In Thailand, B. pseudomallei infections are predominantly manifested as community-acquired septicaemia. Followed by oral antimicrobial therapy comprising of trimethoprim and sulfamethoxazole for 3–6 months. However, despite of adequate antibiotic therapy the pathogen is capable of undergoing latency for decades and relapse in later stages of immune suppressed conditions. No substitutional protecting molecules or human vaccines for the disease currently exist. Therefore, there is a high priority for development of alternative antimicrobial molecules that can efficiently confer passive protection against the disease among the susceptible hosts. To combat the aforementioned challenge, passive antibodymediated protection would be a better alternative as antibodies upon passive administration confer immediate and specific immunity to the susceptible and/or infected host. Additionally, antibodies have minimal toxicity as they are natural in origin. Monoclonal antibodies hold great promise in this view, since the antimicrobial activity conferred by them shall be highly specific. Thus, they are also growing faster as new class of therapeutic and passive protection molecules. Pathogenesis mechanisms of B. pseudomallei are being explored intensively both in vitro and in vivo. As a pathogen, it has several strategies to survive and VX-11e establish pathogenesis in host system. The key factor of its pathogenesis is the ability to survive intracellularly in both phagocytic and non-phagocytic cells. This feature makes the pathogen successful in escaping host immune responses, establish chronic infections, latency and multi-drug resistance. Once invaded into host cells, B. pseudomallei induces cell-to-cell fusion resulting in formation of multinucleated giant cells. This is followed by the induction of apoptosis in infected cells by unknown mechanism. The inherent ability of the pathogen to form biofilm is also likely to be responsible for persistence of infection. B. pseudomallei has demonstrated resistance to antimicrobial drugs when grown in conditions that induce biofilm formation. Development of specific antibodies against the bacterial components involved in adherence and invasion into host cells might possibly prevent the pathogen to establish pathogenesis and in turn confer passive protection in susceptible and infected hosts. Earlier works reported on similar lines implied the promise of structural virulent factors present on the surface of bacteria for the purpose, since location of the antigens plays an important role in determining the effectiveness of the antibodies. Further, the antibodies, when bound to the surface-expressed antigens may enhance phagocytosis or CA-074 Me trigger complement fixation resulting in subsequent killing of internalized bacteria. Targeting a virulence factor that plays a key role in the former mentioned pathogen-mechanisms appears to be promising. However, according to a recent review, passive immunization against B. pseudomallei using mAbs raised against surface expressed molecules including capsular polysaccharide, lipopolysaccharide and exopolysaccharide provide significant but not complete protection in murine models. Also, using mAbs raised against CPS and LPS of B. pseudomallei in different studies have shown partial protection in murine models.