Abstract
The primary reason for skin graft failure and the mortality of burn wound patients, particularly those in burn intensive care centers, is bacterial infection. Several animal models exist to study burn wound pathogens. The most commonly used model is the mouse, which can be used to study virulence determinants and pathogenicity of a wide range of clinically relevant burn wound pathogens. However, animal models of burn wound pathogenicity are governed by strict ethical guidelines and hindered by high levels of animal suffering and the high level of training that is required to achieve consistent reproducible results. In this study, we describe for the first time an invertebrate model of burn trauma and concomitant wound infection. We demonstrate that this model recapitulates many of the hallmarks of burn trauma and wound infection seen in mammalian models and in human patients. We outline how this model can be used to discriminate between high and low pathogenicity strains of two of the most common burn wound colonizers Pseudomonas aeruginosa and Staphylococcus aureus, and multi-drug resistant Acinetobacter baumannii. This model is less ethically challenging than traditional vertebrate burn wound models and has the capacity to enable experiments such as high throughput screening of both anti-infective compounds and genetic mutant libraries.
Highlights
Burn wound infection is one of the main clinical complications associated with burn wound care and is a leading cause of mortality among burn wound patients (Branski et al, 2009; Calum et al, 2017; Akers et al, 2019)
P. aeruginosa was recovered from the hemolymph of these larvae in 92% of cases whereas in the burn only control, P. aeruginosa was never recovered (Figure 3C). This further demonstrates that the infection progression cycle mimics what is observed in mammalian burn wound models and human patients. To determine if this model could be used to study other Gramnegative burn wound pathogens such as A. baumannii, the assay interrogate the capacity of Staphylococcus spp. to cause mortality in this model and demonstrate the role of biofilm formation in infection progression, a strain of S. epidermidis (ATCC 12228) that does not readily form biofilm and has not previously been reported to cause burn wound infections was tested
We show that P. aeruginosa PA14 can colonize G. mellonella burn wounds and that this infection progression cycle is remarkably similar to infection progression in patients and mammalian models (Figures 3A,B)
Summary
Burn wound infection is one of the main clinical complications associated with burn wound care and is a leading cause of mortality among burn wound patients (Branski et al, 2009; Calum et al, 2017; Akers et al, 2019). These murine models can offer robust insights into the host/pathogen processes involved in burn wound colonization and can play a key role in the validation of novel therapeutic strategies They are governed by strict ethical guidelines, associated with high levels of suffering and are limited by the numbers of animals that can be used in a given study. Another complication with mouse burn models is that mice are classified as “loose-skin animals,” meaning that they do not have a similar skin structure to humans and the process of wound healing is different. We outline for the first time a G. mellonella burn wound model that can be used to study burn trauma and wound infection
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