The intimate parasite–host interaction in terms of SL metabolism has been well documented; L. major pathogenic amastigotes isolated from mammalian hosts showed normal IPC levels (Zhang et al. 2005) despite lacking LCB2, a functional SPT and the ability to synthesis CER de novo. Alterations in host, macrophage, cell SL biosynthesis upon infection may compensate for this deficiency (Ghosh et al., 2001, 2002). These studies suggest a complex and multifaceted interplay between host and parasite SL metabolism comprising nutritional factors and signalling pathways that could modulate parasite survival and/or host defence (Zhang et al. 2010). Similar observations have been reported in the apicomplexan parasites (Romano et al. 2013). This highlights the striking potential of host and parasite SL modulation as an anti-protozoal target, as is similarly proposed for pathogenic fungi (Zhang et al. 2010; Ramakrishnan et al. 2013).