Formation of Pseudomonas aeruginosa Biofilms in Full-thickness Scald Burn Wounds in Rats

Abstract

Using Sprague-Dawley rats (350–450 g; n = 61) and the recently updated Walker-Mason rat scald burn model, we demonstrated that Pseudomonas aeruginosa readily formed biofilms within full-thickness burn wounds. Following the burn, wounds were surface-inoculated with P. aeruginosa in phosphate-buffered saline (PBS), while sterile PBS was used for controls. On post-burn days 1, 3, 7, and 11, animals were euthanized and samples collected for quantitative bacteriology, bacterial gene expression, complete blood cell counts, histology, and myeloperoxidase activity. Robust biofilm infections developed in the full-thickness burn wounds inoculated with 1 × 104 CFU of P. aeruginosa. Both histology and scanning electron microscopy showed the pathogen throughout the histologic cross-sections of burned skin. Quantigene analysis revealed significant upregulation of alginate and pellicle biofilm matrix genes of P. aeruginosa within the burn eschar. Additionally, expression of P. aeruginosa proteases and siderophores increased significantly in the burn wound environment. Interestingly, the host’s neutrophil response to the pathogen was not elevated in either the eschar or circulating blood when compared to the control burn. This new full-thickness burn biofilm infection model will be used to test new anti-biofilm therapies that may be deployed with soldiers in combat for immediate use at the site of burn injury on the battlefield.

Comparative Analysis of the Host Response in a Rat Model of Deep-Partial and Full-Thickness Burn Wounds With Pseudomonas aeruginosa Infection

“…Longer implications can include chronic infection of the wound, systemic inflammation, multi-organ failure, sepsis, and/or death (Kallinen et al, 2012;Turner et al, 2014;Greenhalgh, 2017;Lin and Kazmierczak, 2017). Our previous work on FT burn injury with P. aeruginosa infection showed a septic rate of 50-100% at POD 11, depending on the starting inoculum (Brandenburg et al, 2019a). These rates are similar to those found clinically, which can range anywhere from 50 to 84%, depending on age and burn severity (Lopez et al, 2017).…”

“…Compared to the native flora, the clinical isolate of P. aeruginosa appears to be far more invasive, which would explain why these cytokines remained at sham levels in the burn-only controls. Our previous work also noted several cases of sepsis following FT burn injury infected with P. aeruginosa (Brandenburg et al, 2019a). While HYL and FBN followed similar trends to the burnonly group, HMGB-1 was further elevated by the presence of P. aeruginosa in the case of both burn scenarios.…”

Chitosomes-In-Chitosan Hydrogel for Acute Skin Injuries: Prevention and Infection Control

“…Drugs 2021, 19, 269 2 of 21 formation, increasing the complexity of the wounds and leading to chronicity [5]. The escalating threat of antimicrobial resistance and biofilm-producing strains influence the treatment outcome [6]. The incidents of burn injuries are ostensibly decreasing [7]; however, nearly 9 million injuries globally were related to fire, heat, or hot substances, according to the Global Burden of Disease 2017 study [8].…”

The Antibacterial and Anti-Biofilm Activity of Metal Complexes Incorporating 3,6,9-Trioxaundecanedioate and 1,10-Phenanthroline Ligands in Clinical Isolates of Pseudomonas aeruginosa from Irish Cystic Fibrosis Patients

“…Pseudomonas aeruginosa is a ubiquitous Gram-negative human pathogen that can colonise a diversity of sites with severe clinical consequences. Isolates of P. aeruginosa are found in nosocomial infections within immunocompromised patients, ranging from burn sepsis [ 1 ] to ventilator-associated pneumonia [ 2 ], to pulmonary infections of patients with lung afflictions such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) [ 3 ]. CF is an inherited autosomal recessive disorder characterised by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene located on chromosome 7 that primarily affects the lungs.…”