Bacteria involved in implant associated infection mainly include non-
pathogen or opportunistic pathogens. But the species associated differ
considerably based on the site of localisation and sorts of device em-
ployed. 28,59 Staphylococcus spp. (S. epidermidis and S. aureus) and other
Gram-positive cocci usually infect arteriovenus shunts, sutures, vascular
grafts, central venous catheters, sclera buckles and orthopaedic devices. 28,59
Enterobacteriaceae (frequently E. coli) and Enterococcus spp. colonise urinary
catheters. The conversion of opportunistic or non-pathogenic bacteria into

.