The microbiome of diabetic foot ulcers and the role of biofilms

The most common pathway leading to a foot infection in a person with diabetes is through a physical break in the protective barrier of the skin, in the form of a diabetic foot ulcer (DFU). Once the skin is breached, a DFU exposes the underlying soft tissues to potential bacterial colonization with infection arising if certain conditions favor bacterial replication. Further contiguous extension to deeper structures may produce scenarios where failure in controlling the spread of infection leads to extensive damage of host tissue and bone, and this in part may be driven by several aspects of altered immunologic function. Of particular focus is the reduction in polymorphonuclear leukocyte response to bacterial infection and the role of hyperglycemia, all being extensively reviewed. This scenario optimizes the pathway to lower extremity amputation in a person with diabetes. Bacteria that contaminate and colonize wounds likely originate from the surrounding skin flora but other sources include the environment and endogenous mucous membranes, such as the gastrointestinal tract or nares. One reason for this is that DFUs present an ideal environment for harboring microorganisms since they offer a warm, moist, nutritive home, especially if devitalized tissue is present in the wound bed. The longer a wound remains open, the greater the chances of a more diverse and abundant bacterial colonization, with the type, depth, location, level of perfusion and the efficacy of the host immune response dictating the niche of colonizing bacteria.