Biomedical Engineering Reference
In-Depth Information
1
Introduction
1.1 Background on Chronic Wound Infections
Chronic wounds are clinically defined as any wound which fails to heal within
30 days and include diabetic foot ulcers, venous leg ulcers, arterial ulcers, and
pressure ulcers (Bradley et al.
1999
; Falanga
1998
). Ulcer wounds all possess one
similarity, which is that they penetrate deep into the epidermis of the skin (Robin-
son and Lynn
2008
). Wound infections are usually staged with inclination to
severity based on the depth and appearance of the ulcer (The National Pressure
Ulcer Advisory Panel
1989
). These wounds are resistant to natural healing and can
require long-term medical care (Beckrich and Aronovitch
1999
). The chronic
wound environment supports a variety of microorganisms, including a mixture of
gram-negative, gram-positive, aerobic, and anaerobic bacteria, plus fungal cells
(Leake et al.
2009
). Some of the primary bacterial pathogens most commonly
isolated from wound infections are
Staphylococcus aureus, Enterococcus faecalis,
Finegoldia magna,
and
Pseudomonas aeruginosa
(Dowd et al.
2008
). Indeed,
S. aureus
and
P. aeruginosa
are reported to infect up to 88 % and 33 % of leg
ulcers respectively (Hansson et al.
1995
; Schmidt et al.
2000
).
1.2 Biofilm Pathogenesis in Chronic Wounds
Microorganisms are thought to delay wound healing by causing tissue damage and
are difficult to treat because of multidrug resistance and the formation of biofilms
(Percival et al.
2010
). Biofilms are a conglomerate of bacterial cells, DNA, and
proteins intercalated in a sugary slime matrix (Fuxman Bass et al.
2010
). Biofilms
have been implicated to cause many chronic diseases, and when 50 clinical chronic
wounds were evaluated for the presence of biofilm, 60 % of these wounds were
biofilm positive (James et al.
2008
). The continued presence of bacterial biofilms in
wounds is thought to delay wound healing for multiple reasons. The outer coating
of the biofilm, called the exopolysaccharide (EPS) matrix, acts as a mechanical
barrier to antibodies and complement, preventing biofilm penetration and
protecting bacterial cells (Thomson
2011
; Jacobsen et al.
2011
). The EPS may
also prevent fibroblasts, epithelial cells, and keratinocytes from migrating into the
wound bed. As long as the biofilm remains, the immune system will try and remove
it, causing prolonged inflammation and collateral damage to host tissue (Wolcott
et al.
2008
). In addition, oxygen is depleted rapidly in biofilms, supporting the
growth of anaerobic bacteria and impairing host cell growth and repair. In biofilm-
associated chronic wound infections, topical and systemic antibiotics have reduced
efficacy. The bacteria within the biofilms are 500-5,000 times more tolerant to
antimicrobials than planktonic bacteria, making these infections difficult to treat
(Anwar et al.
1990
). The tolerance that biofilms display is distinct from the
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