We review the molecular and epidemiological characteristics of cetacean morbillivirus (CeMV) and the diagnosis and pathogenesis of associated disease, with six different strains detected in cetaceans worldwide. CeMV has caused epidemics with high mortality in odontocetes in Europe, the USA and Australia. It represents a distinct species within the Morbillivirus genus. Although most CeMV strains are phylogenetically closely related, recent data indicate that morbilliviruses recovered from Indo-Pacific bottlenose dolphins (Tursiops aduncus), from Western Australia, and a Guiana dolphin (Sotalia guianensis), from Brazil, are divergent. The signaling lymphocyte activation molecule (SLAM) cell receptor for CeMV has been characterized in cetaceans. It shares higher amino acid identity with the ruminant SLAM than with the receptors of carnivores or humans, reflecting the evolutionary history of these mammalian taxa. In Delphinidae, three amino acid substitutions may result in a higher affinity for the virus. Infection is diagnosed by histology, immunohistochemistry, virus isolation, RT-PCR, and serology. Classical CeMV-associated lesions include bronchointerstitial pneumonia, encephalitis, syncytia, and lymphoid depletion associated with immunosuppression. Cetaceans that survive the acute disease may develop fatal secondary infections and chronic encephalitis. Endemically infected, gregarious odontocetes probably serve as reservoirs and vectors. Transmission likely occurs through the inhalation of aerosolized virus but mother to fetus transmission was also reported.

We present new and revised data for the phocine distemper virus (PDV) epidemics that resulted in the deaths of more than 23 000 harbour seals Phoca vitulina in 1988 and 30 000 in 2002. On both occasions the epidemics started at the Danish island of Anholt in central Kattegat, and subsequently spread to adjacent colonies in a stepwise fashion. However, this pattern was not maintained throughout the epidemics and new centres of infection appeared far from infected populations on some occasions: in 1988 early positive cases were observed in the Irish Sea, and in 2002 the epidemic appeared in the Dutch Wadden Sea, 6 wk after the initiation of the outbreak at Anholt Island. Since the harbour seal is a rather sedentary species, such 'jumps' in the spread among colonies suggest that another vector species could have been involved. We discussed the role of sympatric species as disease vectors, and suggested that grey seal populations could act as reservoirs for PDV if infection rates in sympatric species are lower than in harbour seals. Alternatively, grey seals could act as subclinical infected carriers of the virus between Arctic and North Sea seal populations. Mixed colonies of grey and harbour seal colonies are found at all locations where the jumps occurred. It seems likely that grey seals, which show long-distance movements, contributed to the spread among regions. The harbour seal populations along the Norwegian coast and in the Baltic escaped both epidemics, which could be due either to genetic differences among harbour seal populations or to immunity. Catastrophic events such as repeated epidemics should be accounted for in future models and management strategies of wildlife populations. KEY WORDS: Epizootic · Harbour seal · Mass mortality · Phocine distemper virus Resale or republication not permitted without written consent of the publisherDis Aquat Org 68: [115][116][117][118][119][120][121][122][123][124][125][126][127][128][129][130] 2006 natural reductions in food supply driven by El Niño conditions have led to high levels of mortality (Trillmich & Dellinger 1991).There is also increasing evidence for mortality resulting from infectious disease. In 1988, up to 60% of North Sea harbour seals Phoca vitulina died during an outbreak of a then newly discovered distemper virus identified by inclusion bodies (e.g. Dietz et al. 1989a, Bergman et al. 1990. This virus was isolated and described as a morbillivirus, phocine distemper virus (PDV) (Osterhaus & Vedder 1988). Subsequently, related dolphin and porpoise morbilliviruses were isolated from cetaceans (Barrett et al. 1993), and widespread screenings suggest that many populations of pinnipeds, cetaceans and sirenians in the North Atlantic had been exposed to these viruses prior to and after the 1988 PDV outbreak (Dietz et al. 1989b, Duignan et al. 1995a,b,c, 1997a,b, Van Bressem et al. 2001. Clinical signs of disease were not recorded in many of the populations in which morbillivirus antibodies were detected (Duignan et al. 1995b, Nielsen et al. 20...

Killer whales (Orcinus orca) are among the most highly polychlorinated biphenyl (PCB)–contaminated mammals in the world, raising concern about the health consequences of current PCB exposures. Using an individual-based model framework and globally available data on PCB concentrations in killer whale tissues, we show that PCB-mediated effects on reproduction and immune function threaten the long-term viability of >50% of the world’s killer whale populations. PCB-mediated effects over the coming 100 years predicted that killer whale populations near industrialized regions, and those feeding at high trophic levels regardless of location, are at high risk of population collapse. Despite a near-global ban of PCBs more than 30 years ago, the world’s killer whales illustrate the troubling persistence of this chemical class.

A description and comparison of the four major methods available for studying conservation physiology of large whales, namely analysis of faecal, respiratory vapour, and skin/blubber biopsy samples, and photographs.

A recent rise in the reporting of diseases in marine organisms has raised concerns that ocean health is deteriorating. The goal of this study was to determine whether or not there has been a recent deterioration in marine mammal health by investigating the trends in disease reports over the past 40 years (categorized by the method of study, the species affected, and the etiology of the disease) and by exploring the changes in frequency of mass mortality events among marine mammals reported in the United States since 1978. The number of papers on marine mammal disease published each year has increased since 1966, although the annual publication rate appears to have stabilized since $1992. Those published in the 1960s and 1970s were largely about helminth and bacterial disease, those investigating viruses emerged in the late 1970s and increased in the 1980s and 1990s, whereas protozoal diseases and harmful algal toxins were largely not reported until the 1990s. The annual number of mass mortality events in the U.S. approximately doubled between 1980 and 1990 but since 2000 has been between seven and eight events per year. Causes of mass mortality events have included biotoxins, viruses, bacteria, parasites, human interactions, oil spills, and changes in oceanographic conditions. Events due to biotoxins appear to be increasing, but the change in the frequency of mass mortality events from other causes over the past 40 years cannot be determined from the available published literature due to changes in marine mammal abundance, inconsistencies in effort and extent of resources for pathological investigation, and advances in technology that have allowed improved detection of pathogens and toxins in more recent years. To ensure future information on the true incidence of marine diseases and their underlying causes is more reliable, specific and directed marine health monitoring programs, well-equipped stranding networks, and dedicated diagnostic laboratories are needed.