scholarly journals Stony Coral Tissue Loss Disease in Florida Is Associated With Disruption of Host–Zooxanthellae Physiology

2020 ◽  
Vol 7 ◽  
Author(s):  
Jan H. Landsberg ◽  
Yasunari Kiryu ◽  
Esther C. Peters ◽  
Patrick W. Wilson ◽  
Noretta Perry ◽  
...  
Keyword(s):  
Body Wall ◽  
Chromatin Condensation ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Host Cells ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Crystalline Inclusion ◽  
Periodic Acid Schiff ◽  
Stony Coral

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.

scholarly journals Viral-Like Particles Are Associated With Endosymbiont Pathology in Florida Corals Affected by Stony Coral Tissue Loss Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Thierry M. Work ◽  
Tina M. Weatherby ◽  
Jan H. Landsberg ◽  
Yasunari Kiryu ◽  
Samantha M. Cook ◽  
...  
Keyword(s):  
Host Cell ◽  
Viral Disease ◽  
Host Cells ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Coral Host ◽  
Stony Coral ◽  
Mucus Cells ◽  
Functional Extinction ◽  
Apparently Healthy

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.

scholarly journals Changing Stony Coral Tissue Loss Disease Dynamics Through Time in Montastraea cavernosa

2021 ◽  
Vol 8 ◽  
Author(s):  
Greta Aeby ◽  
Blake Ushijima ◽  
Erich Bartels ◽  
Cory Walter ◽  
Joseph Kuehl ◽  
...  
Keyword(s):  
Common Species ◽  
Disease Prevalence ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Disease Dynamics ◽  
Western Atlantic ◽  
Fort Lauderdale ◽  
Stony Coral ◽  
Montastraea Cavernosa ◽  
Lesion Morphology

Stony coral tissue loss disease (SCTLD) is affecting corals across the Western Atlantic and displays species-specific and regional differences in prevalence, incidence, degree of mortality, and lesion morphology. We examined two Florida sites with different temporal histories of disease emergence; Fort Lauderdale where SCTLD is endemic and the Lower Florida Keys where SCTLD has recently emerged. Our objectives were to (1) assess the potential impact of SCTLD on overall reef condition by surveying reefs in each region, (2) in a single common species, Montastraea cavernosa, examine differences in SCTLD prevalence, colony mortality, and lesion morphology in each region, and (3) look for differences in contagion by conducting transmission experiments using lesions from each region. Reef surveys found sites in both regions had low coral cover, high algae cover, and similar coral species composition. SCTLD prevalence was higher in the Lower Keys than at Fort Lauderdale and two of the common species, M. cavernosa and S. siderea at Fort Lauderdale were dominated by smaller colonies (<5 cm) whereas larger colonies occurred in the Lower Keys. Tagged M. cavernosa SCTLD-affected colonies were followed for 2 years at one site in each region. In both years, Fort Lauderdale colonies showed declining disease prevalence, low colony mortality, and disease lesions were mainly bleached spots lacking tissue loss. In contrast, Lower Keys colonies tagged in the first year maintained 100% disease prevalence with high mortality, and disease lesions were predominantly tissue loss with no bleached edges. However, SCTLD dynamics changed, with year two tagged colonies showing declining disease prevalence, low mortality, and lesion morphology switched to a mixture of bleached polyps and tissue loss with or without bleached edges. Lesion morphology on colonies was a significant predictor of amount of tissue loss. Aquaria studies found the rate of SCTLD transmission using lesions from the different zones (emergent and endemic) were similar. Our study highlights that differences in coral mortality from SCTLD are not necessarily linked to host species, lesion morphology is reflective of subsequent rate of mortality, and disease dynamics change through time on reefs where the disease has newly emerged.

Reef-scale impacts of the stony coral tissue loss disease outbreak

Coral Reefs ◽  
2020 ◽  
Vol 39 (4) ◽  
pp. 861-866 ◽  
Author(s):  
Nuria Estrada-Saldívar ◽  
Ana Molina-Hernández ◽  
Esmeralda Pérez-Cervantes ◽  
Francisco Medellín-Maldonado ◽  
F. Javier González-Barrios ◽  
...  
Keyword(s):  
Disease Outbreak ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Stony Coral

scholarly journals Neuroaxonal Dystrophy in a Group of Related Cats

1993 ◽  
Vol 5 (4) ◽  
pp. 585-590 ◽  
Author(s):  
K. Paige Carmichael ◽  
Elizabeth W. Howerth ◽  
John E. Oliver ◽  
Kurt Klappenbach
Keyword(s):  
Spinal Cord ◽  
Hind Limb ◽  
Coat Color ◽  
Amorphous Material ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Neuroaxonal Dystrophy ◽  
Periodic Acid Schiff ◽  
Dystrophic Axons ◽  
Positive Core

A syndrome resembling previously described feline hereditary neuroaxonal dystrophy (FHND) was diagnosed in a litter of cats. The disorder was characterized by a sudden onset of hind limb ataxia that slowly progressed to hind limb paresis and paralysis. The cats were between 6 and 9 months old when clinical signs were first noted. Histologically, there was marked ballooning of axonal processes, with spheroid formation and vacuolation in specific regions of the brain and spinal cord. Some dystrophic axons contained a central periodic acid-Schiff (PAS)-positive core. Neuronal loss and gliosis were seen in certain brain stem nuclei, spinal cord nuclei, and the cerebellum. Ultrastructurally, there was hypomyelination and dysmyelination of affected axons. The PAS-positive core in dystrophic axons corresponded ultrastructurally with accumulations of electrondense, flocculent, amorphous material. In addition, these axons contained membrane-bound osmiophilic bodies and large nonmembrane-bound vacuoles. The syndrome in this report differs from the previously described FHND in that no inner ear involvement was seen and onset of clinical signs occurred at a later age. In addition, although some of the affected cats did have diluted coat colors, abnormal coat color was not always associated with clinical disease. This disease is similar to juvenile neuroaxonal dystrophy in children and to neuroaxonal dystrophies described in horses, dogs, cattle, and sheep.

scholarly journals Spontaneous Lung Lesions in Aging Laboratory Rabbits (Oryctolagus cuniculus)

2016 ◽  
Vol 54 (1) ◽  
pp. 178-187 ◽  
Author(s):  
T. K. Cooper ◽  
J. W. Griffith ◽  
Z. C. Chroneos ◽  
J. M. Izer ◽  
L. B. Willing ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Periodic Acid ◽  
Genetic Defect ◽  
Clinical Signs ◽  
Heterotopic Bone ◽  
Alpha Smooth Muscle Actin ◽  
Periodic Acid Schiff ◽  
Lung Lesions ◽  
Age Related

Spontaneous age-related lesions of laboratory rabbits are not well documented in the contemporary scientific literature. A retrospective study of diagnostic necropsies of 36 rabbits >2 years of age found a number of common lung lesions. Fibromuscular intimal hyperplasia affected medium and to a lesser extent large pulmonary arteries and was present to a variable extent in all 36 rabbits >2 years of age. The lesions were characterized by fragmentation and/or reduplication of the internal elastic lamina (IEL), proliferation of smoothelin+/alpha-smooth muscle actin (α-SMA)+/vimentin− smooth muscle cells and fewer smoothelin−/α-SMA+/vimentin+ myofibroblasts, and intimal deposition of collagen without thrombosis, embolism, or evidence of pulmonary hypertension. Pulmonary emphysema, present in 30/36 rabbits, was characterized by the loss of alveolar septa; most affected rabbits did not have clinical signs of respiratory disease. In 8/13 rabbits of the inbred EIII/JC audiogenic strain, we identified a unique syndrome of granulomatous pneumonia containing hyaline brown to gray, globular to ring-like acellular material that was Alcian blue and periodic acid-Schiff positive. The material was immunoreactive for surfactant protein-A and had the ultrastructural appearance of multilamellar vesicles, suggesting a genetic defect in surfactant metabolism. Additionally, we found small benign primary lung tumors (fibropapillomas, 5 rabbits) not previously described. Other findings included heterotopic bone (5 rabbits), subacute to chronic suppurative bronchopneumonia, pyogranulomatous pneumonia with plant material, and pulmonary artifacts from barbiturate euthanasia solution.

scholarly journals Epitheliocystis Infection in Cultured White Sturgeon (Acipenser transmontanus): Antigenic and Ultrastructural Similarities of the Causative Agent to the Chlamydiae

1996 ◽  
Vol 8 (2) ◽  
pp. 172-180 ◽  
Author(s):  
Joseph M. Groff ◽  
Scott E. LaPatra ◽  
Robert J. Munn ◽  
Mark L. Anderson ◽  
Bennie I. Osburn
Keyword(s):  
Periodic Acid ◽  
Host Cells ◽  
White Sturgeon ◽  
Acipenser Transmontanus ◽  
Periodic Acid Schiff ◽  
Homogeneous Population ◽  
Cytoplasmic Inclusions ◽  
Individual Host ◽  
Intensive Fish Culture ◽  
Chlamydial Antigen

A mild to moderate branchial epitheliocystis infection was diagnosed in subyearling (11 months old, 250–300 g) white sturgeon ( Acipenser transmontanus) from a private culture facility with a 4–8% mortality in the population. Infected branchial epithelial cells contained the coccoid to coccobacillary epitheliocystis organisms, which appeared as cytoplasmic inclusions composed of a fine, homogeneous, dense, basophilic, granular material. The infected cells were variably enlarged with spherical to oval profiles and were randomly distributed throughout the branchial epithelium. The cytoplasmic inclusions stained positive with Macchiavello stain but negative with Brown and Brenn, periodic acid-Schiff, and Gimenez stains. Expression of chlamydial antigen was demonstrated within the cytoplasmic inclusions using a standard peroxidase-antiperoxidase immunohistochemical technique. Three stages of coordinated intracellular development were recognized by electron microscopy. The reticulate bodies were oval to spherical and 0.4–0.8 × 0.5–1.4 μm but often exhibited a pleomorphic and convoluted appearance because of variable membrane invaginations and evaginations suggestive of uneven fission and budding. Separate host cells contained intermediate bodies that were spherical to oval and 0.2–0.4 × 0.3–0.6 μm although often observed in the process of apparent uneven division. The presence of a cap or plaque composed of hexagonally arrayed fibrillar surface projections was initially recognized in this stage. A homogeneous population of 0.3–0.4 μmoval elementary bodies were observed separately in individual host cells. This developmental stage had a single, dense, compact, eccentrically located cytoplasmic condensation that occurred opposite to the location of the cap of hexagonally arrayed fibrillar surface projections. Morphologic characteristics of the epitheliocystis organism in these white sturgeon were similar to those previously described in other teleosts and expands the species catalogue of epitheliocystis infection. Furthermore, the ultrastructural similarities to the chlamydiae and the immunohistochemical detection of chlamydial antigen provides further evidence that the epitheliocystis agent is related to members of the Chlamydiales. Although the infection was considered mild to moderate and could not be definitively attributed to the mortality in this population, the potential adverse impact of epitheliocystis infection on sturgeon culture should be considered especially in intensive fish culture operations.

Globoid Cell-like Leukodystrophy in a Domestic Longhaired Cat

2002 ◽  
Vol 39 (4) ◽  
pp. 494-496 ◽  
Author(s):  
C. J. Sigurdson ◽  
R. J. Basaraba ◽  
E. M. Mazzaferro ◽  
D. H. Gould
Keyword(s):  
Mononuclear Cells ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Krabbe Disease ◽  
Periodic Acid Schiff ◽  
Nervous Systems ◽  
Central Nervous Systems ◽  
Mental Regression ◽  
Globoid Cell ◽  
Globoid Cells

Globoid cell leukodystrophy (GLD; Krabbe disease), is a rare heritable metabolic disorder in humans, dogs, mutant twitcher mice, and rhesus monkeys that is caused by a deficiency in the lysosomal enzyme galactocerebrosidase (GALC). GALC deficiency results in the accumulation of psychosine, which is toxic to oligodendrocytes and Schwann cells of the central and peripheral nervous systems. Clinical signs include hypotonia, mental regression, and death by 2 years of age in most human patients. Here we describe a domestic longhaired kitten with rapidly progressive neurologic disease and brain and spinal cord lesions characteristic of GLD. Pathologic hallmarks of the disease reflect the loss of oligodendrocytes and include myelin loss, gliosis, and the perivascular accumulation of large mononuclear cells with fine cytoplasmic vacuoles (globoid cells) in the peripheral and central nervous systems. Globoid cells were CD68 and ferritin positive, confirming their monocytic origin, and cytoplasmic contents were nonmetachromatic and periodic acid-Schiff positive.

scholarly journals Stony Coral Tissue Loss Disease biomarker bacteria identified in corals and overlying waters using a rapid field-based sequencing approach

2021 ◽  
Author(s):  
Cynthia C. Becker ◽  
Marilyn Brandt ◽  
Carolyn A. Miller ◽  
Amy Apprill
Keyword(s):  
Coral Disease ◽  
The United States ◽  
Virgin Islands ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Rna Sequences ◽  
Disease Biomarker ◽  
Stony Coral ◽  
Ribosomal Rna Sequences ◽  
Reef Tract

AbstractStony Coral Tissue Loss Disease (SCTLD) is a devastating disease. Since 2014, it has spread along the entire Florida Reef Tract, presumably via a water-borne vector, and into the greater Caribbean. It was first detected in the United States Virgin Islands (USVI) in January 2019. To more quickly identify disease biomarker microbes, we developed a rapid pipeline for microbiome sequencing. Over a span of 10 days we collected, processed, and sequenced coral tissue and near-coral seawater microbiomes from diseased and apparently healthy Colpophyllia natans, Montastraea cavernosa, Meandrina meandrites and Orbicella franksi. Analysis of the resulting bacterial and archaeal 16S ribosomal RNA sequences revealed 25 biomarker amplicon sequence variants (ASVs) enriched in diseased tissue. These biomarker ASVs were additionally recovered in near-coral seawater (within 5 cm of coral surface), a potential recruitment zone for pathogens. Phylogenetic analysis of the biomarker ASVs belonging to Vibrio, Arcobacter, Rhizobiaceae, and Rhodobacteraceae revealed relatedness to other coral disease-associated bacteria and lineages novel to corals. Additionally, four ASVs (Algicola, Cohaesibacter, Thalassobius and Vibrio) were exact sequence matches to microbes previously associated with SCTLD. This work represents the first rapid coral disease sequencing effort and identifies biomarkers of SCTLD that could be targets for future SCTLD research.

scholarly journals Considering Commercial Vessels as Potential Vectors of Stony Coral Tissue Loss Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Nicholas A. Rosenau ◽  
Sarah Gignoux-Wolfsohn ◽  
Richard A. Everett ◽  
A. Whitman Miller ◽  
Mark S. Minton ◽  
...  
Keyword(s):  
Ballast Water ◽  
Management Strategies ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Caribbean Region ◽  
Future Research ◽  
Ship Traffic ◽  
Marine Invasion ◽  
Stony Coral ◽  
Resource Managers

Stony coral tissue loss disease (SCTLD) is a troubling new disease that is spreading rapidly across the greater Caribbean region, but the etiological agent(s) and the mechanisms(s) of spread are both unknown. First detected off the coast of Miami, Florida, major ocean currents alone do not explain the pattern of spread, with outbreaks occurring across geographically disjunct and distant locations. This has raised concerns by researchers and resource managers that commercial vessels may contribute as vectors to spread of the disease. Despite existing regulatory and management strategies intended to limit coastal marine invasion risks, the efficacy of these measures is still unresolved for ship-borne microorganisms, and disease transport via ballast water and hull biofouling are under examination given the high ship traffic in the region. Here, to help inform the discussion of ships as possible vectors of SCTLD, we provide an overview of the current state of knowledge about ships and their potential to transfer organisms in the greater Caribbean, focusing in particular on ballast water, and outline a set of recommendations for future research.

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