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Frogger

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Well in the beginning when I had just one Coral stating to show a STN line few weeks ago it all started. Fast forward, jumped on the wagon of ciliates and did the PC products with some first good results and followed tank treatments, killed fish, did elevated concentrations and ciliates did not eradicated sufficiently. Started to believe again more the real reason that it's bacteria and found this hidden microbe, did all sort of stuff while STN/RTN became worse from day to day and if I do not do anything quickly I will for sure loose the entire tank.

I am sorry to hear of your loss. Just thinking out loud here but could it be possible that the dosing of these products to your tank has destroyed any sense of balance/ bio-diversity in your tank. stressed your corals and just expedited the whole process? It has killed all your fish, what else has it killed or affected.

I cannot say I am an expert on RTN but I have lost quite a few corals to RTN, usually frags that didn't take. I have also over the years lost several colonies to RTN but they could always be routed back to something I screwed up, let the alkalinity get to high, I let the temperature get too high with a faulty heater and bad thermometer. But in all those episodes once the tank perimeters were stabilized, the RTN stopped no other corals were affected and even in once instance a birds nest regrew in the exact spot that it RTN'd and it was about a year later that I noticed it.

I have heard stories of whole tanks going for no apparent reason, but maybe there is something wrong that caused the situation in the beginning and reefer just was not able to figure it out.

Could these ciliates, bacteria and other unidentified parasites only be opportunistic? Could they just likely survive in the tank as saprophyte only to become parasitic when a stressed coral presents itself.
 

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A suggestion for @Prime Coral (or any other sponsor with a new product or idea. Write an article explaining the rationale for the product, the research supporting it (in science), the research (thats not proprietary defending its use). The research showing its safe (and safe for what), The success/failure rate of the product in helping whatever its supposed to help. It seems like many products toss out a thread - which results in pages of back and forth with many repeated questions and answers - and a lot of animosity. I had suggested that R2R 'vet' new sponsors - I think thats too hard - but requiring a written summary as an article might be a good start to avoid arguing. I.e. User Question xxxxx? Sponsor answer see the article paragraph yyyyy. Of course there will still be discussion - but hopefully it will reduce repeats and arguing - just a suggestion.
 

MnFish1

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A suggestion for @Prime Coral (or any other sponsor with a new product or idea. Write an article explaining the rationale for the product, the research supporting it (in science), the research (thats not proprietary defending its use). The research showing its safe (and safe for what), The success/failure rate of the product in helping whatever its supposed to help. It seems like many products toss out a thread - which results in pages of back and forth with many repeated questions and answers - and a lot of animosity. I had suggested that R2R 'vet' new sponsors - I think thats too hard - but requiring a written summary as an article might be a good start to avoid arguing. I.e. User Question xxxxx? Sponsor answer see the article paragraph yyyyy. Of course there will still be discussion - but hopefully it will reduce repeats and arguing - just a suggestion.
BTW - this is not a slam against prime coral - I could also mention T******, N******, C******* A*** ***********. etc etc etc Opinion only - and not limited to those vendors....
 

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Well...as many of you know I backed the doctor from the beginning. For me...the Philaster appeared more than capable of wrecking a large acropora colony within 24 hours or less.

However, then we started to dig into all the studies. Some of these studies were performed using transmission electron microscopy. Transmission electron microscopes are capable of imaging at a significantly higher resolution than light microscopes. This enables the instrument to capture fine detail...even as small as a single column of atoms, which is thousands of times smaller than a resolvable object seen in the light microscope which is what the doctor is using.

After learning about this, looking at the latest studies, receiving feedback from several people, and watching the doctor run from tough questions- I began to rethink my position. I’ve observed a lot of fish die from his product and every report I received stated that the product did not stop RTN. Reef Junkie was the only Reefer that reported his RTN stopped and had not progressed for 18 days at the time of his thread reply. This could have been a coincidence and I suspect it was given all the other reports. He also reported loosing 1/2 his fish during that treatment like many of the others.

I will continue to remain skeptical until I see “real evidence” that the product is indeed working. I want to see dated pictures of corals or detailed Vlogs. These Vlogs should be very easy to make since the doctor claims 99% eradication with his formula and also claims that the Philaster Lucinda is the “only cause” of RTN.

Bottom line: The product is not working now and hasn’t been. The doctor is the only one making these claims.

If anybody has evidence (Pics or Vlogs) of before and after the treatments...please post up or PM me.

I gave you a lot of crap in 38 pages, but this is a stand-up post and also very important. Most people are cowards and just run/disappear and never have the guts to nut-up and write a post like this. Well done. It will also help others who are reading this thread.

If anybody does start another thread with science, please link it here so that we can find it and follow along.
 

robert

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I read a study a while back that looked at how various carbon sources in the water disrupted the coral's resident bacteria - often leading to a delayed necrosis and death of the host. I've also read that "cell free" homogenate of RTN tissue could induce necrosis in an otherwise healthy specimen whereas the same "cell free" homogenate of healthy tissue did not. What the authors speculated was that normally benign resident bacteria could be transformed into killers through a genetic switch triggered by something called "quorum sensing" -

"Quorum sensing is the regulation of gene expression in response to fluctuations in cell-population density. Quorum sensing bacteria produce and release chemical signal molecules called autoinducers that increase in concentration as a function of cell density. The detection of a minimal threshold stimulatory concentration of an autoinducer leads to an alteration in gene expression. Gram-positive and Gram-negative bacteria use quorum sensing communication circuits to regulate a diverse array of physiological activities. These processes include symbiosis, virulence, competence, conjugation, antibiotic production, motility, sporulation, and biofilm formation. In general, Gram-negative bacteria use acylated homoserine lactones as autoinducers, and Gram-positive bacteria use processed oligo-peptides to communicate. Recent advances in the field indicate that cell-cell communication via autoinducers occurs both within and between bacterial species. Furthermore, there is mounting data suggesting that bacterial autoinducers elicit specific responses from host organisms. Although the nature of the chemical signals, the signal relay mechanisms, and the target genes controlled by bacterial quorum sensing systems differ, in every case the ability to communicate with one another allows bacteria to coordinate the gene expression, and therefore the behavior, of the entire community. Presumably, this process bestows upon bacteria some of the qualities of higher organisms." https://www.ncbi.nlm.nih.gov/pubmed/11544353

If such a mechanism were in play as the homogenate experiment suggests, then even Dr. Sweet's research might miss the true culprits as it is no longer a direct observation but must take into account the genetic expression of the various bacterial populations at various densities and combinations. It could be very very difficult to isolate a causative agent without much more elaborate experimentation.

If that is not enough, then it is further complicated by the response of the host and zox themselves. I've been reading about something called DMSP - a sulfur molecule - the presence or absence of which seems to predict the survival probablilty of an individual coral to various stressors. Those corals with the highest levels of DMSP are survivors while those without perish. (DMSP is what gives corals that wonderful smell). Certain bacteria within the coral host are thought to feed on the DMSP produced by the host and zoox - like the coral host feeds the zoox - the host and zoox feed these special bacteria which constitute a sort of immune system for the aggregate.

I'm not a fan of antibiotic use as I'm always afraid of unintended consequences and for similar reasons I find feeding carbon sources to heterotrophic bacteria in the water column for nutrient export a bit sketchy, but perhaps an approach which enhances the production of these host produced compounds could prove productive.

Just throwing things out for consideration -
 

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I read a study a while back that looked at how various carbon sources in the water disrupted the coral's resident bacteria - often leading to a delayed necrosis and death of the host. I've also read that "cell free" homogenate of RTN tissue could induce necrosis in an otherwise healthy specimen whereas the same "cell free" homogenate of healthy tissue did not. What the authors speculated was that normally benign resident bacteria could be transformed into killers through a genetic switch triggered by something called "quorum sensing" -

"Quorum sensing is the regulation of gene expression in response to fluctuations in cell-population density. Quorum sensing bacteria produce and release chemical signal molecules called autoinducers that increase in concentration as a function of cell density. The detection of a minimal threshold stimulatory concentration of an autoinducer leads to an alteration in gene expression. Gram-positive and Gram-negative bacteria use quorum sensing communication circuits to regulate a diverse array of physiological activities. These processes include symbiosis, virulence, competence, conjugation, antibiotic production, motility, sporulation, and biofilm formation. In general, Gram-negative bacteria use acylated homoserine lactones as autoinducers, and Gram-positive bacteria use processed oligo-peptides to communicate. Recent advances in the field indicate that cell-cell communication via autoinducers occurs both within and between bacterial species. Furthermore, there is mounting data suggesting that bacterial autoinducers elicit specific responses from host organisms. Although the nature of the chemical signals, the signal relay mechanisms, and the target genes controlled by bacterial quorum sensing systems differ, in every case the ability to communicate with one another allows bacteria to coordinate the gene expression, and therefore the behavior, of the entire community. Presumably, this process bestows upon bacteria some of the qualities of higher organisms." https://www.ncbi.nlm.nih.gov/pubmed/11544353

If such a mechanism were in play as the homogenate experiment suggests, then even Dr. Sweet's research might miss the true culprits as it is no longer a direct observation but must take into account the genetic expression of the various bacterial populations at various densities and combinations. It could be very very difficult to isolate a causative agent without much more elaborate experimentation.

If that is not enough, then it is further complicated by the response of the host and zox themselves. I've been reading about something called DMSP - a sulfur molecule - the presence or absence of which seems to predict the survival probablilty of an individual coral to various stressors. Those corals with the highest levels of DMSP are survivors while those without perish. (DMSP is what gives corals that wonderful smell). Certain bacteria within the coral host are thought to feed on the DMSP produced by the host and zoox - like the coral host feeds the zoox - the host and zoox feed these special bacteria which constitute a sort of immune system for the aggregate.

I'm not a fan of antibiotic use as I'm always afraid of unintended consequences and for similar reasons I find feeding carbon sources to heterotrophic bacteria in the water column for nutrient export a bit sketchy, but perhaps an approach which enhances the production of these host produced compounds could prove productive.

Just throwing things out for consideration -
I read a similar content article I need to find again about the internal bacteria and it's dependency on carbohydrates, internal electrical signals and it's effect on the symbiotic relationship between coral and ZooX that was very interesting. Will try to find that again.
 

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Quick update, life comes across and I wasn't able to even make some pictures :-(

Sooooooooo.......
Things got better finally.
It seems that TN stopped progressing finally.
Heavily infected frags barely made it or got lost unfortunately.
Colonies seem to handle it better.

I'm observing a few patches of TN that started to appear prior the O3 use and it developed not further as of yesterday. The excessive use of carbon and Ozone as well the Water changes along with UV seem to help.
Water is still not crisp, but I hope it's getting there. Feel whatever is in the water fuel(ed) the pathogens.

I'm having more hope now, that no new infections will occur.
 

MnFish1

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Will try to do so with some close ups. Basically spreading infections and STN as well as RTN appear within hours or simply progressing slowly.
Certain Birdsnests are going from colony to frag size within 2-3 hours.



Well in the beginning when I had just one Coral stating to show a STN line few weeks ago it all started. Fast forward, jumped on the wagon of ciliates and did the PC products with some first good results and followed tank treatments, killed fish, did elevated concentrations and ciliates did not eradicated sufficiently. Started to believe again more the real reason that it's bacteria and found this hidden microbe, did all sort of stuff while STN/RTN became worse from day to day and if I do not do anything quickly I will for sure loose the entire tank.

So yesterday was the worse day and it was very frustrating and exhausting.
Then I decided to use the Ozone full throttle!
I believe there is a pathogenic bacteria outbreak caused by something that fuels the pathogens.

Will know more when I get back home this evening.
Looking for comments on these ideas:

I have theory (just like when people get a cut on coral and get a vibrio infection - which rapidly spreads - an can even kill the person within 24 hours) - that ANY injury to a coral (chemical, physical, environmental) - that allows bacterial entry can set up the start of RTN. In my tank - I have never had the process whereby there is spread from coral to coral unless there has been some stress event. On the other hand I have touched part of a coral by accident - and over the next several days that arm RTN's. I clip it off and it stops. Of course this is all anecdote on my part.

That said, I have also had times when the temp dropped to 65 - and nothing happened. Or the Alk dropped to 5 and nothing happened when it was quickly corrected (supposedly a no-no) - so it is clearly multifactorial or?

PS - I have most often seen RTN when adding a new coral to the tank - and when placing it - I touch another coral with it - I wonder how often neighboring coral injury initiates whatever injury process that happens which then results in bacterial infection - and then ciliate infestation. (or the newly added coral is injured in transport)

PPS - I do not think its ciliates (or bacteria) swimming around randomly attacking other healthy coral - if this were the case, fragging and sealing the living tissue would not stop the process (which it often does)
 

MnFish1

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Looking for comments on these ideas:

I have theory (just like when people get a cut on coral and get a vibrio infection - which rapidly spreads - an can even kill the person within 24 hours) - that ANY injury to a coral (chemical, physical, environmental) - that allows bacterial entry can set up the start of RTN. In my tank - I have never had the process whereby there is spread from coral to coral unless there has been some stress event. On the other hand I have touched part of a coral by accident - and over the next several days that arm RTN's. I clip it off and it stops. Of course this is all anecdote on my part.

That said, I have also had times when the temp dropped to 65 - and nothing happened. Or the Alk dropped to 5 and nothing happened when it was quickly corrected (supposedly a no-no) - so it is clearly multifactorial or?

PS - I have most often seen RTN when adding a new coral to the tank - and when placing it - I touch another coral with it - I wonder how often neighboring coral injury initiates whatever injury process that happens which then results in bacterial infection - and then ciliate infestation. (or the newly added coral is injured in transport)

PPS - I do not think its ciliates (or bacteria) swimming around randomly attacking other healthy coral - if this were the case, fragging and sealing the living tissue would not stop the process (which it often does)

PPPS - my solution to RTN when it happens - no dips, no medications, I just cut off the damaged part immediately - I don't wait and hope that it will stop. Or I cut off multiple healthy pieces off - seal them to the rock - and toss the rest. To me this has been the most successful - getting rid of the dying tissue. Every time Ive tried the watch and wait method I've lost the whole piece.
 

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In this discussion I also wonder if our indescriminate use of corals and fish from different locations world wide exposes them to bacteria, viruses, and other agents that they would never encounter in the wild? It makes me wonder if corals specifically from the same locations might prevent or at least reduce the RTN incidents we see in the aquarium? I know this does not answer WBD incidents in the wild but that may be the result of more environmental forces than biological.

I have noticed the increase in difficulty many face with a mixed aquarium versus a type dominate aquarium (Sps vs. LPS or soft corals). I know some of that is in regard to lighting and nutrient control but it makes me wonder none the less. We certainly have seen some of the hazards with coral flat worms and related outbreaks. In the natural location do natural preditors keep the outbreaks limited? Is this progression and loss similar to the way forests wax and wane on land? The possible interelationships of the various macro and micro communities boggles the mind!

pffft that sound was my mind shorting out. Have a great and productive day everyone!
 

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MnFish1

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Trying to find more stuff about the R&D concerning the "Coral Tissue" I found so far these 2, but more stuff out there.

Wondering how this green microbe I stained did make it into the Tissue next to the ZooX's .....


https://royalsocietypublishing.org/doi/full/10.1098/rsif.2016.1003



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141621/
What was the stain you used. One thing is certain bacteria are susceptible to different stains there may be many more that did t take up that stain.
 

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Trying to find more stuff about the R&D concerning the "Coral Tissue" I found so far these 2, but more stuff out there.

Wondering how this green microbe I stained did make it into the Tissue next to the ZooX's .....


https://royalsocietypublishing.org/doi/full/10.1098/rsif.2016.1003



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141621/
Can you reshare the picture of the bacteria in the coral tissue? Are you sure you know what your looking at? I may be off base but most living bacteria won’t stain. I can’t remember whether this was a dead or living picture
 

Frogger

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Things got better finally.
It seems that TN stopped progressing finally.
Heavily infected frags barely made it or got lost unfortunately.
Colonies seem to handle it better.

I'm observing a few patches of TN that started to appear prior the O3 use and it developed not further as of yesterday. The excessive use of carbon and Ozone as well the Water changes along with UV seem to help.
Water is still not crisp, but I hope it's getting there. Feel whatever is in the water fuel(ed) the pathogens.

It is good to hear that the RTN cycle is in remission.

Here is the million dollar question. Did the progression of RTN stop because?
  1. Solely based on the addition of O3, the use of excessive carbon or UV?
  2. Combination of those 3 things?
  3. The addition of the antibiotics and prime or either one or the other?
  4. The combination of everything that you have done or a couple of the things in tandem?
  5. Because the disease has naturally reached its conclusion
  6. Because of whatever caused it to start in the beginning has been fixed inadvertently.
  7. A combination or none of what you have done?
Unfortunately because you did so much we will never know. Unless of course you were prepared to begin the experiment all over again and leave out certain steps.;)
 

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It is good to hear that the RTN cycle is in remission.

Here is the million dollar question. Did the progression of RTN stop because?
  1. Solely based on the addition of O3, the use of excessive carbon or UV?
  2. Combination of those 3 things?
  3. The addition of the antibiotics and prime or either one or the other?
  4. The combination of everything that you have done or a couple of the things in tandem?
  5. Because the disease has naturally reached its conclusion
  6. Because of whatever caused it to start in the beginning has been fixed inadvertently.
  7. A combination or none of what you have done?
Unfortunately because you did so much we will never know. Unless of course you were prepared to begin the experiment all over again and leave out certain steps.;)
or random stoppage...
 

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Unfortunately this thread has created way more questions than it has answered.
Just wondering out loud again:
  • Is O3 effective at reducing the mobile pathogen(s)?
  • Has anyone had RTN on multiple coral colonies while employing O3?
  • If O3 is effective at reducing the mobile pathogen(s) would a Sochting Oxydator help?
  • What about UV?
 

MnFish1

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Unfortunately this thread has created way more questions than it has answered.
Just wondering out loud again:
  • Is O3 effective at reducing the mobile pathogen(s)?
  • Has anyone had RTN on multiple coral colonies while employing O3?
  • If O3 is effective at reducing the mobile pathogen(s) would a Sochting Oxydator help?
  • What about UV?

H2O2 also kills bacteria - so I don't think it helps decide what is causing RTN. It will also help 'clean away' dead tissue.
 
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