The key role of TLRs in the pathogenesis of melioidosis is underscored by the finding that mice deficient in myeloid-differentiation-primary-response-gene-88 (MyD88), which is the key signalling adaptor protein for all TLRs, except for TLR3, show a strongly accelerated lethality upon intranasal infection with B. pseudomallei [40]. Here, MYD88 is linked to infection.