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Background: Buruli ulcer (BU) is an infectious disease caused by Mycobacterium ulcerans and considered the third most prevalent mycobacterial disease in humans. This skin disease can affect the entire body surface, but primarily the lower extremities, with symptoms varying from nodules to ulcers. Secondary bacterial infections in open BU lesions are the main cause of pain, delayed healing and systemic illness, resulting in prolonged hospital stay. Thus understanding the diversity of bacteria in these open lesions is important for proper treatment. The normal skin flora is known to protect the host through commensal relationships, however, certain factors such as ulceration can shift the skin flora from being primarily commensal to potentially pathogenic. Therefore, the objective of this study was to characterize and compare the skin bacteria from BU ulcers, non-BU ulcers, and similar locations on the skin of healthy individuals. Results: Using 16S rRNA sequencing, we determined the microbial composition of 5 BU lesions, 3 non-BU lesions and 3 healthy skin samples, and compared these using a data analysis pipeline. Our results showed a lower bacterial diversity in both the BU and non-BU lesions compared to the healthy skin. However, no significant differences were found between BU and non-BU lesions. The BU lesions were characterized by an increase of Bacteroidetes compared to the non-BU wounds, which contained more (Gamma)Proteobacteria. Furthermore, the BU lesions also contained significantly more obligate anaerobes. All lesions contained a mixture of gram-positive and gram-negative bacteria, with more gram-negatives present in the BU and non-BU lesions than in healthy skin samples. With this molecular-based study, we were also able to detect bacteria, which were missed by culture-based methods in previous BU studies.Conclusions: Our study suggests that BU leads to changes in the bacterial community within the lesions. These changes are potentially detrimental and may cause a delay in the healing process. In order to determine if the alterations in Bacteroidetes were due to a specific wound environment, underlying pathophysiological conditions created by M. ulcerans, or associated with wound location on the body, further microbiome studies are necessary. |