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INTRODUCTION

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The skin is an essential component of immunity, protecting the host from potential pathogens in the environment. Breaches in this protective barrier thus represent a form of immunocompromise that predisposes the patient to infection. Thermal burns may cause massive destruction of the integument as well as derangements in humoral and cellular immunity, permitting the development of infection caused by environmental opportunists and components of the host’s skin flora.

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EPIDEMIOLOGY

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Over the past decade, the estimated incidence of burn injuries in the United States has steadily declined; still, however, >1 million burn injuries are brought to medical attention each year. While many burn injuries are minor and require little or no intervention, 183,000 cases were reported between 2002 and 2011 to the National Burn Repository from specialized burn care facilities; of the 45,000 persons hospitalized for these injuries, 60% required intensive care and 20,000 had major burns involving at least 25% of the total body surface area. The majority of burn patients are men. Children under the age of 5 account for ~20% of all reported cases. Scalds, structural fires, and flammable liquids and gases are the major causes of burns, but electrical, chemical, and smoking-related sources also are important. Burns predispose to infection by damaging the protective barrier function of the skin, thus facilitating the entry of pathogenic microorganisms, and by inducing systemic immunosuppression. It is therefore not surprising that multiorgan failure and infectious complications are the major causes of morbidity and death in serious burn injury. More than 3000 patients in the United States die of burn-related infections each year, and 6 of the top 10 complications recently identified by the American Burn Association’s 10-year review are infectious: pneumonia (4.6%), septicemia (2.7%), cellulitis/traumatic injury (2.6%), respiratory failure (2.5%), wound infection (2.2%), another infection (2.0%), renal failure (1.5%), line infection (1.4%), acute respiratory distress syndrome (1.2%), and arrhythmia (1.0%).

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PATHOPHYSIOLOGY

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Loss of the cutaneous barrier facilitates entry of the patient’s own flora and of organisms from the hospital environment into the burn wound. Initially, the wound is colonized with gram-positive bacteria from the surrounding tissue, but the number of bacteria grows rapidly beneath the burn eschar, reaching ~8.4 × 103 cfu/g on day 4 after the burn. The avascularity of the eschar, along with the impairment of local immune responses, favors further bacterial colonization and proliferation. By day 7, the wound is colonized with other microbes, including gram-positive bacteria, gram-negative bacteria, and yeasts derived from the gastrointestinal and upper respiratory flora. Invasive infection—localized and/or systemic—occurs when these bacteria penetrate viable tissue. In addition, a role for biofilms has been recognized in experimental animal models of burn-wound infection. (Biofilms are surface-associated communities of bacteria, often embedded in a matrix, that allow the microbes to persist and to resist the effects of host immunity and antimicrobial agents.)

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Streptococci and staphylococci were the predominant causes of ...

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