Evidence for a biofilm based treatment strategy in the management of chronic hidradenitis suppurativa

Abstract

Hidradenitis suppurativa (HS) is a chronic, inflammatory, debilitating skin disease of the hair follicle defined by recurrent, painful, deep‐seated and inflamed lesions.1 Although many aspects of the clinical presentation of HS is suggestive of infection, the role of the microbiology is still the subject of much debate. Polymicrobial‐positive cultures of skin bacteria are common but many cases are culture‐negative. Empirical antibiotic treatment returns mixed results in terms of resolving the disease. Interestingly, there are many similarities with otitis media with effusion (OME) in which there were conflicting data and opinions as to the role of bacteria in the chronic recurrent inflammation and whether the underlying cause was infection or a dysfunctional immune response.2 The bacterial biofilm paradigm of chronic disease may resolve some of these contradictions. Biofilms are aggregates of bacteria living within a protective extracellular polymeric slime matrix that adhere to indwelling devices and host tissue. When bacteria are in the biofilm phenotype they become highly tolerant of antibiotics and host immunity and elicit a chronic inflammatory response that causes damage to host tissue but fails to clear the infection. Chronic inflammation associated with bacterial biofilms is seen in diseases such as OME, the infected cystic fibrosis lung and periprosthetic joint infections (PJI).3 Because biofilm bacteria are notoriously difficult to culture and as there are no biofilm‐specific biomarkers, direct microscopic observation of biofilms is the best way to determine their presence with confocal laser scanning microscopy (CLSM) being the preferred method. Previously it was reported that bacterial biofilms were present in a case study of a patient with HS4 and this might provide a missing link between microbiology and chronic inflammation. In the present issue of the BJD, Ring et al.5 use peptide nucleic acid (PNA)–fluorescence in situ hybridization (FISH) (PNA)–FISH) and CLSM to demonstrate and map the presence of biofilms in chronic lesions of 42 patients with HS. Biofilms were seen in 67% of chronic lesions and 75% of the perilesional samples. The biofilms were heterogeneously distributed in discrete bacterial aggregates ranging from 5‐μm diameter up to more continuous patches > 50 μm, similar to those seen in OME and PJI specimens.2, 3 Importantly, the majority of the sinus tract samples (73%) contained active bacterial cells, which were associated with inflammation, thus suggesting the histology of HS may provide ideal settings for biofilm growth. This important study makes a clear link between a biofilm involvement and chronic inflammation in the late stages of the disease. However, other biofilm studies looking at clinically unaffected HS skin and samples from acute HS found little or no evidence of biofilms,6, 7 thus suggesting that biofilm formation is involved in exacerbating or possibly progressing the disease to later stages (Fig. 1). The mounting evidence that biofilms have an involvement in HS warrants consideration of a biofilm‐based treatment strategy such as is employed in other chronic wound biofilm infections8 in which a combination of high doses of locally administered antibiotics and aggressive early surgical excision or de‐roofing may reflect the most optimal treatment strategy for these patients.

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ORCID for Paul Stoodley: orcid.org/0000-0001-6069-273X

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