title: Cellular responses and disease expression in oysters (Crassostrea virginica) exposed to suspended field contaminated sediments.
abstract: Exposure of oysters to water soluble fractions derived from field-contaminated sediments (FCS) containing predominantly lower molecular weight organic aromatic compounds, has been previously demonstrated to enhance pre-existing infections caused by the protozoan parasite, Perkinsus marinus (Dermo), and the prevalence of experimentally induced infections. To further explore the role of pollution on the onset and progression of disease, effects of suspended FCS from an estuarine creek in Virginia, USA, dominated by higher molecular weight polycyclic aromatic hydrocarbons (PAHs) on cellular responses and Dermo disease expression in oysters (Crassostrea virginica) were examined. Sediments were collected from a PAH polluted estuarine creek in Virginia, USA. To test effects on cellular response, oysters from Maine were exposed daily to 0, 1.0, 1.5, or 2.0 g suspended FCS (corresponding to 0, 70.2, 105, or 140 microg PAHs, respectively) for 5, 10, 20, and 40 days. Hemocyte activities and plasma lipid, protein and lactate dehydrogenase (LDH) levels were then measured. Exposure stimulated neutral red uptake, MTT reduction, and 3H-leucine incorporation in oyster hemocytes at various exposure times, but did not affect the plasma protein, lipid and LDH levels. To test effects on Dermo expression, oysters from a Dermo enzootic area, with an initial estimated infection prevalence of 39%, were exposed daily to 0, 1.0, 1.5, or 2.0 g suspended FCS (corresponding to 0, 75.0, 113, or 150 microg PAHs, respectively) for 30 days. Exposure enhanced disease expression in oysters. However, no significant change was noted in any measured cellular or humoral parameters.
authors.affiliation: Department of Environmental Sciences, Virginia Institute of Marine Science, College of William and Mary, Gloucester Point, VA 23062, USA. chu@vims.edu
authors.forename: Fu-Lin E
authors.initials: FL
authors.lastname: Chu
authors.forename: Aswani K
authors.initials: AK
authors.lastname: Volety
authors.forename: Robert C
authors.initials: RC
authors.lastname: Hale
authors.forename: Yongqin
authors.initials: Y
authors.lastname: Huang
mesh_terms: D000820:Animal Diseases / Q000139:chemically induced*; D000818:Animals; D004196:Disease Outbreaks; D018450:Disease Progression; D004781:Environmental Exposure; D056890:Eukaryota / Q000472:pathogenicity*; D019015:Geologic Sediments / Q000737:chemistry; D010125:Ostreidae / Q000469:parasitology* / Q000502:physiology*; D015995:Prevalence; D011528:Protozoan Infections / Q000209:etiology*; D014873:Water Pollutants / Q000009:adverse effects*
chemical_list: D014873:Water Pollutants