Bacterial Loads - Contamination, Colonization & Infection
The development of any infection can be viewed in relation to the chain of infection - which includes a portal of entry, a susceptible host and virulence of the organisms. Any break in the skin represents the loss of the skin’s protective function and allows for an easy portal of entry for bacteria. The transmission of microbes to the wound bed can be through the endogenous route (i.e. contamination with stool) or exogenous route (e.g. health care worker’s hands or equipment). This underscores the importance of effective hand hygiene and in some cases, the barrier mechanism of occlusive dressings in preventing the spread of infection.
Many chronic wound patients possess impaired host defense mechanisms, thus lowering their body’s ability to respond to bacterial invasion. Individuals may be immuno-compromised due to systemic diseases, malnutrition, immuno-suppressant therapy or advanced age. Poor perfusion impairs the ability of phagocytic cells to reach the affected area. Smoking has been demonstrated to greatly increase the risk of infection for both acute and chronic wounds. Elevated serum glucose levels in diabetic patients impairs the function of white blood cells. Efforts to stabilize chronic medical conditions, promote adequate nutrition, maintaining glycemic control and encouraging smoking cessation, all of which could improve the patient’s ability to fight infection.
The ability of micro-organisms in the wound bed to create a damaging effect on the host is dependent on the relative number of organisms, their virulence and whether or not they invade the tissue. Bacterial levels of 105 colony forming units (CFU) are generally considered infection. Some organisms, such as Beta hemolytic Streptococcus, can cause tissue destruction at 1 CFU/gram of tissue obtained by tissue biopsy. Staphylococcus, Streptococcus and Pseudomonas are the most commonly isolated organisms from chronic wounds although the latter two require far greater numbers (i.e. ≥10 ³ CFU/gm of tissue) to be classified as infection.
The presence of bacteria in a wound can be categorized as four different conditions - contamination, colonization, critical colonization and infection. All chronic wounds are considered contaminated, meaning that they contain non-replicating microorganisms within or on the surface of the wound bed. Host defenses are usually able to clear them and they do not delay wound healing. Colonization is defined as replicating microorganisms that adhere to the wound surface, but do not cause damage to the host.
The term critical colonization, also sometimes referred to as local infection, is a relatively new concept and not clearly defined. It refers to a condition in which the bacterial bioburden in the wound reaches a level in which it interferes with healing, but does not produce the classic signs and symptoms of infection. It was alluded to in the sentinel AHCPR Pressure Ulcer Treatment Guidelines (1994) which recommended “consider initiating a 2-week trail of topical antibiotics for clean pressure ulcers that are not healing or are continuing to produce exudates after 2-4 weeks of optimal patient care” (p. 59). Identification of this threshold between colonization and infection, in which bacterial levels are impairing wound healing, has been the topic of much recent literature, however, no data ( particularly clinical data) correlating it with the gold standard of tissue biopsy have been published.. While classic signs of infection may not be present, symptoms such as delayed healing, increased pain/tenderness, increased exudate, abnormal odor or abnormal or friable granulation tissue might signal critical colonization. Certainly it is an interestingly appealing possibility but until it is supported with research based findings, one should err on obtaining objective evidence to support treatment.
Wound infection is characterized by the presence of replicating microorganisms within a wound resulting in a subsequent host response. Local signs and symptoms of infection include erythema, warmth, swelling, pain, odor and purulent drainage although in chronic wound these may not always be present. If not recognized and treated, in some cases, it can progress to systemic infection with fever, elevated white blood cell count and sepsis. In all cases if a wound infection is objectively validated as present, it will retard wound healing.
While a quantitative tissue biopsy is considered the gold standard for diagnosing wound infection, it is dependent on the availability of a qualified practitioner. Quantitative swab cultures, rapid slide tests and irrigation of the wound and/or adjacent tissue with subsequent aspiration of tissue fluid also provide data regarding the numbers and types of bacterial organisms present in the wound. The most practical, accessible and widely used method to culture wounds remains the semi-quantitative swab culture.
Correct technique for performing the semi-quantitative swab culture is critical for accurate, clinically relevant results. The wound surface should be cleansed with sterile saline or water. The sample should be taken from clean viable tissue, by rolling the sterile swab one complete turn over a 1 cm area. Focal collections of tissue fluid or abscess formation adjacent to a wound may be cultured, but necrotic tissue or purulent exudate from the wound bed should not.
The presence of necrotic tissue in the wound bed delays wound healing. The high levels of bacteria contained in non-viable tissue reduce the host immune response. Sharp debridement of necrotic tissue quickly reduces the bacterial count, and activates the release of growth factors and tissue cytokines.
The need to reduce harmful bacterial counts within chronic wounds must be balanced with measures to reduce antibacterial resistance. It is neither prudent nor advisable to indiscriminately place patients with chronic wounds on prophylactic broad spectrum antibiotics in an effort to prevent infection or promote healing. When critical colonization is suspected, antiseptic agents or topical antimicrobial therapy is usually sufficient to reduce the bacterial bioburden and promote healing. One must always consider; however, the deleterious as well as the beneficial effects of some of these therapies and pick one that is highly effective in reducing bacteria while not at the same time injuring healthy cells.
Although several in vitro studies have suggested that antiseptic agents such as povidone-iodine and Dakin’s solution are cytotoxic to fibroblasts, in vivo studies have failed to demonstrate a delay in wound healing. Short-term (2 weeks or less) use of antiseptic agents, such as dilute Dakin’s solution, can be very effective in reducing local bacterial counts, especially Pseudomonas, but should be followed with topical therapy that is more conducive to would healing. Hydrogen peroxide should be avoided - it has limited antimicrobial properties and is cytotoxic to fibroblasts.
Various formulations of the new silver dressings provide another option for reducing wound bacterial counts. Ionic silver provides broad spectrum antimicrobial coverage against yeast, fungi, viruses and Gram-negative and Gram-positive bacteria, including MRSA and VRE. The development of bacterial resistance to silver is unlikely because silver destroys bacteria through multiple mechanisms. Silver also appears to reduce chronic inflammation, which can interfere with wound healing. Many of the current dressing applications provide sustained release of silver, allowing for longer intervals between dressing changes. Less frequent disruption of the wound bed typically provides faster healing and promotes cost-effective wound care. More research, however, is needed to distinguish therapeutic levels of silver from those that could thwart the wound healing process by being destructive to healing cells ( in particular the fibroblast, macrophage and the epithelial cell).
Systemic antibiotics, either orally or parenterally, are indicated for infection that extends beyond the local wound bed. The presence of erythema extending more than 1 cm from the wound, signs of underlying deep structure infection (i.e. osteomyelitis) or systemic signs and symptoms of infection all warrant systemic antibiotics targeting the identified bacteria.
Understanding the role that bacteria play in the spectrum of wound healing is essential in providing comprehensive, cost-effective care to patients with wounds. All clinicians who treat wounds need to increase their knowledge of the large body of scientific literature existing on this subject. Perhaps no other area of chronic wound care would benefit greatly from ending its basics in tradition and moving towards science.
Bergstrom, N, Bennet, MA, Carlson, CE et al. Treatment of Pressure Ulcers. Clinical Practice Guideline, No. 15. Rockville, MD: U.S. Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research. AHCPR Publication No. 95-0652. December 1994.
This article was written by Carolyn Crumley, MSN RN BC M-SCNS CWOCN, Medical Surgical Clinical Nurse Specialist, St. Mary’s Hospital of Blue Springs