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Buruli Ulcer-Associated Staphylococcus aureus in Burkina Faso
Rym Lalaoui1, Anselme Millogo2,3, Madjid Morsli4
1Laboratoire d'Hématologie et de Biologie Vasculaire, Assistance Publique-Hôpitaux de Marseille, Marseille, France.
None:
The characterization of Staphylococcus aureus (S. aureus) isolates superinfecting cutaneous lesions of Buruli ulcer (BU), a neglected tropical disease caused by non-tuberculous Mycobacterium ulcerans, remains limited. In Burkina Faso, we investigated eight S. aureus isolates from BUs and three from non-BUs using phenotypic analysis, including antibiotic susceptibility testing and genomic analysis (whole genome sequencing, average nucleotide identity, resistome, virulome, multilocus sequence typing, pangenome, and multiple correspondence analysis). All isolates were firmly identified at the species level as S. aureus subsp. aureus but did not cluster according to the group to which they belonged. These 11 isolates were in vitro susceptible to most antibiotics, except for penicillin G, erythromycin, and ciprofloxacin, to which some were resistant (11/11, 3/11, and 3/11, respectively). S. aureus isolates were assigned to different spacer-types (STs) including ST5 (2/11), ST1472 (1/11), ST1 (2/11), ST2434 (1/11), ST152 (3/11), and a previously unreported ST7358 (2/11). The spa types included t8921, t318, t127, t084, t355, t559, and t311. Several phages, antibiotic resistance genes, and virulence factors, including immunomodulators, adhesins, exoenzymes, and toxins such as Panton-Valentine leucocidin, were identified in all groups. No mec genes were detected in any of the S. aureus strains studied. OrthoANI, pangenome, and multiple correspondence analysis did not specify any S. aureus genotype associated with BU. In conclusion, we found no specificity of S. aureus strains to BU, which leads us to speculate that this microorganism behaves only as an opportunistic pathogen of the lesion.
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