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Asterix and the chariot race
Famous for their extensive travels around the Known World, this time Asterix and Obelix are going to meet the people of the Italian peninsula: the Italics! To Obelix's delight, the inhabitants of Ancient Italy are not all Romans! Far from it! The Italics want to keep their independence and take a dim view of Julius Caesar and his Legions' plans for total domination. In Asterix and the Chariot Race, Asterix and Obelix embark upon a great adventure in the extraordinary world of Ancient Italy!
Book
First Record of Black Band Disease in the Hawaiian Archipelago: Response, Outbreak Status, Virulence, and a Method of Treatment
A high number of coral colonies, Montipora spp., with progressive tissue loss were reported from the north shore of Kaua'i by a member of the Eyes of the Reef volunteer reporting network. The disease has a distinct lesion (semi-circular pattern of tissue loss with an adjacent dark band) that was first observed in Hanalei Bay, Kaua'i in 2004. The disease, initially termed Montipora banded tissue loss, appeared grossly similar to black band disease (BBD), which affects corals worldwide. Following the initial report, a rapid response was initiated as outlined in Hawai'i's rapid response contingency plan to determine outbreak status and investigate the disease. Our study identified the three dominant bacterial constituents indicative of BBD (filamentous cyanobacteria, sulfate-reducing bacteria, sulfide-oxidizing bacteria) in coral disease lesions from Kaua'i, which provided the first evidence of BBD in the Hawaiian archipelago. A rapid survey at the alleged outbreak site found disease to affect 6-7% of the montiporids, which is higher than a prior prevalence of less than 1% measured on Kaua'i in 2004, indicative of an epizootic. Tagged colonies with BBD had an average rate of tissue loss of 5.7 cm2/day over a two-month period. Treatment of diseased colonies with a double band of marine epoxy, mixed with chlorine powder, effectively reduced colony mortality. Within two months, treated colonies lost an average of 30% less tissue compared to untreated controls.
Journal Article
To Understand Coral Disease, Look at Coral Cells
Diseases threaten corals globally, but 40 years on their causes remain mostly unknown. We hypothesize that inconsistent application of a complete diagnostic approach to coral disease has contributed to this slow progress. We quantified methods used to investigate coral disease in 492 papers published between 1965 and 2013. Field surveys were used in 65% of the papers, followed by biodetection (43%), laboratory trials (20%), microscopic pathology (21%), and field trials (9%). Of the microscopic pathology efforts, 57% involved standard histopathology at the light microscopic level (12% of the total investigations), with the remainder dedicated to electron or fluorescence microscopy. Most (74%) biodetection efforts focused on culture or molecular characterization of bacteria or fungi from corals. Molecular and immunological tools have been used to incriminate infectious agents (mainly bacteria) as the cause of coral diseases without relating the agent to specific changes in cell and tissue pathology. Of 19 papers that declared an infectious agent as a cause of disease in corals, only one (5%) used microscopic pathology, and none fulfilled all of the criteria required to satisfy Koch’s postulates as applied to animal diseases currently. Vertebrate diseases of skin and mucosal surfaces present challenges similar to corals when trying to identify a pathogen from a vast array of environmental microbes, and diagnostic approaches regularly used in these cases might provide a model for investigating coral diseases. We hope this review will encourage specialists of disease in domestic animals, wildlife, fish, shellfish, and humans to contribute to the emerging field of coral disease.
Journal Article
Localized outbreaks of coral disease on Arabian reefs are linked to extreme temperatures and environmental stressors
The Arabian Peninsula borders the hottest reefs in the world, and corals living in these extreme environments can provide insight into the effects of warming on coral health and disease. Here, we examined coral reef health at 17 sites across three regions along the northeastern Arabian Peninsula (Persian Gulf, Strait of Hormuz and Oman Sea) representing a gradient of environmental conditions. The Persian Gulf has extreme seasonal fluctuations in temperature and chronic hypersalinity, whereas the other two regions experience more moderate conditions. Field surveys identified 13 coral diseases including tissue loss diseases of unknown etiology (white syndromes) in Porites, Platygyra, Dipsastraea, Cyphastrea, Acropora and Goniopora; growth anomalies in Porites, Platygyra and Dipsastraea; black band disease in Platygyra, Dipsastraea, Acropora, Echinopora and Pavona; bleached patches in Porites and Goniopora and a disease unique to this region, yellow-banded tissue loss in Porites. The most widespread diseases were Platygyra growth anomalies (52.9% of all surveys), Acropora white syndrome (47.1%) and Porites bleached patches (35.3%). We found a number of diseases not yet reported in this region and found differential disease susceptibility among coral taxa. Disease prevalence was higher on reefs within the Persian Gulf (avg. 2.05%) as compared to reefs within the Strait of Hormuz (0.46%) or Oman Sea (0.25%). A high number of localized disease outbreaks (8 of 17 sites) were found, especially within the Persian Gulf (5 of 8 sites). Across all regions, the majority of variation in disease prevalence (82.2%) was associated with the extreme temperature range experienced by these corals combined with measures of organic pollution and proximity to shore. Thermal stress is known to drive a number of coral diseases, and thus, this region provides a platform to study disease at the edge of corals’ thermal range.
Journal Article
Patterns of Coral Disease across the Hawaiian Archipelago: Relating Disease to Environment
In Hawaii, coral reefs occur across a gradient of biological (host abundance), climatic (sea surface temperature anomalies) and anthropogenic conditions from the human-impacted reefs of the main Hawaiian Islands (MHI) to the pristine reefs of the northwestern Hawaiian Islands (NWHI). Coral disease surveys were conducted at 142 sites from across the Archipelago and disease patterns examined. Twelve diseases were recorded from three coral genera (Porites, Montipora, Acropora) with Porites having the highest prevalence. Porites growth anomalies (PorGAs) were significantly more prevalent within and indicative of reefs in the MHI and Porites trematodiasis (PorTrm) was significantly more prevalent within and indicative of reefs in the NWHI. Porites tissue loss syndrome (PorTLS) was also important in driving regional differences but that relationship was less clear. These results highlight the importance of understanding disease ecology when interpreting patterns of disease occurrence. PorTrm is caused by a parasitic flatworm that utilizes multiple hosts during its life cycle (fish, mollusk and coral). All three hosts must be present for the disease to occur and higher host abundance leads to higher disease prevalence. Thus, a high prevalence of PorTrm on Hawaiian reefs would be an indicator of a healthy coral reef ecosystem. In contrast, the high occurrence of PorGAs within the MHI suggests that PorGAs are related, directly or indirectly, to some environmental co-factor associated with increased human population sizes. Focusing on the three indicator diseases (PorGAs, PorTrm, PorTLS) we used statistical modeling to examine the underlying associations between disease prevalence and 14 different predictor variables (biotic and abiotic). All three diseases showed positive associations with host abundance and negative associations with thermal stress. The association with human population density differed among disease states with PorGAs showing a positive and PorTrm showing a negative association, but no significant explanatory power was offered for PorTLS.
Journal Article
Gram staining reveals diverse bacterial associations in coral cell-associated microbial aggregates in the Pacific Ocean
Cell-associated microbial aggregates (CAMAs) (also referred to as coral-associated microbial aggregates) have been observed in 24 coral species from the Pacific Ocean, and studies indicate most contain gram-negative bacilli from the genus Endozoicomonas. Here, we used histology with Gram staining to evaluate the morphology and distribution of CAMAs in six species of scleractinian corals from Hawaii and Palmyra. Within CAMAs, we observed the coexistence of bacteria with differing morphologies and Gram-staining properties both within and among coral species. Pocillopora and Acropora had mostly gram-negative bacilli, whereas gram-negative cocci dominated in Porites . Acropora had the highest abundance of gram-positive CAMAs. The anatomical distribution of CAMAs varied by coral species. CAMAs dominated in the tentacles of Pocillopora meandrina , Pocillopora grandis , and Porites evermanni, were mostly in the coenenchyme of Acropora cytherea , and were found equally between tentacles and coenenchyme in Porites compressa and Porites lobata . Tissue-layer distribution also varied, with CAMAs mainly in the epidermis of Pocillopora but in the gastrodermis of Porites and Acropora . The diversity of bacteria in CAMAs and their anatomic distribution in Pacific corals may be more complex than previously understood. This indicates other bacterial species, in addition to Endozoicomonas, are colonizing CAMAs in corals from the Pacific Ocean.
Journal Article
A comparative baseline of coral disease in three regions along the Saudi Arabian coast of the central Red Sea
Coral disease is a growing problem for coral reefs globally and diseases have been linked to thermal stress, excess nutrients, overfishing and other human impacts. The Red Sea is a unique environment for corals with a strong environmental gradient characterized by temperature extremes and high salinities, but minimal terrestrial runoff or riverine input and their associated pollution. Yet, relatively little is known about coral diseases in this region. Disease surveys were conducted at 22 reefs within three regions (Yanbu, Thuwal, Al Lith) in the central Red Sea along the Saudi Arabian coast. Surveys occurred in October 2015, which coincided with a hyperthermal-induced bleaching event. Our objectives were to 1) document types, prevalence, and distribution of coral diseases in a region with minimal terrestrial input, 2) compare regional differences in diseases and bleaching along a latitudinal gradient of environmental conditions, and 3) use histopathology to characterize disease lesions at the cellular level. Coral reefs of the central Red Sea had a widespread but a surprisingly low prevalence of disease (<0.5%), based on the examination of >75,750 colonies. Twenty diseases were recorded affecting 16 coral taxa and included black band disease, white syndromes, endolithic hypermycosis, skeletal eroding band, growth anomalies and focal bleached patches. The three most common diseases were Acropora white syndrome (59.1% of the survey sites), Porites growth anomalies (40.9%), and Porites white syndrome (31.8%). Sixteen out of 30 coral genera within transects had lesions and Acropora , Millepora and Lobophyllia were the most commonly affected. Cell-associated microbial aggregates were found in four coral genera including a first report in Stylophora . Differences in disease prevalence, coral cover, amount of heat stress as measured by degree heating weeks (DHW) and extent of bleaching was evident among sites. Disease prevalence was not explained by coral cover or DHW, and a negative relationship between coral bleaching and disease prevalence was found. The northern-most sites off the coast of Yanbu had the highest average disease prevalence and highest average DHW values but no bleaching. Our study provides a foundation and baseline data for coral disease prevalence in the central Red Sea, which is projected to increase as a consequence of increased frequency and severity of ocean warming.
Journal Article
Stony Coral Tissue Loss Disease in Florida Is Associated With Disruption of Host–Zooxanthellae Physiology
Samples from eight species of corals ( Colpophyllia natans , Dendrogyra cylindrus , Diploria labyrinthiformis , Meandrina meandrites , Montastraea cavernosa , Orbicella faveolata, Pseudodiploria strigosa , and Siderastrea siderea ) that exhibited gross clinical signs of acute, subacute, or chronic tissue loss attributed to stony coral tissue loss disease (SCTLD) were collected from the Florida Reef Tract during 2016–2018 and examined histopathologically. The hallmark microscopic lesion seen in all eight species was focal to multifocal lytic necrosis (LN) originating in the gastrodermis of the basal body wall (BBW) and extending to the calicodermis, with more advanced lesions involving the surface body wall. This was accompanied by other degenerative changes in host cells such as mucocyte hypertrophy, degradation and fragmentation of gastrodermal architecture, and disintegration of the mesoglea. Zooxanthellae manifested various changes including necrosis (cytoplasmic hypereosinophilia, pyknosis); peripheral nuclear chromatin condensation; cytoplasmic vacuolation accompanied by deformation, swelling, or atrophy; swollen accumulation bodies; prominent pyrenoids; and degraded chloroplasts. Polyhedral intracytoplasmic eosinophilic periodic acid–Schiff-positive crystalline inclusion bodies (∼1–10 μm in length) were seen only in M. cavernosa and P. strigosa BBW gastrodermis in or adjacent to active lesions and some unaffected areas (without surface lesions) of diseased colonies. Coccoidlike or coccobacilloidlike structures (Gram-neutral) reminiscent of microorganisms were occasionally associated with LN lesions or seen in apparently healthy tissue of diseased colonies along with various parasites and other bacteria all considered likely secondary colonizers. Of the 82 samples showing gross lesions of SCTLD, 71 (87%) were confirmed histologically to have LN. Collectively, pathology indicates that SCTLD is the result of a disruption of host–symbiont physiology with lesions originating in the BBW leading to detachment and sloughing of tissues from the skeleton. Future investigations could focus on identifying the cause and pathogenesis of this process.
Journal Article
Phase Shift from a Coral to a Corallimorph-Dominated Reef Associated with a Shipwreck on Palmyra Atoll
Coral reefs can undergo relatively rapid changes in the dominant biota, a phenomenon referred to as phase shift. Various reasons have been proposed to explain this phenomenon including increased human disturbance, pollution, or changes in coral reef biota that serve a major ecological function such as depletion of grazers. However, pinpointing the actual factors potentially responsible can be problematic. Here we show a phase shift from coral to the corallimorpharian Rhodactis howesii associated with a long line vessel that wrecked in 1991 on an isolated atoll (Palmyra) in the central Pacific Ocean. We documented high densities of R. howesii near the ship that progressively decreased with distance from the ship whereas R. howesii were rare to absent in other parts of the atoll. We also confirmed high densities of R. howesii around several buoys recently installed on the atoll in 2001. This is the first time that a phase shift on a coral reef has been unambiguously associated with man-made structures. This association was made, in part, because of the remoteness of Palmyra and its recent history of minimal human habitation or impact. Phase shifts can have long-term negative ramification for coral reefs, and eradication of organisms responsible for phase shifts in marine ecosystems can be difficult, particularly if such organisms cover a large area. The extensive R. howesii invasion and subsequent loss of coral reef habitat at Palmyra also highlights the importance of rapid removal of shipwrecks on corals reefs to mitigate the potential of reef overgrowth by invasives.
Journal Article
Viral-Like Particles Are Associated With Endosymbiont Pathology in Florida Corals Affected by Stony Coral Tissue Loss Disease
Stony coral tissue loss disease (SCTLD) was first documented in 2014 near the Port of Miami, Florida, and has since spread north and south along Florida’s Coral Reef, killing large numbers of more than 20 species of coral and leading to the functional extinction of at least one species, Dendrogyra cylindrus . SCTLD is assumed to be caused by bacteria based on presence of different molecular assemblages of bacteria in lesioned compared to apparently healthy tissues, its apparent spread among colonies, and cessation of spread of lesions in individual colonies treated with antibiotics. However, light microscopic examination of tissues of corals affected with SCTLD has not shown bacteria associated with tissue death. Rather, microscopy shows dead and dying coral cells and symbiotic dinoflagellates (endosymbionts) indicating a breakdown of host cell and endosymbiont symbiosis. It is unclear whether host cells die first leading to death of endosymbionts or vice versa. Based on microscopy, hypotheses as to possible causes of SCTLD include infectious agents not visible at the light microscopy level or toxicosis, perhaps originating from endosymbionts. To clarify this, we examined corals affected with SCTLD and apparently healthy corals using transmission electron microscopy. Endosymbionts in SCTLD-affected and apparently healthy corals consistently had varying degrees of pathology associated with elongated particles compatible in morphology with filamentous positive single-stranded RNA viruses of plants termed anisometric viral-like particles (AVLP). There was apparent progression from early to late replication of AVLP in the cytoplasm of endosymbionts adjacent to or at times within chloroplasts, with morphologic changes in chloroplasts consistent with those seen in plant cells infected by viruses. Coral host cell pathology appeared limited to massive proliferation and lysis of mucus cells. Based on these findings, we hypothesize that SCTLD is a viral disease of endosymbionts leading to coral host death. Efforts to confirm the presence of a virus associated with SCTLD through other means would be appropriate. These include showing the presence of a virus through molecular assays such as deep sequencing, attempts to grow this virus in the laboratory through culture of endosymbionts, localization of virus in tissue sections using immunohistochemistry or in situ hybridization, and experimental infection of known-virus-negative corals to replicate disease at the gross and microscopic level.
Journal Article