If you work with an animal, companion or production, you will at some time have to contend with a wound. Regardless of how much we try to protect our animals, it seems they will find a way to injure themselves. It also seems some animals, like some people, are more accident prone than others.

Figure 1.

Some injuries may be as simple as a minor cut or scratch. Others may require emergency veterinary care. Regardless, all of these follow a similar series of events from initial injury through “final” repair. In the initial phase blood coagulates and a clot forms. There is a release of growth factors and cytokines that begins within minutes to hours. During this time, biofilms may begin to form, protecting bacteria from topical or even systemic treatments. Inflammation characterizes the second phase. In this phase, neutrophils and macrophages are recruited to help fight infection. This phase usually occurs within hours of the initial wound and may last for several days. The third phase involves cell migration (movement) and proliferation (increase in cell numbers).  It is during this phase we begin to “see” skin “closure” and this may last for weeks. The fourth and final phase is scar formation and remodeling. This phase may last for several weeks to several months.

Any injury opens a route for bacteria to enter the body. To combat these bacteria, the body utilizes parts of the innate immune system. Antimicrobial peptides (AMPs) are part of the innate immune system and are found on the skin or mucous membranes. These AMPs are the first line of defense and are known to be bactericidal to both gram + and gram- bacteria. Their mode of action is the disruption of the cellular membranes with a release of internal components. Envision a balloon filled with water where the balloon serves as the cell membrane and the water was the cellular components. You puncture the balloon with a knife blade and the water flows from the puncture provides a visual on how AMPs work (figure 1). Not only do the AMPs cause the death of bacteria, they recruit other components of the immune system to help fight the invading bacteria. They send signals to request additional neutrophils and macrophages to come to the site of infection and help kill the bacteria. While this is very important in the inflammatory phase, AMPs also function in the third phase. AMPs induce fibroblast proliferation (increase in numbers), which is important in the rebuilding of the epidermis.

Figure 2.

There are two “types” of bacteria, gram+ and gram-. The major difference between these is gram+ have a single cell membrane (no outer membrane) and gram- have a double cell membrane making them more difficult to control/kill (figure2). Gram- bacteria also seem to induce a more inflammatory response due to lipopolysaccharide (LPS) residing on the outer membrane. AMPs can bind with LPS on the outer membrane of gram- bacteria very quickly, helping to control inflammation and neutralize the negative effects of LPS.

Bacteria are not without means to protect themselves from many types of control. Within minutes of an injury, bacteria begin to form biofilms (figure3). These are made up of multiple organisms that synthesize and secrete a protective matrix that attaches the biofilm to a surface, in this case the wound edges. This biofilm barrier protects the bacteria from external threats. These biofilms delay wound healing by stimulating chronic inflammation. Biofilms not only protect bacteria, they also serve as a reservoir for future infections as bacteria breakoff and move to new regions/areas of the body.

AMPs inhibit biofilms in several ways. They can inhibit bacteria adhesion to a surface via binding to the bacteria themselves; they can kill early surface bacteria; they disrupt bacteria to bacteria communication; they can penetrate and kill the biofilm; and bind/neutralize bacterial endotoxins like LPS.

Figure 3.