• Steven P LaRosa, Steven M Opal, Barbara Utterback, Sau Chi Betty Yan, Jeffrey Helterbrand, Andrew J H Simpson, Wipada Chaowagul, Nicholas J White, and Charles J Fisher.
• Division of Infectious Disease, Rhode Island Hospital, Gerry House 113, 593 Eddy Street, and Infectious Diseases and Microbiologic Divisions of Brown University School of Medicine, Providence, Rhode Island 02903, USA. slarosa@lifespan.org
• Int. J. Infect. Dis. 2006 Jan 1;10(1):25-31.

BackgroundAcute septicemic melioidosis is associated with systemic release of endotoxin and the proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin-1, and interleukin-6. Excessive release of these cytokines may lead to endothelial injury, depletion of naturally occurring endothelial modulators, microvascular thrombosis, organ failure, and death.MethodPlasma samples drawn at baseline and after initial antimicrobial therapy in 30 patients with suspected acute severe melioidosis were assayed for D-dimer levels, protein C and protein S antigen levels, and antithrombin functional activities.ResultsBoth baseline and continued deficiencies of protein C, protein S, and antithrombin were statistically associated with a poor outcome by logistic regression. Baseline D-dimer levels were significantly higher in fatal cases than survivors and correlated inversely with protein C and antithrombin, suggesting both increased fibrin deposition and fibrinolysis.ConclusionThe inflammatory response to systemic Burkholderia pseudomallei infection leads to depletion of the natural endothelial modulators protein C, protein S, and antithrombin. Both baseline and continued deficiency of these endothelial modulators is predictive of poor outcome in melioidosis.

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