Because temperature plays an important role on progression and transmission of disease caused by Perkinsus marinus in the field, the effects of triclosan on the viability of P. marinus meronts (trophozoites) and oyster hemocytes were tested at a range of environmental relevant temperatures. Additionally, we examined the triclosan effect on reactive oxidative intermediate production (ROI) by oyster hemocytes and tested the efficacy of treating infected oysters with triclosan in eliminating/reducing P. marinus infection in a pilot experiment. When P. marinus cultivated at 13°C, 20°C, and 28°C was exposed to triclosan at corresponding temperatures, 2–10 μM triclosan killed 10–30% at 20°C and ≥40% at 28°C, but ≤10% at 13°C. When exposure of P. marinus cultivated at 28°C to triclosan at 26°C, similar mortality was noted as those recorded at 28°C. Treating hemocytes from oysters maintained at 13°C, 20°C, or 26°C with 2, 5, 10 μM triclosan at corresponding temperatures, killed 2% to 13% at 13°C and 6 to16% at 20°C. No mortality occurred in hemocytes exposed to 2–10 μM triclosan at 26°C. However, at the highest temperature and triclosan concentration tested (28°C, 10 μM triclosan), hemocyte mortality exceed 30%. Exposure of hemocytes to triclosan concentrations of 2–10 μM for 4 h at 4°C significantly reduced the ROI production in hemocytes in a dose-dependent response. Treating P. marinus infected oysters with 300 and 600 μg triclosan/oyster daily for 8 wk, significantly slowed the disease progression.