Melioidosis predominantly affects the people who are in regular contact with soil and water. The Burkholderia pseudomallei gains entry through the abrasion of existing wounds or by the aspiration of contaminated water during near-drowning episodes or iatrogenic inoculation and laboratory acquired infection. Among these, the most common mode of infection is inoculation (Cheng and Currie, 2005, Loveleena et al., 2004).

The disease usually presents with a broad clinical spectrum ranging from mild localized infection to rapidly fatal septicemia (Chantratita et al., 2012). The organism has the tendency to remain latent in the host for long periods of time and when conditions become favorable for the bacterium to multiply, the disease may recrudesce clinically (Ashdown and Guard, 1984, Van et al., 1993, Naigowit et al., 1992). In endemic areas, a significant proportion of apparently healthy individuals have antibodies to B. pseudomallei which may result from subclinical infection (Barnes et al., 2004).

Previous studies have demonstrated contradictory results in the role of phagocytes in melioidosis. It has been proved that the organism can survive and multiply within professional phagocytes including macrophages or monocyte and neutrophil cell lines (Jones et al., 1996, Pruksachartvuthi et al., 1990). The organism has the ability to evade phagosome-lysosome fusion and destroy the phagosome membrane as soon as 15 min after ingestion (Harley et al., 1998). In ultra structural studies of the interaction between macrophage and B. pseudomallei , the responses have compared between the patients with melioidosis and healthy controls and it suggests that there is less early phagolysosome fusion in macrophages from melioidosis patients, resulting in higher intracellular bacterial concentrations (Cheng and Currie, 2005).

TNF-α is an early and potent proinflammatory cytokine which is primarily produced by macrophages but also by B cells, T cells and fibroblasts. The increase in the level of TNF-α is associated with mortality. However, the infection can be suppressed by TNF-α and in a mouse model, the neutralization of TNF-α shows increased susceptibility to melioidosis (Santanirand et al., 1997). Another study shows that the interferon-γ plays a vital role in controlling melioidosis and they suggest that the rapid production of IFN-γ, occurring in the innate response to B. pseudomallei , can be achieved not only by the natural-killer cells, but also by the CD8+ cells which are activated by a cytokine-dependent bystander mechanism (Lertmemongkolchai et al., 2001).

The Studies indicate that, individuals develop infection when they fail to mount an adequate cell mediated immunity response where as the individuals who develop strong specific cell mediated immunity response to organism may not develop clinical disease (Barnes et al., 2004).