Effects of Carbon Dioxide Exposure on Intensively Cultured Rainbow Trout Oncorhynchus mykiss: Physiological Responses and Fillet Attributes

Rainbow trout Oncorhynchus mykiss (261.6 × 24.7 g initial weight, mean × SEM) at 13.1 × 0.2 C were exposed for 94 d to one of three CO₂ treatments: control (22.1 × 2.8 mg/L), medium (34.5 × 3.8 mg/L), or high (48.7 × 4.4 mg/L). Trout were checked daily for survival, and fish were sampled at 0, 28, 56, and 84 d for physiological responses, growth, and fillet quality assessments. Trout were also challenged to a 15-min crowding stress at 93 d to assess their ability to initiate a stress response during hypercapnia. Chronically exposed trout showed nearly 100% survival through 84 d exposure (1 of 1,500 fish died). Growth and physiological results showed that increasing elevated CO₂, concentrations result in corresponding decreased growth rates and CO₂specific physiological parameters: The medium and high CO₂ treatments had significantly slower growth and subsequently smaller fish by 84 d. Exposed trout also showed significantly ( P < 0.05) decreased plasma chloride for medium and high CO₂ treatments compared to the control from 28 through 84 d. Decreased growth and smaller fish in the medium and high CO₂ treatments resulted in correspondingly smaller fresh and smoked fillet weights. Chronic CO₂ exposure did not result in notable changes in ultimate muscle pH. Exposure to 15-min crowding stress at 93 d resulted in significant changes in hematocrit, plasma cortisoI, glucose, and chloride for all treatment groups. CO₂-specific changes were detected in hematocrit, plasma cortisoI, and plasma chloride responses following the 15-min crowding stress.     

Seedborne Fusarium on Douglas-fir: Pathogenicity and seed stratification method to decrease Fusarium contamination

Twelve Douglas-fir (Pseudotsuga menziesii (Mirb.) Franco) seedlots from coastal British Columbia were assayed for seedborne Fusarium. All of the seedlots were contaminated with Fusarium. Percent of nonstratified seeds from individual seedlots harboring Fusarium ranged from 0.3% to 95.4%. Sixty-seven percent of the seedlots had Fusarium on less than 2% of the seeds. Post-stratification seedborne Fusarium levels were significantly less for running water imbibition compared to standing water imbibition. However, seedling growth at a container nursery was not consistently different for stratified seed imbibed initially in standing or running water. Fusarium disease symptoms were not observed in the nursery environment. The species of Fusarium isolated from seed were F. acuminatum, F. avenaceum, F. lateritium, F. moniliforme, F. oxysporum, F. poae and F. sambucinum. Twelve Fusarium isolates, comprising six species, were assessed for pathogenicity. Disease symptoms were observed after four weeks incubation and Fusarium isolates ranged in virulence from low to high. Fusarium oxysporum isolates were the most pathogenic.     

Early postmortem biochemical factors influence tenderness and water-holding capacity of three porcine muscles

The objective of this study was to determine whether differences in pork tenderness and water-holding capacity could be explained by factors influencing calpain activity and proteolysis. Halothane-negative (HAL-1843 normal) Duroc pigs (n = 16) were slaughtered, and temperature and pH of the longissimus dorsi (LD), semimembranosus (SM), and psoas major (PM) were measured at 30 and 45 min and 1, 6, 12, and 24 h postmortem. Calpastatin activity; mu-calpain activity; and autolysis and proteolysis of titin, nebulin, desmin, and troponin-T were determined on muscle samples from the LD, SM, and PM at early times postmortem. Myofibrils from each muscle were purified to assess myofibril-bound (mu-calpain. Percentage drip loss was determined, and Warner-Bratzler shear (WBS) force was analyzed. Myosin heavy-chain (MHC) isoforms were examined using SDS-PAGE. The pH of PM was lower (P < 0.01) than the pH of LD and SM at 30 and 45 min and 1 h postmortem. The PM had a higher (P < 0.01) percentage of the MHC type IIa/IIx isoforms than the LD. The-LD had the greatest proportion of (P < 0.01) MHC IIb isoforms of any of the muscles. The PM had the lowest (P < 0.01) percentage of MHC IIb isoforms and a greater (P < 0.05) percentage of type I MHC isoforms than the LD and SM. The PM had less (P < 0.01) drip loss after 96 h of storage than the SM and LD. The PM had more desmin degradation (P < 0.01) than the LD and SM at 45 min and 6 h postmortem. Degradation of titin occurred earlier in the PM than the LD and SM. At 45 min postmortem, the PM consistently had some autolysis of mu-calpain, whereas the LD and SM did not. At 6 h postmortem, some autolysis of mu-calpain (80-kDa subunit) was observed in all three muscles. The rapid pH decline and increased rate of autolysis in the PM paralleled an earlier appearance of myofibril-bound mu-calpain. The SM had higher calpastatin activity (P < 0.05) at 45 min, 6 h, and 24 h and had higher WBS values at 48 h (P < 0.01) and 120 h (P < 0.05) postmortem than the LD. At 48 and 120 h postmortem, more degradation of desmin, titin, and nebulin were observed in the LD than in the SM. These results show that mu-calpain activity, mu-calpain autolysis, and protein degradation are associated with differences in pork tenderness and water-holding capacity observed in different muscles.     

Histological and morphometric lesions in the pre-clinical,developmental phase of insulin-induced laminitis in Standardbred horses

Lamellar pathology in experimentally-induced equine laminitis associated with euglycaemic hyperinsulinaemia is substantial by the acute, clinical phase (～48 h post-induction). However, lamellar pathology of the developmental, pre-clinical phase requires evaluation. The aim of this study was to analyse lamellar lesions both qualitatively and quantitatively, 6, 12 and 24 h after the commencement of hyperinsulinaemia. Histological and histomorphometrical analyses of lamellar pathology at each time-point included assessment of lamellar length and width, epidermal cell proliferation and death, basement membrane (BM) pathology and leucocyte infiltration. Archived lamellar tissue from control horses and those with acute, insulin-induced laminitis (48 h) was also assessed for cellular proliferative activity by counting the number of cells showing positive nuclear immuno labelling for TPX2.Decreased secondary epidermal lamellar (SEL) width and increased histomorphological evidence of SEL epidermal basal (and supra-basal) cell death occurred early in disease progression (6 h). Increased cellular proliferation in SELs, infiltration of the dermis with small numbers of leucocytes and BM damage occurred later (24 and 48 h). Some lesions, such as narrowing of the SELs, were progressive over this time period (6–48 h). Cellular pathology preceded leucocyte infiltration and BM pathology, indicating that the latter changes may be secondary or downstream events in hyperinsulinaemic laminitis.     

FIV diversity: FIV Ple subtype composition may influence disease outcome in African lions

Feline immunodeficiency virus (FIV) infects domestic cats and at least 20 additional species of non-domestic felids throughout the world. Strains specific to domestic cat (FIV(Fca)) produce AIDS-like disease progression, sequelae and pathology providing an informative model for HIV infection in humans. Less is known about the immunological and pathological influence of FIV in other felid species although multiple distinct strains of FIV circulate in natural populations. As in HIV-1 and HIV-2, multiple diverse cross-species infections may have occurred. In the Serengeti National Park, Tanzania, three divergent subtypes of lion FIV (FIV(Ple)) are endemic, whereby 100% of adult lions are infected with one or more of these strains. Herein, the relative distribution of these subtypes in the population are surveyed and, combined with observed differences in lion mortality due to secondary infections based on FIV(Ple) subtypes, the data suggest that FIV(Ple) subtypes may have different patterns of pathogenicity and transmissibility among wild lion populations.