Biofilm infection significantly contributes to wound chronicity. This preclinical model infects full-thickness swine wounds with clinically isolated pathogens to study wound biofilm formation and biofilm-dependent changes in wound outcomes. By including both microbial as well as host factors, we aim to investigate the complex host microbe interactions underlying pathogenic biofilms in chronic wounds.
Although the current literature does not discriminate between the two, wound biofilm aggregates differ significantly from biofilm aggregates found by microbial interactions in the absence of host human defenses. For example, biofilm grown on plastic surface or on say dead skin. The iterative interplay between microbial processes and host immune defense systems leads to wound biofilm aggregate formation.
Since this process takes several days, having a longer term model of wound infection is crucial. Both in vitro and ex vivo systems lack the necessary host immune response required to study wound biofilm. While short-term in vivo studies yield acute response and that do not allow for biofilm maturation, our standardized preclinical experimental system with reported clinically relevant findings addresses these gaps.
While biofilm-infected wound might close structurally, they may not achieve functional wound closure, as the repaired scale often failed to reestablish the barrier function. The breached affected skin with compromised barrier function constitutes an open, invisible wound that is structurally covered, but functionally open. Our study highlights the importance of measuring skin barrier function at the site of wound repair to determine functional wound closure.
The barrier function is measured by clinically validated point of care measurement of transepidermal water loss.
