**10. BU and host susceptibility**

*M. ulcerans* is an environmental pathogen [64]. Several studies have reported *M. ulcerans* DNA target both in BU endemic and non-endemic regions [21]. In addition, Sero-epidemiological studies have also shown that antibodies for the immuno-dominant protein, 18 kDa shsp is present in healthy controls [100]. This has raised numerous questions and hypotheses on host genetics and susceptibility [36]. From previous reports, it appears not all those exposed to *M. ulcerans* develop overt disease [36]. Some genetic marks such as solute carrier family 11, member 1 (*SLC11A1*) [36], autophagyrelated genes E3 ubiquitin-protein ligase (PARK2) and autophagy-related protein 16–1 (ATG16L1) [36] nucleotide-binding oligomerization domain-containing 2 (NOD2) have been suggested as key players in BU susceptibility [36]. If host susceptibility is at play, it could change our perception on the mode of transmission and treatment of BU.
