Uncontrollable infection increases the risk of bacteremia, sepsis, multi-system organ failure and death. To provide better care and avoid payment denials, learn the signs of chronic infections and develop a multi-pronged approach to effective treatment.

Infection occurs when homeostatic balance among the host, organism and environment is disrupted. It depends on if and how organisms adhere to the host's body.

Of all factors controlling infection, host resistance is the most important. Poor resistance, due to general debility or a prior surgical or traumatic insult, significantly reduces the capacity to fight off infection.^1,2

Host resistance is lowered by poor tissue perfusion; poor nutritional intake; local edema; smoking; drug or alcohol abuse; and the presence of foreign material in the wound (necrotic debris or retained packing materials).

Microorganism Levels
All wounds are colonized with bacteria. During treatment, don't destroy the surface homeostasis of the skin with products that remove the slight acidic pH of the skin or occlude the skin from vapor permeability. For example, topical agents that contain alcohol can actually burn or dry out the skin, causing cracking and fissure to serve as portals for infection.

Colonization becomes contamination if non-replicating organisms are present in a wound. Some wounds are contaminated with bacteria, but the immune system of the cells around and within a wound can still fight off adverse affects.

When the immune system can no longer maintain balance with an increasing number of bacteria, the wound has critical colonization.³ Contaminating microorganisms arise from the external environment, surrounding skin and endogenous sources like the gastrointestinal tract or oral mucosa,^4,5 especially when a wound on the trunk is exposed to urine and stool. That's why the outdated philosophy of leaving wounds open to air to heal is dangerous: it only predisposes the wound site to exposure to toxins and contaminants that can cause infection.

A truly infected wound possesses a quantifiable microorganism count >105.6 Determine this via culture techniques, which will quantify the number of bacteria present, and identify type of bacteria, sensitivity and resistance to antibiotic management.

A tissue biopsy will display bacteria, but it also reveals the pathology of the cells, which can include cancer, vasculitis, necrotizing fasciitis or pyoderma gangrenosum. 

Other Infections
Venous stasis tends to produce fungal infections, eczema and allergic dermatitis. Fungal infections can be spread from other locations like skin folds or perineal surfaces that are moist.

While the perineal fungal infection may present as regions of erythema and satellite papules, the fungus of the leg manifests as redness.⁷ Classic signs of fungus to the feet can be seen in the toes, where there is cracking of the skin and an accumulation of hyperkeratinized adherent tissue. The flaking, dead tissue holds the fungus in place.

The use of systemic or topical antifungal agents to the venous stasis wound site is a relatively new recommendation based upon recognition that these wounds don't heal with compression and absorptive dressings alone.

The flora in chronic venous leg ulcers is polymicrobial with anaerobes in 30 percent of total number of isolates. The most common bacteria present is staph aureus. Tengrove reported no single microorganism or group of bacteria was more detrimental to healing than any other, and the probability for healing was significantly lower if four or more bacterial groups were present in the ulcer.⁸

Diabetic Wounds
Patients with diabetes have compromised immunity that leads to a reduced resistance to infection. Diabetes can also suppress the classical signs of infection. Infected diabetic ulcerations have been categorized as 

• infected neuropathic foot, i.e., plantar ulcerations;
• ischemic gangrenous foot, most likely the toes and lateral regions of the feet;
• infected foot with diabetic polyneuropathy and peripheral arterial disease;
• infection of the foot with diabetic pathobolism and no evidence relevant to neuropathy or angiopathy.⁹

The diabetic foot of mixed angiopathy and neuropathic genesis, and the neuropathic ulceration may always be regarded as infected. The chance for spreading the infection is high owing to the differential structure of the connective tissue in the foot region. Systemic therapy with antibiotics has proven effective in treating these types of infections.

Biofilm
Biofilm identification further complicates infection management, particularly in the chronic wound. The biofilm is a self-produced polymeric matrix, referred to as a glycocalyx or slime. Biofilms adhere to inert and living surfaces that may be single species or a mixture of bacterial species. Biofilms account for 80 percent of infections.¹⁰

Cell-to-cell adhesion to the conditioning film occurs, with continued adhesion of micro-organisms to form a multilayered colony of cells. The biofilm has a rough, irregular surface containing many individual colonies of non-uniform columns surrounded by fluid-filled channels in which nutrients, enzymes and waste products circulate.

Bacteria in biofilms are commonly responsible for recurring infections after repeated trials of antibiotics. The microorganisms can remain dormant for weeks or years before causing local or systemic signs of infection to develop. Biofilms may dilute, bind or entrap all or part of the antimicrobial, preventing therapeutic levels of antibiotics, antibodies or phagocytes from reaching the bacteria, and thus limiting therapy effectiveness.¹¹