For clinicians across acute, post-acute, and community settings, few topics in wound care create more uncertainty than biofilm. These structured communities of microorganisms encased in a protective matrix drive inflammation, delay epithelialization, and contribute to recalcitrant infection, yet their behavior in the wound bed is often misunderstood. Below, we debunk common myths with current evidence and offer practical takeaways for day-to-day care.

Myth 1: You can see biofilm with the naked eye.

In routine practice, you cannot reliably identify a wound biofilm by visual inspection alone. Biofilms are microscopic; definitive visualization typically requires laboratory tools such as confocal or electron microscopy, while in-clinic clues (eg, recurring slough, excessive exudate, delayed granulation) are indirect and nonspecific. A 2023 review emphasizes that biofilm is invisible to the naked eye and should be suspected based on clinical trajectory and risk factors rather than appearance alone.¹ Diagnostic limitations matter clinically: culture and light microscopy frequently miss biofilms, whereas advanced molecular assays and imaging are more sensitive but not widely available at the point of care.²   

Myth 2: One-time cleansing or a single sharp debridement removes biofilm.

Mechanical disruption is essential but rarely curative by itself or in a single episode. Biofilm communities demonstrate marked tolerance to host defenses, topical agents, and even physical removal, rapidly re-establishing in a wound. Experimental work shows biofilms can form within hours, highlighting why serial debridement and ongoing hygiene are required rather than “one-and-done” approaches.^3-4 Preclinical wound models also show that combining debridement with biofilm-dispersing enzymes can significantly enhance clearance and improve responsiveness to topical antibiotics: evidence that adjunctive, repeated strategies outperform a single intervention.⁵ 

Myth 3: Antibiotics alone will clear a wound biofilm.

Systemic antibiotics penetrate biofilms poorly and often fail against biofilm-adapted phenotypes. Biofilm-associated bacteria exhibit profound antibiotic tolerance and can survive otherwise adequate antimicrobial exposures. Contemporary reviews underscore that standard antimicrobial monotherapy is frequently ineffective against biofilm, mandating a multifaceted plan anchored in debridement, aggressive wound bed preparation, and targeted topical/antibiofilm measures (eg, antiseptics, surfactant-containing or chelator-enhanced dressings) alongside antimicrobial stewardship.^6,7 

Myth 4: If a swab culture is negative, there’s no biofilm.

Don’t equate a negative or low-yield swab with the absence of a biofilm. Microbiologic methods under-sample sessile communities, and swab results can deviate from tissue sampling or sequencing. A 2021 study comparing cultivation with 16S sequencing in matched swabs and biopsies from chronic wounds found substantial differences in detected taxa, underscoring culture’s blind spots for complex communities.⁸ In parallel, a 2025 review notes that routine culture and light microscopy often fail to detect biofilms, pushing clinicians to rely on longitudinal assessment and adjunctive technologies when available.² For diabetic foot ulcers specifically, high-quality guidelines advise against treating clinically uninfected wounds with antibiotics; they also emphasize obtaining appropriate deep samples when osteomyelitis is suspected—reminders that sampling strategy and clinical context, rather than a single swab result, should drive decisions.⁹ 

Myth 5: Biofilms are only a chronic-wound problem.

Chronicity amplifies biofilm recalcitrance, but early biofilm establishment can occur in acute wounds as well. In vitro and ex vivo wound models demonstrate that common pathogens (eg, Staphylococcus aureus, Pseudomonas aeruginosa) initiate biofilm formation within hours to a day in host-like conditions, supporting early, proactive wound bed preparation to prevent maturation into a tolerant, entrenched state.^3,4 Population data on prevalence vary, but recent clinical reviews estimate biofilm across a substantial portion of chronic wounds and implicate it as a key barrier to healing.¹ 

Myth 6: All antimicrobial dressings perform the same against biofilm.

Head-to-head, open-access work in wound-relevant biofilm models shows meaningful performance differences among antimicrobial dressings. Matrix-disrupting chemistries, surfactants, and specific active agents can change outcomes, which is why product selection should be evidence-based and paired with thorough wound bed preparation.¹⁰ 

What does this mean at the bedside?

For a hard-to-heal wound that stalls or repeatedly “resloughs,” assume biofilm presence until proven otherwise. Optimize host factors and perfusion, then plan care as a process, not a one-time event. Start with effective disruption—sharp, mechanical, or enzymatic debridement—followed by antimicrobial/antibiofilm cleansers and/or dressings that suit the bioburden, exudate, and patient goals. Reassess frequently and repeat debridement as indicated, recognizing that biofilms re-establish quickly in wound environments. Use deeper samples or advanced diagnostics when infection is suspected, and reserve systemic antibiotics for clinically infected wounds to align with stewardship principles. Taken together, this biofilm-aware approach—debride, disrupt, dress, and diligently reassess—improves the odds of progression to healing while minimizing unnecessary antibiotic exposure.^3–7,9,10

References

1. Goswami AG, Basu S, Banerjee T, Shukla VK. Biofilm and wound healing: from bench to bedside. Eur J Med Res. 2023;28(1):157. Published 2023 Apr 25. doi:10.1186/s40001-023-01121-7. 
2. Almuhanna Y. Microbial Biofilms as Barriers to Chronic Wound Healing: Diagnostic Challenges and Therapeutic Advances. J Clin Med. 2025;14(22):8121. Published 2025 Nov 17. doi:10.3390/jcm14228121 
3. Pai L, Patil S, Liu S, Wen F. A growing battlefield in the war against biofilm-induced antimicrobial resistance: insights from reviews on antibiotic resistance. Front Cell Infect Microbiol. 2023;13:1327069. Published 2023 Dec 19. doi:10.3389/fcimb.2023.1327069 
4. Rubio-Canalejas A, Baelo A, Herbera S, Blanco-Cabra N, Vukomanovic M, Torrents E. 3D spatial organization and improved antibiotic treatment of a Pseudomonas aeruginosa-Staphylococcus aureus wound biofilm by nanoparticle enzyme delivery. Front Microbiol. 2022;13:959156. Published 2022 Nov 16. doi:10.3389/fmicb.2022.959156
5. Tan X, Cheng X, Hu M, et al. Transcriptional analysis and target genes discovery of Pseudomonas aeruginosa biofilm developed ex vivo chronic wound model. AMB Express. 2021;11(1):157. Published 2021 Nov 27. doi:10.1186/s13568-021-01317-2
6. Schneider RE, Hamdan JV, Rumbaugh KP. Biofilm Dispersal and Wound Infection Clearance With Preclinical Debridement Agents. Int Wound J. 2025;22(3):e70145. doi:10.1111/iwj.70145
7. Darvishi S, Tavakoli S, Kharaziha M, Girault HH, Kaminski CF, Mela I. Advances in the Sensing and Treatment of Wound Biofilms. Angew Chem Int Ed Engl. 2022;61(13):e202112218. doi:10.1002/anie.202112218
8. Mahnic A, Breznik V, Bombek Ihan M, Rupnik M. Comparison Between Cultivation and Sequencing Based Approaches for Microbiota Analysis in Swabs and Biopsies of Chronic Wounds. Front Med (Lausanne). 2021;8:607255. Published 2021 Jun 4. doi:10.3389/fmed.2021.607255 
9. Senneville É, Albalawi Z, van Asten SA, et al. IWGDF/IDSA guidelines on the diagnosis and treatment of diabetes-related foot infections (IWGDF/IDSA 2023). Diabetes Metab Res Rev. 2024;40(3):e3687. doi:10.1002/dmrr.3687 
10. Stuermer EK, Plattfaut I, Dietrich M, et al. In vitro Activity of Antimicrobial Wound Dressings on P. aeruginosa Wound Biofilm. Front Microbiol. 2021;12:664030. Published 2021 May 14. doi:10.3389/fmicb.2021.664030