Polymer identification of plastic marine debris can help identify its sources, degradation, and fate. We optimized and validated a fast, simple, and accessible technique, attenuated total reflectance ...Fourier transform infrared spectroscopy (ATR FT-IR), to identify polymers contained in plastic ingested by sea turtles. Spectra of consumer good items with known resin identification codes #1–6 and several #7 plastics were compared to standard and raw manufactured polymers. High temperature size exclusion chromatography measurements confirmed ATR FT-IR could differentiate these polymers. High-density (HDPE) and low-density polyethylene (LDPE) discrimination is challenging but a clear step-by-step guide is provided that identified 78% of ingested PE samples. The optimal cleaning methods consisted of wiping ingested pieces with water or cutting. Of 828 ingested plastics pieces from 50 Pacific sea turtles, 96% were identified by ATR FT-IR as HDPE, LDPE, unknown PE, polypropylene (PP), PE and PP mixtures, polystyrene, polyvinyl chloride, and nylon.
Display omitted
•We validate ATR FT-IR to identify polymers of weathered and ingested plastics.•We outline criteria to differentiate HDPE from LDPE samples.•Cutting or cleaning ingested plastics with water improves identification.•A database of standards is not required for polymer identification.•Collaborations of life and materials sciences address plastic debris issues.
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.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Fibropapillomatosis (FP) is a tumor disease associated with a herpesvirus (chelonid herpesvirus 5 ChHV5) that affects mainly green turtles globally. Understanding the epidemiology of FP has been ...hampered by a lack of robust serological assays to monitor exposure to ChHV5. This is due in part to an inability to efficiently culture the virus
for neutralization assays. Here, we expressed two glycoproteins (FUS4 and FUS8) from ChHV5 using baculovirus. These proteins were immobilized on enzyme-linked immunosorbent assay plates in their native form and assayed for reactivity to two types of antibodies, full-length 7S IgY and 5.7S IgY, which has a truncated Fc region. Turtles from Florida were uniformly seropositive to ChHV5 regardless of tumor status. In contrast, in turtles from Hawaii, we detected strong antibody reactivity mainly in tumored animals, with a lower antibody response being seen in nontumored animals, including those from areas where FP is enzootic. Turtles from Hawaii actively shedding ChHV5 were more seropositive than nonshedders. In trying to account for differences in the serological responses to ChHV5 between green turtles from Hawaii and green turtles from Florida, we rejected the cross-reactivity of antibodies to other herpesviruses, differences in viral epitopes, or differences in procedure as likely explanations. Rather, behavioral or other differences between green turtles from Hawaii and green turtles from Florida might have led to the emergence of biologically different viral strains. While the strains from turtles in Florida apparently spread independently of tumors, the transmission of the Hawaiian subtype relies heavily on tumor formation.
Fibropapillomatosis (FP) is a tumor disease associated with chelonid herpesvirus 5 (ChHV5) that is an important cause of mortality in threatened green turtles globally. FP is expanding in Florida and the Caribbean but declining in Hawaii. We show that Hawaiian turtles mount antibodies to ChHV5 mainly in response to tumors, which are the only sites of viral replication, whereas tumored and nontumored Floridian turtles are uniformly seropositive. Tumor viruses that depend on tumors for replication and spread are rare, with the only example being the retrovirus causing walleye dermal sarcoma in fish. The Hawaiian strain of ChHV5 may be the first DNA virus with such an unusual life history. Our findings, along with the fundamental differences in the life histories between Floridian turtles and Hawaiian turtles, may partly explain the differential dynamics of FP between the two regions.
Ingestion of marine debris is an established threat to sea turtles. The amount, type, color and location of ingested plastics in the gastrointestinal tracts of 55 sea turtles from Pacific longline ...fisheries from 2012 to 2016 were quantified, and compared across species, turtle length, body condition, sex, capture location, season and year. Six approaches for quantifying amounts of ingested plastic strongly correlated with one another and included: number of pieces, mass, volume and surface area of plastics, ratio of plastic mass to body mass, and percentage of the mass of gut contents consisting of plastic. All olive ridley (n=37), 90% of green (n=10), 80% of loggerhead (n=5) and 0% of leatherback (n=3) turtles had ingested plastic; green turtles ingested significantly more than olive ridleys. Most debris was in the large intestines. No adverse health impacts (intestinal lesions, blockage, or poor body condition) due directly to plastic ingestion were noted.
•Ingested plastic marine debris was found in 91% of pelagic Pacific sea turtles.•Green sea turtles ingested the most, and immature leatherbacks ingested none.•Six methods of quantifying plastic ingestion amounts gave similar results.•Most plastic was found in the large intestines.•No obvious health impacts were observed by plastic debris ingestion.
Sea star wasting disease (SSWD) refers to a suite of poorly described non-specific clinical signs including abnormal posture, epidermal ulceration, and limb autotomy (sloughing) causing mortalities ...of over 20 species of sea stars and subsequent ecological shifts throughout the northeastern Pacific. While SSWD is widely assumed to be infectious, with environmental conditions facilitating disease progression, few data exist on cellular changes associated with the disease. This is unfortunate, because such observations could inform mechanisms of disease pathogenesis and host susceptibility. Here, we replicated SSWD by exposing captive
Pisaster ochraceus
to a suite of non-infectious organic substances and show that development of gross lesions is a basal-to-surface process involving inflammation (e.g. infiltration of coelomocytes) of ossicles and mutable collagenous tissue, leading to epidermal ulceration. Affected sea stars also manifest increases in a heretofore undocumented coelomocyte type, spindle cells, that might be a useful marker of inflammation in this species. Finally, compared to purple morphs, orange
P. ochraceus
developed more severe lesions but survived longer. Longer-lived, and presumably more visible, severely-lesioned orange sea stars could have important demographic implications in terms of detectability of lesioned animals in the wild and measures of apparent prevalence of disease.
Invasive rodents on islands have adverse effects on native birds in island ecosystems, and rats are the most common culprits. Recently, house mice (Mus musculus) in the South Atlantic were found ...preying on three species of albatross chicks. Here, we show that house mice can also prey on nesting adult Laysan Albatross (Phoebastria immutabilis) on Midway Atoll National Wildlife Refuge (US). In contrast to mouse attacks on albatross in the South Atlantic, where mice targeted the rump and crown of chicks, on Midway, mice targeted nesting adults mainly on the back. For both regions, the outcome was similar with reduced nesting success. In the case of Midway, reduced nesting success was due to nest abandonment or mortality of one or both parents because of secondary bacterial infections. Mouse-induced mortality of adult albatross has the potential to have a more potent demographic effect because of their much higher natural survivorship once they reach adulthood.
A need exists for additional methods to examine cnidaria at the cellular level to aid our understanding of health, anatomy, and physiology of this important group of organisms. This need is ...particularly acute given that disease is emerging as a major factor in declines of ecologically important functional groups such as corals. Here we describe a simple method to process cnidarian cells for microscopic examination using the model organism Exaiptasia. We show that this organism has at least 18 cell types or structures that can be readily distinguished based on defined morphological features. Some of these cells can be related back to anatomic features of the animal both at the light microscope and ultrastructural level. The cnidome of Exaiptasia may be more complex than what is currently understood. Moreover, cnidarian cells, including some types of cnidocytes, phagocytize cells other than endosymbionts. Finally, our findings shed light on morphologic complexity of cell-associated microbial aggregates and their intimate intracellular associations. The tools described here could be useful for other cnidaria.
Microbial disease and the coral holobiont Bourne, David G; Garren, Melissa; Work, Thierry M ...
Trends in microbiology (Regular ed.),
12/2009, Letnik:
17, Številka:
12
Journal Article
Recenzirano
Tropical coral reefs harbour a reservoir of enormous biodiversity that is increasingly threatened by direct human activities and indirect global climate shifts. Emerging coral diseases are one ...serious threat implicated in extensive reef deterioration through disruption of the integrity of the coral holobiont – a complex symbiosis between the coral animal, endobiotic alga and an array of microorganisms. In this article, we review our current understanding of the role of microorganisms in coral health and disease, and highlight the pressing interdisciplinary research priorities required to elucidate the mechanisms of disease. We advocate an approach that applies knowledge gained from experiences in human and veterinary medicine, integrated into multidisciplinary studies that investigate the interactions between host, agent and environment of a given coral disease. These approaches include robust and precise disease diagnosis, standardised ecological methods and application of rapidly developing DNA, RNA and protein technologies, alongside established histological, microbial ecology and ecological expertise. Such approaches will allow a better understanding of the causes of coral mortality and coral reef declines and help assess potential management options to mitigate their effects in the longer term.
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.
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.
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