Expression of immune-regulatory genes in juvenile Chinook salmon following exposure to pesticides and infectious hematopoietic necrosis virus (IHNV).

Impairment of fish immune function as a consequence of polluted aquatic environments can result in changes in susceptibility to disease. In this study, we investigated the effects of two widely used insecticides, chlorpyrifos (CP) and esfenvalerate (EV), and a pathogen, infectious hematopoietic necrosis virus (IHNV), singly and in combination, on survival and cytokine (Mx protein, IL-1beta, TGF-beta and IGF-1) expression in juvenile Chinook salmon. Fish were exposed for 96 h to sublethal concentrations of CP (3.7 microg L(-1)) or EV (0.08 microg L(-1)), allowed to recover in clean water for seven days, then exposed to IHNV (6.4x10(5)TCID(50)mL(-1)) for 1.5h. Mortality was recorded daily, and spleen and anterior kidney samples were collected on day 4 (after CP or EV treatment), day 20 and day 60 (after CP or EV treatment and subsequent IHNV exposure) of the experiment. Significant mortality after 60 days was observed following exposure to EV (17%) or IHNV (20%), and prior insecticide exposure did not synergize the acute effects of pathogen treatment. By day 4, exposure to CP as well as EV led to a significant decrease of Mx protein and IL-1beta expression; by day 20, EV-exposed fish significantly overexpressed IL-1beta. Mx protein transcription was up-regulated in spleen and kidney of all IHNV-exposed fish groups by day 20. All but one treatment (EV) led to significantly decreased IGF-1 transcription in spleen on days 20 and 60, whereas a short-term increase was seen after CP exposure (day 4). In kidney, decreases of IGF-1 transcription were less pronounced. TGF-beta transcription was up-regulated in CP/IHNV and EV/IHNV exposure groups. Our results indicate that CP and EV alter the expression of cytokines, but this did not negatively affect the ability of fish to survive a subsequent exposure to IHNV. Induced TGF-beta transcription indicated that the combined stressors affected fish in a synergistic manner, but the consequences are unknown. Increased transcription of Mx protein was a reliable indicator of virus exposure.

Synergistic effects of esfenvalerate and infectious hematopoietic necrosis virus on juvenile chinook salmon mortality.

Sublethal concentrations of pollutants may compromise fish, resulting in increased susceptibility to endemic pathogens. To test this hypothesis, juvenile chinook salmon (Oncorhynchus tshawytscha) were exposed to sublethal levels of esfenvalerate or chlorpyrifos either alone or concurrently with infectious hematopoietic necrosis virus (IHNV). Three trials were performed with fish exposed to concentrations of IHNV between 0.8 x 10(2) and 2.7 x 10(6) plaque-forming units/ml and to 5.0 microg/L of chlorpyrifos or 0.1 microg/L of esfenvalerate. The presence and concentration of IHNV in dead fish were assayed by virus isolation and plaque assay techniques, respectively. Among groups exposed to both esfenvalerate and IHNV, 83% experienced highly significant (p < 0.001) mortality, ranging from 20 to 90% at 3 d post-virus exposure, and cumulatively died from 2.4 to 7.7 d sooner than fish exposed to IHNV alone. This trend was not seen in any other treatment group. Virus assays of dead fish indicate a lethal synergism of esfenvalerate and IHNV. Chlorpyrifos had no observed effect on total mortality or IHNV susceptibility. The present results suggest that accepted levels of pollutants may be seemingly nonlethal to fish but, in fact, be acting synergistically with endemic pathogens to compromise survivorship of wild fish populations through immunologic or physiologic disruption.

Assessment of hepatic motion secondary to respiration for computer assisted interventions.

This article reviews the published efforts to characterize hepatic motion secondary to respiration, with the specific goal of defining the limitations and potential applications of image-guided systems in percutaneous liver interventions (computer assisted interventions). Hepatic motion and deformation due to respiration remain obstacles to applying stereotactic localization techniques to the liver. Respiratory-associated hepatic motion is complex. Nine studies using diagnostic imaging or modeling are reviewed, and their findings are tabulated herein. The significant variations in their findings are discussed, including cranio-caudal translation, anterior-posterior and lateral translation, movement secondary to tissue deformation, and motion with respect to surrounding tissue. Techniques for correcting for hepatic respiratory motion are then described, including gating techniques, modeling approaches, real-time liver tracking, and magnetic tracking technology.