It's hard to say where this acronym, "RTN," came from.

I have heard that it originated from Stan Brown, honorable "pioneer" of the Breeder's Registry. I have also heard it began among some of the hobbyists on CompuServe's FishNet forum.

Regardless, this term has become one of the most recognized terms in reef aquarium keeping over the past several years. This is quite ironic considering it is a "non-term,"

...that is to say, it is only a description of a mode of coral death that affects certain species.

Descriptive and accurate, to be sure - but a term which gives a certain air of authenticity to a condition which is still very far from being understood or accepted as other than a non-sequitur.

It's nice to be here, and we hope you enjoy tonight's presentation. I (Eric) will be delivering the text first, so the lecture may sound a bit one-sided - it isn't! <g>

Our History with this Coral Malady

In 1992, I acquired my first colony of Acropora from a small pet shop in Birmingham, Alabama.

I didn't know much about the requirements of this coral, as this was not exactly the stuff of captive propagation at the time. Acropora occasionally appeared on mail order price lists, but was rarely available.

I put this smallish, brownish colony mid-way up in a 55 gallon tank lit by four 40 watt fluorescent bulbs. The coral did not seem to be doing well for almost a month - a little recession, poor polyp expansion, etc.

One morning, I awoke to find the coral completely white.

Wow! What happened? I had lost corals before, but not so fast!!

Several other tries with this coral genus, as well as some Pocillopora damicornis, resulted in roughly the same fate - sometimes survival was a couple months, sometimes less than a few days.

I never had more than one specimen in the tank at a time as these guys cost darn near $75.00 each in those days, so they were expensive sacrifices. I continued to see this type of death even after acquiring metal halides (2 x 150 watt 6500K) a year or so later, but eventually I found a few colonies to survive and look quite healthy for some time.

But, invariably, I would add another couple pieces to the tank, usually quite near the others (as I had figured out they preferred high light and water flow), and I noticed that if one died in this overnight macabre fashion, sometimes more than one would die with them.

Guilt weighed heavily on my conscience. I tried dips and antibiotic pastes and baths and all sorts of odd treatments but never found a good "recipe" for success - occasionally saving one, usually losing them in a cloudy quarantine tank full of stinky mucus and medicine.

A few years later, other aquarists started talking about this phenomena, and the catch phrase "RTN" was coined. I thought, at the time, it was a pretty good description of what I had been seeing.

At about the same time, Jonathan was onboard a research vessel in the Florida Keys doing studies on coral reef recovery following a hurricane, and was using Acropora cervicornis as one of the coral models.

He had subjected these colonies to various stressors, including chemical stress, temperature stress, sedimentation, etc., and had logged various levels that would cause the death of the coral - nothing too fancy, but enough to assess the impact of the hurricane in the study.

A few years later, he did some other studies on coral tissue necrosis for another reason - neither at all related to aquariums or "RTN." Jonathan was not really an aquarium hobby person at the time (and really still isn't).

We met as pet hosts for the Fish and Marine Life Forum on America Online and eventually started sharing some stories. Having hashed out this mysterious problem, we found that we both shared some similar thoughts and observations - mine based on aquarium husbandry, his on his own work.

We half-heartedly bantered about it, eventually beginning to use the term "RTN," along with the rest of the world. Imagine our surprise when we heard some mumblings that a bacteria had been found that caused "RTN."

Wow! This "disease" displayed very little that exemplified bacterial disease, especially in terms of common observations of the masses - not to mention our own.

We kept asking each other , "Well, if its bacterial, then why doesn't it respond to antibiotics?" And, "If its bacterial, why does it act like this, and why doesn't it do that, and what about when this happens, and have you ever noticed that....." You all get the point, and they are the exact same points that bother hobbyists today, and which are discussed periodically with fervor.

Not to mention, we had already been planning on trying to elucidate what causes "RTN," and if there was a bacteria that caused it, it would sure throw a monkey wrench in our plans! <gg>

Furthermore, a bacteria like this, if it existed, would form the basis of some disease etiology that would certainly be the first of its kind in all the world - the bacteria and the "founders" would be famous - cover of Science, no doubt!

By this time, though, I had already long acquired an almost obsessive interest in coral disease and was starting to amass a substantial amount of literature on coral immunology. I started sending Jonathan boxes of papers and we started going to work........But we'll save that for later...hang tight!

RTN as a Coral "Dis-Ease "

We hesitate to use the word disease to describe "RTN," except in the sense that it is a breakdown of the normal function of the organism. Unfortunately, we of Western thought tend to equate disease with such things as a flu virus, cancer, leprosy, etc.

As such, we also tend to think in terms of: cause--->disease--->cure.

Not only is this often incorrect with both human and veterinary disease, but it appears to hold true for corals, as well. "RTN" is not a disease - at least not a recognized one. "RTN" is only considered to be a disease by the cumulative anecdote of the aquarium hobby.

To repeat - outside of our hobby, there is no such thing as "RTN."

Coral diseases are well recognized. The first coral disease was recognized in 1973 by Arnfried Antonius and was called Black Band Disease, or BBD. Since then, and up to even a few months ago, new diseases are being reported with increasing frequency.

Some of these are:

• BBD - Black Band Disease
• WBD - White Band Disease
• YBD - Yellow Band Disease
• BBD - Brown Band Disease
• RBD - Red Band Disease
• YLD - Yellow Line Disease
• RWD - Rapid Wasting Disease
• WP - White Plague
• WP Type II - White Plague Type 2
• White Pox
• Yellow Blotch Disease
• Patchy Necrosis
• Stress Related Necrosis
• Shut Down Reaction
• Aspergillosis

Corals can also get protozoan infections (brown jelly), succumb to bleaching related necrosis, and can even get true neoplastic tumors!

"Coral Cancer!"

With most of the above diseases, there is a very distinct appearance to corals with the respective disease, and they show fairly regular signs of disease.

For some, accumulations of microbes and other organisms may be found responsible for, or present on, diseased corals. For example, BBD always has a self perpetuating band of organisms that include Beggiatoa sp. - sulfur oxidizing bacteria, Phormidium sp. cyanobacteria, various bacteria, algae, and a host of other organisms who come to dine on "coral off the bone, saut饤 in a light sulfur reduction."

Most of the diseases have environmental or stress-related issues that factor into the appearance of the disease, with some of the causative organisms not even being typical of the reef or even marine systems.

Necrosis, if present, is often found in bands and local areas of eroding skeleton, or is simply partially digested and sloughing tissue. The rate is variable, but rarely are entire sheets of intact tissue simply lost from the skeleton as we see in "RTN." Most microbes tend to dine on coral tissue, not cause it to simply release from its skeletal attachment.

Once sloughed, further tissue digestion and decomposition takes place rapidly, however.

In terms of "RTN," the most interesting diseases are White Band Disease and Shut Down Reaction.

WBD can become an SDR under chronic and/or acute stress, and the descriptions of SDR (except the most often reported species it affects) are remarkably similar to what we call "RTN."

SDR, like "RTN," is contagious, rapid, and very fatal. Also, no pathogen has been isolated from SDR cases.

Furthermore, Jonathan and I have reversed the process, having many "RTN" affected corals slow to signs that resemble a WBD type disease.

I keep using "resemble" and "looks like" because we do not know the relation, if any, that the condition we call "RTN" has to any known coral disease, or if necrosis is a just a common sign of many diseases.

There are only so many ways for a coral to die.

In fact, there are many reports of coral mortality in the wild that have remarkably similar descriptions to what we call "RTN," and these have been often attributed to various environmental stressors such as heat, oil, sedimentation, UV light, transplantation, allelochemicals, etc.

In many of these cases, the sensitive Acropora spp. and Pocillopora spp. are most affected and often the first to die.

Furthermore, there are many studies - including those with the aformentioned SDR - that have attempted to explain the mortality as disease, yet have found no causative agent or organism outside the stress. This also holds largely true with WBD, which Jonathan will cover in a moment.

Finally, we cover the bacteria.

Coral mucus, as I discussed in my last talk here, is the site of a plethora of marine microbes, many of which have the potential to be pathogenic.

One of the most common inhabitants of coral mucus is Vibrio alginolyticus, which can be pathogenic. Of course, coral larvae may also settle in response to the biofilm produced by V. alginolyticus, so what does that tell us? <gg> Yet, there is not a single disease, even under stress, which is attributed to the action of this microbe.

In fact, corals produce a variety of antibiotic substances (perhaps secondarily) against various bacterial species - it has been proposed that those which are most "non-native" are the most affected, with gram-positive strains being most affected.

Oddly, the gram-negatives seem to pose the greatest threat, yet corals don't seem to mind their presence, and the bacteria growing on their surface actually play very significant on their normal metabolic activities - many positive ones, too.

Yet, under stress, the pathogenic tendencies, the number and types of species present, as well as their rapid growth on excess mucus secreted by stressed corals, can all affect the overall health of corals. BUT, the condition we call "RTN," despite possibly having bacterial components, is not caused by any single type of marine microbe. Jonathan will take it from here.

What RTN Isn't...

In a necessarily skeptical world, one must look at proof - the evidence of a statement. What we were attempting to prove was that the condition of RTN is possibly immunological, and not bacterial or viral in nature.

Taking a similarly skeptical approach, I developed a multi-step process to show what RTN isn't. One of science's original means of proving biological disease is called Koch's postulates.

This is a series of steps that must show all of the following:

a) the microbe in question must be present in all diseased hosts (not one or two cases)
b) the microbe must be isolated and grown in pure culture.
c) upon reintroduction, the microbe must produce disease, and
d) re-isolation of the organism, grown in pure culture, must be the same as the original organism.

Based on these postulates, I have conducted numerous studies into the origins of RTN. It is not bacterial.
To be bacterial, we would expect to find an abundance of pathogenic bacteria on sick colonies. In fact, we would expect to find the same bacteria on all sick colonies.

Also, we would expect that if we took a sick colony and a healthy one, and filtered out all bacteria, that transmission of the disease would stop.

My experiments showed that a variety of bacteria exist on healthy and diseased corals. Statistically, no one type of bacteria were present in higher numbers on sick colonies.

Some unusual species were found on both sick and healthy corals that were non-native to marine environments. In addition, there was less bacterial diversity on sick corals than found on healthy corals, although the total bacterial numbers in some cases was higher or lower.

Of the species cultured, some were considered to be 'pathogenic,' but were also found in moderate numbers on healthy corals. Interestingly enough, the 'bad bugs' were found in fewer numbers on many sick colonies, with more 'good' bugs present.

These experiments were conducted with controls, and using aseptic (sterile) techniques. A variety of microbiological culture media was utilized, including Tryptic Soy Agar/Salt, TCBS, Photobacterium Agar, Blood agar/salt, Nutrient agar/salinity tolerances, TSA agar, and in lesser numbers a variety of other media in accordance with various protocol.

Samples of over 400 individual colonies were taken in numerous studies, representing many species of Acroporid and Pocilloporid corals.

The results closely matched those conducted by Kim Ritchie in independent analyses looking at normal flora on coral mucus in both healthy and diseased (WBD) colonies.

She had found a trend from Psuedomonas --->Vibrio in necrotic areas near the "band" and suggested that Vibrios seem more capable of and successful in utilizing the dying tissue as substrate material, but did not suggest that they were responsible for disease. She also found fewer bacteria in type on necrotic tissue than on healthy tissue - similar to what I found.

Interestingly, Dr. Ritchie also recently appeared on a Scientific America "Frontiers" episode and discussed coral disease. She is now also focusing on immunity as a potential cause of other forms of disease that afflict corals.

Other experimentation showed that a bacterial vector may be blocked and still allow transmission of disease. Although these tests ruled out bacteria, they are inconclusive for the causative agent.

They did filter some virus, but not all, and they allowed all bioorganic and inorganic molecules to pass though unfiltered. These experiments involved induction of 'RTN' in healthy conspecifics and congenerics (same species and/or same genus) using contaminated mucus and water from a tank with a diseased specimen.

Using a variety of micron filters, sieves, and UV sterilization, we showed in two concurrent and independent studies that water from the diseased corals COULD induce "RTN" in healthy corals. Water column bacterial counts and cultures showed a nearly sterile environment, so no free floating bacteria could have caused the disease.

We do not rule out the potential that any of a myriad of bacteria could be acting as primary or secondary agents of disease, or as stressors in certain cases, especially those corals exuding excess and unflushed mucus (such as during shipping in stagnant water bags).

However, based on these series of experiments, we can assume that "RTN" is NOT caused by bacteria, but by another agent, event, or combination. The necrosis event is somewhat easier to explain by models involving the loss of cell adhesion (heat stress, polyp bail outs, etc.), but the contagion among certain sensitive species is the most interesting.

There would seem to be an effector of the necrotic reaction, much as with "SDR." Furthermore, the necrosis is unusual in both its rate and its pattern - quite different from most true coral disease. Further research is ongoing in an attempt to classify the potential substance that initiates "RTN" in healthy colonies.

One hypothesis we feel shows merit and is supported by many studies is the production of a bioorganic molecule(s) that elicits an immune response from another coral.

Additional research is also needed in applying Koch's postulates to such an unknown 'biological' vector. This vector could be a small virus, or bioorganic molecule. As research continues, we will gather new information.

We are also attempting to show a cellular mechanism for the necrosing reaction, which we feel may involve the reversal of the calcification enzyme, carbonic anhydrase, followed perhaps by the invasive action of the many normally present microorganisms.

What can be done

It is apparent through our trials and the reports of many who have attempted to treat "RTN" corals that antibiotic therapy will not work in most cases.

Some therapies to try are dilution, absorption and isolation. We have found them to be reasonably successful in slowing or stopping "RTN."

However, there also seems to be a point in the progression of the condition where the coral is no longer able to be saved. Many observations allowed us to find a number of pre-necrotic changes that seem to occur with some regularity - these include thickened mucus, some darkening or a pinkish-brown hue to the tissue, and an increased odor.

In addition, it's good to check all water quality parameters and look for signs of stress. If a biological trigger is present, dilution will potentially lessen the concentration and/or stop the reaction. Much the same as a human suffering from chronic allergies feels relief as they move indoors away from the pollen, the reaction seems to subside in corals with "RTN" when isolated or subjected to dilution.

Absorption is another possible action we have used with some success, possibly from the ability of media to remove certain bioorganic molecules. We will also be attempting to use various blockers of CA activity in future work.

Lastly, isolation works quite well. This is just a means of taking dilution to an extreme. Keeping regard to proper husbandry and care, isolation of an affected coral in freshly made circulating sea water seems to have the best effect. By placing the coral in a totally new environment, it accomplishes much of what the first two methods do, but to a greater degree.

Fragmentation also works, and is especially effective when the fragment is made well ahead of the advancing necrosis and then isolated from the affected system. If left in the same system, the chances for survival are much less.

Antibiotic therapy and dips, we have found, are mostly hit or miss, but seem more likely to be beneficial where conditions of stagnation have been present. Such therapies also further stress the coral, possibly lowering its own ability to naturally combat disease.

Lest anyone lose hope if they have an outbreak of "RTN," it is very possible for a healthy system to have an outbreak and have it resolve naturally.

I have two colonies that have survived such an event outside of experimental work, and I track their progress. In fact, after a recent addition of new corals following a move, a previous "RTN" survivor experienced "RTN" again, but only on the branch with new growth.

The old growth and recovered tissue loss regions remained unaffected - is this immune memory?
Corals have been shown to have short term immunological memory, and so this is a possibility.

The coral has since responded to dilution and absorption protocol, and is regaining lost tissue daily.

Summary

Like Jonathan, I have seen similar results with spontaneous recovery, slowing of the "RTN" response, and mortality despite all efforts. There are many questions to be answered yet, and we both feel the implications of "RTN" are far-reaching.

We feel this response to be mostly a reaction to various stressors - chronic or acute.

We do not feel that "RTN," is a single disease, and we know it is not caused by any particular agent. Some cases may indeed have a single agent as the impetus for the reaction, but it is not universally present in the hundreds of corals we have examined.

We also feel that the hobby may have provided for the observations of conditions rarely seen in the wild, but which may have real meaning to wild coral disease, especially as natural reefs become subjected to ever increasing stress.

For this reason, we have begun contacting many authorities in the field hoping to gain new insights. We will be continuing our work as time and funds allow, and hope our abilities and the aide of others will soon provide more definite answers to what we all have come to know as Rapid Tissue Necrosis.............

..............it is kind of catchy, isn't it?

Thanks, everyone!

Eric -n- Jonathan

When starting these studies did you come up with a 'protocol' for inducing RTN or did you just use corals as they came down with it?

Eric: both - some of Jonathan's early work was inducing disease - others studies we did as we saw or obtained corals with active RTN

Jonathan: Well, as was mentioned, my first research was not aimed at RTN per se, but other natural stressors on corals.
The protocols developed were to test stressors on corals. Later, we did develop a protocol to test RTN induction.
We also used MANY samples of corals that were showing clinical signs of the disease.

Dana Riddle showed some pictures of corals with bacteria living inside the tissue. What studies have been performed on them and can they be causative?

Jonathan: Well, we know what species many are. Besides us, many other coral researchers have cultured 'normal flora' in corals. Again, the work we did involves culture of the various bacteria on sick and healthy corals. As for pathogenicity, this was material referenced from work done by others.

Eric: This gets back to the core issue... what exactly are we looking at - are they all the same instance or different. Bacteria are normal to corals, and sick corals may well have opportunistic bacteria in the necrotic areas - this does not imply causation. I would like to hear full details of this, and I could perhaps comment better.

Is there any possibility that RTN is like the common cold, i.e. it is caused by a variety of agents, therefore no specific agent can be found, but it is still bacterial/viral in origin?

Jonathan: Actually- the common cold is caused by a Rhinovirus, although many forms of it. So, relating in that sense COULD be misleading. We have ruled out a virus to some extent. Also, based on vector studies, it seems not to be a virus.

Eric: Given the amount of literature documenting similar necrosing events under stress, it is not likely. If, for example, one applies significant heat to a colony, it will lose cell adhesion much like "RTN" - our studies isolated bacteria and yet we could still induce the reaction - the role of bacteria/virus is probably important, but is almost certainly not required.

What environmental factors seem to contribute to RTN?

Eric: the important thing is that this reaction can be caused by many factors, yet the mechanism, susceptibility, and each case may be quite individual in nature. Certainly things like shipping stress weigh heavily and overcrowding, substrate stirring ( redox/O2 changes), power failures, etc. I am sure most who have experienced RTN have noticed that this is often a time when you see "RTN" and, of course, after adding new corals.

Jonathan: In nature, you don't commonly see this type of problem.... But in a closed system you do, yet often the stressors can be similar. You can get temp flux, sediment stirring, poor water, etc. IME, the new coral can cause it in older corals, or the new coral can be afflicted.

Does RTN occur more often with newly introduced specimens?

Eric: Yes and no - we often see the reaction in older colonies after a new one has been added. Also, after something "wrong" happens in the tank. Sensitive species are affected first. But, the most reported time is after new additions - I think statistically because that is the most common stressful event.

Is it very likely that a well established tank with no new specimens will have an "RTN" outbreak?

Jonathan: Well, that is not an accurate way to quantify how RTN occurs. It is less likely if the corals are situated in regions that do not encroach on one another. Yes, it CAN happen, but usually there has to be a 'triggering' event, such as a coral being moved, or introduction of new corals. Sadly, this type of study relies on anecdotal evidence supplied by hobbyists and can be hard to compile.

Eric: provided that the tank maintains stability, the chances of this happening, IME, are markedly lower.

What's a dealer to do to prevent "RTN" for new arrivals?

Jonathan: Quarantine. If possible, keep corals in constantly circulating water with replenishment (the dilute factor) . This is not practical for many however. Knowledge about what species to mix in what tanks, and proving stable husbandry for the species will also reduce outbreaks.

Eric: To be honest, I think that new arrivals have the highest likelihood of having bacterial cause of RTN - the bacterial numbers in the stagnant water increase dramatically as the coral produces a ton of unflushed mucus. The bacteria present can overwhelm the metabolism of the coral and cause necrosis. It does not imply that bacteria are the ones actually causing RTN, but act as secondary agents, perhaps so, my advice would be flush them well outside of any main system, dips may be advisable for some cases, and, of course, quarantine if possible.

Jonathan: I have also cultured bag water from new arrivals, and found a similar flora to that of a healthy coral.

Is RTN strictly seen in what we call SPS corals, or this occur with LPS corals as well?

Eric: There seem to be certain corals that are almost always affected first both in the wild and captivity. Among these are, obviously, the Acroporid and Pocillopriods. Yes, these do seem highly susceptible, and I think part of the reason is that their polyps are not deeply imbedded as with, say Montipora sp. But "SPS' is a misnomer because some "SPS" corals seem very resistant to sloughing events, while some "LPS" seem very susceptible - the relation is not known. But some corals, like Trachyphyllia, seem to get what appears to be an "RTN' type reaction quite often and, if you look at descriptions of SDR, and, in fact, many of the more well studied true coral diseases they mostly affect what we call "LPS" corals. So, until we know if "RTN" is a true event or a sign of stressed coral and merely "coral death" it is not possible to say except in that certain corals are far more sensitive .

Eric, you mention dips, can you delve more into that, mixtures, species to dip, times etc etc?

Eric: gosh, I strongly hesitate to recommend any protocol at this point, because it is so experimental. If you have a coral that has been in a bag for a long time, without water movement, looks stressed, bag full of mucus, a standard Lugol's type dip might help reduce the total bacterial numbers, but is NOT a treatment. Outside of that, I do not want it being misconstrued that I am advising dips for RTN ;-)

Where can we read further on coral diseases?

Eric: One of the best discourses and up-to-date places is the chapter by Esther Peters in "Life and Death of Coral Reefs", ed. Charles Birkeland. There is also a very good review in the Proceedings of the 8th International Coral Reef Symposium by Esther Peters and DL Sanatavy. If you want just about every coral disease article ever done, email me after this, and I can send you a very looooong list.

No environmental factors seem more guilty than others for RTN?

Jonathan: Well most of my work was conducted at stable temperatures, but anecdotally this has played a role with others. As for other factors, the obvious poor lighting, husbandry (ammonia, pH, lack of Ca, etc) play a role with all disease.

Eric: I cannot add to that - one of the areas I would like to address in future work is the type/level of various stressors to bring about necrotic events on different species.

This goes along with the recent article in Aquarium Frontiers, but what about this idea if sand stirring causing RTN? I was under the impression that many people feel that stirring sand is beneficial to many corals as it released nutrients into the water column.

Jonathan: I have not yet had the chance to read the AF article, so I cannot comment just yet. I can add that sand stirring is a natural process that occurs FREQUENTLY on reefs in nature.

Eric: Sand stirring causes a host of things to happen in the tank. One of them is a perturbation in all sorts of water parameters. Certainly detritus is an important food source, but stirring sand messes the intrinsic stability of the sand community - all sorts of havoc can result, not the least of which is dramatic drops in redox, release of H2S if present and a host of microbes not native to the water column - the action of sand stirring is probably not the best way to get detritus in the system - good water flow, coupled with reduced filtration, is probably a better solution, IMO.

Why is it that increased water motion seems to counteract the progression of RTN?

Jonathan: The dilution factor. In short, the fact that the water is moving about the coral, any 'vectors' present will be diluted rather than remain in-between coral branches, etc. Also, higher circulation implies greater DO levels, and more water volume with many systems, and that will help.

Eric: Agreed, flushing is very important to the health of corals for many reasons, and some corals, such as P. meandrina, will die without strong water flow, even in transplantation studies in the wild. Some of these corals will become much more stressed without the delivery/removal of products, and is important for all types of metabolic activity.

Do you know if RTN is similar to the coral bleaching we are experiencing on the GBR?

Eric: Bleaching and necrosing events are sometimes related in the wild - usually because bleaching causes enough of a nutritional deficit that the coral expires. However, there is no relation that can be made between "RTN" and bleaching.

Jonathan: In nature, bleaching events are well studied by scientists as well, and they have found no connection.

Any indicators that any certain method(s) of filtration for a reef system (along the lines of nutrient export) would be preferential for preventing RTN?

Jonathan: Ok, I run a skimmerless system. I am of the school that says FOOD in water column is good for corals. I also feed LIVE plankton and Artemia daily to my tank, so I dump a ton of food into the water, and do not do a lot of export, other than harvest of macroalgaes. As for if this is 'better'? This has not been studied under controlled settings. Anecdotally one could guess, but until its researched, its premature to say for sure.

Eric: Whatever method allows for the greatest water quality and stable environment for the species. I think carbon may be important, but that is EXTREME anecdote at this point. The more closely you can get to replicating the conditions where the corals came from, the better off you will be, obviously. I think that J is right, though, in that allowing corals access to proper nutrition sources is important in maintaining health and immunity.

Jonathan: Ad/absoption media MAY be beneficial in stopping RTN, but it has little to do wit the nutrient uptake.

Eric: Agreed.

You mentioned RTN not being seen in the wild, any ideas why it would afflict captive aquaria only?

Jonathan: Hmmmm, yes. But its a LONG LONG answer. It begins with our talk at MACNA about bioorganic molecules. To summarize BRIEFLY (please email for more detail)... Captive systems are CLOSED. Same old water circulating. Open ocean reef has ultimate dilution factors. So, in a closed system, we have a MUCH higher concentration of EVERYTHING.
In addition, we are subjecting animals to artificial light, foreign foods, and often foreign animals they have never encountered. Its a hodgepodge soup of 'newness' for them in a typical home aquarium. Because of this magnification of bio-products, lack of dilution, and artificial eco-systems, it makes comparison between an aquarium and natural ocean very difficult, and makes a number of bias' against home systems for disease.

Eric: Even a well run reef is inherently more stressful that a stressed reef community simply because of the nature of aquaria - at least at the level we are now - our light, water flow, food availability, dilution, etc. are all dreadfully inadequate, even as good as we have gotten at keeping these animals alive. We put very sensitive animals together and expect them to "get along" in immediate proximity. These animals are exquisitely chemosensitive to each other and for all practical purposes, an aquarium is like grafting mortal enemies together, even in large tanks - as J said, comparison is difficult and all we can do is look at the literature for cases that may have some comparison.

OK, the last question before we open the forum: If you could turn back the clock a few years, what would you call this, instead of "RTN"?

Jonathan: heeheeheehee. Nice question. Let me consider for a sec...

Eric: Great question. If you ask me, we are witness to the very elusive condition in the wild called "Shut Down Reaction" - I am of the personal opinion that it, and perhaps Peter's "stress related necrosis " and Sorokins "Pull in of Polyps" are one and the same. I wish I could coin a better name, but I feel that there are some very exceptional attributes to this malady that need to be addressed and, as far as I am concerned, "RTN" is a fitting name. Perhaps as we understand it more, a better name will arise.

Jonathan: I guess I will agree here with Eric. I am not happy with the term RTN, but until we understand the etiology better, it is difficult to describe it properly and do it justice.

Thanks for the great talk, Eric and Jonathan!