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Changing the Paradigm of Critical Colonization

David G. Armstrong, DPM, MD, PhD

I’m happy to present to the audience a recent study from my colleagues, Tom Serena, Mike Edmonds, and me. Long ago, critical limb ischemia (CLI) was adopted as if there was some sort of critical point over which someone descended into ischemia. We know that this is not how it works for our patients with diabetes. This is chronic. These patients don’t show up with an acute cold limb. This developed into what we now call chronic limb threatening ischemia, or CLTI.
 
We think that the same thing might be true for what was once called “critical colonization.” It now might be called “chronic inhibitory bacterial load,” or CIBL.
 
Bottom line: just as we have chronic limb threatening ischemia (CLTI), we likely have chronic inhibitory bacterial load (CIBL). If it is inhibiting healing and inflammation on one end or pushing over the edge toward a frank and obvious infection on the other, it is very likely important but presently not visible.

The good thing now is that this can be detected, and we can likely knock it back with consistent debridement and maybe ultimately effective antimicrobials. Let me share more about the recent article published in the International Wound Journal.1

We know that increased bacteria, including biofilm, contribute to wound infection and delayed healing. However, one should note that there is a lack of clinical terminology and diagnostic tools that apply specifically to asymptomatic high bacterial loads. In our study across multiple care centers, we investigated the role of fluorescence imaging in 138 diabetic foot ulcers with respect to detecting biofilm-encased and planktonic bacteria in wounds at high loads using quantitative tissue culture.1 We found the presence of bacteria in 131/138 ulcers and loads >104 CFU/g in nearly 94% of them. These wounds, for the most part, had no symptoms of infection. Fluorescence imaging increased sensitivity in our study for detecting bacteria in load of 104–109, with the peak at those >108 CFU/g. We also found that over 84% of the ulcers imaged had high bacterial loads in the periwound area.1
 
Using a new term, chronic inhibitory bacterial load (CIBL), my co-authors and I believe we can describe these frequently asymptomatic, high bacterial loads in diabetic ulcers and periwound tissues. Thus, clinicians can then intervene at this stage to prevent infection and its consequences. We anticipate this way of thinking could indeed spark a paradigm shift to support better outcomes through earlier intervention.1

Dr. Armstrong is Professor of Surgery at the Keck School of Medicine at the University of Southern California. He is the Director of the Southwestern Academic Limb Salvage Alliance (SALSA).

Editor’s note: This blog originally appeared here. It is adapted with permission from the author.

Reference

1.     Armstrong DG, Edmonds ME, Serena TE. Point-of-care fluorescence imaging reveals extent of bacterial load in diabetic foot ulcers. Int Wound J. 2023;20(2):554-566.

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