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Questioning the use of an acute porcine wound model to assess antibiofilm activity of dressings

To the Editor, Our understanding of biofilm and its role in wound chronicity is developing rapidly, and there has been a proliferation of wound care products aiming to address biofilm and test models attempting to support claims and predict clinical performance. Although great progress is being made, it is important to maintain critical thinking and to crosscheck against other sources of information. Given that the porcine wound model is accepted as a gold standard for studying acute healing, I read with great interest the Davis et al's paper using an adaptation of this model to investigate biofilm. Unfortunately, I concluded that this was not a reliable representation of a chronic wound and that the authors had not considered alternate interpretations or checked conflicting evidence from other sources. By definition, infected and chronic wounds are nonhealing, populated by polymicrobial bioburden, where biofilm structure has matured and stabilized over days, weeks, and even months. This in vivo model differed in species and maturity from the referenced validated model, as it used a single bacterial species and allowed only 24 hours for bioburden development. The presence of biofilm or infection was not confirmed as the use of a DNA stain and total viable counts are not sufficient and do not differentiate between planktonic and biofilm phenotypes. Additionally, typical histological microscopy is of insufficient magnification to confirm biofilm structure. Initial bacterial counts were low, and the no-treatment control showed a 2-log increase in the first 2 days, suggesting biofilm was still developing. All wounds fully epithelialized in 5 days (including the no-treatment control), and therefore remained fundamentally acute in nature. Biofilm-colonized wounds are predominantly associated with ongoing elevated rates of exudation compared to acute wounds where rates are low and reduce to near zero with epithelialization. In this model, the dressings were minimally hydrated at the beginning of the study (different volumes used for the different dressings), and although a secondary film dressing was used, it is highly probable that dressings became dehydrated. Dehydration compromises antimicrobial activity, and if they become adhered (as is observed for gelling fibre dressings with silver (GFD); Exufiber Ag+ in vitro), this may have resulted in the bacterial detachment observed in histological samples. Planktonic and bacteria in thin, immature biofilm will be more susceptible to the effects of antimicrobial agents. Therefore, in a dehydrating system, any dressing with a bolus antimicrobial release will be perceived to be more effective, particularly where the test bacteria are susceptible to the antimicrobial as in the case of Pseudomonas aeruginosa to ionic silver. This therefore does not necessarily reflect the clinical situation where the chronic wound will contain a mixed-species bioburden in a mature biofilm where sustained antimicrobial activity is a key. This then questions the value of the small differences observed in the semiquantitative histology evaluations, the uninterpreted white cell infiltrates, and bacterial counts— particularly those at day 7 which is after epithelialization. The conclusion suggests that the synergistic action of the Hydrofiber dressing with silver, benzethonium chloride and ethylenediaminetetraacetic acid; AQUACEL Ag+ Extra dressing to disrupt biofilm and expose microorganisms to the antimicrobial action of silver is not demonstrated, but this is unfounded as synergy is not tested and requires comparison to the effects of the individual components. The authors miss the opportunity to reference or discuss alternative peer-reviewed published data such as the in vitro models on which the synergistic claim is based; the in vivo, validated, ischemic, nonhealing, mixed biofilm model, which links directly biofilm reduction to wound closure, or the clinical studies in which healing and/or wound progression was observed for 90% of realworld, nonhealing wounds. On this basis, I suggest that the overarching conclusion “Overall our study confirmed the effectiveness of a new GFD Ag+ dressing on wounds with established P. aeruginosa biofilm infection” was not proven and that, in this instance, a fair and balanced test has not been performed and the relevance of results has been overstated.