MicrobiologyBytes

Melioidosis, which can present as an acute septic illness or as a chronic low-grade infection, was first described in Burma more than 100 years ago. 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 recent years as more and more research groups are working on this disease. The global distribution boundaries of melioidosis continue to expand well beyond the traditionally recognized endemic region of southeast-Asia and northern-Australia. For instance, new cases have been described in Brazil and southeast-Africa, although it has to be clarified whether melioidosis is indeed endemic in these regions. Of interest, phylogenetic studies have recently hypothesized that B. pseudomallei has originated in tropical Australia with subsequent spread to southeast-Asia (dubbed as the Gondwana hypothesis). Pneumonia with bacterial dissemination to distant sites and abscess formation is a common presentation. Current treatment recommendations on the basis of clinical trial evidence are parental ceftazidim or carbapenem for 10–14 days or longer as clinically indicated, followed by oral trimethoprim–sulfamethoxazole ± doxycycline for at least 12–20 weeks. This review summarizes present knowledge on the molecular characterization of B. pseudomallei and the immunology of melioidosis with a special emphasis on its potential therapeutic implications.

Immunity to Burkholderia pseudomallei. Curr Opin Infect Dis. 2009 22(2): 102-108
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. 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. 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.

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