Bacterial biofilm in chronic lesions of hidradenitis suppurativa. (19th February 2017)

• Record Type: Journal Article
• Authors: Ring, H.C.; Bay, L.; Nilsson, M.; Kallenbach, K.; Miller, I.M.; Saunte, D.M.; Bjarnsholt, T.; Tolker‐Nielsen, T.; Jemec, G.B.
• Is Part Of: British journal of dermatology. Volume 176:Number 4(2017)
• Page Start: 993
• Page End: 1000
• Publication Date: 2017-02-19
• Subjects: Dermatology -- Periodicals; Skin -- Diseases -- Periodicals; 616.5
• DOI: 10.1111/bjd.15007
• Languages: English
• ISSNs: 0007-0963

Abstract

Abstract : What's already known about this topic? Chronic lesions of hidradenitis suppurativa (HS) exhibit several similarities with well‐known biofilm infections. Biofilms have previously been found in approximately 20% of lesions. What does this study add? Biofilm aggregates occur in 67–75% of sinus tracts and infundibula, and are larger in lesional skin than in perilesional skin, suggesting they are associated with established chronic lesions. Abundant keratinous debris may provide the nidus that promotes biofilm formation by commensal cocci in chronic HS lesions. What is the translational message? This study supports the association between bacterial biofilms and chronic HS lesions. Combining medical therapy with early surgical excision of chronic HS lesions or even simple deroofing may reflect the effective removal of otherwise intractable biofilms. Respond to this article Linked Comment:Stoodley. Br J Dermatol 2017;176 :855–856 Summary: Background: Chronic nonhealing or recurrent inflammatory lesions, reminiscent of infection but recalcitrant to antibiotic therapy, generally characterize biofilm‐driven diseases. Chronic lesions of hidradenitis suppurativa (HS) exhibit several characteristics, which are compatible with well‐known biofilm infections. Objectives: To determine and quantify the potential presence of bacterial aggregates in chronic HS lesions. Methods: In 42 consecutive patients with HS suffering from chronic lesions, biopsies were obtained from lesional as well as from perilesional skin. Samples were investigated using peptide nucleic acid–fluorescence in situ hybridization in combination with confocal laser scanning microscopy. In addition, corresponding histopathological analysis on haematoxylin and eosin slides was performed. Results: Biofilms were seen in 67% of the samples of chronic lesions and in 75% of the perilesional samples. The mean diameter of aggregates in lesional skin was significantly greater than in perilesional skin ( P = 0·01). Large biofilms (aggregates > 50 μm in diameter) were found in 42% of lesional samples and in only 5% of the perilesional samples ( P = 0·009). The majority of the large biofilms were situated in sinus tracts (63%) or in the infundibulum (37%). The majority of the sinus tract samples (73%) contained active bacterial cells, which were associated with inflammation. Conclusions: This study suggests that biofilm formation is associated with inflammation of chronic HS lesions. The aggregates most likely occur as a secondary event, possibly due to predisposing local anatomical changes such as sinus tracts (tunnels), keratinous detritus and dilated hair follicles.