A study of the lesions of beaked whales (BWs) in a recent mass stranding in the Canary Islands following naval exercises provides a possible explanation of the relationship between anthropogenic, acoustic (sonar) activities and the stranding and death of marine mammals. Fourteen BWs were stranded in the Canary Islands close to the site of an international naval exercise (Neo-Tapon 2002) held on 24 September 2002. Strandings began about 4 hours after the onset of midfrequency sonar activity. Eight Cuvier's BWs (Ziphius cavirostris), one Blainville's BW (Mesoplodon densirostris), and one Gervais' BW (Mesoplodon europaeus) were examined postmortem and studied histopathologically. No inflammatory or neoplastic processes were noted, and no pathogens were identified. Macroscopically, whales had severe, diffuse congestion and hemorrhage, especially around the acoustic jaw fat, ears, brain, and kidneys. Gas bubble-associated lesions and fat embolism were observed in the vessels and parenchyma of vital organs. In vivo bubble formation associated with sonar exposure that may have been exacerbated by modified diving behavior caused nitrogen supersaturation above a threshold value normally tolerated by the tissues (as occurs in decompression sickness). Alternatively, the effect that sonar has on tissues that have been supersaturated with nitrogen gas could be such that it lowers the threshold for the expansion of in vivo bubble precursors (gas nuclei). Exclusively or in combination, these mechanisms may enhance and maintain bubble growth or initiate embolism. Severely injured whales died or became stranded and died due to cardiovascular collapse during beaching. The present study demonstrates a new pathologic entity in cetaceans. The syndrome is apparently induced by exposure to mid-frequency sonar signals and particularly affects deep, long-duration, repetitive-diving species like BWs.

No abstract

No abstract

No abstract

No abstract

No abstract

Substitution of marine ingredients (FM‐FO) by plant protein and oil sources can modify selenium (Se) levels in feeds. Se plays an important role in the antioxidative defence by forming part of selenoproteins. Se requirements of gilthead sea bream are not accurately determined; therefore, this study was conducted to define Se supplementation levels in low FM‐FO practical diets for sea bream fingerlings. A plant‐based diet containing 0.45 mg Se/kg diet was used as the basal diet. Four other diets were supplemented to contain 0.68, 0.86, 1.00 or 1.70 mg Se/kg diet, supplied as sodium selenite. Sea bream, weighing 12.6 ± 1.4 g, were distributed in triplicate groups per diet and fed for 42 days. Se supplementation up to 1.00 mg Se/kg significantly improved the growth of sea bream, whereas further increase up to 1.70 mg Se/kg diet reduced growth. The results of this study suggest that the optimum dietary levels of sodium selenite in diets with low FM‐FO with basal levels of 0.45 mg Se/kg are around 0.94 mg Se/kg to promote growth of gilthead sea bream juveniles. On the contrary, dietary levels of 1.70 mg Se/kg were found to be excessive and caused growth reduction, increased catalase expression and hydropic degeneration in the liver.

In the present work Hafnia alvei was isolated from laying hens displaying a reduction in egg production, loss of appetite, opisthotonus, and death. Multifocal necrotizing hepatitis and splenitis were the most prominent lesions. The organism was identified microbiologically. Laying hens were experimentally inoculated by the oral and intraperitoneal route to show the pathogenicity of the organism. A very similar clinicopathologic effect resulted from this trial. Several experimentally infected laying hens died due to septicemia. We conclude that H. alvei may cause a septicemia similar to that reportedly caused by Salmonella spp. in avian species.