Shark depredation: future directions in research and management.

Shark depredation is a complex social-ecological issue that affects a range of fisheries worldwide. Increasing concern about the impacts of shark depredation, and how it intersects with the broader context of fisheries management, has driven recent research in this area, especially in Australia and the United States. This review synthesises these recent advances and provides strategic guidance for researchers aiming to characterise the occurrence of depredation, identify the shark species responsible, and test deterrent and management approaches to reduce its impacts. Specifically, the review covers the application of social science approaches, as well as advances in video camera and genetic methods for identifying depredating species. The practicalities and considerations for testing magnetic, electrical, and acoustic deterrent devices are discussed in light of recent research. Key concepts for the management of shark depredation are reviewed, with recommendations made to guide future research and policy development. Specific management responses to address shark depredation are lacking, and this review emphasizes that a "silver bullet" approach for mitigating depredation does not yet exist. Rather, future efforts to manage shark depredation must rely on a diverse range of integrated approaches involving those in the fishery (fishers, scientists and fishery managers), social scientists, educators, and other stakeholders.

Comparison of flock characteristics, journey duration and pathology between flocks with a normal and a high percentage of broilers 'dead-on-arrival' at abattoirs.

This study investigated high mortality in broilers transported to slaughter in Norway by comparing data from flocks with normal and high mortality during transportation. The data sources consisted of necropsy findings in 535 broilers dead-on-arrival (DOA), production data and slaughterhouse data, along with average journey duration for the 61 associated flocks. The mean Norwegian DOA% for 2015 was 0.10. In this study, normal-mortality flocks were defined as flocks with a mean DOA% up to 0.30 and high mortality as flocks with a mean DOA% above 0.30. DOA% was calculated per flock. The most frequent pathological finding was lung congestion which was observed in 75.5% of the DOA broilers. This postmortem finding was significantly more common in broilers from high-mortality flocks (89.3%) than in DOA broilers from normal-mortality flocks (58%). The following variables had a significantly (P<0.05) higher median in the high-mortality flocks: flock size, 1st week mortality, foot pad lesion score, carcass rejection numbers and journey duration. The results indicate that high broiler mortality during transportation to the abattoir may be linked to several steps in the broiler production chain. The results suggest that preventive measures are to be considered in improvement of health and environmental factors during the production period and throughout the journey duration.

Entry of coronavirus into primate CNS following peripheral infection.

A previous report demonstrated that intracerebrally inoculated coronavirus produced CNS disease in two species of primates (Murray RS, Cai G-Y, Hoel K, et al., Virol 1992; 188: 274-84). We were therefore interested in testing the potential of coronaviruses to infect primate CNS tissue following peripheral inoculation. Four Owl monkeys (Aotus trivirgatus) were inoculated intranasally and ocularly and four were inoculated intravenously with coronavirus JHM OMp1 (Murray RS, Cai G-Y, Hoel K, et al., Virol 1992; 188: 274-84). Two intranasally and two intravenously inoculated animals received a second intravenous inoculum at 153 days post-infection. The animals were sacrificed 16, 35, 194, and 215 days post-infection. Tissue sections from brain and spinal cord were screened for viral products by in sity hybridization and immunostaining. Virus RNA and/or antigen was detected in the brains of all animals and the distribution corresponded to areas of inflammation and edema. Viral products were predominantly found in blood vessels and perivascular regions, suggesting hematogenous spread with entry into the central nervous system through endothelium.

Coronavirus JHM OMP1 pathogenesis in owl monkey CNS and coronavirus infection of owl monkey CNS via peripheral routes.

Two separate studies are described in this report. First, 5 Owl monkeys were inoculated intracerebrally (IC) with coronavirus JHM OMP1; this virus isolate was cultured from the brain of an animal inoculated with uncloned MHV JHM. Two of the animals became neurological impaired and were sacrificed; these animals had developed severe encephalomyelitis as previously described. Two of the remaining 3 healthy animals were inoculated IC again at 90 days post-inoculation (DPI) and all 3 were sacrificed approximately 5 months after the first virus inoculation. Despite the lack of detectable infectious virus, viral RNA and antigen, all 3 animals had significant white matter inflammation and areas of demyelination in the spinal cord. In the second study 4 Owl monkeys were inoculated intranasally (IN) and ocularly and 4 inoculated intravenously (i.v.) with JHM OMP1. The animals were sacrificed between 16 and 215 DPI with 2 IN and 2 i.v. animals receiving a second i.v. inoculum at 152 DPI. Viral RNA and/or antigen was detected in the brains of all animals and the distribution corresponded to areas of inflammation and edema. One of the animals that received the second inoculum developed neurological impairment and subsequent analysis of tissues showed viral antigen in both brain and spinal cord. Viral products were predominantly found in blood vessels suggesting hematogenous spread with entry into the central nervous system (CNS) through endothelium.

Coronavirus infects and causes demyelination in primate central nervous system.

Two species of primates, Owl and African green monkeys, were inoculated intracerebrally with either the neurotropic mouse hepatitis virus JHM or the putative multiple sclerosis brain coronavirus isolate SD. These viruses caused an acute to subacute panencephalitis and/or demyelination in the infected animals. The course of pathogenesis and sites of detected viral RNA and antigen was dependent both on animal species and virus strain but the results clearly showed that these viruses replicated and disseminated in the central nervous system (CNS) of these primates. This study suggests that human CNS may be susceptible to coronavirus infection.