Simulating particle organic matter dispersal beneath Atlantic salmon fish farms using different resuspension approaches.

An accurate representation of the particle organic matter (POM) footprint is necessary in order to effectively predict impacts upon benthic communities and the risk of excessive organic enrichment beneath aquaculture sea-cages. Consequently, bottom-related processes such as particle resuspension must be adequately parametrized and evaluated in the available numerical models. We implemented two approaches to model POM resuspension in a Lagrangian particle tracking model and compared their influence on footprint extension and gradients of depositional flux against a no-resuspension scenario. We performed simulations in both exposed and protected aquaculture locations, and at different stages of the Atlantic Salmon (Salmo salar) production cycle in Norway. Our results indicate that the use of sediment-dependent thresholds for resuspension has the potential to regulate the high levels of erosion produced when selecting a low critical value in constant-threshold approaches, particularly in dynamic environments with mixed sediment types.

Environmental change influences the life history of salmon Salmo salar in the North Atlantic Ocean.

Annual mean total length (LT) of wild one-sea-winter (1SW) Atlantic salmon Salmo salar of the Norwegian River Imsa decreased from 63 to 54 cm with a corresponding decrease in condition factor (K) for cohorts migrating to sea from 1976 to 2010. The reduction in LT is associated with a 40% decline in mean individual mass, from 2 to 1·2 kg. Hatchery fish reared from parental fish of the same population exhibited similar changes from 1981 onwards. The decrease in LT correlated negatively with near-surface temperatures in the eastern Norwegian Sea, thought to be the main feeding area of the present stock. Furthermore, S. salar exhibited significant variations in the proportion of cohorts attaining maturity after only one winter in the ocean. The proportion of S. salar spawning as 1SW fish was lower both in the 1970s and after 2000 than in the 1980s and 1990s associated with a gradual decline in post-smolt growth and smaller amounts of reserve energy in the fish. In wild S. salar, there was a positive association between post-smolt growth and the sea survival back to the River Imsa for spawning. In addition, among smolt year-classes, there were significant positive correlations between wild and hatchery S. salar in LT, K and age at maturity. The present changes may be caused by ecosystem changes following the collapse and rebuilding of the pelagic fish abundance in the North Atlantic Ocean, a gradual decrease in zooplankton abundance and climate change with increasing surface temperature in the Norwegian Sea. Thus, the observed variation in the life-history traits of S. salar appears primarily associated with major changes in the pelagic food web in the ocean.

Marine downscaling of a future climate scenario in the North Sea and possible effects on dinoflagellate harmful algal blooms.

Two hydrodynamic and ecological models were used to investigate the effects of climate change-according to the IPCC A1b emission scenario - on the primary productivity of the North Sea and on harmful algal blooms. Both models were forced with atmospheric fields from a regional downscaling of General Circulation Models to compare two sets of 20-year simulations representative of present climate (1984-2004) conditions and of the 2040s. Both models indicated a general warming of the North Sea by up to 0.8°C and a slight freshening by the 2040s. The models suggested that the eastern North Sea would be subjected to more temperature and salinity changes than the western part. In addition, the ecological modules of the models indicated that the warming up of the sea would result in a slightly earlier spring bloom. The one model that also computes the distribution of four different phytoplankton groups suggests an increase in the abundance of dinoflagellates, whereas the abundance of diatoms, flagellates and Phaeocystis sp. remains comparable to current levels, or decrease. Assuming that Dinophysis spp. would experience a similar increase in abundance as the modelled group of dinoflagellates, it is hypothesised that blooms of Dinophysis spp. may occur more frequently in the North Sea by 2040. However, implications for shellfish toxicity remain unclear.

A single-base change in the tyrosine kinase II domain of ovine FGFR3 causes hereditary chondrodysplasia in sheep.

Ovine hereditary chondrodysplasia, or spider lamb syndrome (SLS), is a genetic disorder that is characterized by severe skeletal abnormalities and has resulted in substantial economic losses for sheep producers. Here we demonstrate that a non-synonymous T>A transversion in the highly conserved tyrosine kinase II domain of a positional candidate gene, fibroblast growth factor receptor 3 (FGFR3), is responsible for SLS. We also demonstrate that the mutant FGFR3 allele has an additive effect on long-bone length, calling into question the long-standing belief that SLS is inherited as a strict monogenic, Mendelian recessive trait. Instead, we suggest that SLS manifestation is determined primarily by the presence of the mutant FGFR3 allele, but it is also influenced by an animal's genetic background. In contrast to FGFR3 mutations causing dwarfism in humans, this single-base change is the only known natural mutation of FGFR3 that results in a skeletal overgrowth phenotype in any species.

5-Hydroxytryptophan toxicosis in dogs: 21 cases (1989-1999).

OBJECTIVE: To determine epidemiologic characteristics, clinical findings, and treatment outcome of 5-hydroxytryptophan (5-HTP) toxicosis in dogs. DESIGN: Retrospective study. ANIMALS: 21 dogs with evidence of accidental 5-HTP ingestion. PROCEDURE: Information was retrieved from the National Animal Poison Control Center database. Records of dogs ingesting 5-HTP between January 1989 and February 1999 were reviewed for information on signalment, dose ingested, clinical signs (onset, severity, duration), treatments administered, and outcome. RESULTS: Clinical signs of toxicosis developed in 19 of 21 (90%) dogs. Neurologic signs included seizures (9 dogs), depression (6), tremors (5), hyperesthesia (5), and ataxia (4). Gastrointestinal tract signs included vomiting or diarrhea (12 dogs), signs of abdominal pain (3), and hypersalivation (2). Other clinical signs were hyperthermia (7 dogs) and transient blindness (3). Three dogs died. No important clinical laboratory or necropsy findings were reported. The doses of 5-HTP ingested ranged from 2.5 to 573 mg/kg (1.1 to 260 mg/lb) of body weight; the minimum toxic dose reported in our study was 23.6 mg/kg (10.7 mg/lb), and the minimum lethal dose was 128 mg/kg (58.1 mg/lb). Onset of signs ranged from 10 minutes to 4 hours after ingestion, and signs lasted up to 36 hours. Of 17 dogs with clinical signs of toxicosis that received treatment, 16 recovered; treatment consisted of decontamination, seizure control, thermoregulation, fluid therapy, and supportive care. CONCLUSIONS AND CLINICAL RELEVANCE: Ingestion of 5-HTP in dogs can result in a potentially life-threatening syndrome resembling serotonin syndrome in humans, which requires prompt and aggressive care.

Evaluation of castor bean toxicosis in dogs: 98 cases.

Castor beans (Ricinus communis) contain ricin. Ricin is a glycoprotein reported to cause hypotension, gastroenteritis, depression, and death. However, few deaths are reported following castor bean ingestion in animals. From January 1987 to December 1998, the American Society for the Prevention of Cruelty to Animals-National Animal Poison Control Center received 98 incidents of castor bean ingestion in dogs. The most commonly reported clinical signs were vomiting, depression, and diarrhea. Death or euthanasia occurred in 9% of the cases. The severity of clinical signs following castor bean ingestion may depend on whether the beans were chewed or swallowed whole.

Localization of the locus causing Spider Lamb Syndrome to the distal end of ovine Chromosome 6.

Spider Lamb Syndrome (SLS) is a semi-lethal congenital disorder, causing severe skeletal abnormalities in sheep. The syndrome has now been disseminated into several sheep breeds in the United States, Canada, and Australia. The mode of inheritance for SLS is autosomal recessive, making the identification and culling of carrier animals difficult due to their normal phenotype. Two large pedigrees segregating for the SLS mutation were established, and a genome scan with genetic markers from previously published genome maps of cattle and sheep was used to map the locus causing SLS. Genetic linkage between SLS and several microsatellite markers, OarJMP8, McM214, OarJMP12, and BL1038, was detected, thereby mapping the SLS locus to the telomeric end of ovine Chromosome (Chr) 6. Alignment of ovine Chr 6 with its evolutionary ortholog, human Chr 4, revealed a positional candidate gene, fibroblast growth factor receptor 3 (FGFR3).

Cycad palm toxicosis in dogs: 60 cases (1987-1997).

OBJECTIVE: To report clinical and epidemiologic information, summarize characteristic clinical signs and laboratory results, and describe the expected course of cycad toxicosis in dogs. DESIGN: Retrospective study. ANIMALS: 60 dogs with evidence of cycad ingestion. PROCEDURE: The National Animal Poison Control Center's case record database was searched for records of dogs ingesting cycad plants from January 1987 to November 1997. Data were retrieved on clinical signs, laboratory test results, exposure history, and physical examination findings. Cases were assessed as toxicosis, suspected toxicosis, or possible toxicosis. RESULTS: Records from 60 dogs were retrieved; 89.7% of the dogs were from the southern United States, 38.7% ingested seeds, 95% developed liver and gastrointestinal tract problems, and 53.3% had abnormal neurologic signs. High serum bilirubin concentration and alkaline phosphatase and alanine aminotransferase activities were the most common serum biochemical abnormalities. Although clinical signs were observed within 1 day, laboratory values did not change for 24 to 48 hours after cycad ingestion. Mortality rate was reportedly 32.1%. CLINICAL IMPLICATIONS: 68% of dogs responded well to treatment and supportive care. Dogs ingesting seeds are likely to develop more serious problems. Clinical signs can develop within 1 to 3 days and can last for several days. A tentative diagnosis should be made on the basis of history of ingestion, clinical signs, and duration of signs. Because of the nature of these toxins, cycad ingestion is serious and should be treated aggressively.