1. Kravitz, Steven DPM, FAPWCA, FACFAS

Article Content

The time has come to consider modifying the way we define "infection" in the wound care arena. Based on my clinical experience, conversations with other wound care practitioners, and reports in the literature, I believe the term infection should include the presence of bacteria and the degree of compromise to its host because these factors impact the virulence of bacteria in any type of wound. In short, a decreased immune response increases the wound's relative bacterial virulence.


Different types of bacteria carry different characteristics, one of these being varying degrees of innate virulence.1-3 When treating patients with nonhealing wounds, I propose that we consider the relative virulence of any specific wound surface organism. That would include the host's ability to contain the bacteria. With this in mind, the definition of infection would address the presence of bacteria that prevent a wound from healing. Such a definition would take into account the bacterial count and the compromised host, both of which affect the relative virulence of the bacteria.


Classifying the Wound

Currently, we think of infection in terms of bioburden, which refers to the presence of bacteria in a wound and the number of microorganisms that contaminate an object.1,2,4 Bioburden is subdivided into 4 categories reflecting a wide continuum,2 including the following:


* contamination-bacteria within a wound without host reaction2


* colonization-bacteria within the wound that multiply or initiate a host reaction2


* critical colonization-bacteria that multiply to cause a delay in wound healing, often with increased pain but not with an acute host reaction2,5,6


* infection-bacteria that multiply and cause a host reaction.2



I perceive 2 problems in applying this standard approach to the chronic wound patient. First, an impaired immune response can be associated with many conditions, such as diabetes, vascular supply, nutritional deficit, and cancer and its related therapies. A decreased immune response precludes the expected local and systemic host reaction.7 Therefore, using "host reaction" as an assessment criterion to determine the presence of infection can be misleading.


Additionally, the classically accepted concept that infection is associated with a bacterial count of 105 does not account for the degree of host compromise. This is not appropriate for nonhealing chronic wounds. Indeed, a bacterial count of far less than 105 can prevent wound healing in patients with a deficient immune response.1,2 In addition, some bacteria, such as beta-hemolytic streptococci, are injurious at levels far below 105.8,9


Time for a Change?

In summary, a new "working" definition of infection might be stated as the presence of bacteria in any quantity sufficient to prevent a wound from healing. The identification of infection in wounds requires a high index of suspicion and a complete patient assessment. We cannot rely solely on wound appearance.


The goal of the health care professional is to identify the type and the amount of bacterial load; the virulence of the dominant bacteria; and the host's resistance, or the ability of the patient to mount a reasonable defense to the growing bacterial load on the wound. After establishing that information, we should direct patient therapies to reduce the bioburden to host-manageable levels.1




1. Lindfors J. A comparison of an antimicrobial wound cleanser to normal saline in reduction of bioburden and its effect on wound healing. Ostomy Wound Manage 2004;50(8):28-41. [Context Link]


2. Ovington L. Bacterial toxins and wound healing. Ostomy Wound Manage 2003;49(7A): 8-12. [Context Link]


3. Kaito C, Kurokawa K, Matsumoto Y, et al. Silkworm pathogenic bacteria infection model for identification of novel virulence genes. Mol Microbiol 2005;56:934-44. [Context Link]


4. Sterile and Materials Processing Department Glossary. University of Rochester Medical Center. (C)1999-2006. Available at: Accessed February 23, 2006. [Context Link]


5. Falanga V, Grinnell F, Gilchrest B, Maddox YT, Moshell A. Workshop on the pathogenesis of chronic wounds. J Invest Dermatol 1994;102:125-7. [Context Link]


6. Kingsley A. A proactive approach to wound infection. Nurs Stand 2001;15(30):50-54, 56, 58. [Context Link]


7. Armstrong DG, Perales TA, Murff RT, Edelson GW, Welchon JG. Value of white cell count with differential in the acute diabetic foot infection. J Am Podiatr Med Assoc 1996;86:224-7. [Context Link]


8. Gardner SE, Frantz RA, Doebbeling BN. The validity of the clinical signs and symptoms used to identify localized chronic wound infection. Wound Rep Reg 2001;9:178-86. [Context Link]


9. Robson MC. Lessons gleaned from the sport of wound watching. Wound Rep Reg 1999;7:2-6. [Context Link]