The review is limited to mostly colour vision and to mostly reef fishes. This ignores a large body of work, both from other marine environments and freshwater systems, but the reef contains examples of many of the challenges to vision from the aquatic environment. It is also a concentrate of life, perhaps the most specious and complex on earth, suffering now catastrophically from the consequences of our lack of action on climate change. Volume 95 , Issue 1. The full text of this article hosted at iucr. If you do not receive an email within 10 minutes, your email address may not be registered, and you may need to create a new Wiley Online Library account.
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Institutional Login. This dinoflagellate lives in epiphytic association with bushy red, brown and green seaweeds and also occurs free in sediments and coral rubble Hallegraeff et al. The dead coral and marine algae thriving in tropical and subtropical reef systems are eaten by herbivorous fish; these fish accumulate and concentrate the toxins produced by the dinoflagellate.
The herbivorous fish are eaten by larger carnivorous fish. During the passing through the food chain there is an oxidative biotransformation of the less oxidized gambiertoxins to the more oxidized and more toxic ciguatoxins Durborow, ; Lehane and Lewis, In the stomach of herbivorous fish, incomplete biotransformation of gambiertoxins to ciguatoxins could be seen. After accumulation in herbivores the toxins are transferred to carnivorous fish. Carnivorous fish have been shown to contain ciguatoxins and no gambiertoxins, indicating that any remaining gambiertoxins present in the herbivorous prey is completely biotransformed in the carnivorous fish Burgess and Shaw, In the literature, other dinoflagellates were also mentioned, which may play a role in the production of toxins associated with ciguatera poisoning such as Prorocentrum concavum , P.
The Caribbean C-CTXs and Pacific toxins P-CTXs possess closely related structures but are chromatographically distinguishable from each other, indicating that the ciguatoxins from the Caribbean Sea are members of another family of ciguatoxins. The presence of different families of toxins may underlie the differences in ciguatera symptoms found between the Pacific and Caribbean region.
It is likely that the Caribbean ciguatoxins arise from a small number of precursor toxins, similar to ciguatera in the Pacific where one gambiertoxin GTX-4A can give rise to at least four ciguatoxins which accumulate in fish. Probably different strains of G. It appears to be most prolific in the shallower waters away from terrestrial influences, with most ciguateric endemic areas being characterized by oceanic salinity waters De Fouw et al. Low salinity and high light intensities adversely affected G. Research on G.
De Fouw et al. Environmental studies suggested that the development of G. Population densities of G. Such growth patterns presumably underlie the spatial and temporal variability of ciguatera outbreaks. However, little is known of the precise environmental conditions that result in increased gambiertoxin production in nature De Fouw et al. In the Puerto Rico area maximum toxicity of the benthic dinoflagellate Ostreopsis lenticularis was seen in October to December preceded by several months August to September of exposure to sustained elevated sea surface temperatures lasting to an average of 20 days.
Spyraenea barracuda caught in this area in October to December showed maximum toxicity following 24 days of exposure to elevated sea surface temperatures during the preceding months August to October. Several factors may account for the correlation between increased sea surface temperatures and ciguatoxicity in fish.
Changes of two or three degrees in ambient temperatures would be expected to produce marked responses in respiration and metabolic rates, circulating hormones and predatory activity in a variety of fishes Tosteson et al. From February to December , Gambierdiscus spp. A total of 58 blooms were recorded of which 65 percent occurred in and alone. Seasonality in cell densities was found from February to May During this period Gambierdiscus spp. In contrast, salinity did not appear to be a determining factor in the seasonal abundance of this dinoflagellate.
The noticeable increase in both peak densities and frequency of blooms further noticed in and was preceded by unusually high water temperatures in January to April , concomitant with a severe coral-bleaching episode. Toxicity screening revealed that toxin production was maximum from October through December and no correlation was found between toxicity of the blooms and their biomass, nor the seasonal pattern of temperatures Chinain et al.
Lehane stated that the presence of G. Some research indicates that certain bacteria are found symbiotically associated with dinoflagellates and play a role in the elaboration of toxins by the symbiont dinoflagellates.
Coral and micro-benthic assemblages from reef habitats in Moreton Bay
It was suggested that bacteria might produce nutrients that were assimilated by dinoflagellates and were necessary for producing toxins. Another suggestion was the synthesis by bacteria of toxins which are then phagocytosed by dinoflagellates Lehane, Over the last decades, evidence has been accumulating that reef disturbance by military and tourist developments increase the risk of ciguatera by increasing benthic substrate for dinoflagellate growth Hallegraeff et al.
Although there seems no seasonal variation in the occurrence of ciguatera intoxication, according to some authors the frequency of ciguatoxic barracuda caught, varied seasonally, with peak values 60 to 70 percent toxic fish in the late winter-early spring January to May and autumn August to November.
Minimal frequencies 0 to 10 percent toxic fish were observed in summer June and July and December. The seasonal variations in barracuda ciguatoxicity may reflect variability in the toxicity of their immediate prey, as well as the capacity of their detoxification system the detoxification mechanism is inhibited by hormones produced in the reproductive cycle, and at reduced temperatures De Fouw et al.
The uptake and distribution of ciguatoxins was determined in Caribbean fish caught from to on the island of St. Barthelemy French Caribbean. Extracted lipids from several parts of these fish were analysed by mouse bioassays. The fish species belonged to the families of Muraenidae, Serranidae, Scombridae, Carangidae , and Sphyraedinae. The ciguatoxin concentration was highest in the viscera, particularly in the liver, spleen, and kidney, and lowest in the bones. The ratios of the toxin concentrations in the liver or viscera to that in the flesh were high and varied with the species suggesting that the toxin is distributed in different ways in different fish.
The fact that highly vascularized organs such as liver, spleen, and kidney retained the highest quantity of ciguatoxin per unit weight suggests that blood is involved in the distribution of ciguatoxin to other tissues De Fouw et al. Ciguatoxin becomes more concentrated as it moves up the food chain and its level is up to 50 to times more concentrated in the viscera, liver and gonads of affected fish than in other tissues.
It is not known why the fish are asymptomatic after toxin ingestion and how affected fish can remain toxic for years De Fouw et al. Toxins in tissues from the herbivorous surgeonfish Ctenochaetus striatus collected in the Great Barrier Reef were characterized by mouse bioassay and chromatography. The biodetritus on turf algae on which the fish feeds, were collected and the toxins present were compared with those found in C. It appeared that levels of gambiertoxins entering the fish were typically higher than levels found later in the liver.
Many species and many families of reef fishes are involved in ciguatera globally. These include the herbivorous Acanthuridae and corallivorous Scaridae parrot fish , which are considered key vectors in the transfer of ciguatoxins to carnivorous fish. Many more species of carnivorous fish cause ciguatera. These include Muraenidae moray eels and Lutjanidae snappers such as red bass which are notorious in the Pacific, Serranidae groupers including coral trout from the Great Barrier Reef, Epinephelidae , Lethrinidae , Scombridae mackerel , Carrangidae jacks and Sphyraenidae barracudas.
The latter two families are a particular problem in the Caribbean Crump et al. More than species of bony fish have been reported in the literature to have caused ciguatera poisoning. The larger carnivores such as moray eels, snappers, groupers, carrangs, Spanish mackerels, emperors, certain inshore tunas and barracuda are the most toxic IPCS, Along the southwest coast of Puerto Rico, the caught barracuda is involved in ciguatera poisoning.
Head, viscera and flesh tissue components of barracudas tissue samples were screened for their toxicity during the period March through May Twenty nine percent of these fish yielded toxic preparations in at least one of their tissue components De Fouw et al. In the continental United States, the grouper, red snapper, jack, and barracuda are the most commonly reported fish species associated with ciguatera poisoning De Fouw et al.
In Florida, in the majority of cases, the great barracuda has been involved in ciguatera poisonings between and Apart from the barracuda, other commonly reported species are snapper, hogfish, jack, and grouper De Fouw et al. In Hawaii, jack, black snapper and surgeonfish are most frequently involved with ciguatera toxin De Fouw et al.
In the Mascareignes archipelago, 34 fish species have been identified to be involved in ciguatera poisoning. Large predators such as grouper Serranidae 53 percent, Carangidae 10 percent, Lethrinidae 15 percent are mostly involved in CFP. Most toxic fish were caught by fishing offshore on coral banks located north of Mauritius De Fouw et al. An incomplete list of fish species associated with ciguatera is presented in Table 7.
A complete list would be nearly impossible because in some areas hundreds of fish species may be involved in CFP. Although the vast majority of ciguatera fish poisoning is seen after ingestion of carnivorous fish, other marine species are suspect in human ciguatera intoxication. Notably ciguatoxin was found in the viscera of a turban shell Turbo argyrostoma , a marine snail. This snail has occasionally caused ciguatera-like intoxication in humans IPCS, Invertebrates small shrimps and crabs may also be a vector in the transfer of gambiertoxins to carnivorous fish.
This suggestion was made based on a study with the often ciguateric blotched javelin fish Pomadasys maculatus which was found to feed predominantly on small shrimps and crabs in Platypus Bay, Queensland. Only shrimps contained detectable levels of ciguatoxin-like toxins detected by mouse bioassay. It remains to be established if shrimps are capable of biotransformation of the gambiertoxins to ciguatoxins or if this capacity is exclusive for fish De Fouw et al.
In Platypus Bay, inside Fraser Island, Queensland Australia , Alpheidae shrimps appeared to be an important vector transferring ciguatoxins to the small carnivore Pomadasys maculatus. Given the diversity of prey preferences among the families of carnivores, it seems likely that additional herbivore vectors of ciguatoxins will be identified in the future Lewis, The mechanism of action of ciguatoxins is related to its direct effect on excitable membranes.
Such membranes are critical to the function of nerve and muscle, mainly in their ability to generate and propagate action potentials. Ciguatoxins are characterized by their affinity binding to voltage sensitive sodium channels, causing them to open at normal cell resting membrane potentials. This results in alteration of bioenergetic mechanisms, cell and mitochondrial swelling and bleb formation on cell surfaces.
Cardiovascular effects of ciguatoxins were thought to result from a positive inotropic effect on the myocardium. Calcium is the intracellular trigger for muscle contraction. Although much of the increased calcium is buffered by the sarcoplasmic reticulum, it is likely that locally increased calcium concentrations increase the force of cardiac muscle contraction as is observed at ciguatoxin poisoning. A similar mechanism of ciguatoxin-induced intracellular transport of calcium occurs in intestinal epithelial cells. The increased concentration of intracellular calcium caused by ciguatoxin acts as a second messenger in the cell, as it disrupts important ion-exchange systems.
This results in fluid secretion, which presents itself as diarrhoea Lehane and Lewis, Maitotoxins are also produced by G. However, maitotoxins are approximately times less potent by the oral route compared with the intraperitoneal route, whereas the ciguatoxins are equipotent De Fouw et al. No specific blocker has been identified for this maitotoxin-induced channel. However, the primary target of MTXs remains still undefined.
It is strongly suggested that these toxins have no ionophoretic activity. Among natural products, maitotoxins have the largest molecular weight Da compared with any natural product known, besides biopolymers like proteins or polysaccharides. Maitotoxins also accumulate in the viscera of herbivorous fish, but obviously are not accumulated at sufficiently high doses in carnivorous fish to cause problems at human consumption. If maitotoxins were involved in CFP, qualitative differences in symptomatology might be expected, given that the pharmacology of maitotoxins is quite different from that of ciguatoxins Lewis, Various species of parrot fish have previously been reported to contain a toxin less polar than CTX-1, named scaritoxin.
Poisoning with scaritoxin is not well described. The name is derived from the poisonous fish Scarus gibus. Poisonings have two phases of symptoms, the first set of symptoms resembling typical ciguatera poisoning, the other, developing five to ten days after onset with failure of equilibration and marked locomotor ataxia De Fouw et al. Ciguatoxins are fat soluble and absorption from the gut is rapid and substantial, although an early onset of vomiting and diarrhoea may exist in expelling some of the toxins before they are absorbed.
Since cleaning ciguateric fish can cause tingling of the hands and eating them can cause altered sensation in the oral cavity and dysphagia, it would appear that ciguatoxins can penetrate the skin and mucous membranes. The related brevetoxins also have this property. Ciguatoxins are carried in the blood bound to human serum albumin and moderate unspecified levels of ciguatoxin in serum of a patient were reported 22 weeks after consuming ciguatoxic fish.
Ciguatoxins are also transmitted in breast milk and are able to cross the placenta and affect the foetus Lehane and Lewis, Sexual transmission of ciguatera from female to male penile pain after intercourse and vice versa pelvic and abdominal pain after intercourse has been described De Fouw et al. Dysuria, or painful urination, suggest that ciguatoxins are excreted at least in part and possibly unchanged in urine. However, such excretion could be neither rapid nor complete given the serum levels 22 weeks after poisoning. As ciguatoxins accumulate in the body, they may reactivate clinical symptoms from time to time.
If stored in adipose tissue, ciguatoxins are probably not a problem unless the tissue is rapidly broken down for example at rapid weight loss Lehane and Lewis, Because of their similar structure, ciguatoxins are supposed to behave in a similar pharmacokinetic manner to brevetoxins. To determine the origin of watery secretion and type of diarrhoea seen at ciguatoxin poisoning a study with male mice was carried out. Semi-pure ciguatoxin This definition deviates from the definition given below and in Table 7. To estimate the potency of CTX causing diarrhoea, it was compared with diarrhoea caused by the cholera toxin.
CTX was administered by gastric tube and intraperitoneal route at different doses. Diarrhoea and morphological influences on digestive tracts caused by CTX were observed microscopically. The results of the study revealed that:. Diarrhoea occurred by intraperitoneal treatment but not by per os treatment. It is likely that CTX given per oral route was absorbed and metabolised in a slightly different manner from that of intraperitoneal route, and therefore did not cause diarrhoea.
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Diarrhoea probably resulted from hypersecretion of mucus in the colon and accelerated excretion at the rectum, so only the lower portion of the intestine was affected. Diarrhoea stopped within one hour, the mucus secretion was stimulated even after 24 hours accompanied by an abnormal increase in the number of goblet cells. The type of diarrhoea was similar to that seen at choleratoxicosis.
The potency of CTX to cause diarrhoea was suggested to be about 1 to 8 times stronger than that of cholera toxin De Fouw et al. In mice, symptoms are well defined and hypothermia is a characteristic response. However, whether ciguatoxin has direct effects on the central nervous system and what its targets in the brain may be are not known. The action of intraperitoneally administered ciguatoxin 0. As a marker for neuroexcitability c- fos was used.
The effect of CTX on c- fos mRNA was investigated to establish a time course of action on the brain and its effect on the c- fos translation product was examined to identify specific neuronal pathways activated by this toxin. A pronounced decrease in body temperature was seen between 10 and 20 minutes after administration. Ciguatoxin causes a rapid induction of c- fos mRNA in the brain that corresponds with the decrease in body temperature. The primary targets of CTX appeared to be the hypothalamus and brain stem.
The results indicate that CTX has neuroexcitatory actions on brain stem regions receiving vagal afferents and ascending pathways associated with visceral and thermoregulatory responses De Fouw et al. Table 7. MTXs can induce slight watery anal secretion, but do not cause diarrhoea.
From Table 7. However the maitotoxins are about fold less toxic by the oral route than by i. Male ICR mice were given ciguatoxin or ciguatoxin-4c at a dose level of 0. Ciguatoxin-4c was not specified. Histopathological and ultrastructural changes of various organs and the modifying effects of several antagonists on the membrane permeability of sodium were examined.
The heart, medulla of adrenal glands, autonomic nerves and the penis appeared to be the target organs. There were no differences in clinical signs or histopathological changes in mice receiving ciguatoxin or ciguatoxin-4c. Ultrastructural changes in the heart after the administration were characteristic. Marked edema between myofibrils and other organelles was prominent. It is of interest that antagonists to cholinergic and adrenergic autonerves used in this experiment had no effect on cardiac injuries.
Therefore, the effect of ciguatoxin on cardiac muscle may be based on its direct activity on cardiac muscles. Despite the severe diarrhoea, there were no morphological changes in the mucosal layer of the small intestine but the autonomic nerve system in muscle layers of the small intestine was sensitive to the toxins. Pre-treatment with atropine prevented the diarrhoea caused by the toxins and therefore it was suggested that the diarrhoea is probably induced by a direct action of these toxins on the autonomic system in the small intestine.
No changes were seen in the cortical layer of the adrenal glands but degeneration of the medulla of the adrenal glands was prominent. Erect penises of treated mice were observed even after death. The precise mechanism is unknown, but direct or indirect effects of the toxins on penile cavernous bodies via autonomic endings as well as the formation of thrombi in the cavernous bodies may play a role De Fouw et al. The morphologic response of the mouse heart was examined after repeated 15 days low dose 0.
Furthermore the sequential changes of the heart injuries up to 14 months after either repeated low doses or after a single high dose 0. A single dose of 0. The effects seen after repeated exposure are similar to those observed after the administration of one single high dose. The prominent swelling of the endothelial lining cells is likely to cause serious alteration of the permeability, which may result in plasma migration from the degenerated endothelial lining cells into the interstitial space.
Within one month after the administration, myocytes and capillaries appeared to be normal.
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The effusion in the interstitial spaces resulted in bundles of dense collagen, which persisted for 14 months. The results indicate that ciguatoxin and ciguatoxin-4c have a cumulative effect on the cardiac tissue. This means that if there are repeated exposures to low doses of ciguateric fish, even the ingestion of fish slightly contaminated by ciguatoxin may play a role in the development of the heart disease De Fouw et al.
Experiments were carried out on nodes of Ranvier of myelinated nerve fibres isolated from the sciatic nerve of adult frogs. CTX-1b, the major toxin involved in ciguatera fish poisoning, was extracted and highly purified from moray-eel liver and viscera. The authors did not explain why they defined the ciguatoxin as CTX-1b. CTX-1b produced swelling of the nodes of Ranvier. D-mannitol caused shrinkage of nodes of Ranvier previously swollen by CTX-1b.
The papillary muscles were less sensitive to the toxic effects of ciguatoxin than those of the atrium. This corresponded to a fold difference in their sensitivity to positive inotropic doses of ciguatoxin De Fouw et al. After consumption of ciguatoxin contaminated fish, the onset of the first symptoms can be as short as 30 minutes for severe intoxications, while in milder cases onset may be delayed for up to 24 hours to occasionally 48 hours.
The first symptoms can be either gastrointestinal or neurological in nature e. Gastrointestinal symptoms usually last only a few days, while some neurological symptoms can take several days to develop. Ciguatera symptoms typically last for several weeks to several months. In a small percentage of cases less than 5 percent , certain symptoms may persist for a number of years.
These symptoms and a profound feeling of fatigue 90 percent of cases can occur throughout the illness. Severe cases can involve hypotension with bradycardia, respiratory difficulties and paralysis but deaths are uncommon less than 1 percent according to Lehane, The low fatality rate 2 percent appears to arise because fish rarely accumulate sufficient levels of ciguatoxin to be lethal at a single meal, perhaps because fish succumb to the lethal effects of higher ciguatoxin levels Lewis, Lehane and Lewis noted that most cases of CFP in the Pacific involved the consumption of fish containing 0.
Neurological disturbances usually resolve within weeks of onset, although some symptoms may persist for months or even years. Symptoms such as pruritus, arthralgia and fatigue can also persist for months or years. Analysis of ciguatoxins in blood samples suggests that the toxin can be stored in adipose tissue and that symptoms may recur during periods of stress, such as exercise, weight loss, or excessive alcohol consumption.
Sensitivity to alcohol may also persist for years after the first attack Lehane, The phenomenon of sensitization has been observed where persons who previously were intoxicated with ciguatoxin may suffer a recurrence of typical ciguatera symptoms after eating fish that do not cause symptoms in other persons. It was also noted that individuals who had suffered from CFP, often have symptoms after eating any seafood and often nuts, nut oils and alcoholic beverages as well.
Therefore patients suffering from CFP are recommended to avoid these food products. Eating fish with low levels of toxin over several years in the absence of symptoms could eventually result in sensitization to the toxin. This may be a matter of accumulation of ciguatoxin in the host or possibly an induction of an immunological reaction De Fouw et al. Large variations are noted in the frequency and severity of the symptoms after ciguatera poisoning. Ciguatera case reports from the Hawaii State Department of Health were examined for patterns of symptomatology in relation to the types of fish consumed.
It may be postulated that the carnivores feed on different herbivores or metabolise the toxins from the same prey to more or less active forms De Fouw et al. Though variation in symptomatology is possibly the result of inconsistent reporting, it has also been speculated that it relates to differences in toxins within the same contaminated fish. Some authors reported that the symptoms correlated with ethnic groups. It appeared that Melanesians more commonly had pruritis, ataxia, abdominal pain and weakness, that Europeans experienced more neck stiffness, lachrymation, arthralgia and reversal of temperature sensation, and that Asians had more diarrhoea and abdominal pain De Fouw et al.
In the Pacific Ocean, neurological symptoms predominate, while in the Caribbean Sea, gastrointestinal symptoms are a dominant feature of the disease. These differences in symptoms provide clear evidence that different ciguatoxins may underlie ciguatera in Pacific and Caribbean waters. A third class of ciguatoxins is likely to underlie the different pattern of symptoms observed in the Indian Ocean where ciguateric fish cause a cluster of symptoms reminiscent of hallucinatory poisoning including lack of coordination, loss of equilibrium, hallucinations, mental depression and nightmares, in addition to symptoms typical of ciguatera.
Ciguateric fish in the Indian Ocean are also more frequently contaminated by lethal levels of toxin Lewis, Neurological symptoms: paresthesia is found in 36 percent of cases in US Virgin Islands, 70 to 76 percent in Australia and Miami, and in 87 to 89 percent of cases in French Polynesia, Fiji and the Caribbean area De Fouw et al. Gastrointestinal symptoms: diarrhoea appears to be common in 32 percent of cases in Fiji to 86 percent in other regions De Fouw et al. Cardiac manifestations: Bradycardia and hypotension are reported in French Polynesia 16 percent and Fiji 9 percent De Fouw et al.
The toxin responsible for ciguatera in the Gove region of Northern Australia is the same as the major toxin responsible for poisoning from carnivorous fishes in the Pacific Ocean but differs from the toxins involved in the Indian Ocean and the Caribbean Sea De Fouw et al. Four men became ill after the ingestion of freshly caught trevally and coral trout a few hours before the characteristic symptoms of ciguatera poisoning developed.
Ciguatoxin is transferred across the placenta from mother to foetus. It does not affect foetal development but has been attributed to accelerated foetal movements. It can also pass from mother to infant via breast milk. Mothers who breast fed their babies had reported excessive pain of their nipples. The babies showed diarrhoea.
Excellent otherwise. What is the point of having a Liberal government in Austrailia or a Republican one in the USA if they pursue bad policy based on lousy science. Does Mr. Turnbull have an answer? We found ours last go round.
Best Wishes to our Aussie friends. Reblogged this on Wolsten and commented: An excellent analysis of Hughes Probably not surprising that the impact of falling sea levels was ignored when the prevailing dogma has them rising inexorably. SPS corals which make up most of the corals you see in these bleach images are very sensitive to light spectrum changes and falling sea level would cause such a problem which the corals naturally adjust to.
One of my MSc students undertook a research project a decade ago looking at managing the coral reef fish resources for the Federated States of Micronesia. One of the local concerns was about the impacts of global warming on the coral reefs. The focus was on bleaching due to elevated temperatures, particularly following a severe event in We compiled all available data for Pohnpei on ocean and atmospheric conditions and bleaching events. The students analysis showed that severe bleaching coincided with a shift in dominant wind direction with an associated change in wave patterns, a drop in sea surface and air temperatures, a decrease in rainfall and a large decrease in sea level 30 cm below MSL.
Our conclusion was that the bleaching was primarily due to sea level fall exposing the upper reef to the atmosphere and UV. It was not a well received conclusion. A thought for Jim Steele to follow; The Australian tectonic plate is moving towards New Guinea at around 24mm per year and has been doing so since it broke away from Antarctica. As it does so, it is rising against the northern plate so that the Torres Strait is one of the shallowest seaways in the world. This movement could cause the sea levels to fall the further north you go.
If you look at the Great Barrier Reef Marine Park Authority colour coded chart, this seems to be represented with most bleaching to the north and least to the south. It would be interesting to see if the sea levels at the various monitoring stations reflect this. As you know, technically southern New Guinea is on the Australian Plate.
This big, continental plate meets a bunch of little plates in northern New Guinea, forming the Highlands, and the Bismarck arc, site of some big, active volcanoes. The FALL, even a regional one, is extremely inconvenient. Thank you for your most insightful article on corals. Jim, you may be interested that there was a mass mortality of mangroves in the Gulf of Carpentaria last year also caused in part by a temporary drop in sea level associated with El Nino.
It was a huge event. I should add that I have looked at many of the videos of the bleaching taken from aircraft and it is difficult to see how the figures that Hughes presents are credible. In addition a parallel survey of GBR bleaching done by tourist operators indicated far lower levels than reported by Hughes team.
It looks like another example of results we cannot trust. The effect of lower sea level on mangroves is definitely interesting. If you could send me the original paper I would be grateful. Its always refreshing to see a scientific article which looks at the data first, and then makes hypotheses second.
There is not a lot of that approach in the climate fraternity. It even more refreshing when that study explodes a dogma well past its use-by date. On a scientific point, a m sea level rise in the last 20ky after the last ice age peak means that all current corals down to m didnt exist 20k years ago, and the shallower colonies are very young.
Isotopic age studies on corals must be particularly illuminating. I have snorkeled out there twice and it is breathtaking as you dive down deeper. The GBR is a living thing. In ideal conditions the coral grows wider and higher until it gets close to the surface where it is exposed to the sun more often during low tide. Naturally its vivid colours will become bleached. But of course there is no funding in this sort of story. Have there been studies of coral exposure on the eastern pacific coastal areas Baja, or wherever coral is found?
Do La Nina periods leave corals along the western Americas exposed? If so, perhaps there is complementary bleaching in opposition to the bleaching in the western pacific. Anyway, thanks Jim Steele for another intriguing science piece. Seems like a strong case to explain surface bleaching. So sea level rise is levelling off and the Climagesterium is trying to conceal the fact. This could get interesting. The information I think the public needs includes the alternative causes for a particular effect.
It is only when you have an idea of the other things besides warming that can have an effect that you can counter their arguments successfully. This article provided that information. And you are so right — no one has heretofore even mentioned sea level in relation to coral bleaching on the GBR — no one. They also fail to mention that it is almost exclusively near-surface corals that are affected by bleaching events — those at what I call snorkel-depths — less than 15 meters. Not only do most tropical reefs include vast areas deeper than 20 meters 60 feet , but huge areas of deep sea reefs exist in all oceans — which can be found as deep as 2, feet.
As someone who lives in Cairns, the main GBR tourist city, it was very disappointing to see the immense media coverage that Hughes et al received. It did a lot of damage to tourism. About the same time as the bleaching event I read a very brief news story of mass mortality of mangrove tress on the south-east corner of the Gulf of Carpentaria, i.
The reason given for the mortality was extreme low sea levels. There is a tidal gauge at my local pier Palm Cove so its not as it sea level information was not available to Hughes et al. This is a very popular pier with locals in northern Cairns and is only a few kilometres from JCU, so Hughes and his colleagues will know of its existence. To Jim Steele, Guardian has an April 9 article declaring another bleaching event in No mention of falling sea level.
Includes aerial photos of coral exposed above the water, and bleaching primarily on the tops of the coral. This appears to be propaganda if the original authors knowingly ignore data that refuted last years claims, and double down this year.
And, the same on the BBC news this evening with an interview of Hughes and, what seemed to me, a nervous woman from, who I think was, from Bristol Uni being a little more cautious. JS A well worked piece. Most informative indeed. Thank you for your efforts. You have set me quite a task to read and understand all of the references.
Today the BBC fawned all over Huges in a piece which is pure warmist propaganda. Flawed work produced either willfully or incompetently is certainly no impediment to funding or career as long as it promotes the religion! I am not a conspiracy theorist but the frequency with which bad research on this subject despite being shown to be flawed continues to be promoted, seemingly immune to critical question suggests some very powerful forces are at work.
The fact that so many sheep believe in this fiction is sad. Bleached corals do not grow, they do not reproduce, they have lost their food source and energy. Starving not worrisome? The fact that the denialists are so hopeful that widescale bleaching is not glaring obvious example of the destruction of climate change that they prop up Jim Steele, a nature walk expert, is unseemly. He is a charlatan, and pretending that the Great Barrier Reef is not bleaching due to anything but climate change is poppycock.
Tripp also worked in government relations for The Washington Group and The Livingston Group where he represented Fortune companies, trade associations, and non-profit organizations. Tripp received his M. Other than surroundign himself with people who on this coral foundation, he appears to have no scientific training, unlike Jim Steele, otherwise he would not have to resort to to ad hom attacks on Mr. Given coral is his sole source of employment, this famous quote is applicable to Tripp.
Trip is a business major overseeing their operations. The tremendous loss of staghorn and other Acropora sp coral in the Caribbean due to disease and predation makes it difficult for those species to recover because they reproduce mostly by fragmentation. A complete loss of staghorn on a reef usually means that reef needs to be colonized from a fragment from another reef. Coral Restoration Foundation collects living staghorns breaks them up into many smaller pieces and grows them and then replants them. Thanks for this info, Jim.
I just sent this to the Coral Restoration Foundation. The Australian mainstream media slavishly follow the alarmist meme — to the detriment of genuine and meaningful understanding of our precious marine ecosystems. Jim I am very sorry you had to put up with such childish behaviour.
If bleaching persists then mortality will follow. If bleaching is temporary, then observation after observation reports recovery to pre-bleaching conditions and every thing Trip is worried about is no longer a problem. Not being a biologist such simple facts elude him. A must read to educate and prevent further misleading great barrier reef hysteria and subsequent ad-hoc and misguided Coral conservation policies…. Like this: Like Loading Related posts. Not enough stars for an exceptionally clear rebuttal.
Thank you.! JS … they probably did the aerial survey at low tide with the sps exposed. Doom and gloom? I suspect GBR is well and in good shape then! Best wishes to you! It would appear Hughes et al. Jim Thank you very much for your outstanding research. How long does it take a coral to evolve? Because they have all evolved to use bleaching as a survival tool…….. Coral use forest fires to survive? I looked into the subject very superficially last year because it appeared to me that the places in the Pacific where El Nino coral bleaching was being reported seemed a rather dubious match to the elevated El Nino sea surface temps that were purportedly responsible I came away feeling that: 1.
So, how good are the numbers? Thanks, Beliaik. Cheers, Beliaik FNQ. Why is that better than pumping cold water in? Hi Peter, The effect of lower sea level on mangroves is definitely interesting. Just bought his book. People who can think critically need to be encouraged IMHO.
Oh my goodness. Yer a real badass Mr. Steele ;. So… Do La Nina periods leave corals along the western Americas exposed? Excellent article. Duly bookmarked. Science is a truly wonderful thing but politically adulterated science is abominable. Trip is now calling my house, dropping F bombs and launching insulting rants. And this brings me to the reason for my message to you today. Sorry, your blog cannot share posts by email.