The pathological
significance of the presence of bacteria within wound tissue and its
impact on healing is controversial. Even healing chronic wounds tend
to be colonised with a number of microorganisms and a continuum extends
from colonisation to infection with a laboratory-based definition of
infection being difficult to achieve (Bowler, 2001). It is without doubt
that clinical infection will delay healing when the number of colonising
species increases (Trengove, 1996) and the total bioburden passes threshold
values thought to be greater than 105 organisms/gm of tissue (Robson,
1997), although for b-haemolytic Streptococci the threshold may be as
low as 103 for impairment of healing. Regardless of a precise definition
of infection it is clear that granulation tissue of most chronic wounds
will be exposed to bacteria in some degree. Bacteria can interact with
the healing process in a number of different ways. They may produce
molecular species (virulence factors) such as proteases that directly
affect the healing process or bioactive molecules such as lipopolysaccharide
(LPS or endotoxin) that are potent stimulators of inflammatory cells.
Additionally when phagocytosed as part of the innate inflammatory response
to infection they will stimulate macrophages and neutrophils to synthesise
and release pro-inflammatory cytokines and proteases.
Elimination
of bacteria from the wound environment is clearly desirable from a number
of different perspectives and this objective provides an immediate therapeutic
target. Efforts to restrict indiscriminate antibiotic use and prevent
development of bacterial antibiotic resistance has driven the development
of wound dressings that deliver antibacterials which minimise the risk
of resistance. The latest generation utilise silver formulations which
have the advantage that high levels of antibacterial agent generated
at the wound site with a minimal systemic effect, there is reduced toxicity
and the dressings can be multi-functional and manage odour and exudate
simultaneously (White, 2003).
Whilst antibacterials
may be used to treat infected wounds they are unlikely to be used for
prophylaxis of colonised wounds without signs of infection so the situation
remains that most chronic wounds will have some level of bacterial bioburden
interacting with the healing process. The consequence of persisting
low levels of bacteria in the wound is an accumulation of bacterial
products and prolonged stimulation of inflammation. This is a contributing
factor to high levels of protease activity and a disordered cytokine
and growth factor profile found in compromised wounds.
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