Melioidosis: Clinical impact and public health threat in the tropics
Fig 2
Schematic representation showing the virulence and pathogenesis of melioidosis infection.
B. pseudomallei is transmitted from its environmental reservoir to lung epithelial cells, where it initially attaches, possibly through bacterial components such as the capsule and type IV pili. Following invasion of epithelial cells, the T3SS-3 effectors assist in vacuolar escape and intracellular motility due to BimA-mediated actin polymerization. The activation of TLR-2, TLR-4, and TLR-5 by bacterial LPS and flagella results in recruitment of innate immune cells, such as neutrophils, macrophages, and natural killer cells. IRAK-M, interleukin-1-associated kinase 3; TLR, toll-like receptor; LPS, lipopolysaccharide; CD14, cluster of differentiation; NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells; IL, interleukin; TNF-α, tumor necrosis factor alpha; NLRC-4, NRL family CARD domain-containing protein 4; NLRP3, NACHT, LRR, and PYD domain-containing protein 3; ACS, acetyl-CoA synthetases; PCR, polymerase chain reaction.