Mass mortalities due to disease outbreaks have recently affected major taxa in the oceans. For closely monitored groups like corals and marine mammals, reports of the frequency of epidemics and the number of new diseases have increased recently. A dramatic global increase in the severity of coral bleaching in 1997—98 is coincident with high El Nino temperatures. Such climate-mediated, physiological stresses may compromise host resistance and increase frequency of opportunistic diseases. Where documented, new diseases typically have emerged through host or range shifts of known pathogens. Both climate and human activities may have also accelerated global transport of species, bringing together pathogens and previously unexposed host populations. T he oceans harbor enormous biodiver- sity by terrestrial terms (1), much of which is still poorly described taxo- nomically. Even less well known are the dy- namics of intermittent, ephemeral, threshold phenomena such as disease outbreaks. De- spite decades of intense study of the biolog- ical agents structuring natural communities, the ecological and evolutionary impact of diseases in the ocean remains unknown, even when these diseases affect economically and ecologically important species. The paucity of baseline and epidemiological information on normal disease levels in the ocean chal- lenges our ability to assess the novelty of a recent spate of disease outbreaks and to de- termine the relative importance of increased pathogen transmission versus decreased host resistance in facilitating the outbreaks. Our objectives here are to review the prevalence of diseases of marine taxa to evaluate wheth- er it can be concluded that there has been a recent increase. We also assess the contribut- ing roles of human activity and global cli- mate, and evaluate the role of the oceans as incubators and conveyors of human disease agents. Is There an Increase in Diseases in the Ocean?

/pdf/emerging-marine-diseases-climate-links-and-anthropogenic-24nqep16se.pdf

Emerging Marine Diseases--Climate Links and Anthropogenic Factors

The long-term consequences of climate change and potential environmental degradation are likely to include aspects of disease emergence in marine plants and animals. In turn, these emerging diseases may have epizootic potential, zoonotic implications, and a complex pathogenesis involving other cofactors such as anthropogenic contaminant burden, genetics, and immunologic dysfunction. The concept of marine sentinel organisms provides one approach to evaluating aquatic ecosystem health. Such sentinels are barometers for current or potential negative impacts on individual- and population-level animal health. In turn, using marine sentinels permits better characterization and management of impacts that ultimately affect animal and human health associated with the oceans. Marine mammals are prime sentinel species because many species have long life spans, are long-term coastal residents, feed at a high trophic level, and have unique fat stores that can serve as depots for anthropogenic toxins. Marine mammals may be exposed to environmental stressors such as chemical pollutants, harmful algal biotoxins, and emerging or resurging pathogens. Since many marine mammal species share the coastal environment with humans and consume the same food, they also may serve as effective sentinels for public health problems. Finally, marine mammals are charismatic megafauna that typically stimulate an exaggerated human behavioral response and are thus more likely to be observed.

https://journals.sagepub.com/doi/pdf/10.1177/0300985810388525

Marine Mammals as Sentinel Species for Oceans and Human Health

Echinoderms play a key role in structuring many marine ecosystems and are notorious for large population density variations in so-called “outbreak” or “dieoff” events. In a review of this phenomenon, we assess the causal factors and ecological and evolutionary consequences. We identified 28 species (6 Asteroidea, 8 Echinoidea, 10 Holothuroidea, 4 Ophiuroidea) that exhibit large (more than two population doublings or halvings) population density changes. Three generalized patterns were identified and named for exemplary species: (1) rapid decreases followed by no or slow recovery (Diadema–Paracentrotus Model), (2), rapid increase and apparent stability at a new population density (Amperima–Amphiura Model), and (3) population density fluctuations (Acanthaster–Asterias Model). Echinoderms identified were distributed from the shallow intertidal to the deep sea, and from tropical to temperate regions. In most cases, significant impacts on the respective ecosystems were observed. The most striking similarity among all species identified was possession of the ancestral-type planktotrophic larva. This larval type was significantly overrepresented in species identified within the Asteroidea, Echinoidea, Holothuroidea, and for the combined data set. We suggest three main factors that render a life history with planktotrophic larvae a high-risk–high-gain strategy: (1) a strong nonlinear dependency of larval production on adult densities (Allee effects), (2) a low potential for compensatory feedback mechanisms, and (3) an uncoupling of larval and adult ecology. The alternative (derived) lecithotrophic larva occurs in 68% of recent echinoderm species, suggesting an evolutionary trend toward this larval type. Lecithotrophic development represents a more buffered life history because compensatory feedback between adult densities and larval output is likely to be more efficient. For lecithotrophic developers, direct nutritive coupling from adult to larva to the early benthic juvenile provides a buffer against starvation. Lecithotrophic larvae are independent of the vagaries of planktonic food supply, and their short planktonic duration may promote local recruitment. Anthropogenic influences contributed to the population density variations in most cases, including increased primary productivity through eutrophication or global change, disease, overfishing, and species introductions. We suggest that anthropogenic disturbance, through its influence on the frequency and/or amplitude of echinoderm population density changes, may go beyond present ecosystem impacts and alter future evolutionary trends.

https://esajournals.onlinelibrary.wiley.com/doi/pdf/10.1890/07-2136.1

A boom–bust phylum? Ecological and evolutionary consequences of density variations in echinoderms

Morbilliviruses comprise measles virus, canine distemper virus, rinderpest virus, and several other viruses that cause devastating human and animal diseases accompanied by severe immunosuppression and lymphopenia. Recently, we have shown that human signaling lymphocyte activation molecule (SLAM) is a cellular receptor for measles virus. In this study, we examined whether canine distemper and rinderpest viruses also use canine and bovine SLAMs, respectively, as cellular receptors. The Onderstepoort vaccine strain and two B95a (marmoset B cell line)-isolated strains of canine distemper virus caused extensive cytopathic effects in normally resistant CHO (Chinese hamster ovary) cells after expression of canine SLAM. The Ako vaccine strain of rinderpest virus produced strong cytopathic effects in bovine SLAM-expressing CHO cells. The data on entry with vesicular stomatitis virus pseudotypes bearing measles, canine distemper, or rinderpest virus envelope proteins were consistent with development of cytopathic effects in SLAM-expressing CHO cell clones after infection with the respective viruses, confirming that SLAM acts at the virus entry step (as a cellular receptor). Furthermore, most measles, canine distemper, and rinderpest virus strains examined could any use of the human, canine, and bovine SLAMs to infect cells. Our findings suggest that the use of SLAM as a cellular receptor may be a property common to most, if not all, morbilliviruses and explain the lymphotropism and immunosuppressive nature of morbilliviruses.

Morbilliviruses Use Signaling Lymphocyte Activation Molecules (CD150) as Cellular Receptors

textDisease outbreaks with high mortality rates among seals and dolphins
have recently attracted considerable public and scientific
interest. Allhouyh in most cases morbillivirus infections were
shown to be the primary cause of the disease outbreaks, it was
speculated that pollution-induced immunosuppression had playat:!
a contributory role. Here we present results of a prospective
study under semifield conditions, in which two groups of harbor
seals (Phoca vitulina) were fed herring from marine regions with
different contamination levels; the highly polluted Baltic Sea and
the relatively unpolluted Atlantic Ocean. During a period of 93
weeks, parameters related to immune function were monitored
and compared between the two groups. We found that natural
killer-cell activity and mitogen-induced proliferative T -cell responses
from the seals feeding on herring from the Baltic Sea
were significantly lower. In addition, we observed higher levels of
circulating polymorphonuclear granulocytes in these animals,
which may indicate an increase in the occurrence of bacterial infections.
This is the first demonstration of impaired immunological
functions in mammals associated with chronic exposure to environmental
contaminants accumulated through the marine food
chain.

/pdf/impairment-of-immune-function-in-harbor-seals-phoca-vitulina-5gpnzsk4h8.pdf

A. Marco

Papers

Morbillivirus in dolphins.