General Factors About Bacterial Involvement in HS Pathogenicity

The series of events in HS pathogenesis are unclear and the exact role of bacteria in the etiology of the disease remains controversial. Shelley and Cahn [49] were able to reproduce HS lesions by applying atropine-impregnated adhesive tape to a manually depilated axillary region. They noticed subsequent dilatation, inflammation, and bacterial invasion of the apocrine duct and concluded that HS is a bacterial infection of an obstructed apocrine sweat gland with the causative bacteria deriving from the normal flora of the skin.

However, today it is largely accepted that apocrine gland involvement is not essential to the pathogenesis, and that the inflammatory processes and involvement of apocrine glands are secondary events [6, 28]. The disease starts with follicular hyperkeratosis and dilatation of the infundibula and most authors believe that the bacterial contribution is a secondary event in the disease process [27, 48]. The retention of keratin in follicles and chronic sinusoids is subject to subsequent bacterial infection. Follicular occlusion leads to dilatation followed by rupture and spillage of the keratin and bacteria into the dermis. This induces a strong chemotactic response with an inflammatory cellular infiltrate consisting of neutrophils, lymphocytes, and histiocytes [50]. In chronic lesions, bacteria can be found in and around the glands and lymphatics [34]. In later stages of HS, bacterial infection is a risk factor for extension of the lesions. Sinus tracts are formed in the dermis and subcutis from the ruptured follicular epithelium in an attempt by the tissue to confine the inflammation, and there is a high risk for secondary infections [34, 50].

Systemic infections such as bacterial meningitis, bronchitis or pneumonia are possible, due to the spread of microorganisms [27]. In the case of coagulase-negative staphylococci, the recently found inflammatory peptides called phenol-soluble modulins (microbial products that stimulate cytokine production in host cells) play a role in the pathogenesis and systemic manifestations of sepsis [42].

Polypeptides from Propionibacterium acnes were found to stimulate a specific immune response in acne patients [26]. Jemec et al. [29] tried to detect a specific serologic response to a possible staphylococcal or streptococcal infection but the results were inconclusive.

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