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There are no convincing data to suggest that HS is primarily an infectious disease (see Chap. 11). The polymicrobial infection (or colonization) of HS - Staphylococcus aureus, Gram-negative rods, anaerobic bacteria - is quite different from the usual colonization of acne by Propionibacte-rium acnes and coagulase-negative staphylococci. The role of bacteria in HS may therefore be either secondary to some as yet unknown mechanism, or purely secondary once anatomical disruptions are established. HS is not a primary infectious disease; yet the initial inflammatory changes can be produced by a bacterial colonization of the follicular area similar to the triggering event of acne. The amount of inflamma tion and related pain is however quite different from what is observed in acne, even in the nodular variety. This may be due to the localization of the lesions but may also point to either a specific non-infectious inflammatory phenomenon, or a sequential series of events in which bacterial involvement occurs at specific points. Early involvement of pathogenic bacteria may be responsible for establishing inflammation, which leads to destructive scarring and extension of the disease independently of bacteria. Eventual secondary bacterial superinfections would then maintain the inflammatory process without the need for permanent colonization with pathogenic bacteria. The dramatic improvement observed in some patients with severe HS following a 3-month course of clinda-mycin-rifampicin treatment suggests a role for infection in advanced disease (see Chap. 15). However, it does not rule out the possibility that this polymicrobial infection is only a secondary 9 phenomenon, or that these antibiotics exert a predominantly anti-inflammatory effect. A specific anti-inflammatory role of some antibiotics - including tetracyclines, clindamycin and ri-fampicin - has been demonstrated in in vitro experiments. Whether this action is relevant in vivo and independent from any anti-infectious activity remains to be established.

of HS, the efficacy of anti-inflammatory drugs, of anti-tumor necrosis factor (TNF) drugs, and the significant association with Crohn's disease all point to an abnormality of immune and/or inflammatory mechanisms in HS. The number of "candidates" is large, including abnormalities of innate immunity, e.g., NOD, TLR, and deficiencies of natural antibacterial substances such as defensins and cathelicidins (see Chaps. 6, 12). The potential usefulness of anti-inflammatory and immunosuppressive therapy in HS may therefore have a broader scope than is reflected in existing literature.

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