Head and Lateral Line Erosion (HLLE)

[Jay Hemdal Verified Community Expert]

I just started carbon after the addition of my first tang - a Tomini. I am using large diameter pelletized carbon in a reactor with no fluidized motion or grinding. The reactor output is fed into a 5 micron filter sock. I am monitoring the fish each day and report any HLLE within 30 days. Not scientific, but maybe a good anecdote.

You have a number of things going for you here; tomini's don't easily get HLLE, using pelleted carbon, and then, the post-filtration. The only downside is that 30 days is almost always too soon to tell. Four months is a better time test.

Jay

 

[chadfish]

You have a number of things going for you here; tomini's don't easily get HLLE, using pelleted carbon, and then, the post-filtration. The only downside is that 30 days is almost always too soon to tell. Four months is a better time test.

Jay

Great. So if he develops HLLE then I surely screwed up!

 

[Cory]

Ive used small amounts of carbon sparingly but haven't used it in a month or so now. I have 5 fish, a fully grown emperor angelfish, a fully grown orange spot rabbitfish, and a yellow tang, scopas tang, and panther grouper. None of them except the scopas tang has developed HLLE near the head.

The scopas tang always had minor abrasions near his head, i suspected from carbon use but until I started using ozone on the system has his conditon gotten much worse. I dont use carbon with my ozone, just ozone. I wonder why its getting worse with ozone and no carbon use? Im running 200mg/l on 150ish gallons for 9 minute's every hour via apex control.

Im curious if ozone is destroying the organics making the heavy metal toxicity theory work here too.

I was reading something about glutamine and fishes lateral line. Now i wonder if activated carbon is removing glutamine and ozone destroying it? Do fish need glutamine to develope a slime coat or something?

"The mechanoreceptive hair cells of the lateral line structure are integrated into more complex circuits through their afferent and efferent connections. The synapses that directly participate in the transduction of mechanical information are excitatory afferent connections that utilize glutamate.[18] "

I used poly lab pro carbon before fwiw.

 

[Cory]

A non-toxic dose of cobalt chloride blocks hair cells of the zebrafish lateral line

Abstract

Experiments on the flow-sensitive lateral line system of fishes have provided important insights into the function and sensory transduction of vertebrate hair cells. A common experimental approach has been to pharmacologically block lateral line hair cells and measure how behavior changes. Cobalt chloride (CoCl2) blocks the lateral line by inhibiting calcium movement through the membrane channels of hair cells, but high concentrations can be toxic, making it unclear whether changes in behavior are due to a blocked lateral line or poor health. Here, we identify a non-toxic treatment of cobalt that completely blocks lateral line hair cells. We exposed 5-day post fertilization zebrafish larvae to CoCl2 concentrations ranging from 1–20 mM for 15 minutes and measured 1) the spiking rate of the afferent neurons contacting hair cells and 2) the larvae’s health and long-term survival. Our results show that a 15-minute exposure to 5 mM CoCl2 abolishes both spontaneous and evoked afferent firing. This treatment does not change swimming behavior, and results in >85% survival after 5 days. Weaker treatments of CoCl2 did not eliminate afferent activity, while stronger treatments caused close to 50% mortality. Our work provides a guideline for future zebrafish investigations where physiological confirmation of a blocked lateral line system is required.

 

[Cory]

Mechanical overstimulation causes acute injury and synapse loss followed by fast 2 recovery in lateral-line neuromasts of larval zebrafish

Abstract 18 Excess noise damages sensory hair cells, resulting in loss of synaptic connections with 19 auditory nerves and hair-cell death. The cellular mechanisms underlying mechanically induced 20 hair-cell damage and subsequent repair are not completely understood. Hair cells in 21 neuromasts of larval zebrafish are structurally and functionally comparable to mammalian hair 22 cells but undergo robust regeneration following damage. We therefore developed a model for 23 mechanically induced hair-cell damage in this highly tractable system. Free swimming larvae 24 exposed to strong water current for 2 hours displayed mechanical injury to neuromasts, 25 including afferent neurite retraction, damaged hair bundles, and reduced mechanotransduction. 26 Synapse loss was observed in apparently intact exposed neuromasts, and this loss was 27 exacerbated by inhibiting glutamate uptake. Mechanical damage also elicited an inflammatory 28 response and macrophage recruitment. Remarkably, neuromast morphology, synapse number, 29 and hair-cell function fully recovered within 2 days following exposure. Our results indicate 30 functional changes and synapse loss in mechanically damaged lateral-line neuromasts that 31 appear similar to damage observed in noise-exposed mammalian ear yet are completely 32 repaired. 33 34 Keywords: Hair cell, mechanical damage, ribbon synapse, inflammation, regeneratio

 

[Cory]

Larval Zebrafish Lateral Line as a Model for Acoustic Trauma

Finally, we used the zebrafish lateral line as a tool to screen a select redox library for compounds that prevent acoustic stimulation-induced damage. Four compounds (glutathione, baicalein, D- α-tocopherylquinone, and ferulic acid ethylester) significantly protected lateral line hair cells from acoustic stimulation-induced hair cell damage (Fig. 11B), only one of which (glutathione) has been previously identified as a potential therapy to prevent NIHL (Ohinata et al., 2000).

 

[Jay Hemdal Verified Community Expert]

Larval Zebrafish Lateral Line as a Model for Acoustic Trauma

Finally, we used the zebrafish lateral line as a tool to screen a select redox library for compounds that prevent acoustic stimulation-induced damage. Four compounds (glutathione, baicalein, D- α-tocopherylquinone, and ferulic acid ethylester) significantly protected lateral line hair cells from acoustic stimulation-induced hair cell damage (Fig. 11B), only one of which (glutathione) has been previously identified as a potential therapy to prevent NIHL (Ohinata et al., 2000).

I know little about glutamine. As an amino acid, would the uptake and processing of it all be through the food cycle? I don't see how anything in the water would have an effect on amino acids.

The trouble is, zebrafish don't exhibit HLLE. I tried to locate the histopathology reports from my study fish to see if they reported hair cell damage, but I couldn't find them.

Ozone has only anecdotally been tied to HLLE - we run ozone but no carbon and we have no cases of HLLE in our systems.

Jay

 

[Projects with Sam]

I have an Emperor angelfish that was given to me just starting to develop HLLE around the eyes and in a few months intense feeding with various prepackaged frozen foods + homemade food + Brightwell Angelixir and endless nori clips he seems to be healing.
also, I've had decent success with some Hippo Tangs I got on discount because they were so bad:
https://www.reef2reef.com/threads/h...ess-from-january-22-2022-march-5-2022.897378/They are also doing much better. The small one grew to about the size of the other since then. He is still permanently disfigured but is much better then before.

 

[Jay Hemdal Verified Community Expert]

I have an Emperor angelfish that was given to me just starting to develop HLLE around the eyes and in a few months intense feeding with various prepackaged frozen foods + homemade food + Brightwell Angelixir and endless nori clips he seems to be healing.
also, I've had decent success with some Hippo Tangs I got on discount because they were so bad:
https://www.reef2reef.com/threads/h...ess-from-january-22-2022-march-5-2022.897378/They are also doing much better. The small one grew to about the size of the other since then. He is still permanently disfigured but is much better then before.

One key thing - moving fish to a new tank has been shown to cause reversal of HLLE in many cases. Moving the fish and then changing the diet introduces two variables at the same time. This was the reason why there was the "natural sunlight" cures HLLE came about...a public aquarium moved fish from one system to another and saw the HLLE go away. The difference they thought, was natural sunlight. However, years later, that was determined not to be the causative factor.

The same was the flaw in the early "vitamin C cures HLLE" study - where the researcher ran no controls, and one of the aspects of his study was to first move his study fish to new tanks (grin). It took decades for people to stop using vitamin C to try and cure HLLE.... I think I posted this story here, but it bears repeating; about 15 years ago, a researcher in Florida ran a study to examine vitamins and HLLE. She had things properly set up with controls, etc. However, her study was cancelled when her control fish developed HLLE. Turns out one of her assistants thought the water looked a bit dingy, so they put a carbon filter on the tank.....

I once had a concrete vat that I could use to induce HLLE - move fish into it and the fish developed, move them out to our reef system and it would go away. I finally stripped the vat down and changed everything and stopped using carbon and it no longer induced HLLE.

Jay

 

[Ricardo Miozzo]

Hello. At this point, so many years after the first discussion about it, I’d like to ask if HLLE cause was found. Cientifically, I mean. What is really found in the erosion itself, or the scar? Is there any irrefutable proof that it is lignite activated carbon? A lot of people suggest HLLE is about high NO3, also. I believe that adequate and varied diet plays a role to avoid it. So… Any proven conclusion? TIA

 

[Jay Hemdal Verified Community Expert]

Hello. At this point, so many years after the first discussion about it, I’d like to ask if HLLE cause was found. Cientifically, I mean. What is really found in the erosion itself, or the scar? Is there any irrefutable proof that it is lignite activated carbon? A lot of people suggest HLLE is about high NO3, also. I believe that adequate and varied diet plays a role to avoid it. So… Any proven conclusion? TIA

What is “proven”? Two peer-reviewed studies have shown that lignite carbon use causes HLLE. These studies were published back in 2011. There have been no published studies since then that I know about.
There was another study that looked at heavy metals causing “epithelial thinning”, but that is not quite the same. Freshwater fish HLLE is also different.

High nitrate as a cause has never been proven. In my study, Nitrate-nitrogen was below 10 mg/l in the study tanks.

 

[Projects with Sam]

My Nitrates have not been below 50 for any number of days in the 4 years since my tanks been up; I, anecdotally, don't think nitrates are a significant factor in HLLE.

 

[IrezumiHurts]

I was aware of this study, but never knew about this post on R2R. I decided to read the post starting in 2020 and couldn't get past page 3 - the ignorance of the comments section was absolutely mind numbing. Classic example of great information squandered on fools and only speaks to further reinforce why the anecdotal suggestions from hobbyists on HLLE should be met with an incredibly high degree of skepticism. To suggest that a controlled study has less credibility than the misinformed cuasal inferences drawn from the masses blows my mind. I've been met with equal amounts of ignorance discussing toxic nitrate levels in marine fish and the status quo makes my draw drop at times. I digress.

@Jay Hemdal do you know if during your study, the size of carbon fines was ever measured or suggested?

The reason im asking is I wanted to explore my theory that diatom filtration - or even pleated, low micron filtration - could potentially reduce suspended carbon fines even further. Your study suggests that pelletized, higher quality carbons reduce the severity of HLLE but histopathology showed the mechanical action was still occurring, and some cases presented or progressed after the study, albeit with significantly less severity.

I know diatom filtration has fallen out of favor in the hobby but I am a big proponent of it's merits for certain applications - I use it, in conjunction with flow tuned, oversized UV, as just one layer in my chemoprophylaxis protocols for fish QT, and have found it makes my entire strategy more efficient, predictable and reliable. I have recently been starting to wonder if diatom filtration placed downstream of pelletized, low flow carbon might have appreciable benefits for systems where aquarists such as myself have previously eschewed the use of carbon altogether due to housing surgeonfish and angelfish. This, combined with foam fractioning, could theoretically make the carbon a non-issue

Edit: Since we're speaking about anecdotes here, I recently did an annual water change on my tank - Hanna HR readings were ~650ppm nitrate (*NO3-, not NO3-N), of course I had to use dilution to derive this result as it topsnout at 75.0ppm. I have tangs and angels in the system, some with HLLE and some that have none, and a wide range - one zebrasoma with significant HLLE (which had already started before intake), 3x zebrasoma with absolutely none, a captive bred imperator with moderate, a few centropyge with mild and none, ctenochaetus with none and one with mild, etc etc. Anyways my point is unless there is a genetic predisposition towards nitrate sensitivity as it relates to HLLE, or a relationship with age or development, I can attest with almost full certainty that nitrates, in and of themselves, are NOT the primary factor for causing HLLE. My systems average 250-750ppm nitrate throughout the year and I have some angels and tangs which do/dont have the issue, some within the same genus - but given the fact I have so many examples in my systems without HLLE and such high nitrates really suggests unless there are other compounds whose abundance may have a relationship with nitrates such as phenols, i think i have found it difficult to entertain theories that nitrates "cause HLLE". I know you arent suggesting that, but i know many other aquarists do.

Of note almost every fish with HLLE I own presented during intake or immediately following QT, of which i predominantly use formalin, copper, and prazi. I have used limited carbon in the past during post-QT observation (i no longer do) and i did not start using diatom filtration until about a year ago, so I dont have enough data from this to draw additional conclusions

 

[Jay Hemdal Verified Community Expert]

I was aware of this study, but never knew about this post on R2R. I decided to read the post starting in 2020 and couldn't get past page 3 - the ignorance of the comments section was absolutely mind numbing. Classic example of great information squandered on fools and only speaks to further reinforce why the anecdotal suggestions from hobbyists on HLLE should be met with an incredibly high degree of skepticism. To suggest that a controlled study has less credibility than the misinformed cuasal inferences drawn from the masses blows my mind. I've been met with equal amounts of ignorance discussing toxic nitrate levels in marine fish and the status quo makes my draw drop at times. I digress.

@Jay Hemdal do you know if during your study, the size of carbon fines was ever measured or suggested?

The reason im asking is I wanted to explore my theory that diatom filtration - or even pleated, low micron filtration - could potentially reduce suspended carbon fines even further. Your study suggests that pelletized, higher quality carbons reduce the severity of HLLE but histopathology showed the mechanical action was still occurring, and some cases presented or progressed after the study, albeit with significantly less severity.

I know diatom filtration has fallen out of favor in the hobby but I am a big proponent of it's merits for certain applications - I use it, in conjunction with flow tuned, oversized UV, as just one layer in my chemoprophylaxis protocols for fish QT, and have found it makes my entire strategy more efficient, predictable and reliable. I have recently been starting to wonder if diatom filtration placed downstream of pelletized, low flow carbon might have appreciable benefits for systems where aquarists such as myself have previously eschewed the use of carbon altogether due to housing surgeonfish and angelfish. This, combined with foam fractioning, could theoretically make the carbon a non-issue

Edit: Since we're speaking about anecdotes here, I recently did an annual water change on my tank - Hanna HR readings were ~650ppm nitrate (*NO3-, not NO3-N), of course I had to use dilution to derive this result as it topsnout at 75.0ppm. I have tangs and angels in the system, some with HLLE and some that have none, and a wide range - one zebrasoma with significant HLLE (which had already started before intake), 3x zebrasoma with absolutely none, a captive bred imperator with moderate, a few centropyge with mild and none, ctenochaetus with none and one with mild, etc etc. Anyways my point is unless there is a genetic predisposition towards nitrate sensitivity as it relates to HLLE, or a relationship with age or development, I can attest with almost full certainty that nitrates, in and of themselves, are NOT the primary factor for causing HLLE. My systems average 250-750ppm nitrate throughout the year and I have some angels and tangs which do/dont have the issue, some within the same genus - but given the fact I have so many examples in my systems without HLLE and such high nitrates really suggests unless there are other compounds whose abundance may have a relationship with nitrates such as phenols, i think i have found it difficult to entertain theories that nitrates "cause HLLE". I know you arent suggesting that, but i know many other aquarists do.

Of note almost every fish with HLLE I own presented during intake or immediately following QT, of which i predominantly use formalin, copper, and prazi. I have used limited carbon in the past during post-QT observation (i no longer do) and i did not start using diatom filtration until about a year ago, so I dont have enough data from this to draw additional conclusions

The carbon dust hypothesis was not clearly proven in either study. The studies did prove that carbon use itself causes HLLE in ocean surgeons (the model used in both studies). The Disney study concluded that the process was that carbon use removed organics from the water that would otherwise be bond to heavy metals, and that in turn allowed the heavy metals to become more toxic to the fish, causing the HLLE. I do not think that is borne out because ICP analysis does not show excess heavy metals in these tanks. My hypothesis of course, is that carbon fines are the cause. I base this on anecdotal cases where I had systems that had previously used carbon, but in which 100% of the water was changed, carbon use stopped, yet the HLLE continued - until I did a complete strip down of the tank, changing all of the substrate, etc. I did have a researcher tell me they found carbon dust in the lateral lines of affected fish using electron microscopy. That was never published, so I don't know if it was a valid observation or not.

The trouble with singling out "nitrate" as a cause is that high nitrates are just a "marker" for senescent systems that have gone beyond their water change frequency. As nitrate builds up, so do other compounds, and still other compounds are depleted. It may well not be nitrate itself, but rather, something else in "old water" that causes HLLE.

Oddly, I've had people implicate diatom powder in the same way as carbon dust. I never studied that, so I can't say if that's an issue or not.

 

[IrezumiHurts]

The carbon dust hypothesis was not clearly proven in either study. The studies did prove that carbon use itself causes HLLE in ocean surgeons (the model used in both studies). The Disney study concluded that the process was that carbon use removed organics from the water that would otherwise be bond to heavy metals, and that in turn allowed the heavy metals to become more toxic to the fish, causing the HLLE. I do not think that is borne out because ICP analysis does not show excess heavy metals in these tanks. My hypothesis of course, is that carbon fines are the cause. I base this on anecdotal cases where I had systems that had previously used carbon, but in which 100% of the water was changed, carbon use stopped, yet the HLLE continued - until I did a complete strip down of the tank, changing all of the substrate, etc. I did have a researcher tell me they found carbon dust in the lateral lines of affected fish using electron microscopy. That was never published, so I don't know if it was a valid observation or not.

The trouble with singling out "nitrate" as a cause is that high nitrates are just a "marker" for senescent systems that have gone beyond their water change frequency. As nitrate builds up, so do other compounds, and still other compounds are depleted. It may well not be nitrate itself, but rather, something else in "old water" that causes HLLE.

Oddly, I've had people implicate diatom powder in the same way as carbon dust. I never studied that, so I can't say if that's an issue or not.

Thank you for the thoughtful response. I didn't realize the fines were still an inference, and not an inexorable part of the findings in and of themselves. Although personally i find it hard to see it any other way, given the parameters of the test. I didn't notice if it was mentioned that the pelletized carbon was anthracite or bituminous? I don't know much about carbon manufacturer for marine aesthetic applications, so maybe they just pellets lignite and call it a day, but the lack of unpolished surfaces makes it less likely to produce fines.

Regarding the nitrate theory, i guess that is my point - i run tanks with "old water" but feel like if that was a significant concern, most of my population should have HLLE, yet many (if not most), do not. Of course HLLE may not always present with gross visual analysis, as you say the damage may be smaller than can easily be seen but still present. I also run 2x protein skimmers, fleece, UV, and now recently now diatom, so if there's is a relationship between HLLE and nitrates and undesirable "old water" compounds which index off nitrates, it's possible I've been fractioning most of them out. Of course that's assuming there was an HLLE relationship of concern to begin with.

One last thing of consideration on the Disney study, since you mention that it struck me...i seem to recall reading somewhere that you no longer use ozone, due to HLLE-like effects you observed. Any thoughts on how ozone could be interacting with the water in similar ways to carbon, which might tie into that theory, it the one you are putting forward on the fines? I know you did the ICP tests to rule out the heavy metal issue, but as you say maybe if other compounds aren't available in the water anymore, it changes how they might interact? I

And for the diatoms i was wondering if you were going to mention that - diatoms are "fines" in and of themselves, so if the issue is a mechanical one related to particle size, it would be interesting if they were capable of the same action. Though the filter, if my understanding is correct, essentially works on the basis of a continual clogging action, so in theory the amount of suspended diatoms in the column should be short lived relative to their assembly and impaction in the filter pleats... Assuming a significant amount aren't continually "slipping through".

Anyways, thank you again for the earlier feedback, respond in your own time if/as you feel

 

[Jay Hemdal Verified Community Expert]

Thank you for the thoughtful response. I didn't realize the fines were still an inference, and not an inexorable part of the findings in and of themselves. Although personally i find it hard to see it any other way, given the parameters of the test. I didn't notice if it was mentioned that the pelletized carbon was anthracite or bituminous? I don't know much about carbon manufacturer for marine aesthetic applications, so maybe they just pellets lignite and call it a day, but the lack of unpolished surfaces makes it less likely to produce fines.

Regarding the nitrate theory, i guess that is my point - i run tanks with "old water" but feel like if that was a significant concern, most of my population should have HLLE, yet many (if not most), do not. Of course HLLE may not always present with gross visual analysis, as you say the damage may be smaller than can easily be seen but still present. I also run 2x protein skimmers, fleece, UV, and now recently now diatom, so if there's is a relationship between HLLE and nitrates and undesirable "old water" compounds which index off nitrates, it's possible I've been fractioning most of them out. Of course that's assuming there was an HLLE relationship of concern to begin with.

One last thing of consideration on the Disney study, since you mention that it struck me...i seem to recall reading somewhere that you no longer use ozone, due to HLLE-like effects you observed. Any thoughts on how ozone could be interacting with the water in similar ways to carbon, which might tie into that theory, it the one you are putting forward on the fines? I know you did the ICP tests to rule out the heavy metal issue, but as you say maybe if other compounds aren't available in the water anymore, it changes how they might interact? I

And for the diatoms i was wondering if you were going to mention that - diatoms are "fines" in and of themselves, so if the issue is a mechanical one related to particle size, it would be interesting if they were capable of the same action. Though the filter, if my understanding is correct, essentially works on the basis of a continual clogging action, so in theory the amount of suspended diatoms in the column should be short lived relative to their assembly and impaction in the filter pleats... Assuming a significant amount aren't continually "slipping through".

Anyways, thank you again for the earlier feedback, respond in your own time if/as you feel

Sorry - did I write that I thought ozone can cause HLLE? I don't recall that. We still use a lot of ozone and have very little HLLE. It showed up as a possible cause in the public aquarium survey that I did, but that survey was just of people's opinions....

I found the survey results in my files, here they are, The survey was done prior to the publication of the two carbon papers:


Online survey of 100 aquarists concerning Head and Lateral Line Erosion (HLLE)
Jay Hemdal


1) What do you think are the POSSIBLE causes of Head and Lateral Line Erosion (HLLE)? (Check all that apply)

Bacterial infection 31.3%
Carbon (by removing essential elements) 30.3%
Carbon (Dust - as an irritant) 28.3%
Copper medication 19.2%
Diet, lack of vitamin C 62.6%
Diet, lack of HUFA's 40.4%
Diet, lack of fiber 20.2%
Electrical grounding problems 32.3%
General stress from captivity 55.6%
Iodine, lack of 10.1%
Protozoan infections, Hexamita, 31.3%
Nitrate, high levels 36.4%
Sunlight, lack of 32.3%
Viral infection 19.2%



Other causes not listed above:

Ozone, ozone-oxidants (3)
Lack of trace elements (3)
Heavy metals other than copper (4)
Poor lighting (2)
Stress from tankmates (4)
Water temperature (1)
Undetermined water quality problem (6)
Pump noise (2)
Global warming (1)
Lack of vitamin A (1)
Genetic predisposition (1)
Dinoflagellates (1)
Starvation during supply chain (1)



2) What do you feel is the SINGLE most important cause of this syndrome in fish? Pick just one answer:

Bacterial infection 2.1%
Carbon (by removing essential elements) 4.1%
Carbon (Dust - as an irritant) 5.2%
Copper medication 6.2%
Diet, lack of vitamin C 15.5%
Diet, lack of HUFA's 11.3%
Diet, lack of fiber 4.1%
Electrical grounding problems 5.2%
General stress from captivity 24.7%
Iodine, lack of 0.0%
Protozoan infections, Hexamita 4.1%
Nitrate, high levels 4.1%
Sunlight, lack of 10.3%
Viral infection 3.1%


3) Have you ever been able to completely resolve a case of HLLE? If so, indicate methods used:

Moved fish to a new tank 37.5%
Kept fish in same tank, changed diet 19.4%
Moved fish, changed diet 29.2%
Removed carbon 12.5%
Removed copper 5.6%
Added grounding probe 5.6%
Changed water 18.1%
Added supplements 20.8%
Did nothing, went away on its own 5.6%


Other methods used to completely resolve HLLE, not listed above

Regranex treatments (8)
Water changes ( 1)
Moving fish combined with other changes (8)
Treated with Metronidazole (4)
Selcon food additive (1)
Algae added to diet (2)
Garlic (1)
Cured fish of velvet (1)
Added protein skimmer (1)
Reduced ozone oxidants (1)
Reduced stress from tankmates (1)


4) Please indicate your aquarium experience: (choose single best answer)

Beginning home aquarist 0%
Intermediate home aquarist 12%
Advanced home aquarist 15%
Retail pet store employee / owner 3%
Public aquarist 37%
Public aquarium manager / director 29%
Marine / fisheries biologist