This paper reports the output of the Biofilm Workgroup at ICM 2018 (Philadelphia), the largest orthopedic infection consensus meeting in history. 28 biofilm experts used Delphi methodology to reach consensus on 13 questions covering biofilm biology, diagnostics, antimicrobial susceptibility, surface modifications, and emerging therapies. The focus is on what every orthopedic surgeon managing implant infections needs to understand about why biofilm is fundamentally different from planktonic infection.
When you send a culture and susceptibility report on a patient with a chronic periprosthetic joint infection, the MIC value on that report tells you nothing about whether your antibiotic will work against the biofilm on the implant surface. Biofilm bacteria are hundreds to thousands of times less susceptible than the planktonic bacteria that grew in the lab.
This changes how you frame surgical decision-making: antibiotics alone cannot eradicate an established biofilm infection, and the absence of a positive culture does not exclude biofilm-mediated disease. When you debride, you are not helping the antibiotics — you are doing the work the immune system cannot do.
When using a two-stage revision with an ALBC spacer, recognize that the spacer surface becomes colonizable once local antibiotic levels fall below MIC, and sub-therapeutic levels can persist for years. The spacer interval is a window of vulnerability, not protection.
No current imaging modality can tell you where the biofilm is on an implant before or during surgery. SPECT-CT and PET-CT identify zones of active infection but cannot distinguish biofilm from planktonic bacteria. You are always debriding without a map.
This paper reports the output of the Biofilm Workgroup at ICM 2018 (Philadelphia), the largest orthopedic infection consensus meeting in history. 28 biofilm experts used Delphi methodology to reach consensus on 13 questions covering biofilm biology, diagnostics, antimicrobial susceptibility, surface modifications, and emerging therapies. The focus is on what every orthopedic surgeon managing implant infections needs to understand about why biofilm is fundamentally different from planktonic infection.
When you send a culture and susceptibility report on a patient with a chronic periprosthetic joint infection, the MIC value on that report tells you nothing about whether your antibiotic will work against the biofilm on the implant surface. Biofilm bacteria are hundreds to thousands of times less susceptible than the planktonic bacteria that grew in the lab.
This changes how you frame surgical decision-making: antibiotics alone cannot eradicate an established biofilm infection, and the absence of a positive culture does not exclude biofilm-mediated disease. When you debride, you are not helping the antibiotics — you are doing the work the immune system cannot do.
When using a two-stage revision with an ALBC spacer, recognize that the spacer surface becomes colonizable once local antibiotic levels fall below MIC, and sub-therapeutic levels can persist for years. The spacer interval is a window of vulnerability, not protection.
No current imaging modality can tell you where the biofilm is on an implant before or during surgery. SPECT-CT and PET-CT identify zones of active infection but cannot distinguish biofilm from planktonic bacteria. You are always debriding without a map.