How To Differentiate Between Infected Wounds And Colonized Wounds

By Jason R. Hanft, DPM, and Brigette Smith, DPM

   Since every wound has the potential for infection, it is important to differentiate between infection and colonization.1 There is no textbook that depicts all the possible appearances of wounds that contain bacteria. Indeed, the potential of wounds to heal or become infected depends on many variables. Wound care specialists have a responsibility to become familiar with the these variables as well as develop a trained eye for the clinical appearance of a wound so they may render the appropriate treatment.    There is an enormous amount of information concerning the treatment, staging and physiology of wounds and healing. The influx of emerging research is constantly affecting the current thinking on classifying wounds and providing appropriate treatment. Accordingly, one must be able to differentiate between contaminated and infected wounds, and understand how bioburden, critical colonization and the effects of bacteria affect the wound environment.    The human body harbors over 200 species of bacteria on the skin.2 At any time, one of these bacteria can be inoculated into the wound. Once the skin is injured, the body is vulnerable to contamination from the environment, surrounding skin and mucous membranes.1 The longer the wound is exposed, especially if it is devitalized or compromised, the easier it is for bacteria to colonize.1    In fact, wounds are an ideal place for bacteria to colonize and proliferate since they have a warm, moist nutritive environment. The type of bacteria present and whether the bacteria has infected the wound depends on the type, depth, location, level of perfusion and the efficacy of the host response.1 Consider the following equation relating to infection.3,4 Infection = bacteria dose x virulence host resistance

How Local And Systemic Factors Can Lead To Infection

   The interaction of bacteria with the host influences wound healing.3 Some vulnerabilities that can leave the host open to infection are age, obesity, malnutrition, chronic steroid use and immune defects. Systemic diseases such as diabetes and local issues such as venous hypertension are just some examples of the contributing factors that DPMs need to address at the initial assessment.    Diabetes is a known factor in the host response, especially if the patient’s blood sugar is not well controlled. When the patient has uncontrolled blood sugar levels, there is evidence of a decrease in the function of polymorphonuclear cells that help with chemotaxis.4 Keeping the host defenses at peak efficiency can prevent infection in many cases.5    Some local factors that affect a wound’s defense mechanisms are necrotic tissue, perfusion, foreign bodies, hematomas and dead space. If the tissue at the base or periphery of the wound is hypoxic, then fibrosis and/or necrosis will result. The longer bacteria are exposed to necrotic or fibrotic tissue, the more advantageous it is for the proliferation and colonization of bacteria.1    The quality of perfusion of the wound is vital to healing. Microbial proliferation is greatly increased at PO2 < 20 mmHg.6 It is beneficial to optimize tissue perfusion as this has a direct impact upon the ability of bacteria to proliferate. Demonstrating the positive impact of perfusion, one study showed anal wounds heal faster than lower extremity wounds due to the increased perfusion in the anal region. Despite the fact that the amount and type of bacteria are more difficult to control in this region, the anal wounds healed more rapidly.    When examining the possible contributing factors to infection, one should also consider the wound location, the duration of the wound, the mechanism of injury and the presence of dead space. The age of the wound can be an important factor when considering bacterial burden and infection. Surgical wounds that are exposed less than 30 minutes have an average rate of infection of 3.6 percent. In contrast, wounds exposed for greater than five hours have an increased infection rate of 16.4 percent.5    The mechanism of injury also plays a role in the incidence of infection. With all variables being equal, a laceration with minimal skiving has a minimal chance of infection when one compares this to a “torn” wound or a crush injury, which is 100 times more likely to become infected.4 Dead space, undermining and tunneling are also factors. These situations can harbor bacteria and encourage anaerobic growth.

Defining Colonization And Infection

   Recent literature has begun to differentiate between colonization and infection. There is much discussion as to when colonization stops and infection begins. Colonization is defined as the presence of proliferating bacteria without a host response.2,3 These bacteria may be present due to the natural flora, environmental or endogenous factors. Colonization generally does not impede healing and has been shown in small amounts to accelerate healing.6 Identifying and measuring host response is still difficult.    Infection is the invasion of proliferating bacteria not only on the surface of the wound but into deeper, healthy viable tissue on the periphery of the wound. Infection will elicit a host response. In the presence of infection, the host’s immune response is not sufficient to eliminate or overcome the effect of the bacteria.2 At this point, the equilibrium now favors bacterial proliferation and infection will impede healing.    Recently, researchers have postulated that there is a critical point between colonization and infection, which is termed critical colonization.2,6 Again, critical colonization is more of a theoretical concept at this point as it has not yet been established in the scientific literature. The ability to differentiate clinically between colonization and critical colonization is nearly impossible in today’s environment. Future tests and research may improve the practitioner’s ability to make this important distinction. For now, however, critical colonization has yet to be quantified.

Assessing The Impact Of Bioburden

   Bioburden is the local response that bacteria cause by colonizing a wound. Research has shown it is not the presence of organisms that is important but the level of bacterial growth.5 Bioburden is the number of microorganisms that inhabit a wound. Researchers have shown that when bioburden reaches levels >105 bacteria per gram of tissue, it can cause wound infection.5,6 When bioburden levels >106, wound healing is impeded.5 Other authors found that wounds with a bioburden >106 had a healing rate of 0.05 cm per week.3 When bioburden ranged between 105 to 106, the wound healing rate was 0.15 cm per week. When patients had no bioburden in the wound, the healing rate was 0.2 cm of epithelialization per week.3    Clinically evaluating the quantity of bacteria present can be difficult. A delay in wound healing may be the clinician’s only finding in a wound with a high bioburden.6 A wound with a high bioburden may have more exaggerated clinical symptoms than that of a similar wound. Hypergranular tissue that is bright pink and bleeds easily can also be a sign of high bioburden.    Early during the inflammatory stage when the neutrophils are clearing debris, they are also recruiting inflammatory cells. Neutrophils are only present for a few days unless the bioburden is high. If this is the case, inhibitors of the neutrophils turn off and the wound is delayed or trapped in the inflammatory phase.    A high bioburden also influences the concentration of matrix metalloproteinases (MMPs). Matrix metalloproteinases are released by various cells including inflammatory cells. Macrophages are responsible for releasing MMPs as well.7,8 A high bioburden retards the wound in the inflammatory phase, thus recruiting more inflammatory cells. This in turn increases the concentration of MMPs. When the concentration of MMPs is unusually high, tissue inhibitors of metalloproteinases (TIMP) are outnumbered.    MMPs are responsible for the destruction of the extracellular matrix (ECM). In a healthy wound, this would facilitate the migration of cells through the ECM and allow for granulation. In the chronic or highly bacteria-burdened wound, the MMPs can digest all of the ECM and growth factors present.7,8

Assessing Infected Wounds And Selecting An Appropriate Treatment Course

   Once the bacteria have gained advantage over the host’s defenses and have started a host response, then infection has occurred. When clinically assessing any infection, one must look for the classic signs; rubor, calor, dolor, tumor and loss of function.    Mildly infected wounds may present with signs of necrosis, decreased or no granulation tissue, erythema, edema, increased temperature of the surrounding skin, purulent drainage (although not always), and less than 2 cm of cellulitis from the wound.9    In the moderate to severely infected wound, one may see a deep wound base, liquefaction, purulence, odor and cellulitis of >2 cm. In these wounds, one will also likely note leukocytosis and constitutional signs.2 In some patient populations, visual signs of an immune response may be delayed or even absent.    Qualitative testing is beneficial when determining which bacteria is present in the wound. This test is appropriate when choosing antibiotic therapy. A gram stain can also offer a rudimentary quantitative assessment of the wound. If one organism is visible on the slide, then research has shown that there are at least 105 bacteria.    When it comes to treatment, one should address the level of bacteria present within the wound. If the wound is colonized and progressing through the stages of healing or appears without infection or bioburden, clinicians should emphasize supportive therapy. It is imperative to relieve any mechanical stress on the wound. Mechanical stress can impede perfusion and increase the presence of non-viable tissue, thus predisposing the wound to an increased bacterial burden.    When wounds appear to have a high bioburden, topical antibiotics and antiseptics have been shown to decrease the bacterial load.1,5 It has also been suggested that metronidazole may aid the chronic wound by disrupting the synergy between bacteria.1    If a wound is clinically infected, wound healing will be delayed. One may proceed with empiric treatment pending culture results. Upon getting the culture results, clinicians may employ appropriate oral or intravenous antibiotics.

Understanding The Progression Of Wound Healing

   The stages of wound healing overlap and the wound can revert to a prior stage if damaged. This is why bioburden becomes important.    Wound healing begins with coagulation. Once there has been an injury, the damaged tissue releases clotting factors which lead to the formation of a fibrin clot that will act as a scaffold.    Neutrophils enter early during the inflammation stage. Neutrophils destroy bacteria and recruit other inflammatory cells through chemotaxis. They are also responsible for breaking down debris and foreign material in the wound. These cells are present for a few days and then macrophages emerge in the wound. Macrophages are vital in that they help convert the wound from an inflammatory state to a granulation state. These cells are responsible for facilitating debridement of the wound as well as controlling fibroblasts and endothelial cells.    The third stage of healing is the granulation phase. In this phase, fibroblasts emerge and lay down extracellular matrix, setting the stage for angiogenesis. Epithelialization also takes place at this time.    The final stage is the maturation stage. At this point, the wound closes with fragile epithelium. The tissue deep to the fragile epithelium will begin to be replaced by scar tissue. This tissue eventually evolves into a sturdy avascular collagen scar. Scar tissue will initially have 20 percent strength of the original skin and will only advance to 70 percent of original strength.7

In Conclusion

   Differentiating between colonized and infected wounds is difficult at best. Using the tools available to today’s wound care specialist, one must emphasize clinical evaluation with assistance from quantitative testing in order to properly diagnose the wound and provide appropriate treatment. Until we have more information on the exact definition of critical colonization and an objective measuring tool with which to measure the level and activity of bacteria in wounds, practitioners must rely on clinical observation to assist them in this difficult task. Dr. Hanft is the Director of Podiatric Medical Education within the South Miami Hospital/Baptist Health Systems. He is a Fellow of the American College of Foot and Ankle Surgeons. Dr. Smith is a second-year resident within the South Miami Hospital Foot And Ankle Program. For a related article, see “How To Detect And Treat Infected Wounds” in the July 2004 issue or check out the archives at References 1. Bowler PG, Duerden BI, Armstrong DG. 2001.Wound Microbiology and Associated Approaches to Wound Management. Clinical Microbiology Reviews, 14.2:244-269. 2. Ovington L. 2003. Bacterial Toxins and Wound Healing. Ostomy Wound Management, 49.7A:8-12. 3. Brone AC, Vearncombe M, Sibbald RG. 2001. High Bacterial Load in Asymptomatic Diabetic Patients with Neurotrophic Ulcers Retards Wound Healing after Application of Dermagraft. Ostomy Wound Management, 47.10:44-49. 4. Eron LJ. Targeting Lurking Pathogens in Acute Traumatic and Chronic Wounds. J Emer Med, 17,1:189-195, 1999. 5. Robson MC. Wound Infection A Failure of Wound Healing Caused by an Imbalance of Bacteria. Surgical Clinics of North America, 77.3:637-650, 1997. 6. Edwards R, Harding K. Bacteria and Wound Healing. Current Opinion in Infectious Diseases, 17,2:91-96, 2004. 7. Georgina C. Wound Repair: advanced dressing materials. Nursing Standard, 17,4:49-53, 2002. 8. Ovington L. Overview of Matrix Metalloprotease Modulation and Growth Factor Protection in Wound Healing. Ostomy/Wound Management, 48,6supp:3-7, 2002. 9. Joseph W. 2003. Handbook of Lower Extremity Infections, 2nd Edition. Churchill Livingstone. 109-125. Additional References 10. Perry CR, Pearson RL, Miller GA. Accuracy of Cultures of Material from swabbing of the superficial Aspect of the Wound and Needle Biopsy in the Peoperative Asessment of Osteomyelitis. JBJS, 73-A,5:745-749, 1991. 11. Vincent JL. Infection/Inflammation and Hemostasis. Current Hematology Reports 2:407-410, 2003. 12. Lobmann R, Ambrosch A, Schultz G, Waldmann K, Schiweck S, Lehnert H. Expression of matrix-metalloproteinases and their inhibitors in the wounds of diabetic and non-diabetic patients. Diabetologia, 45:1011-1016, 2002.



CE Exam #132 Choose the single best response to each question listed below: 1. The human body harbors over ___ species of bacteria on the skin. a) 400 b) 200 c) 253 d) None of the above Instructions for Submitting Exams Fill out the enclosed card that appears on the following page or fax the form to NACCME at (610) 560-0502. Within 60 days, you will be advised that you have passed or failed the exam. A score of 70 percent or above will comprise a passing grade. A certificate will be awarded to participants who successfully complete the exam. Responses will be accepted up to 12 months from the publication date. 2. Microbial proliferation is greatly increased at PO2 levels … a) >50mmHg b) >30mmHg c) <20mmHg d None of the above 3. Some vulnerabilities that can leave the host open to infection are … a) Age b) Obesity c) Malnutrition d) All of the above 4. Wounds that are exposed for greater than five hours have an infection rate of … a) 25 percent b) 16.4 percent c) 32.1 percent d) None of the above 5. Colonization is defined as … a) The presence of proliferating bacteria without a host response b) The invasion of proliferating bacteria only on the surface of the wound c) Proliferating bacteria that always generates a host response d) None of the above 6. What amount of bacteria impedes wound healing? a) >102 b) >104 c) >106 d) None of the above 7. Which of the following statements is true about bioburden? a) It is the local response that bacteria cause by colonizing a wound. b) A high bioburden may influence the concentration of matrix metalloproteinases (MMPs). c) It is the number of microorganisms that inhabit a wound. d) All of the above 8. True or false: In the chronic or highly bacteria-burdened wound, the MMPs can digest all of the extracellular matrix (ECM) and growth factors present. a) True b) False 9. Mildly infected wounds may present with … a) Ample granulation tissue b) Edema c) Decreased temperature of the surrounding skin d) All of the above 10. In the moderate to severely infected wound, one may note … a) Purulence b) Odor c) A deep wound base d) All of the above Instructions for Submitting Exams Fill out the enclosed card that appears on the following page or fax the form to NACCME at (610) 560-0502. Within 60 days, you will be advised that you have passed or failed the exam. A score of 70 percent or above will comprise a passing grade. A certificate will be awarded to participants who successfully complete the exam. Responses will be accepted up to 12 months from the publication date.


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