Figure 2.

The intracellular adaptation and spread of B. pseudomallei from cell-to-cell. Following phagosomal escape B. pseudomallei switches its metabolic pathways to allow for the greatest energy production within the cytoplasmic environment. Additionally, secretion of the toxin BLF1 and the T3SS effector CHBP modulate host cell processes, halting host protein synthesis. Host cell actin is polymerised by BimAC and B. pseudomallei cells rapidly propel to the cellular membrane upon which their T6SS–1 is expressed and Hcp1 causes membrane fusion and the formation of multinucleated giant cells (MNGCs). MNGC formation facilitates rapid spread of bacterial infection to neighbouring cells while escaping recognition by the immune response.