PURPOSE OF REVIEW: Largely due to its recognition as a biological threat agent, 
current knowledge on melioidosis, caused by the Gram-negative bacterium 
Burkholderia pseudomallei, has increased tremendously over the last years. This 
review summarizes current understanding on the molecular characterization of B. 
pseudomallei and the immunology of melioidosis.
RECENT FINDINGS: The genome of B. pseudomallei is composed of two chromosomes of 
which the largest part represents the B. pseudomallei core genome, whereas the 
remaining accessory genome has been associated with bacterial virulence. 
Virulence factors, most notably quorum sensing, type III secretion system, 
lipopolysaccharide and other surface polysaccharides, flagella and various 
factors essential for the intracellular life cycle of B. pseudomallei, have been 
further characterized. The neutrophils play a critical in host defense, which is 
initiated by the Toll-like receptors. The proinflammatory immune 
response--including the activation of coagulation-- and its regulation have been 
further dissected.
SUMMARY: Severe melioidosis can probably be seen as the clinical manifestation 
of a pathogen recognition receptor mediated dysregulation of the immune response 
to invading B. pseudomallei. B. pseudomallei employs numerous tactics to evade 
the immune response. Studies on host-pathogen interactions in melioidosis have 
identified a whole range of potential new treatment targets.