scholarly journals White Syndrome-Affected Corals Have a Distinct Microbiome at Disease Lesion Fronts

2016 ◽  
Vol 83 (2) ◽  
Author(s):  
F. Joseph Pollock ◽  
Naohisa Wada ◽  
Gergely Torda ◽  
Bette L. Willis ◽  
David G. Bourne
Keyword(s):  
Disease Ecology ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Health States ◽  
Host Coral ◽  
Tissue Samples ◽  
Content Type ◽  
White Syndrome ◽  
Community Profiling

ABSTRACT Coral tissue loss diseases, collectively known as white syndromes (WSs), induce significant mortality on reefs throughout the Indo-Pacific, yet definitive confirmation of WS etiologies remains elusive. In this study, we integrated ecological disease monitoring, bacterial community profiling, in situ visualization of microbe-host interactions, and cellular responses of the host coral through an 18-month repeated-sampling regime. We assert that the observed pathogenesis of WS lesions on acroporid corals at Lizard Island (Great Barrier Reef) is not the result of apoptosis or infection by Vibrio bacteria, ciliates, fungi, cyanobacteria, or helminths. Histological analyses detected helminths, ciliates, fungi, and cyanobacteria in fewer than 25% of WS samples, and helminths and fungi were also observed in 12% of visually healthy samples. The abundances of Vibrio-affiliated sequences (assessed using 16S rRNA amplicon sequencing) did not differ significantly between health states and never exceeded 3.3% of reads in any individual sample. In situ visualization detected Vibrio bacteria only in summer WS lesion samples and revealed no signs of these bacteria in winter disease samples (or any healthy tissue samples), despite continued disease progression year round. However, a 4-fold increase in Rhodobacteraceae-affiliated bacterial sequences at WS lesion fronts suggests that this group of bacteria could play a role in WS pathogenesis and/or serve as a diagnostic criterion for disease differentiation. While the causative agent(s) underlying WSs remains elusive, the microbial and cellular processes identified in this study will help to identify and differentiate visually similar but potentially distinct WS etiologies. IMPORTANCE Over the past decade, a virulent group of coral diseases known as white syndromes have impacted coral reefs throughout the Indian and Pacific Oceans. This article provides a detailed case study of white syndromes to combine disease ecology, high-throughput microbial community profiling, and cellular-scale host-microbe visualization over seasonal time scales. We provide novel insights into the etiology of this devastating disease and reveal new diagnostic criteria that could be used to differentiate visually similar but etiologically distinct forms of white syndrome.

scholarly journals Pengamatan Laju Penyakit White Syndrome Pada Montipora sp. Di Pulau Pramuka, Taman Nasional Laut Kepulauan Seribu, DKI Jakarta

2018 ◽  
Vol 5 (1) ◽  
pp. 22
Author(s):  
Abdur Rosyid ◽  
Oktiyas Muzaky Luthfi
Keyword(s):  
National Park ◽  
Coral Disease ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Progression Rate ◽  
White Syndrome ◽  
Coral Surface ◽  
Pathogenic Vibrio ◽  
Imagej Software ◽  
Main Factor

Coral disease now became main factor of coral degradation in the world. There is still a few report about coral disease in Kepulauan Seribu Marine National Park (TNKPS) include of white syndrome (WS) in Montipora sp. WS was characterized by white area on coral surface at several stages. WS had caused coral tissue loss and leaved bare CaCO3 skeleton that was caused by pathogenic Vibrio coralliitycus associated with other microorganisms. In this study the progress of WS calculated by measurement of the distances of WS that moved from diseased to healty coral surface. All calculations was performed used ImageJ Software. Our result showed that WS progression rate in first week was 9.06 cm2 and the second week was 2.37 cm2. Total coral tissue mortality was 12.03% for 2 weeks.

scholarly journals Vibrio coralliilyticus Strain OCN008 Is an Etiological Agent of Acute Montipora White Syndrome

2014 ◽  
Vol 80 (7) ◽  
pp. 2102-2109 ◽  
Author(s):  
Blake Ushijima ◽  
Patrick Videau ◽  
Andrew H. Burger ◽  
Amanda Shore-Maggio ◽  
Christina M. Runyon ◽  
...  
Keyword(s):  
Type Strain ◽  
Disease Onset ◽  
Tissue Loss ◽  
Temperature Dependent ◽  
Content Type ◽  
Infectious Dose ◽  
White Syndrome ◽  
Porites Compressa ◽  
Sensing Systems ◽  
Vibrio Coralliilyticus

ABSTRACTIdentification of a pathogen is a critical first step in the epidemiology and subsequent management of a disease. A limited number of pathogens have been identified for diseases contributing to the global decline of coral populations. Here we describeVibrio coralliilyticusstrain OCN008, which induces acuteMontiporawhite syndrome (aMWS), a tissue loss disease responsible for substantial mortality of the coralMontipora capitatain Kāne‘ohe Bay, Hawai‘i. OCN008 was grown in pure culture, recreated signs of disease in experimentally infected corals, and could be recovered after infection. In addition, strains similar to OCN008 were isolated from diseased coral from the field but not from healthyM. capitata. OCN008 repeatedly induced the loss of healthyM. capitatatissue from fragments under laboratory conditions with a minimum infectious dose of between 107and 108CFU/ml of water. In contrast,Porites compressawas not infected by OCN008, indicating the host specificity of the pathogen. A decrease in water temperature from 27 to 23°C affected the time to disease onset, but the risk of infection was not significantly reduced. Temperature-dependent bleaching, which has been observed with theV. coralliilyticustype strain BAA-450, was not observed during infection with OCN008. A comparison of the OCN008 genome to the genomes of pathogenicV. coralliilyticusstrains BAA-450 and P1 revealed similar virulence-associated genes and quorum-sensing systems. Despite this genetic similarity, infections ofM. capitataby OCN008 do not follow the paradigm forV. coralliilyticusinfections established by the type strain.

scholarly journals 3D Photogrammetry Reveals Dynamics of Stony Coral Tissue Loss Disease (SCTLD) Lesion Progression Across a Thermal Stress Event

2020 ◽  
Vol 7 ◽  
Author(s):  
Sonora Meiling ◽  
Erinn M. Muller ◽  
Tyler B. Smith ◽  
Marilyn E. Brandt
Keyword(s):  
Thermal Stress ◽  
Disease Ecology ◽  
The United States ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Critical Parameters ◽  
Bleaching Event ◽  
Stony Coral ◽  
Wide Range ◽  
Loss Rates

Stony coral tissue loss disease (SCTLD) was first observed in the United States Virgin Islands in January 2019 on a reef at Flat Cay off the island of St. Thomas. A year after its emergence, the disease had spread to several reefs around St. Thomas causing significant declines in overall coral cover. Rates of tissue loss are an important metric in the study of coral disease ecology, as they can inform many aspects of etiology such as disease susceptibility and resistance among species, and provide critical parameters for modeling the effects of disease among heterogenous reef communities. The present study quantified tissue loss rates attributed to SCTLD among six abundant reef building species (Colpophyllia natans, Montastraea cavernosa, Diploria labyrinthiformis, Pseudodiploria strigosa, Orbicella annularis, and Porites astreoides). Field-based 3D models of diseased corals, taken approximately weekly, indicated that the absolute rates of tissue loss from SCTLD slowed through time, corresponding with the accumulation of thermal stress that led to mass bleaching. Absolute tissue loss rates were comparable among species prior to the bleaching event but diverged during and remained different after the bleaching event. Proportional tissue loss rates did not vary among species or through time, but there was considerable variability among M. cavernosa colonies. SCTLD poses a significant threat to reefs across the Caribbean due to its persistence through time, wide range of susceptible coral species, and unprecedented tissue loss rates. Intervention and management efforts should be increased during and immediately following thermal stress events in order maximize resource distribution when disease prevalence is decreased.

scholarly journals Reef Sediments Can Act As a Stony Coral Tissue Loss Disease Vector

2022 ◽  
Vol 8 ◽  
Author(s):  
Michael S. Studivan ◽  
Ashley M. Rossin ◽  
Ewelina Rubin ◽  
Nash Soderberg ◽  
Daniel M. Holstein ◽  
...  
Keyword(s):  
Infectious Agent ◽  
Coastal Development ◽  
Ex Situ ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Conservation Strategies ◽  
Dade County ◽  
Tissue Samples ◽  
Stony Coral ◽  
The Individual

Stony coral tissue loss disease (SCTLD) was first observed in 2014 near Virginia Key in Miami-Dade County, Florida. Field sampling, lab experiments, and modeling approaches have suggested that reef sediments may play a role in SCTLD transmission, though a positive link has not been tested experimentally. We conducted an ex situ transmission assay using a statistically-independent disease apparatus to test whether reef sediments can transmit SCTLD in the absence of direct contact between diseased and healthy coral tissue. We evaluated two methods of sediment inoculation: batch inoculation of sediments collected from southeast Florida using whole colonies of diseased Montastraea cavernosa, and individual inoculations of sediments following independent, secondary infections of ∼5 cm2 coral fragments. Healthy fragments of the coral species Orbicella faveolata and M. cavernosa were exposed to these diseased sediment treatments, as well as direct disease contact and healthy sediment controls. SCTLD transmission was observed for both batch and individual diseased sediment inoculation treatments, albeit with lower proportions of infected individuals as compared to disease contact controls. The time to onset of lesions was significantly different between species and among disease treatments, with the most striking infections occurring in the individual diseased sediment treatment in under 24 h. Following infection, tissue samples were confirmed for the presence of SCTLD signs via histological examination, and sediment subsamples were analyzed for microbial community variation between treatments, identifying 16 SCTLD indicator taxa in sediments associated with corals experiencing tissue loss. This study demonstrated that reef sediments can indeed transmit SCTLD through indirect exposure between diseased and healthy corals, and adds credence to the assertion that SCTLD transmission occurs via an infectious agent or agents. This study emphasizes the critical need to understand the roles that sediment microbial communities and coastal development activities may have on the persistence of SCTLD throughout the endemic zone, especially in the context of management and conservation strategies in Florida and the wider Caribbean.

scholarly journals Corals Form Characteristic Associations with Symbiotic Nitrogen-Fixing Bacteria

2012 ◽  
Vol 78 (9) ◽  
pp. 3136-3144 ◽  
Author(s):  
Kimberley A. Lema ◽  
Bette L. Willis ◽  
David G. Bourne
Keyword(s):  
Bacterial Communities ◽  
Coral Species ◽  
Community Diversity ◽  
Coral Tissue ◽  
Terrestrial Plants ◽  
Tissue Samples ◽  
Coral Mucus ◽  
Content Type ◽  
Mutualistic Relationship ◽  
Bacterial Groups

ABSTRACTThe complex symbiotic relationship between corals and their dinoflagellate partnerSymbiodiniumis believed to be sustained through close associations with mutualistic bacterial communities, though little is known about coral associations with bacterial groups able to fix nitrogen (diazotrophs). In this study, we investigated the diversity of diazotrophic bacterial communities associated with three common coral species (Acropora millepora,Acropora muricata, andPocillopora damicormis) from three midshelf locations of the Great Barrier Reef (GBR) by profiling the conserved subunit of thenifHgene, which encodes the dinitrogenase iron protein. Comparisons of diazotrophic community diversity among coral tissue and mucus microenvironments and the surrounding seawater revealed that corals harbor diversenifHphylotypes that differ between tissue and mucus microhabitats. Coral mucusnifHsequences displayed high heterogeneity, and many bacterial groups overlapped with those found in seawater. Moreover, coral mucus diazotrophs were specific neither to coral species nor to reef location, reflecting the ephemeral nature of coral mucus. In contrast, the dominant diazotrophic bacteria in tissue samples differed among coral species, with differences remaining consistent at all three reefs, indicating that coral-diazotroph associations are species specific. Notably, dominant diazotrophs for all coral species were closely related to the bacterial group rhizobia, which represented 71% of the total sequences retrieved from tissue samples. The species specificity of coral-diazotroph associations further supports the coral holobiont model that bacterial groups associated with corals are conserved. Our results suggest that, as in terrestrial plants, rhizobia have developed a mutualistic relationship with corals and may contribute fixed nitrogen toSymbiodinium.

Australian subtropical white syndrome: a transmissible, temperature-dependent coral disease

2010 ◽  
Vol 61 (3) ◽  
pp. 342 ◽  
Author(s):  
S. J. Dalton ◽  
S. Godwin ◽  
S. D. A. Smith ◽  
L. Pereg
Keyword(s):  
Direct Contact ◽  
Field Experiments ◽  
Coral Disease ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Management Tool ◽  
Change Models ◽  
White Syndrome ◽  
Marine Park ◽  
South Wales

Since 2000, a disease displaying white-syndrome characteristics has been observed affecting corals from the genus Turbinaria in the Solitary Islands Marine Park, New South Wales, Australia. Recently termed Australian subtropical white syndrome, this disease is transmissible through direct contact and by a predatory vector, but transmission through the water column has not been observed. In aquarium experiments, progressive tissue loss, extending from the region where healthy Turbinaria mesenterina fragments were in direct contact with samples of diseased coral, was noted in 66% of treatments. No tissue loss occurred in any of the controls or when healthy fragments were not in direct contact with diseased corals. Field experiments confirmed that the disease was infectious through direct contact. Further experiments showed that the rate of tissue loss was significantly higher when corals were exposed to summer temperatures (26°C). These results suggest that temperature increases predicted in most climate change models could lead to the loss of dominant coral species, displacing other organisms that rely on corals for food and shelter. Finally, the present study showed that removal of the disease margin provides a management tool to minimise coral tissue loss during an epizootic.

In situ microprobe quantitation of inorganic particle burden in paraffin sections of lung tissue

1988 ◽  
Vol 46 ◽  
pp. 990-991
Author(s):  
Jerrold L. Abraham
Keyword(s):  
Lung Tissue ◽  
Quantitative Information ◽  
Particulate Material ◽  
Paraffin Sections ◽  
Tissue Samples ◽  
Qualitative And Quantitative ◽  
The Past ◽  
Quantitative Analyses ◽  
Data Result

Inorganic particulate material of diverse types is present in the ambient and occupational environment, and exposure to such materials is a well recognized cause of some lung disease. To investigate the interaction of inhaled inorganic particulates with the lung it is necessary to obtain quantitative information on the particulate burden of lung tissue in a wide variety of situations. The vast majority of diagnostic and experimental tissue samples (biopsies and autopsies) are fixed with formaldehyde solutions, dehydrated with organic solvents and embedded in paraffin wax. Over the past 16 years, I have attempted to obtain maximal analytical use of such tissue with minimal preparative steps. Unique diagnostic and research data result from both qualitative and quantitative analyses of sections. Most of the data has been related to inhaled inorganic particulates in lungs, but the basic methods are applicable to any tissues. The preparations are primarily designed for SEM use, but they are stable for storage and transport to other laboratories and several other instruments (e.g., for SIMS techniques).

A PILOT STUDY OF HER-2/NEU GENE AMPLIFICATION ASSESSED BY FLUORESCENCE IN SITU HYBRIDIZATION (FISH) IN GASTRIC CANCER

2014 ◽  
pp. 15-20
Author(s):  
Van Huy Tran ◽  
Thi Minh Thi Ha ◽  
Trung Nghia Van ◽  
Viet Nhan Nguyen ◽  
Phan Tuong Quynh Le ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Cancer Patients ◽  
Gene Amplification ◽  
Cancer Tissue ◽  
Tissue Samples ◽  
Her 2 ◽  
Gastric Cancer Patients

Background: HER-2/neu is a predictive biomarker for treatment of gastric cancer using trastuzumab in combination with chemotherapy. This study aimed to evaluate the status of HER-2/neu gene amplification using fluorescence in situ hybridization (FISH) in gastric cancer. Patients and methods: thirty six gastric cancer patients were assessed HER-2/neu gene amplification by FISH using PathVysionTM HER-2 DNA Probe kit (including HER-2/neu probe and CEP-17 probe) with biopsy and surgical specimens. Results: The HER-2/neu gene amplification was observed in three cases (8.3%), the HER-2/neu gene amplification rate in Lauren’s intestinal-type and diffuse-type were 11.8% and 5.2%, respectively. Conclusion: We applied successfully FISH technique with gastric cancer tissue samples. This technique could be performed as routine test in gastric cancer in order to select patients that benefit from trastuzumab in combination with chemotherapy.

Pituitary adenoma producing growth hormone and adrenocorticotropin: a histological, immunocytochemical, electron microscopic, and in situ hybridization study

1998 ◽  
Vol 88 (6) ◽  
pp. 1111-1115 ◽  
Author(s):  
Kalman Kovacs ◽  
Eva Horvath ◽  
Lucia Stefaneanu ◽  
Juan Bilbao ◽  
William Singer ◽  
...  
Keyword(s):  
Growth Hormone ◽  
In Situ Hybridization ◽  
Pituitary Adenoma ◽  
Immunoelectron Microscopy ◽  
Secretory Granules ◽  
Cell Types ◽  
Content Type ◽  
Separate Cell ◽  
Fine Print

✓ The authors report on the morphological features of a pituitary adenoma that produced growth hormone (GH) and adrenocorticotropic hormone (ACTH). This hormone combination produced by a single adenoma is extremely rare; a review of the available literature showed that only one previous case has been published. The tumor, which was removed from a 62-year-old man with acromegaly, was studied by histological and immunocytochemical analyses, transmission electron microscopy, immunoelectron microscopy, and in situ hybridization. When the authors used light microscopy, the tumor appeared to be a bimorphous mixed pituitary adenoma composed of two separate cell types: one cell population synthesized GH and the other ACTH. The cytogenesis of pituitary adenomas that produce more than one hormone is obscure. It may be that two separate cells—one somatotroph and one corticotroph—transformed into neoplastic cells, or that the adenoma arose in a common stem cell that differentiated into two separate cell types. In this case immunoelectron microscopy conclusively demonstrated ACTH in the secretory granules of several somatotrophs. This was associated with a change in the morphological characteristics of secretory granules. Thus it is possible that the tumor was originally a somatotropic adenoma that began to produce ACTH as a result of mutations that occurred during tumor progression.

scholarly journals Competition between Metals for Binding to Methanobactin Enables Expression of Soluble Methane Monooxygenase in the Presence of Copper

2014 ◽  
Vol 81 (3) ◽  
pp. 1024-1031 ◽  
Author(s):  
Bhagyalakshmi Kalidass ◽  
Muhammad Farhan Ul-Haque ◽  
Bipin S. Baral ◽  
Alan A. DiSpirito ◽  
Jeremy D. Semrau
Keyword(s):  
Methane Monooxygenase ◽  
High Specificity ◽  
Copper Uptake ◽  
Content Type ◽  
Soluble Methane Monooxygenase ◽  
Sds Page ◽  
Genes Encoding ◽  
Key Factor ◽  
Membrane Bound

ABSTRACTIt is well known that copper is a key factor regulating expression of the two forms of methane monooxygenase found in proteobacterial methanotrophs. Of these forms, the cytoplasmic, or soluble, methane monooxygenase (sMMO) is expressed only at low copper concentrations. The membrane-bound, or particulate, methane monooxygenase (pMMO) is constitutively expressed with respect to copper, and such expression increases with increasing copper. Recent findings have shown that copper uptake is mediated by a modified polypeptide, or chalkophore, termed methanobactin. Although methanobactin has high specificity for copper, it can bind other metals, e.g., gold. Here we show that inMethylosinus trichosporiumOB3b, sMMO is expressed and active in the presence of copper if gold is also simultaneously present. Such expression appears to be due to gold binding to methanobactin produced byM. trichosporiumOB3b, thereby limiting copper uptake. Such expression and activity, however, was significantly reduced if methanobactin preloaded with copper was also added. Further, quantitative reverse transcriptase PCR (RT-qPCR) of transcripts of genes encoding polypeptides of both forms of MMO and SDS-PAGE results indicate that both sMMO and pMMO can be expressed when copper and gold are present, as gold effectively competes with copper for binding to methanobactin. Such findings suggest that under certain geochemical conditions, both forms of MMO may be expressed and activein situ. Finally, these findings also suggest strategies whereby field sites can be manipulated to enhance sMMO expression, i.e., through the addition of a metal that can compete with copper for binding to methanobactin.

Sign in / Sign up

Export Citation Format

Share Document