“…The most important predisposing factors for EP are DM and UTI [2] . The compromised host-defense mechanism and associated EP leading to peritonitis explain the pathogenesis [3] . The various cascades of reactions mediated by interleukin 1,6, tumor necrosis factor, leukotrienes, platelet-activating factor, complement 3A, and 5A further led to splenic abscess formation, which on rupture resulted in pleural empyema secondary to tuberculosis through the pleuroperitoneal communication in the form of DPS [4] .…”