Effects of tributyltin and hypoxia on the progression of Perkinsus marinus infections and host defence mechanisms in oyster, Crassostrea virginica (Gmelin)

Oysters, Crassostrea virginica (Gmelin), naturally infected by the protozoan parasite Perkinsus marinus in the field were exposed for 6 weeks to tributyltin (TBT), hypoxia, or to both stressors simultaneously. The TBT-exposed oysters continuously bioaccumulated TBT, reaching about 4 mg kg^??1 dry weight by 6 weeks; hypoxic oysters were exposed to water containing an average dissolved oxygen level of about 3 mg L^??1. Untreated control oysters suffered about 30% cumulative mortality by 6 weeks as a result of the progression of their P. marinus infections. The TBT treatment alone produced no additional mortality; however, cumulative mortality in hypoxic oysters was elevated. Mortality among oysters receiving both TBT and hypoxia significantly exceeded that caused by either stressor alone, suggesting a synergistic effect. In an attempt to identify immunotoxicological mechanisms underlying stress-related augmentation of P. marinus infections, defence-related immune functions were measured at 3 and 6 weeks in control and treated oysters. In general, the total number of haemocytes increased as the infections progressed, and the TBT and hypoxic treatments also caused significant additional increments in some samples. However, oxygen-dependent (reactive oxygen species) and oxygen-independent (lysozyme) antimicrobial host defence mechanisms appeared to be largely unaffected by TBT and/or hypoxia. This may be explained by the death of those oysters with marked immunological lesions prior to sampling or by the actual lack of treatment effects.