Connection between iron and coral STN/RTN

[Hungarian_reefer]

Possible connection between iron and RTN/STN

Many people report RTN/STN in their corals after aggressive phosphate reduction. Unfortunately, I have experienced this myself several times. However, I have observed that tissue necrosis is most severe and affects the greatest number of corals when I used GFO—even though it was not what caused the fastest phosphate reduction.

Of course, I also consider rapid phosphate reduction to be partly responsible for RTN/STN in such cases, but as a physician I also assume another mechanism that may be specifically related to GFO.

Iron has important functions in all living organisms, but bacteria in particular utilize it in large amounts. Therefore, in more complex organisms a widely spread defense mechanism against bacterial infection is the reduction of tissue iron levels. In humans, for example, it has long been known that free (more precisely, non–hemoglobin-bound) iron levels decrease significantly during bacterial infections, and there is ongoing debate about whether iron supplementation is appropriate during such infections.

Another peculiarity of iron is that there is no true excretory mechanism for it in the animal kingdom; only the rate of uptake can be reduced. (Although I could not find specific data for corals, I would be surprised if they functioned differently.) As a result, iron can accumulate—and this may be even more pronounced in an aquatic organism that is adapted to an environment known to be very low in iron.

Therefore, I hypothesize that one important component of the RTN/STN mechanism observed after the use of large amounts of GFO is that iron accumulated in coral tissue promotes (by bacteria) necrosis of coral tissue that has been weakened—possibly due to changing water parameters—especially in the case of GFO products that generate large amounts of dust.

What do you think?
Have you experienced something similar?

 

[mmorrison55]

Following. Sounds like an interesting discussion

 

[Randy Holmes-Farley]

It’s possible it may happen in some tanks, but lots of people dose iron, sometimes in very large amounts, without seeing such a correlation.

 

[Hungarian_reefer]

It’s possible it may happen in some tanks, but lots of people dose iron, sometimes in very large amounts, without seeing such a correlation.

Thank you, Randy. Yes, I also think that dosing iron on its own (even in large amounts) does not cause problems in an aquarium with healthy microbiome. However, based on my observations, once STN/RTN has already started, its progression seems to be more severe if a large amount of iron was dosed into the aquarium beforehand in some way (solution or GFO). That’s why I was considering the possibility mechanism.

 

[Randy Holmes-Farley]

Thank you, Randy. Yes, I also think that dosing iron on its own (even in large amounts) does not cause problems in an aquarium with healthy microbiome. However, based on my observations, once STN/RTN has already started, its progression seems to be more severe if a large amount of iron was dosed into the aquarium beforehand in some way (solution or GFO). That’s why I was considering the possibility mechanism.

That is certainly possible. I just do not remember anyone pointing the blame in this way before.

 

[Reef Rhino]

Thank You for your timely post. I will reply with my situation as anecdotal information as it was also suggested to me by others that Iron and RTN/STN could be linked:

I have suddenly (Nov / Dec) faced a mass casualty event, primarily RTN/STN of a significant number of Acropora. Close to wipe out of most Acro Frags and colonies. Add in some receding Hydnophora, Montipora RTN/STN, and some receding LPS as well. Goni and Torches seem great.

Things had been going great all Fall - better then ever for Acro color / growth, and my quarterly Fall ICP (10/2/25) was the best I could hope for. I thought I had arrived ....

My tank has OG live rock dating back to the late 90s so I have always assumed some degree of "healthy", or at least established, biome. (It also percolated as a cess pool for about a decade so who knows what grew in there). Given mass casualty and coral health and appearance, and absent other good explanation, I suspect Bad bacteria is my underlying cause and I will list a few possible other recent changes that could be contributing factors:

1. Alkalinity had some fluctuation for a few months, as low as 7.3 but otherwise between 7.5-8.5.
2. Phosphate was historically .03-.05 but increased in the past year to .1
I view this as a good thing and was happy to run higher at .08-.1. Nitrate was ~20.
3. I was weening off and then stopped Amino acids (due to concern over usefulness and feeding "bad bacteria" per Salem Clemens) and was also cutting back a bit on Tank feeding as my nutrients had increased. Perhaps ceasing this feeding was the cause (?), but Nitrate and Phosphate remained in solid range).
4. Frequent fall leaf blowing outside may have blown organic garbage in the slightly open window and down into the tank below ....
5. As far as dosing, my only change post-ICP was that I switched practices and products for dosing Iron and Iodide and although I followed a recommended dose for Iron my addition of Iron was certainly more than it had been before. Last ICP had it at 1.4 ug/l and my additions then likely took it higher.

A LFS (Reef Store) happened to ask me about Iron and also suggested a link to RTN/STN. I stopped Iron dosing a few weeks ago and I am just now sending out a new ICP so what it will show regarding Iron then and now may be a bit useless and dated.

But absent other significant variables or explanations, I do wonder if the increased Iron fueled an increase in bacteria that caused a significant RTN/STN mass casualty event in my tank?

 

[Salem-Novel Aquatics]

Possible connection between iron and RTN/STN

Many people report RTN/STN in their corals after aggressive phosphate reduction. Unfortunately, I have experienced this myself several times. However, I have observed that tissue necrosis is most severe and affects the greatest number of corals when I used GFO—even though it was not what caused the fastest phosphate reduction.

Of course, I also consider rapid phosphate reduction to be partly responsible for RTN/STN in such cases, but as a physician I also assume another mechanism that may be specifically related to GFO.

Iron has important functions in all living organisms, but bacteria in particular utilize it in large amounts. Therefore, in more complex organisms a widely spread defense mechanism against bacterial infection is the reduction of tissue iron levels. In humans, for example, it has long been known that free (more precisely, non–hemoglobin-bound) iron levels decrease significantly during bacterial infections, and there is ongoing debate about whether iron supplementation is appropriate during such infections.

Another peculiarity of iron is that there is no true excretory mechanism for it in the animal kingdom; only the rate of uptake can be reduced. (Although I could not find specific data for corals, I would be surprised if they functioned differently.) As a result, iron can accumulate—and this may be even more pronounced in an aquatic organism that is adapted to an environment known to be very low in iron.

Therefore, I hypothesize that one important component of the RTN/STN mechanism observed after the use of large amounts of GFO is that iron accumulated in coral tissue promotes (by bacteria) necrosis of coral tissue that has been weakened—possibly due to changing water parameters—especially in the case of GFO products that generate large amounts of dust.

What do you think?
Have you experienced something similar?

This is something I hope to get data on eventually - there is certainly a link between virulence in vibrio and iron acquisition in the literature and I have kicked around the idea of "GFO bad because pathogens" due to this. But of course there's many questions with such lines of thought that must be answered to confidently make such a claim.

Essentially it would boil down to - inorganic? chelated? if so what chelated form? and how much of said form(s) to trigger pathogenic gene expression and in what species or strains would that expression occur and at what % of expression could that translate to disease?

Lots of data needed from a multiomics point of view - but an interesting hypothesis the literature could theoretically support.