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Hidradenitis suppurativa is a chronic inflammatory skin disease, with a poor therapeutic response and a significant impact on the patient's quality of life. The aim of this review-type article is to assess the role of bacterial infections in both the pathogenesis and evolution of the hidradenitis suppurativa, but also to evaluate the convenience of antibiotherapy in the management of the disease. Antibiotherapy plays an important role in its longterm management, mainly due to the anti-inflammatory action of the frequently recommended agents from the schemes of treatment. The therapy's initiation ought to be consistent with the antibiotic sensitivity profile of microorganisms isolated in the laboratory, personalized depending on the disease’s severity, history of antibiotic use, the risk of drug interactions and the patient's comorbidities. Moreover, the association of antibiotics with anti-TNF-α (tumour necrosis factor) biologic therapy represents a valid therapeutic alternative that can significantly enhance the quality of life, of great utility especially in severe disease stages. In order to elucidate the pathogenesis, we propose two main research directions. Firstly, the profile analysis of virulence of microorganisms and its correlation with the host response to bacterial insult. Secondly, the description of the bacterial biofilm communities, both architecturally and physiologically in-depth analyzes of inter-cellular communication mechanisms. These steps are necessary for the discovery of new therapeutic agents. [ABSTRACT FROM AUTHOR]

Hidradenitis suppurativa (HS) is a chronic inflammatory disease affecting intertriginous skin areas of young adults. Although HS was historically defined as an infectious disease, the role of microorganisms in its pathogenesis is now controversial. We investigated the lesion microbiota of a recently diagnosed 24-year-old male patient with axillary HS, who shared features of the metabolic syndrome. The microbiological analysis of the patient's lesion was indicative of colonization with bacteria including aerobes - Staphylococcus (S.) aureus, S. lugdunensis, S. epidermidis, anaerobes - Anaerococcus (A.) octavius, and microaerophiles - Cutibacterium (C.) acnes; this last one was also isolated in monoculture from a patient's healthy skin control sample. In vitro antibiotic susceptibility evaluation revealed Methicillin-resistant S. aureus (MRSA) and highly susceptible S. lugdunensis and S. epidermidis. Profiles of A. octavius and C. acnes showed that both strains were susceptible to Vancomycin, Clindamycin, Doxycycline and Linezolid; the anaerobe was Benzylpenicillin-resistant and Tetracycline and the microaerophile was intrinsically Metronidazole-resistant. We conclude that the intralesional microbial diversity in this case shows low variety of species and similarities to healthy skin microbiota, although the presence of S. aureus, particularly MRSA, S. lugdunensis or C. acnes - frequently involved in chronic skin pathologies - may be relevant for the disease severity. MRSA carriage in the patient's lesion represents a significant epidemiological risk for the healthcare environment. Antibiotic treatment in the early stages of HS should be administered with caution. Extended studies of HS microbiota could identify relevant colonization patterns for the outcome of the disease and offer important keys for selecting personalised, efficient therapeutic schemes. [ABSTRACT FROM AUTHOR]

Hidradenitis suppurativa represents a chronic, recurrent inflammatory disease, characterized by the formation of painful abscesses, sinuous tracts, foul smelling secretions, vicious scaring, with a severe reduction of the patients' quality of life. The pathophysiology of hidradenitis suppurativa is complex, follicular hyperkeratosis being regarded as the main pathogenetic mechanism. Bacterial colonization and follicular dysbiosis are of secondary importance in the pathogenesis of the disease, by triggering immunemediated inflammation. The formation of bacterial biofilms in sinuous tracts inhibits the efficacy of antibiotics, thus inducing chronic lesions. This article aims to highlight the role of bacterial colonization in the pathophysiology of hidradenitis suppurativa, as well as therapeutic options that act by regulating follicular dysbiosis. [ABSTRACT FROM AUTHOR]