Abstract
ABSTRACT Surgical site infection risk continues to increase due to lack of efficacy in current standard of care drugs. New methods to treat or prevent antibiotic-resistant bacterial infections are needed. Multivalent Adhesion Molecules (MAM) are bacterial adhesins required for virulence. We developed a bacterial adhesion inhibitor using recombinant MAM fragment bound to polymer scaffold, mimicking MAM7 display on the bacterial surface. Here, we test MAM7 inhibitor efficacy to prevent Gram-positive and Gram-negative infections. Using a rodent model of surgical infection, incision sites were infected with antibiotic-resistant bioluminescent strains of Staphylococcus aureus or Pseudomonas aeruginosa. Infections were treated with MAM7 inhibitor or control suspension. Bacterial abundance was quantified for nine days post infection. Inflammatory responses and histology were characterized using fixed tissue sections. MAM7 inhibitor treatment decreased burden of S. aureus and P. aeruginosa below detection threshold. Bacterial load of groups treated with control were significantly higher than MAM7 inhibitor-treated groups. Treatment with inhibitor reduced colonization of clinically-relevant pathogens in an in vivo model of surgical infection. Use of MAM7 inhibitor to block initial adhesion of bacteria to tissue in surgical incisions may reduce infection rates, presenting a strategy to mitigate overuse of antibiotics to prevent surgical site infections.
Highlights
Surgical site infections (SSIs) have become the most common and costly of hospital-acquired infections
We explored the efficacy of Multivalent adhesion molecule 7 (MAM7) bacterial adhesion inhibitor against bacterial infections of Pseudomonas aeruginosa and Staphylococcus aureus in an in vivo model of surgical site infection
Bacterial burden in animals inoculated with bacteria, but left untreated showed a similar profile to those treated with GST control beads (Figure 1(d))
Summary
Surgical site infections (SSIs) have become the most common and costly of hospital-acquired infections. Of the in-hospital mortalities with an SSI at the time of death, 77% of cases are directly attributable to the surgical site infection [1,2]. Due to drug efflux mechanisms and genetically acquired drug resis tance, antibiotic tolerance has increased in these species [9]. These characteristics have led to the rise of multidrugresistant isolates that are observed in patients and trans ferred between patients through healthcare personnel or hospital equipment [6,10,11].
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