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- Rodgers, C.J., Mohan, C.V., and Peeler, E.J. The spread of pathogens through trade in aquatic animals and their products. Revue scientifique et technique de l'Office international des Epizooties 30(1): 241-256, 2011.
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It is well known that the transboundary spread of infectious diseases is aided by trade in live animals and the consequences can be severe if, as a result, a pathogen broadens its host range to new species. Trade in aquatic animal species is increasing, and aquaculture is also expanding to meet the growing human population's demands for animal protein. Moreover, it is clear that aquaculture has created potential new pathways by which pathogens and diseases may be introduced or spread to new areas. The risk of pathogen transfer is generally considered greater for the movement of live aquatic animals than for the movement of processed and dead products. The currently available health standards support the concept of minimising the risk of disease and pathogen incursion while, at the same time, avoiding unjustifiable or unnecessary impediments to trade. Nevertheless, the international spread of diseases through the movement of animals still occurs, despite these standards.
- Verbrugghe, E., Boyen, F., Gaastra, W., Bekhuis, L., Leyman, B., Van Parys, A., Haesebrouck, F., and Pasmans, F. The complex interplay between stress and bacterial infections in animals. Veterinary Microbiology 155(2-4): 115-127, 2012.
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Over the past decade, an increasing awareness has arisen of the role of neuroendocrine hormones in the susceptibility of mammalian hosts to a bacterial infection. During a stress response, glucocorticoids, catecholamines and neuroendocrine factors are released into the circulation of the host. For a long time the effects of stress on the course of an infection have been exclusively ascribed to the direct effect of stress-related hormones on the immune system and the intestinal barrier function. Chronic stress is known to cause a shift from T helper 1-mediated cellular immunity toward T helper 2-mediated humoral immunity, which can influence the course of an infection and/or the susceptibility to a microorganism. Bacteria can however also respond directly to stress-related host signals. Catecholamines can alter growth, motility, biofilm formation and/or virulence of pathogens and commensal bacteria, and as a consequence influence the outcome of infections by these bacteria in many hosts. For some bacteria, such as Salmonella, Escherichia coli and Pseudomonas aeruginosa it was shown that this influence is regulated by quorum sensing mechanisms. In this manuscript an overview of how and when stress influences the outcome of bacterial infections in animals is provided.
- Brito, D., Moreira, D.O., Coutinho, B.R., and Oprea, M. Ill nature: Disease hotspots as threats to biodiversity. Journal for Nature Conservation 20(2): 72-75, 2012.
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Diseases are part of the natural world, but human activities may affect and disrupt the natural dynamics of diseases, threatening wildlife species and human welfare. We listed the number of species threatened by diseases and compiled their distributional ranges. Based on such data we identify global disease hotspots, regions where disrupted disease dynamics threaten to decimate several species into extinction. The number of species threatened by disease may increase, and climate change may act synergistically increasing the severity of disease incidence in the hotspots, and drive the emergence of new disease hotspots. Until now diseases were thought to play a secondary role in the biodiversity extinction crisis, but the global threat scenario is so dynamic that if we do not bring diseases to the forefront of conservation actions and policies, they may not only bring species into extinction but they may also affect human populations as well.
- Porter, J.W., Torres, C., Sutherland, K.P., Meyers, M.K., Callahan, M.K., Ruzicka, R., and Colella, M. Prevalence, severity, lethality, and recovery of dark spots syndrome among three Floridian reef-building corals. Journal of Experimental Marine Biology and Ecology 408(1-2): 79-87, 2011.
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Disease affects the growth and survival of reef building corals. Prevalence, severity, lethality, and recovery of dark spots syndrome (DSS) was measured on three common scleractinian corals, Montastraea annularis complex, Siderastrea siderea, and Stephanocoenia michelinii on seven reefs in the Florida Keys. Between 2002 and 2004, DSS was the most common disease, responsible for 71.2% ± 5.7 S.E. of all disease infections in the total coral population. Prevalence ranged from 26.3% ± 17.6 S.E. for M. annularis, 7.5% ± 2.9 for S. siderea to 3.0% ± 0.1 for S. michelinii. DSS severity (expressed as the percent of diseased colony surface area) ranged from 0.55% ± 0.12 S.E. for M. annularis, 4.8% ± 0.63 for S. siderea to 0.83% ± 0.31 for S. michelinii. DSS rarely caused whole colony mortality (0.0% yr-1 for Montastraea annularis, 0.3% yr-1 for Siderastrea siderea, and 3.8% yr-1 for Stephanocoenia michelinii), but was a significant source of partial mortality. During the 2002-2003 survey period, net tissue loss per annum due to DSS was 0.3% yr-1 for M. annularis, 1.0% yr-1 for S. siderea, and 8.8% yr-1 for S. michelinii. Total net tissue loss for these three species, from all sources of mortality, was 0.45%, 1.0%, and 8.8% respectively, demonstrating that DSS was the only source of mortality for S. michelinii and S. siderea during this period, and accounted for two-thirds of all tissue loss from M. annularis colonies. DSS recovery rates were variable, depending on the target species. DSS signs in 86.8% of M. annularis colonies and 73.3% of S. michelinii colonies identified in 2002 and 2003 persisted through the end of the survey (2004). By contrast, among S. siderea only 33.3% of colonies affected in 2002 and 2003 continued to exhibit disease signs by 2004. Annual recovery rates from DSS were also species-dependent: 32.9% of DSS-affected S. siderea colonies recovered annually, but, by contrast, only 6.6% and 10.0% of DSS-affected M. annularis and S. michelinii colonies had done so. DSS appears to be a significant source of both whole and partial mortality for S. michelinii, but not for the other two species during this survey.
- Thurber, R.L.V. and Correa, A.M.S. Viruses of reef-building scleractinian corals. Journal of Experimental Marine Biology and Ecology 408(1-2): 102-113, 2011.
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Viruses are ubiquitous and abundant pathogens that likely infect and disrupt all cellular organisms. Although a high diversity of viral types has been characterized from corals over the last decade, we are only beginning to understand the distribution, dynamics, and roles of viral consortia in reef ecosystems. This review synthesizes previous work on the viruses associated with corals and their cnidarian relatives, and highlights some strengths and limitations of the methods commonly used for viral analysis. Based on these foundational studies, we present a current working model for stony coral virology. We hypothesize that viruses are present on and within corals and that these consortia commonly include representatives of the Herpesviridae, Phycodnaviridae, and phages and archaeal viruses. Our working model posits that these different viral groups target distinct hosts, specifically the coral itself, its endosymbiotic algae (Symbiodinium spp.), and its resident microbiome, respectively. Corals may also harbor additional viral diversity (e.g., members of the Iridoviridae) that is pathogenic to reef-associated organisms. Viral infections likely underlie some coral diseases and may be responsible for reef epizootics, but evidence for viral-mediated coral disease is currently inconclusive. Future efforts in coral viral ecology should focus on determining if and how viral infection contributes to reduced coral fitness and/or benthic community shifts in reef ecosystems.
- Yasuda, N., Nakano, Y., Yamashiro, H., and Hidaka, M. Skeletal structure and progression of growth anomalies in Porites australiensis in Okinawa, Japan. Diseases of Aquatic Organisms 97(3): 237-247, 2011.
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Growth anomalies (GAs), one of the diseases recently reported for scleractinian corals, are characterized by an abnormal skeletal structure and reduced zooxanthella density. The pathological characteristics of GAs were studied in colonies of Porites australiensis on a reef in Kayo, Okinawa, Japan. Corallites in the GA region lost the skeletal architecture characteristic of P. australiensis, and polyp density had decreased in the GAs due to enlargement of both calices and the coenosteum. The gross productivity of isolated GA samples was lower than in healthy samples and decreased to almost 0 within 11 d after isolation. However, when GA samples were brought into contact with healthy-looking samples from the same colony, they fused and both the GA and healthy regions grew. Healthy samples fused with GA samples grew more slowly than those fused with healthy samples. For in situ GAs surrounded by healthy tissue, tissue death usually started at the center of the GA, probably due to a deficiency in the translocated energy supply from the surrounding tissue. The total area of the GA region and the dead area increased at a rate of 5.3 ± 2.9 cm2 yr-1. These results suggest that GA regions are maintained by energy supplies from surrounding healthy tissues and that GAs may have a negative impact on host corals.
- Roff, G., Kvennefors, E.C.E., Fine, M., Ortiz, J., Davy, J.E., and Hoegh-Guldberg, O. The ecology of 'Acroporid white syndrome', a coral disease from the southern Great Barrier Reef. PLoS ONE 6(12): art. e26829, 2011.
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Outbreaks of coral disease have increased worldwide over the last few decades. Despite this, remarkably little is known about the ecology of disease in the Indo-Pacific Region. Here we report the spatiotemporal dynamics of a coral disease termed 'Acroporid white syndrome' observed to affect tabular corals of the genus Acropora on the southern Great Barrier Reef. The syndrome is characterised by rapid tissue loss initiating in the basal margins of colonies, and manifests as a distinct lesion boundary between apparently healthy tissue and exposed white skeleton. Surveys of eight sites around Heron Reef in 2004 revealed a mean prevalence of 8.1 ± 0.9%, affecting the three common species (Acropora cytherea, A. hyacinthus, A. clathrata) and nine other tabular Acropora spp. While all sizes of colonies were affected, white syndrome disproportionately affected larger colonies of tabular Acroporids (>80 cm). The prevalence of white syndrome was strongly related to the abundance of tabular Acroporids within transects, yet the incidence of the syndrome appears unaffected by proximity to other colonies, suggesting that while white syndrome is density dependant, it does not exhibit a strongly aggregated spatial pattern consistent with previous coral disease outbreaks. Acroporid white syndrome was not transmitted by either direct contact in the field or by mucus in aquaria experiments. Monitoring of affected colonies revealed highly variable rates of tissue loss ranging from 0 to 1146 cm-2 week-1, amongst the highest documented for a coral disease. Contrary to previous links between temperature and coral disease, rates of tissue loss in affected colonies increased threefold during the winter months. Given the lack of spatial pattern and non-infectious nature of Acroporid white syndrome, further studies are needed to determine causal factors and longer-term implications of disease outbreaks on the Great Barrier Reef.
- Burns, J.H.R. and Takabayashi, M. Histopathology of growth anomaly affecting the coral, Montipora capitata: implications on biological functions and population viability. PLoS ONE 6(12): art. e28854, 2011.
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Growth anomalies (GAs) affect the coral, Montipora capitata, at Wai'ōpae, southeast Hawai'i Island. Our histopathological analysis of this disease revealed that the GA tissue undergoes changes which compromise anatomical machinery for biological functions such as defense, feeding, digestion, and reproduction. GA tissue exhibited significant reductions in density of ova (66.1–93.7%), symbiotic dinoflagellates (38.8–67.5%), mesenterial filaments (11.2–29.0%), and nematocytes (28.8–46.0%). Hyperplasia of the basal body wall but no abnormal levels of necrosis and algal or fungal invasion was found in GA tissue. Skeletal density along the basal body wall was significantly reduced in GAs compared to healthy or unaffected sections. The reductions in density of the above histological features in GA tissue were collated with disease severity data to quantify the impact of this disease at the colony and population level. Resulting calculations showed this disease reduces the fecundity of M. capitata colonies at Wai'ōpae by 0.7–49.6%, depending on GA severity, and the overall population fecundity by 2.41 ± 0.29%. In sum, GA in this M. capitata population reduces the coral's critical biological functions and increases susceptibility to erosion, clearly defining itself as a disease and an ecological threat.
- Weil, E., Irikawa, A., Casareto, B., and Suzuki, Y. Extended geographic distribution of several Indo-Pacific coral reef diseases. Diseases of Aquatic Organisms 98(2): 163-170, 2012.
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Other than coral bleaching, few coral diseases or diseases of other reef organisms have been reported from Japan. This is the first report of lesions similar to Porites ulcerative white spots (PUWS), brown band disease (BrB), pigmentation response (PR), and crustose coralline white syndrome (CCWS) for this region. To assess the health status and disease prevalence, qualitative and quantitative surveys (3 belt transects of 100 m2 each on each reef) were performed in March and September 2010 on 2 reefs of the Ginowan-Ooyama reef complex off Okinawa, and 2 protected reefs off Zamani Island, in the Kerama Islands 40 km west of Okinawa. Overall, mean (±SD) disease prevalence was higher in Ginowan-Ooyama (9.7 ± 7.9%) compared to Zamami (3.6 ± 4.6%). Porites lutea was most affected by PUWS at Ooyama (23.1 ± 10.4 vs. 4.5 ± 5.2%). White syndrome (WS) mostly affected Acropora cytherea (12. 5 ± 18.0%) in Zamami and Oxipora lacera (10.2 ± 10%) in Ooyama. Growth anomalies (GA) and BrB were only observed on A. cytherea (8.3 ± 6.2%) and A. nobilis (0.8%) at Zamami. Black band disease affected Pachyseris speciosa (6.0 ± 4.6%) in Ooyama only. Pigmentation responses (PR) were common in massive Porites in both localities (2.6 ± 1.9 and 5.6 ± 2.3% respectively). Crustose coralline white syndrome (CCWS) was observed in both localities. These results significantly expand the geographic distribution of PUWS, BrB, PR and CCWS in the Indo-Pacific, indicating that the northernmost coral reefs in the western Pacific are susceptible to a larger number of coral diseases than previously thought.
- Böckerman, I., Wiik-Nielsen, C. R., Sindre, H., Johansen, R., and Tengs, T. Prevalence of piscine myocarditis virus (PMCV) in marine fish species. Journal of Fish Diseases 34(12): 955-957, 2011.
- Oidtmann, B. Review of biological factors relevant to import risk assessments for epizootic ulcerative syndrome (Aphanomyces invadans). Transboundary and Emerging Diseases 59(1): 26-39, 2012.
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Epizootic ulcerative syndrome (EUS) is a disease affecting both wild and farmed fish in freshwater and estuarine environments. After it was first described in Japan in 1971, the disease has spread widely across Asia and to some regions of Australia, North America and Africa. In Asia and Africa, the spread of the disease has substantially affected livelihoods of fish farmers and fishermen. No reports are yet published showing the presence of the disease in Europe or South America. Given its epizootic nature and its broad susceptible fish species range, it would appear that the disease has the potential for further spread. This study provides a review of the scientific literature on several biological factors of the pathogen, Aphanomyces invadans, associated with the disease EUS and aspects of the disease that are relevant to undertaking import risk assessments (IRA) covering (i) Life cycle and routes of transmission; (ii) Minimum infectious dose; (iii) Tissue localization and pathogen load; (iv) Predisposing factors for infection and factors influencing expression of disease; (v) Carrier state in fish; (vi) Diagnostic methods; (vii) Survival in the environment; (viii) Permissive temperature range; (ix) Stability of the agent in aquatic animal products; (x) Prevalence of infection; and (xi) Affected life stages. Much of the biological information presented is relevant to a broad range of risk questions. Areas where data are lacking were identified, and the information provided is put into context with other aspects that need to be addressed in an IRA.
- de Eyto, E. et al. Varying disease-mediated selection at different life-history stages of Atlantic salmon in fresh water. Evolutionary Applications 4(6): 749-762, 2011.
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Laboratory studies on associations between disease resistance and susceptibility and major histocompatibility (MH) genes in Atlantic salmon Salmo salar have shown the importance of immunogenetics in understanding the capacity of populations to fight specific diseases. However, the occurrence and virulence of pathogens may vary spatially and temporally in the wild, making it more complicated to predict the overall effect that MH genes exert on fitness of natural populations and over several life-history stages. Here we show that MH variability is a significant determinant of salmon survival in fresh water, by comparing observed and expected genotype frequencies at MH and control microsatellite loci at parr and migrant stages in the wild. We found that additive allelic effects at immunogenetic loci were more likely to determine survival than dominance deviation, and that selection on certain MH alleles varied with life stage, possibly owing to varying pathogen prevalence and/or virulence over time. Our results highlight the importance of preserving genetic diversity (particularly at MH loci) in wild populations, so that they have the best chance of adapting to new and increased disease challenges as a result of projected climate warming and increasing aquaculture.
- Waltzek, T.B. et al. Systemic iridovirus from threespine stickleback Gasterosteus aculeatus represents a new megalocytivirus species (family Iridoviridae). Diseases of Aquatic Organisms 98(1): 41-56, 2012.
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Megalocytiviruses have been associated with epizootics resulting in significant economic losses in public aquaria and food-fish and ornamental fish industries, as well as threatening wild fish stocks. The present report describes characteristics of the first megalocytivirus from a wild temperate North American fish, the threespine stickleback Gasterosteus aculeatus. Moribund and dead fish sampled after transfer to quarantine for an aquarium exhibit had amphophilic to basophilic intracytoplasmic inclusions (histopathology) and icosahedral virions (transmission electron microscopy) consistent with an iridovirus infection. Phylogenetic analyses of the major capsid, ATPase, and DNA polymerase genes confirmed the virus as the first known member of the genus Megalocytivirus (family Iridoviridae) from a gasterosteid fish. The unique biologic and genetic properties of this virus are sufficient to establish a new Megalocytivirus species to be formally known as the threespine stickleback iridovirus (TSIV). The threespine stickleback is widely distributed throughout the northern hemisphere in both freshwater and estuarine environments. The presence of megalocytiviruses with broad host specificity and detrimental economic and ecologic impacts among such a widely dispersed fish species indicates the need for sampling of other stickleback populations as well as other North American sympatric marine and freshwater ichthyofauna.
- Repetto, M. and Griffen, B.D. Physiological consequences of parasite infection in the burrowing mud shrimp, Upogebia pugettensis, a widespread ecosystem engineer. Marine and Freshwater Research 63(1): 60-67, 2012.
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The burrowing mud shrimp, Upogebia pugettensis, is an important ecosystem engineer throughout bays and estuaries along the Pacific coast of North America. Populations of U. pugettensis have recently declined throughout its range. A likely reason for this decline is the arrival of an invasive bopyrid isopod parasite, Orthione griffenis, which has colonised the system and increased in prevalence. We tested the following three hypotheses regarding this host-parasite system: (1) parasite infection is correlated with the volume of water processed by the host; (2) infection negatively affects host's energetic state; and (3) infection causes feminisation in male hosts. We used several physiological and morphological measures to quantify the effects of this parasite infection on U. pugettensis. The parasite appears to have different physiological effects on male and female hosts. Our study provides mixed support for the previous theory that predicted the mechanistic interactions between this host and its new parasite. Recent examples from other systems have demonstrated that invasive parasites can have far-reaching influences when they infect ecosystem engineers. Given the negative effects of O. griffenis on U. pugettensis, this invasive parasite may have similarly large impacts on Pacific North-west estuaries throughout its invaded range.
- Kruse, I., Hare, M., and Hines, A. Genetic relationships of the marine invasive crab parasite Loxothylacus panopaei: an analysis of DNA sequence variation, host specificity, and distributional range. Biological Invasions 14(3): 701-715, 2012.
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Host specificity is a key variable of the niche breath of parasites that can be an important determinant of a parasite's ability to invade new areas. There is increasing evidence that many parasite species may comprise a variety of genetically variable lineages, which differ in host specificity and geographic range. In this study, we (1) explored the extent of diversity in the invasive parasitic barnacle Loxothylacus panopaei (Rhizocephala) infecting mud crabs (2) examined the geographic origin for the invasive lineage and (3) assessed if further southward spread of the parasite may be impeded. Along the US Atlantic coast, L. panopaei infects different hosts in its invaded range (Chesapeake Bay to north of Cape Canaveral) compared to one portion of the native range in Southeast Florida. This difference was reflected in genetic lineages on two independent loci, mitochondrial cytochrome oxidase I and nuclear cytochrome c. Both loci were concordant in that they showed one lineage infecting crabs of the genus Panopeus in the native range and one lineage infecting Eurypanopeus depressus and Rhithropanopeus harrisii hosts in the invaded range and in the Gulf of Mexico , thus indicating Gulf of Mexico populations as the most likely source of introduction into Chesapeake Bay. Interestingly, the nuclear marker resolved an additional lineage of parasites infecting panopeid hosts in the native range. All three parasite lineages were well supported, but a decision about species status must await further analyses. Since its introduction in the 1960s, the invasive L. panopaei lineage has expanded its range southward along the US Atlantic coast, now almost reaching the northern limit of native Panopeus-infecting lineages at Cape Canaveral, Florida. We hypothesized that parasite-free E. depressus in Southeast Florida, living in sympatry with infected panopeid populations, might be resistant to infection by the invasive lineage. Our infection experiments rejected this hypothesis, suggesting that any impediment to further southward range expansion might be expected from temperature regimes of the subtropical zoogeographic region south of Cape Canaveral.
- Carrasco, N., Roque, A., Andree, K.B., Rodgers, C., Lacuesta, B., and Furones, M.D. A Marteilia parasite and digestive epithelial virosis lesions observed during a common edible cockle Cerastoderma edule mortality event in the Spanish Mediterranean coast. Aquaculture 321(3-4): 197-202, 2011.
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The presence of a Marteilia parasite, potentially M. refringens, was observed by histology and by 18S rDNA Marteilia genus specific in situ hybridisation on common edible cockles Cerastoderma edule growing at the Ebro Delta bays during a mortality event in 2008. Marteilia parasites, such as M. refringens, are marine invertebrate pathogens affecting commercial bivalve species such as the flat oyster Ostrea edulis and the mussels Mytilus edulis and M. galloprovincialis. However, occasionally, Marteilia parasites including M. refringens, have also been observed in other commercial bivalve species such as Chamalea gallina, Solen Marginatus and C. edule among others. In the case of the cockle C. edule, a single notification of the presence of Marteilia sp., in 1975, based on histological and ultrastructural studies, has been reported up to date. Parasite prevalence observed in the present study was not negligible (40%) and was potentially associated to the cockle mortality event. Parasite infection intensity was high and moderate, and, in general, developmental stages observed reminded M. refringens infecting flat oysters and mussels. Furthermore, lesions, similar to those produced by digestive epithelial virosis, were observed by first time in cockles. The viral lesions were observed in all the examined specimens in moderate and high intensity. The in situ hybridisation assay for detection of Marteilia sp. using an 18S rDNA probe (SMART2) showed the affinity of the cockle parasite to the Marteilia genus probe. This is the first report of a Marteilia parasite in cockles in Spain and the second report in the world. The potential impact, of both observed pathogens, on the cockle industry and shellfish aquaculture needs to be urgently addressed.
- Morgan, E., O'Riordan, R.M., Kelly, T.C., and Culloty, S.C. Influence of disseminated neoplasia, trematode infections and gametogenesis on surfacing and mortality in the cockle Cerastoderma edule. Diseases of Aquatic Organisms 98(1): 73-84, 2012.
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Cerastoderma edule is a widely distributed bivalve mollusc, commercially exploited throughout Europe and is also an important food source for birds and crustaceans. Recently, mass surfacing and mortalities of cockles have been observed and reported at sites in Ireland and elsewhere, particularly in the summer months. One such site is Flaxfort Strand, Courtmacsherry Bay, County Cork, Ireland, an important feeding area used by many seabirds during the summer months. For the past few years large numbers of surfaced cockles have been observed at the site in a moribund condition. Samples of cockles from this area were collected over the summer months and their health status assessed. Cockles that had surfaced (moribund) and those still buried in the sediment were quantified and screened: sex, gonadal maturity and size class of cockles were also determined. Disseminated neoplasia and trematodes were observed in screened cockles. The most significant finding during the study was that mortalities and surfacing of cockles was related to a greater incidence of disseminated neoplasia. No neoplasia was observed in the smallest and largest size classes. There was a significantly higher prevalence of neoplasia in moribund cockles than in buried cockles, whereas in both groups a similar concentration of trematode metacercariae was observed in the screened tissues. Also, most of the cockles that had surfaced were either in the process of spawning or were spent. Overall a much larger percentage of moribund cockles exhibited both trematode infections plus neoplasia compared with buried cockles. A combination of the presence of neoplasia and trematodes, along with stress related to spawning, may immunocompromise the cockless, causing the animals to surface and become moribund.
- Feehan, C., Scheibling, R.E., and Lauzon-Guay, J.S. An outbreak of sea urchin disease associated with a recent hurricane: Support for the 'killer storm hypothesis' on a local scale. Journal of Experimental Marine Biology and Ecology 413: 159-168, 2012. OA
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The frequency of epizootics causing mass mortality of sea urchins (Strongylocentrotus droebachiensis) along the coast of Nova Scotia, Canada has increased over the past three decades. Laboratory and field studies show that outbreaks of disease are caused by the amoeba Paramoeba invadens, and are associated with hurricane activity and warm seawater temperatures. A statistical model indicates that the probability of a mass mortality event increases with the proximity of a hurricane to the coast and the maximum sustained wind speed, and is greater when post-storm seawater temperature is above a threshold for disease propagation. To assess the reliability of the model in predicting mass mortality events on an annual scale, and to examine spatial variability in mortality (in the event of a disease outbreak) on a local scale (meters to kilometers), we transplanted sea urchins into cages in kelp beds at 6 sites around St. Margarets Bay, Nova Scotia, where localized outbreaks of paramoebiasis have been observed following hurricanes in the past. On 4 September 2010 a Category 1 hurricane (Earl) made landfall 110 km SSW of the experimental area. Based on the parameters of the storm, the model forecasted a 43% probability of a disease outbreak. Morbidity of caged animals was first documented on 6 September 2010, and morbidity and mortality in the cages was ~50% by the end of September and ~85% two months after the storm. Laboratory experiments indicated that the temperature-dependent transmission or induction of morbidity was consistent with paramoebiasis. Our findings provide support for the efficacy of the model to predict the occurrence of disease outbreaks, although the source population(s) of the pathogenic agent and oceanographic mechanisms affecting its introduction and spread along the coast of Nova Scotia remain poorly understood.
- Harms, N.J. Avian cholera in the eastern Canadian Arctic: investigating disease origins and reservoirs. Arctic 64(4): 501-505, 2011.
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- Descamps, S., Jenouvrier, S., Gilchrist, H.G., and Forbes, M.R. Avian cholera, a threat to the viability of an arctic seabird colony? PLoS ONE 7(2): art. e29659, 2012.
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Evidence that infectious diseases cause wildlife population extirpation or extinction remains anecdotal and it is unclear whether the impacts of a pathogen at the individual level can scale up to population level so drastically. Here, we quantify the response of a Common eider colony to emerging epidemics of avian cholera, one of the most important infectious diseases affecting wild waterfowl. We show that avian cholera has the potential to drive colony extinction, even over a very short period. Extinction depends on disease severity (the impact of the disease on adult female survival) and disease frequency (the number of annual epidemics per decade). In case of epidemics of high severity (i.e., causing >30% mortality of breeding females), more than one outbreak per decade will be unsustainable for the colony and will likely lead to extinction within the next century; more than four outbreaks per decade will drive extinction to within 20 years. Such severity and frequency of avian cholera are already observed, and avian cholera might thus represent a significant threat to viability of breeding populations. However, this will depend on the mechanisms underlying avian cholera transmission, maintenance, and spread, which are currently only poorly known.
- Sonne, C., Alstrup, A.K.O., and Therkildsen, O.R. A review of the factors causing paralysis in wild birds: Implications for the paralytic syndrome observed in the Baltic Sea. Science of The Total Environment 416: 32-39, 2012.
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We reviewed paralysis in wild birds with a special focus on the Baltic Sea paralytic syndrome recently described by Balk et al. (2009) by assessing multiple causative factors. The review showed that paralysis may occur in various species and that the aetiology can be divided into biotoxins, nutritional deficiencies, environmental contaminants and infectious diseases. The review also showed that the symptoms are influenced by age, sex and species of the affected individual. It seemed that paralysis may be treated or relieved by e.g. thiamine injections or additives. Due to a lack of extensive diagnostic studies, the potentially negative effects of paralysis at the population level of wild birds remain unsolved. We recommend that when investigating paralysis in wild birds, a holistic study approach including multiple factors are undertaken in order to pinpoint cause-and-effect relationships as well as the potential impacts on wild bird populations including those in the Baltic Sea.
- Sturm, N., Abalos, P., Fernandez, A., Rodriguez, G., Oviedo, P., Arroyo, V., and Retamal, P. Salmonella enterica in pinnipeds, Chile. Emerging Infectious Diseases 17(12): 2377-2378, 2011.
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- Di Guardo, G., Di Cesare, A., Otranto, D., Casalone, C., Iulini, B., Mignone, W., Tittarelli, C., Meloni, S., Castagna, G., Forster, F., Kennedy, S., and Traversa, D. Genotyping of Toxoplasma gondii isolates in meningo-encephalitis affected striped dolphins (Stenella coeruleoalba) from Italy. Veterinary Parasitology 183(1-2): 31-36, 2011.
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This study reports the occurrence of Toxoplasma gondii in the brain of three striped dolphins (Stenella ceoruleoalba) found stranded on the Ligurian Sea coast of Italy between 2007 and 2008. These animals showed a severe, subacute to chronic, non-purulent, multifocal meningo-encephalitis, with the cerebral parenchyma of two dolphins harbouring protozoan cysts and zoites immunohistochemically linked to T. gondii. Molecular, phylogenetic and mutation scanning analyses showed the occurrence of Type II and of an atypical Type II T. gondii isolates in one and two dolphins, respectively. In spite of the different molecular patterns characterizing the above T. gondii genotypes, the brain lesions observed in the three animals showed common microscopic features, with no remarkable differences among them. The role of T. gondii in causing the meningo-encephalitis is herein discussed.
- Dubey, J.P. and Thomas, N.J. Sarcocystis neurona retinochoroiditis in a sea otter (Enhydra lutris kenyoni). Veterinary Parasitology 183(1-2): 156-159, 2011.
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Sarcocystis neurona is an important cause of fatal disease in sea otters in the USA. Encephalitis is the predominant lesion and parasites are confined to the central nervous system and muscles. Here we report retinochoroiditis in a sea otter (Enhydra lutris kenyoni) found dead on Copalis Beach, WA, USA. Salient lesions were confined to the brain and eye. Multifocal nonsuppurative meningoencephalitis was present in the cerebrum and cerebellum associated with S. neurona schizonts. The retina of one eye had a focus of inflammation that contained numerous S. neurona schizonts and merozoites. The focus extended from the retinal pigment epithelium inward through all layers of the retina, but inflammation was most concentrated at the inner surface of the tapetum and the outer retina. The inner and outer nuclear layers of the retina were disorganized and irregular at the site of inflammation. There was severe congestion and mild hemorrhage in the choroid, and mild hemorrhage into the vitreous body. Immuno-histochemistry with S. neurona-specific polyclonal rabbit antibodies stained schizonts and merozoites. To our knowledge this is the first report of S. neurona-associated retinochoroiditis in any naturally infected animal.
- Bellière, E.N., Esperón, F., and Sánchez-Vizcaíno, J.M. Genetic comparison among dolphin morbillivirus in the 1990-1992 and 2006-2008 Mediterranean outbreaks. Infection, Genetics and Evolution 11(8): 1913-1920, 2011.
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In 1990, dolphin morbillivirus (DMV) killed thousands of striped dolphins in the Mediterranean. Subsequently, the prevalence of the infection declined in this species. In 2006-2008, the virus killed not only numerous striped dolphins but also long-finned pilot whales. All partial sequences of the phosphoprotein and nucleoprotein genes obtained thus far from different host species during the 2006-2008 outbreak show 100% identity, suggesting that a single virus was involved, and these sequences are nearly identical to the 1990 Spanish strain. Here our first objective was to determine the sequence identity between the morbillivirus from the 2006-2008 outbreak and the 1990 Spanish strain by sequencing more extensive genomic regions of strains from one pilot whale and one striped dolphin stranded in 2007. The second objective was to investigate the relationship between the 1990 and 2007 strains by constructing a phylogenetic tree based on the phosphoprotein gene to compare several Cetacean morbilliviruses, and another tree based on the nearly complete genomes of Mediterranean DMV. The third objective was to identify the most variable regions in the DMV genomes. Results showed that the two 2007 Spanish strains were 99.9% identical over 9050 bp and should be considered the same virus, and that this virus is 99.3-99.4% similar to the 1990 Spanish strain. The phylogenetic trees, together with the common geographical area for the two outbreaks, suggest that the 2007 DMV strains evolved from the 1990 DMV strain. Pilot whales do not seem to have been exposed or infected during the 1990-1992 epidemic, since these populations appeared to be immunologically naive in 2006-2008. Our results suggest that the virus may have evolved in striped dolphin populations prior to the 2006-2008 outbreak, after which it entered the long-finned pilot whale, perhaps aided by an alanine to valine mutation in the N-terminal domain of the fusion protein.
- Soto, S. et al. Post-epizootic chronic dolphin morbillivirus infection in Mediterranean striped dolphins Stenella coeruleoalba. Diseases of Aquatic Organisms 96(3): 187-194, 2011.
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Dolphin morbillivirus (DMV) has caused 2 epizootics with high mortality rates on the Spanish Mediterranean coast, in 1990 and 2006–07, mainly affecting striped dolphins Stenella coeruleoalba. Following the first epizootic unusual DMV infections affecting only the central nervous system of striped dolphins were found, with histological features similar to subacute sclerosing panencephalitis and old dog encephalitis, the chronic latent localised infections caused by defective forms of measles virus and canine distemper virus, respectively. Between 2008 and 2010, monitoring by microscopic and immunohistochemical (IHC) studies of 118 striped dolphins stranded along Catalonia, the Valencia Region and Andalusia showed similar localised DMV nervous system infections in 25.0, 28.6 and 27.4% of cases, respectively, with no significant differences among regions or sex. The body length of DMV-infected dolphins was statistically greater than that of non-infected dolphins (196.5 vs. 160.5 cm; p < 0.001). Molecular detection of DMV was performed by 2 different RT-PCR techniques amplifying a 429 bp fragment and a 78 bp fragment both within the phosphoprotein (P) gene. The 429 bp RT-PCR results contradicted the IHC-DMV results as only 3 of 6 dolphins with positive IHC-DMV had positive PCR results. All 6 cases were positive with the 78 bp RT-PCR. These findings contraindicate the use of the 429 bp RT-PCR protocol based on the P gene to detect this specific form of DMV. DMV localised nervous infection constitutes the most relevant single cause of stranding and death in Mediterranean striped dolphins in the years following a DMV epizootic, and it might even overwhelm the effects of the epizootic itself, at least in 2007.
- Bossart, G. D. et al. Clinicoimmunopathologic findings in Atlantic bottlenose dolphins Tursiops truncatus with positive cetacean morbillivirus antibody titers. Diseases of Aquatic Organisms 97(2): 103-112, 2011.
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Sera from free-ranging Atlantic bottlenose dolphins Tursiops truncatus inhabiting the Indian River Lagoon (IRL), Florida were tested for antibodies to cetacean morbilliviruses from 2003 to 2007 as part of a multidisciplinary study of individual and population health. A suite of clinicoimmunopathologic variables were evaluated in morbillivirus-seropositive dolphins (n = 14) and seronegative healthy dolphins (n = 49). Several important differences were found. Serum alkaline phosphatase, creatine phosphokinase, chloride, albumin and albumin/globulin ratios were significantly lower in seropositive dolphins. Innate immunity appeared to be upregulated with significant increases in lysozyme concentration and marginally significant increases in monocytic phagocytosis. Adaptive immunity was also impacted in dolphins with positive morbillivirus antibody titers. Mitogen-induced T lymphocyte proliferation responses were significantly reduced in dolphins with positive morbillivirus antibody titers, and marginally significant decreases were found for absolute numbers of CD4+ lymphocytes. The findings suggest impairment of cell-mediated adaptive immunity, similar to the immunologic pattern reported with acute morbillivirus infection in other species. In contrast, dolphins with positive morbillivirus antibody titers appeared to have at least a partially upregulated humoral immune response with significantly higher levels of gamma globulins than healthy dolphins, which may represent an antibody response to morbillivirus infection or other pathogens. These data suggest that subclinical dolphin morbillivirus infection in IRL dolphins may produce clinicoimmunopathologic perturbations that impact overall health.
- Fury, C.A. and Reif, J.S. Incidence of poxvirus-like lesions in two estuarine dolphin populations in Australia: Links to flood events. Science of The Total Environment 416: 536-540, 2012.
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We report on the incidence of poxvirus-like lesions assessed by photographic identification in two estuarine populations of bottlenose dolphins (Tursiops aduncus) in Australia over a 3-year period. Poxvirus infections of odontocetes are characterized by pinhole or ring-like skin lesions that appear as solitary or coalesced circular gray blemishes. Environmental and physiological stressors are believed to contribute to their manifestation. A total of 187 boat-based surveys were completed from October 2003 to September 2006 in the Clarence River (CR) and Richmond River (RR) estuaries, with 720 dolphins sighted. Forty-six individuals, including calves, were identified in the CR and 23 in the RR. We investigated the temporal relationship between four flood events that occurred in the region during the study period and the occurrence of poxvirus-like skin lesions. Dolphin poxvirus-like lesions were not observed in these populations prior to 2004. Following flood events in 2004, 2005 and 2006, a total of 10 new cases were observed, 6 in the CR and 4 in the RR. Our data suggest that the occurrence of dolphin poxvirus-like lesions may be an indicator for climatic events such as flooding. Long-term follow-up of these estuarine populations is required to further clarify the factors leading to 'outbreaks' of poxvirus infections.
- Stone, B.M., Blyde, D.J., Saliki, J.T., and Morton, J.M. Morbillivirus infection in live stranded, injured, trapped, and captive cetaceans in southeastern Queensland and northern New South Wales, Australia. Journal of Wildlife Diseases 48(1): 47-55, 2012.
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We report serologic evidence of cetacean morbillivirus (CMV) infection in five of eight cetacean species found live stranded, injured, or trapped along the coast of southeastern Queensland and northern New South Wales, Australia between December 2005 and January 2011. Antibody to CMV was detected in 13 of 27 (48%) wild cetaceans sampled. Antibody prevalence was significantly higher in clinically diseased (69%) compared to nondiseased (18%) animals (P = 0.018). There was high antibody prevalence (83%, n = 6) in melon-headed whales (Peponocephala electra). Two of 13 (15%) captive cetaceans sampled between November 2005 and January 2011 had CMV antibodies and, as infection was unlikely to have occurred while in captivity, CMV infection appears to have been present in Australian wild cetaceans since at least 1985. These results indicate that morbillivirus infection is occurring without widespread cetacean mortality in this region. However, as the deaths of two immature Australian offshore bottlenose dolphins (Tursiops truncatus) were attributed to CMV infection, morbillivirus infection should be included in the differential diagnosis of disease in cetaceans in Australia. Captive cetacean populations may be prone to significant mortality as a result of CMV introduction, so strict quarantine procedures should be enforced when injured or stranded cetaceans are hospitalized and rehabilitated at Australian zoos and marine parks.
- Tseng, M., Fleetwood, M., Reed, A., Gill, V.A., Harris, R.K., Moeller, R.B., Lipscomb, T.P., Mazet, J.A.K., and Goldstein, T. Mustelid herpesvirus-2, a novel herpes infection in northern sea otters (Enhydra lutris kenyoni). Journal of Wildlife Diseases 48(1): 181-185, 2012.
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Oral ulcerations and plaques with epithelial eosinophilic intranuclear inclusions were observed in northern sea otters (Enhydra lutris kenyoni) that died or were admitted for rehabilitation after the 1989 Exxon Valdez oil spill (EVOS) in Alaska, USA. Transmission electron microscopy demonstrated the presence of herpesviral virions. Additionally, a serologic study from 2004 to 2005 found a high prevalence of exposure to a herpesvirus in live-captured otters. Tissues from 29 otters after the EVOS and nasal swabs from 83 live-captured otters in the Kodiak Archipelago were tested for herpesviral DNA. Analysis identified a novel herpesvirus in the gamma subfamily, most closely related to Mustelid herpesvirus-1 from badgers. Results indicated that this herpesvirus is associated with ulcerative lesions but is also commonly found in secretions of healthy northern sea otters.
- Kersh, G.J., Lambourn, D.M., Raverty, S.A., Fitzpatrick, K.A., Self, J.S., Akmajian, A.M., Jeffries, S.J., Huggins, J., Drew, C.P., Zaki, S.R., and Massung, R.F. Coxiella burnetii infection of marine mammals in the Pacific Northwest, 1997–2010. Journal of Wildlife Diseases 48(1): 201-206, 2012.
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Q fever is a zoonotic disease caused by the bacterium Coxiella burnetii. Humans are commonly exposed via inhalation of aerosolized bacteria derived from the waste products of domesticated sheep and goats, and particularly from products generated during parturition. However, many other species can be infected with C. burnetii, and the host range and full zoonotic potential of C. burnetii is unknown. Two cases of C. burnetii infection in marine mammal placenta have been reported, but it is not known if this infection is common in marine mammals. To address this issue, placenta samples were collected from Pacific harbor seals (Phoca vitulina richardsi), harbor porpoises (Phocoena phocoena), and Steller sea lions (Eumetopias jubatus). Coxiella burnetii was detected by polymerase chain reaction (PCR) in the placentas of Pacific harbor seals (17/27), harbor porpoises (2/6), and Steller sea lions (1/2) collected in the Pacific Northwest. A serosurvey of 215 Pacific harbor seals sampled in inland and outer coastal areas of the Pacific Northwest showed that 34.0% (73/215) had antibodies against either Phase 1 or Phase 2 C. burnetii. These results suggest that C. burnetii infection is common among marine mammals in this region.
- Simon, A. et al. Spatio-temporal variations and age effect on Toxoplasma gondii seroprevalence in seals from the Canadian Arctic. Parasitology 138(11): 1362-1368, 2011.
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Toxoplasmosis is a significant public health threat for Inuit in the Canadian Arctic. This study aimed to investigate arctic seals as a possible food-borne source of infection. Blood samples collected from 828 seals in 7 Canadian Arctic communities from 1999 to 2006 were tested for antibodies using a direct agglutination test. Polymerase chain reaction (PCR) was used to detect T. gondii DNA in tissues of a subsample of seals. Associations between seal age, sex, species, diet, community and year of capture, and serological test results were investigated by logistic regression. Overall seroprevalence was 10·4% (86/828). All tissues tested were negative by PCR. In ringed seals, seroprevalence was significantly higher in juveniles than in adults (odds ratio = 2.44). Overall, seroprevalence varied amongst communities (P = 0·0119) and by capture year (P = 0·0001). Our study supports the hypothesis that consumption of raw seal meat is a significant source of infection for Inuit. This work raises many questions about the mechanism of transfer of this terrestrial parasite to the marine environment, the preponderance of infection in younger animals and the natural course of infection in seals. Further studies to address these questions are essential to fully understand the health risks for Inuit communities.
- Rohr, J.R., Dobson, A.P., Johnson, P.T.J., Kilpatrick, A.M., Paull, S.H., Raffel, T.R., Ruiz-Moreno, D., and Thomas, M.B. Frontiers in climate change-disease research. Trends in Ecology and Evolution 26(6): 270-277, 2011.
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The notion that climate change will generally increase human and wildlife diseases has garnered considerable public attention, but remains controversial and seems inconsistent with the expectation that climate change will also cause parasite extinctions. In this review, we highlight the frontiers in climate change-infectious disease research by reviewing knowledge gaps that make this controversy difficult to resolve. We suggest that forecasts of climate-change impacts on disease can be improved by more interdisciplinary collaborations, better linking of data and models, addressing confounding variables and context dependencies, and applying metabolic theory to host-parasite systems with consideration of community-level interactions and functional traits. Finally, although we emphasize host-parasite interactions, we also highlight the applicability of these points to climate-change effects on species interactions in general.
- Hueffer, K., O'Hara, T.M., and Follmann, E.H. Adaptation of mammalian host-pathogen interactions in a changing arctic environment. Acta Veterinaria Scandinavica 53: art. 17, 2011.
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Many arctic mammals are adapted to live year-round in extreme environments with low winter temperatures and great seasonal variations in key variables (e.g. sunlight, food, temperature, moisture). The interaction between hosts and pathogens in high northern latitudes is not very well understood with respect to intra-annual cycles (seasons). The annual cycles of interacting pathogen and host biology is regulated in part by highly synchronized temperature and photoperiod changes during seasonal transitions (e.g., freezeup and breakup). With a warming climate, only one of these key biological cues will undergo drastic changes, while the other will remain fixed. This uncoupling can theoretically have drastic consequences on host-pathogen interactions. These poorly understood cues together with a changing climate by itself will challenge host populations that are adapted to pathogens under the historic and current climate regime. We will review adaptations of both host and pathogens to the extreme conditions at high latitudes and explore some potential consequences of rapid changes in the Arctic.
- Larsen, M.H., Jensen, K.T., and Mouritsen, K.N. Climate influences parasite-mediated competitive release. Parasitology 138(11): 1436-1441, 2011.
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Parasitism is believed to play an important role in maintaining species diversity, for instance by facilitating coexistence between competing host species. However, the possibility that environmental factors may govern the outcome of parasite-mediated competition has rarely been considered. The closely related amphipods Corophium volutator and Corophium arenarium both serve as second intermediate host for detrimental trematodes. Corophium volutator is the superior competitor of the two, but also suffers from higher mortality when exposed to infective trematode stages. Here, we report parasite-mediated competitive release of C. arenarium in an intertidal habitat, in part triggered by unusually high temperatures linked to the North Atlantic climate oscillation (NAO). The elevated temperatures accelerated the transmission of cercariae from sympatric first intermediate hosts (mud snails) to amphipods, causing a local collapse of the parasite-sensitive C. volutator population and concordant increase in the abundance of the competitively inferior C. arenarium.
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