Diatom filter for treating external parasites?

Brew12

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How about taking tank water and setting up a smaller tank with the water from the DT- place the molly in there and see if the signs appear. That way, you know if the DT still has active velvet but not re-setting the fallow period? THoughts?
I've thought about that, and I've thought about putting the fish in the tank for a day and then pulling it to watch for symptoms. The downside is that any active parasites may not have found the fish in that period of time. There isn't an easy answer, unfortunately. Both ways would likely show a severe infestation, but may not detect a few stragglers.
 
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The real question is whether the fallow periods prescribed are sufficient to fully eradicate the parasite. Recent evidence is that under some conditions found in our tanks, the tomont phase can be substantially extended, potentially resulting in a re-infestation six, seven or eight months after encystment.

I’ve read of this happening in cold water (~53°F), but can you provide evidence of this occurring in reef conditions?
 

Arvind Arya

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I've thought about that, and I've thought about putting the fish in the tank for a day and then pulling it to watch for symptoms. The downside is that any active parasites may not have found the fish in that period of time. There isn't an easy answer, unfortunately. Both ways would likely show a severe infestation, but may not detect a few stragglers.
I thought that the parasites would be able to find the fish fairly quick since their numbers are quite large.... this goes back to my initial question about the DF lowering the swimming populations
 

robert

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@Arvind Arya - I live down in morgan hill but work up near great america in santa clara. DF will certainly lower the swimming populations - it takes ~300 throphants per gram of fish to be lethal - so the time to deploy DF in-tank would have been right when you first saw you had an issue. DF in the quarantine could still be of help.

The infectivity of throphants is highly variable. Not all trophants find a fish, some that do can't attach and some of those do not successfully drop and adhere to produce tomonts.
Taking HF's numbers as a reference - even if you don't take out all free-swimmers and droppers - if you can reduce the infectivity rate below 200:1 - the parasitic cycle will break.

Working in your favor is the natural immunity building in the fish coupled with the senescence of the cell line. Keep the attachment rate below the lethal loading - and the parasite more or less self eradicates. It's simple math. DF also reduces bacterial load and helps prevent secondary infection - which is also a plus.

We tend to naively interpret lab results and try to apply them to our systems, sometimes without considering the fact that lab tanks are in many ways different from the tanks we run at home. There are many aspects of the life-cycle if ich and velvet that have not been explored and are not well understood but which are bit-by bit being figured out.

Senescence of cilliate lines was observed and described over a hundred years ago - and it is reliably observed in virtually every study of marine ich. In the lab - it can be a significant challenge to maintain a viable cell line - so much so that special techniques have had to be developed just to complete a study will a single strain before it dies off on its' own from old age even though it is "fed" a diet of fish which have never had any exposure and have acquired no immunity. Turns out there is a limit to how many times a cell can reproduce by budding as it typically takes place in the tomont under laboratory conditions. How is this observed senescence avoided in the wild - or as some here suggest - in our reef systems? No one knows for sure.

The are researchers looking for the genetic loci of ich's ability to enter into deep hibernation states. Of course they are looking based on its impact on fisheries and the observed seasonality of outbreaks. Is it entering or exiting these hibernation states, which revitalizes the cell line and restores infectivity? Sexual and/or autogamous reproduction which clears DNA damage and restores shortened telomeres - is that the missing piece of the life-cycle which keeps ich and velvet from disappearing through senescent eradication? Looks possible. Looks probable as a matter of fact.

So what are the trigger(s) for deep hibernation? Are they the same for autogamous or sexual reproduction? What are the environmental conditions in a "lab" tank which precludes these states. We know temperature can have an effect - but if this were the only agent - then senescence should be the rule in our tanks as well. It turns out that there is (at least) one other environmental trigger. Hypoxic conditions with O2 levels < 23% have also been seen to be inductive of deep hibernation states. These regions do exist in our tanks - notably areas of the substrate. Tomonts of ich can be revived from hypoxic induced hibernation six, seven or eight months later after exposure to an oxygen rich environment. Thermoclines and/or hypoxia? Thermoclines in our systems - no. Areas of Hypoxia - yes.

Ich or velvet hibernating in sand beds or other regions of reduced 02 saturation - very possible. Maybe part of the fallow protocol should involve addressing potential hypoxic areas of the system? Or we may find that there are other potential facilitators of Deep hibernation - maybe in some cases it just a matter of chance.

At any rate - there is that old saw that "all tanks have ich" - It might be truer than we thought making management the only sure-fired strategy. I personally would prefer a tank design which assumes the worst and deals with it than one which relies on quarantine perfection.
 
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Arvind Arya

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@Arvind Arya - I live down in morgan hill but work up near great america in santa clara. DF will certainly lower the swimming populations - it takes ~300 throphants per gram of fish to be lethal - so the time to deploy DF in-tank would have been right when you first saw you had an issue. DF in the quarantine could still be of help.

The infectivity of throphants is highly variable. Not all trophants find a fish, some that do can't attach and some of those do not successfully drop and adhere to produce tomonts.
Taking HF's numbers as a reference - even if you don't take out all free-swimmers and droppers - if you can reduce the infectivity rate below 200:1 - the parasitic cycle will break.

Working in your favor is the natural immunity building in the fish coupled with the senescence of the cell line. Keep the attachment rate below the lethal loading - and the parasite more or less self eradicates. It's simple math. DF also reduces bacterial load and helps prevent secondary infection - which is also a plus.

We tend to naively interpret lab results and try to apply them to our systems, sometimes without considering the fact that lab tanks are in many ways different from the tanks we run at home. There are many aspects of the life-cycle if ich and velvet that have not been explored and are not well understood but which are bit-by bit being figured out.

Senescence of cilliate lines was observed and described over a hundred years ago - and it is reliably observed in virtually every study of marine ich. In the lab - it can be a significant challenge to maintain a viable cell line - so much so that special techniques have had to be developed just to complete a study will a single strain before it dies off on its' own from old age even though it is "fed" a diet of fish which have never had any exposure and have acquired no immunity. Turns out there is a limit to how many times a cell can reproduce by budding as it typically takes place in the tomont under laboratory conditions. How is this observed senescence avoided in the wild - or as some here suggest - in our reef systems? No one knows for sure.

The are researchers looking for the genetic loci of ich's ability to enter into deep hibernation states. Of course they are looking based on its impact on fisheries and the observed seasonality of outbreaks. Is it entering or exiting these hibernation states, which revitalizes the cell line and restores infectivity? Sexual and/or autogamous reproduction which clears DNA damage and restores shortened telomeres - is that the missing piece of the life-cycle which keeps ich and velvet disappearing through senescent eradication? Looks possible. Looks probable as a matter of fact.

So what are the trigger(s) for deep hibernation? Are they the same for autogamous or sexual reproduction? What are the environmental conditions in a "lab" tank which precludes these states. We know temperature can have an effect - but if this were the only agent - then senescence should be the rule in our tanks as well. It turns out that there is (at least) one other environmental trigger. Hypoxic conditions with O2 levels < 23% have also been seen to be inductive of deep hibernation states. These regions do exist in our tanks - notably areas of the substrate. Tomonts of ich can be revived from hypoxic induced hibernation six, seven or eight months later after exposure to an oxygen rich environment. Thermoclines and/or hypoxia? Thermoclines in our systems - no.

Ich or velvet hibernating in sand beds or other regions of reduced 02 saturation - very possible.
Robert
Thanks for the info. Lots of science here. What do you mean by Hypoxic conditions? Does that mean it hibernates in the sand and when right conditions appear, it reappears? that is kind of scary.
SO when I siphone my sand, if I stir the bed too much, it can release the tomonts and get them alive again?
 

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Robert
Thanks for the info. Lots of science here. What do you mean by Hypoxic conditions? Does that mean it hibernates in the sand and when right conditions appear, it reappears? that is kind of scary.
SO when I siphone my sand, if I stir the bed too much, it can release the tomonts and get them alive again?

yes, but technically the tomonts don't die - they enter a reduced metabolic state - perhaps autophagic - but they can survive, emerge and infect at a much later date than our fallow protocol anticipates.
 

Arvind Arya

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yes, but technically the tomonts don't die - they enter a reduced metabolic state - perhaps autophagic - but they can survive, emerge and infect at a much later date than our fallow protocol anticipates.
there seems to be no escaping them, bar they never are in your system to begin with.
In the wild, I am sure it hardly appears as fish do not live in a trapped space. Sometimes I wonder about the ethics of fish keeping. Of course, not when my fish are healthy, only when they die. :(
 
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The are researchers looking for the genetic loci of ich's ability to enter into deep hibernation states. Of course they are looking based on its impact on fisheries and the observed seasonality of outbreaks. Is it entering or exiting these hibernation states, which revitalizes the cell line and restores infectivity? Sexual and/or autogamous reproduction which clears DNA damage and restores shortened telomeres - is that the missing piece of the life-cycle which keeps ich and velvet from disappearing through senescent eradication? Looks possible. Looks probable as a matter of fact.

So what are the trigger(s) for deep hibernation? Are they the same for autogamous or sexual reproduction? What are the environmental conditions in a "lab" tank which precludes these states. We know temperature can have an effect - but if this were the only agent - then senescence should be the rule in our tanks as well. It turns out that there is (at least) one other environmental trigger. Hypoxic conditions with O2 levels < 23% have also been seen to be inductive of deep hibernation states. These regions do exist in our tanks - notably areas of the substrate. Tomonts of ich can be revived from hypoxic induced hibernation six, seven or eight months later after exposure to an oxygen rich environment. Thermoclines and/or hypoxia? Thermoclines in our systems - no. Areas of Hypoxia - yes.

Ich or velvet hibernating in sand beds or other regions of reduced 02 saturation - very possible. Maybe part of the fallow protocol should involve addressing potential hypoxic areas of the system? Or we may find that there are other potential facilitators of Deep hibernation - maybe in some cases it just a matter of chance.

Do you have any citations to support this? Proven studies??
 

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Do you have any citations to support this? Proven studies??

Support what? Any proven studies or citations which demonstrate the effectiveness of 76 day fallow period? I would only need one > 76 days to disprove the theory right?

I for one believe that in a well oxygenated system devoid of hypoxic zones and kept at typical reef temperatures, absent reintroduction - the fallow period could be much, much shorter and still be effective. I also believe, that in such a system, ich will likely self-eradicate through senescence in ~30-50 cellular divisions whether you remove fish or not with an average around 25.

Which particular aspect are you questioning? Is it senescence, autogamy, autophagy, deep hibernation and its triggers? I have do have citations -
 
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@robert I’m asking to see the “recent evidence” that ich/velvet can “hibernate” in areas of reduced 02 saturation. Basically, I’m looking for proof to back up the assertion you made below:

Recent evidence is that under some conditions found in our tanks, the tomont phase can be substantially extended, potentially resulting in a re-infestation six, seven or eight months after encystment.
 

Arvind Arya

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From the article:
Final thoughts:The outbreak of Amyloodinium I am still treating for, occurred during a period where no fish were added to the tank (last fish added over 6 months ago), and no significant change in water quality was reported. This means that the parasite was either dormant in the substrate or imbedded on fish tissue with no outward signs of infection. Either or could be the case, and it’s important to understand that research has shown that some fish develop an interesting immune response to Amyloodinium. The parasite will embed and begin feeding, but the fish’s body produces something that nullifies the parasite. This means that even if all fish are removed from the display for an extended period of time, there is still a chance of parasitic reoccurrence. Quarantine and prevention, as always, is the best medicine, but even under the best circumstances, it’s not uncommon to come face to face with this common parasite. In wide spread aqua culture, Amyloodinium has been a serious threat to fisheries, and even with modern day technology proves difficult to entirely prevent or eradicate. An infestation of Amyloodinium doesn’t signal poor husbandry practices and many forum users like to believe, just an unfortunate scenario that will test your skills as an aquarist.
 
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From the article:
Final thoughts:The outbreak of Amyloodinium I am still treating for, occurred during a period where no fish were added to the tank (last fish added over 6 months ago), and no significant change in water quality was reported. This means that the parasite was either dormant in the substrate or imbedded on fish tissue with no outward signs of infection. Either or could be the case, and it’s important to understand that research has shown that some fish develop an interesting immune response to Amyloodinium. The parasite will embed and begin feeding, but the fish’s body produces something that nullifies the parasite. This means that even if all fish are removed from the display for an extended period of time, there is still a chance of parasitic reoccurrence. Quarantine and prevention, as always, is the best medicine, but even under the best circumstances, it’s not uncommon to come face to face with this common parasite. In wide spread aqua culture, Amyloodinium has been a serious threat to fisheries, and even with modern day technology proves difficult to entirely prevent or eradicate. An infestation of Amyloodinium doesn’t signal poor husbandry practices and many forum users like to believe, just an unfortunate scenario that will test your skills as an aquarist.

The author doesn't mention if any corals/inverts had been added recently ;): https://www.reef2reef.com/ams/how-to-quarantine-coral-and-inverts.228/

Or rock/sand that possibly had encysted tomonts. Or cross contamination (wet hands, shared equipment, water change hoses, feeding apparatus, etc.) from a quarantine or other infected tank. There's even aerosol transmission to consider: https://www.reef2reef.com/threads/aerosol-transmission.190292/

My point is infected fish aren't the only way to get velvet in a tank. Anything wet can do it. ;Nailbiting
 

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HF

Is leaving contaminated equipment in tap water outside in a bucket for 48 hrs enough to kill any Velvet?
 
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Humblefish

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HF

Is leaving contaminated equipment in tap water outside in a bucket for 48 hrs enough to kill any Velvet?

I can't say for sure, but I wouldn't trust that because in an older study velvet survived for a time in filtered tap water:

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Source: https://www.jstor.org/stable/3282348?seq=1#page_scan_tab_contents

Using bleach and/or complete drying for 24 hours is a better choice for disinfection.
 

Arvind Arya

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Thanks I will air dry my equipment....
This fallow period really sucks. I hate looking at my tank - minus a yellow tang and triggerfish- some of my faves
 
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Thanks I will air dry my equipment....
This fallow period really sucks. I hate looking at my tank - minus a yellow tang and triggerfish- some of my faves

Sorry to hear. Ain't nothing easy about this hobby. There's always something to deal with.
 

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Nice find Arvind...the oft reported failure of fallow periods to totally eliminate ich and velvet from a reef system has been the subject of heated debate for years. Some, will reject observations such as the one offered by Gosnell, insisting that some form of cross contamination had to take place. I think however that those who do, have a shallow grasp of the subject area and over-estimate what we (collectively) really know.

Differential Gene Expression (DGE) analysis is a fairly new technique which has been used to investigate ich's life-cycle alterations to cold water. It turns out that the cold changes the encystment of the tomonts in such a way so as to allow the tomont to extend encystment for many months. See: Transcriptome analysis of dormant tomonts of the marine fish ectoparasitic ciliate Cryptocaryon irritans under low temperature. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4867990/ Read the article and you'll get some appreciation of the mechanisms involved and how the loci were identified resulting in four to five months of dormancy.

After that read: Dormancy induced by a hypoxic environment in tomonts of Cryptocaryon irritans, a parasitic ciliate of marine teleosts.
"When transferred into the hypoxic environment after incubation in an oxic environment (air-saturated, 8.7–8.9 mg/L O2) for 1–4 days, their development stopped in 1 day. However, when dormant tomonts generated in the hypoxic environment were transferred to the oxic environment, they resumed development and released theronts. These results indicate that tomonts can become dormant when exposed to a hypoxic environment, but can resume development when exposed to an oxic environment at any developmental stage. When exposed to the oxic environment, tomonts recovered from 1-month dormancy and released as many theronts as control tomonts constantly incubated in the oxic environment. The infectivity of theronts from the recovered tomonts was similar to the control tomonts."

The main take-aways from this study are:
1. that tomonts of Cryptocaryon irritans become dormant in hypoxic environments.
2.that Dormant tomonts resume development in oxic environments at any developmental stages.
None of this would be surprising to anyone with a general exposure to the study of dormancy in ciliates and protozoa. In fact it would be more surprising that such organisms would *not* have a DGE to environmental stress.

 

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