Wow, that is very interesting.
Spindle Leg Syndrome- Possible Cause?
Check this out. An earlier post lead us to the British Dendroboad and their Newsletters. In one of them is an article on spidle-leg....
I would be interested in what Ed thinks of this.
This was written in approx. 1990SPINDLY-LEG SYNDROME
Dendrobatid breeding has been plagued by the spindly-leg syndrome in recent years, in the U.S.A. and Europe as well as in Britain. Breeders have been very disappointed to find, after spawning their frogs and carefully rearing the tadpoles, that they develop this condition, necessitating euthanasia immediately after metamorphosis. The symptoms are small and ineffective forelimbs, though usually these are perfectly formed. Conversely, the hind limbs are normal. The causes of this condition have been debated and many varying reasons for its occurrence have been suggested. The have included a lack of some factor in the diet of either the parent frogs or the tadpoles, an incorrect environmental parameter, or genetic problem. I have discounted the possibility of the syndrome being genetic in origin as it has occurred in clutches from frogs producing previously healthy larvae, occurring only after intensive breeding. I have also discounted the environmental factor, as I find it hard to believe an environmental parameter occurring in breeder's vivarium but not in the wild state, to result in such handicapping condition. As the forelimbs are the last to develop in the process of metamorphosis, this implies a lack or depletion of some factor that has been exhausted in the previous developmental stages. The larval diet consists generally of good-quality fIsh-food. Whilst not a natural diet mimic, this food should provide all possible nutrients including minerals or all but one. The natural larval diet of non egg-feeders must consist of decaying plant and insect matter (detritus feeders), these items falling into the water body in which the larvae are living, be this a living bromeliad in the treetops, mud puddle on the forest floor or the water in a discarded Coke can. It is possible that the female frog supplies the necessary developmental factors since the adult diet is far less restricted an, thus vital vitamins and minerals may be passed on via the egg yolk. I do not feel a lack of vitamins is responsible since I as well as others who have experienced this syndrome dust livefood will multi-vitamin preparations. My search for a missing factor led me back to my biology text books. The development and metamorphosis of the tadpole into a frog involves complex, morphological changes that are controlled by hormones. These hormones promote the development of certain cells to produce the new limbs and organs of the frog. The main hormone concerned with this cell differentiation is thyroxine, produced by the thyroid gland. Thyroxine contains iodine. If the diet of the parent or the tadpole were deficient in iodine, then there would be a deficiency of thyroxine, the hormone responsible for metamorphosis. There may be enough thyroxine for development up to a point, but not enough for the later developmental stage, that of forelimb growth. I have started to use the iodine nibbles used for cage birds, added to the tadpoles' water and also dusted on the food for adult frogs. In a batch of D. tinctorius that had previously shown 100% offspring with spindly-leg, those tadpoles that had not started to develop limbs prior to iodine addition have developed into perfect frogs. I am still investigating iodine deficiency and would like to show recurrence of the syndrome when iodine is discontinued. However, the immediate correction after the addition of iodine suggests strongly that iodine deficiency is the cause of spindly-leg syndrome. STEVE HALFPENNY
I would be interested in what Ed thinks of this.
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This was on another page.........
SPINDLY-LEG SYNDROME
In my colony of D. auratus West Coast I must lose some 60% of larvae to spindly leg. It is particularly frustrating because this insidious condition only shows itself during what amounts to be the last five minutes of tadpole's development. It is sad enough to have to dispose of a young tadpole but I find having to dispose of a young frog just a it is showing its first beautiful colours even more distressing. I have tried everything I can think of to try to counteract the effects of this condition. Frozen foods for tropical fish; live foods; dried foods; mineral supplements as well as plain cuttlefish. Bearing all this in mind, then, I'm afraid Steve Halfpenny's idea of iodine supplement did not come as an earthshattering revelation to me. I rang one or two people up to discuss the idea with them and, not surprisingly, they shared my scepticism. However, not wanting to put a damper on things before giving it a fair trial, I proceeded to try out Steve's idea on my current batch of ten larvae. They were a couple of weeks old, from two different spawnings, but still do not have their hind legs. They seemed ideal candidates for the trial. I looked after the tadpoles exactly as before except that, after each daily water change, I added to each container a couple of droppers-full of ground iodine block as manufactured for cage birds, mixed with a little water (Johnson's Iodised Condition Pek [sic]). Some of this sank to the bottom in a fine powder, while it seemed clear that a proportion had dissolved. The food was, as before, TetraMin flake (type: Staple food, yellow drum, dark brown lid); the Tradescantia shoots were still present as before. I kept rigidly to this regime... and waited... and waited. I finally got to the point where the first larvae were due to push through their front legs. Up to this point, their development had been completely as it had been in hundreds of larvae before them. Good appetites. Good growth rates. In other words, text book offspring. Out of ten larvae, I expected to lose at least six. Imagine my surprise when, one by one, the larvae developed absolutely normal, healthy front legs. I have a 50% success rate with these at the moment, and don't doubt for one minute that I will have similar successes with the remainder. I have several batches of eggs incubating at the moment, and can't wait for another chance to try this technique, just to make sure it isn't just
a fluke. I'm now sure in my own mind that it is not. Suffice it to say that my thanks must go to Steve for his observations - but I can't help but ask myself: having tried just about everything I could think of, why did I not think of iodine myself. Just goes to show... JOHN SKILLCORN
Wow that is amazing. I agree..where's Ed?
Busy,
There have been many conjectures on the cause of SLS and just as many cures. There have people who have tried the iodine supplement and did not have a change in the incidence of SLS. (I have a copy of this article already) and other people did get a reduction or elimination.
One of the items that I thought was interesting was that iodine is typically restricted to marine sources and deep earth so I was surprised that the iodine looked to be the cure given that in the wild the places they live would be iodine poor habitats.
I am also not convinced that there wasn't one or more other micronutrients that were required that the supplement supplied (for example as a general analysis the product used by the second article contains snip "Contains iodine, grits, seaweed extract, calcium,
yeast, vitamins and minerals, etc." endsnip which includes just about everything....)
Metamorphosis is a complex feedback mechanism that would allow for disruptions to occur at multiple points with the same result.
As a side point, this is also an insufficient definition of SLS and if you review all of the literature, the description varies from no front legs to one front leg to abnormal front legs (in some cases only one developing abnormally or at all) and cases in which the front and hind limbs are deformed or absent.
Some comments,
Ed
PS: I will be doing a workshop/discussion group on SLS at the 2007 IAD....
There have been many conjectures on the cause of SLS and just as many cures. There have people who have tried the iodine supplement and did not have a change in the incidence of SLS. (I have a copy of this article already) and other people did get a reduction or elimination.
One of the items that I thought was interesting was that iodine is typically restricted to marine sources and deep earth so I was surprised that the iodine looked to be the cure given that in the wild the places they live would be iodine poor habitats.
I am also not convinced that there wasn't one or more other micronutrients that were required that the supplement supplied (for example as a general analysis the product used by the second article contains snip "Contains iodine, grits, seaweed extract, calcium,
yeast, vitamins and minerals, etc." endsnip which includes just about everything....)
Metamorphosis is a complex feedback mechanism that would allow for disruptions to occur at multiple points with the same result.
As a side point, this is also an insufficient definition of SLS and if you review all of the literature, the description varies from no front legs to one front leg to abnormal front legs (in some cases only one developing abnormally or at all) and cases in which the front and hind limbs are deformed or absent.
Some comments,
Ed
PS: I will be doing a workshop/discussion group on SLS at the 2007 IAD....
Thanks for your input Ed. I wish I could attend IAD t hear your workshop. Can you make the material accesable to us after the IAD? say in .pdf format.
Here is one more item from the BD about SLS, (it's a long one, but worth reading) not to confuse the issue, it just gives us very good ideas to think about...
[/quote]DEVELOPMENTS IN THE STUDY OF SPINDLE LEG SYNDROME
Spindle leg syndrome, a condition that was identified as a problem many years ago, affects the front legs of metamorphosing tadpoles. The result is froglets which have weak, deformed limbs and which are seldom able to feed effectively and thus die. Last year I attended the "Anuren Taggung 1998" in Germany where I gained further information about Spindle Legs which I have investigated and now produce my conclusions.
A German vet, Dr. Thomas Wohrmann, from the University of Aachen, has examined, by histology, hundreds of affected Dendrobatids and has found the following:
1) The thyroid gland is always normal
2) The fore-legs always have muscular atrophy
3) The spinal column has subtotal dystrophy
4) The medulla oblongata is not closed
Because I am an amateur, but wanted to fully understand what this meant, I spoke with veterinary professors in Belgium and the Netherlands and these are the conclusions:
1. Whilst the thyroid is histologically normal this does not confirm normal secretion of hormones which requires further investigation.
2. This muscular atrophy is the histological examination of the visible effect of spindle leg. The 'elbows' are fixed and the musculature has too few fibres, which are also small (Gouda & Hak, University of Utrecht, 1995).
3. The spinal column has subtotal dystrophy, it is not completely closed.
4. The medulla oblongata is not closed at all (this is the section of the brain that connects with the spinal chord).
THE BIOLOGY:
(Development stages are the standard stages of early development of anurans according to Gosner, 1960)
In the development of frogs eggs the closing of the spinal column starts at stage 13, when the neural plate is formed. This closing is complete at stage 15 when a neural tube is completely formed. The medulla oblongata stays open which is normal for amphibians. The closing of the spinal column and the formation of the forelegs are controlled by a gene, the homeobox gene XLHBox 1. If there is a disturbance of this gene, the frogs develop spindly legs. The German investigators were able to generate this in the laboratory and each time they introduced a disrupter the frogs developed spindly legs. The external influences on that gene are not known, but it is possible that the disrupter is introduced by the parents, by high temperature or radiation (perhaps UV?), after the eggs have been laid, but prior to the tadpoles becoming free swimming at Stage 25.
If this is true, it means that it is too late to change the process once tadpoles have formed as the genetic information to produce spindly legs is set in the egg. Only the influences of temperature or radiation can generate a further disruption of the gene making it impossible to repair a disruption that has existed from stages 13 to 15. Therefore, in my opinion, if we wish to find the reasons for spindly leg, and its cure, we must look at the parents, not the tadpoles.
The human condition, spina bifida, in which babies are born with a spinal column not completely closed is also caused by the XLHBox 1 gene. The incidence of the condition has been demonstrated to be reduced by giving, the mother large quantities of folic acid, and often vitamin E, as a prophylactic. Both spindly legs and spina bifida are conditions generated by a disruption of the same gene making it feasible that the same prophylactic could work, a possibility which must be worth trying with frog parents.
The Question:
It is questionable how the frogs obtain these substances in the wild but it should be possible to give the frogs fruit flies dusted with folic Acid and vitamin E powders but how, and in what quantities, as there is no information on dosage for amphibians? Pregnant women are frequently given a medication called OMNIBIOTA Prenatal which gives a dose of folic acid of 5mg and 12mg of vitamin E for a woman of 55kg body weight. This equates to 0.lmg and 0.22mg/kg respectively.
Folic Acid: Because folic acid is one of the vitamins from the B complex, there is little risk of hypervitaminosis (overdosing). Information for fish and poultry gives a dosage of about 10 to 20 mg folic acid /kg food. Daily
doses of 20 mg/kg body weight would seem to be sufficient for fish and poultry but this is over 100 times the level indicated for humans.
Vitamin E: In a professional fish food for Tillapia and Trout, a dosage of 50-100mg/kg bodyweight of fish is given. This is again, at least, 200 times the level indicated for humans. Vitamin E prevents the formation of free radicals that can initiate the disruption of the relevant gene.
As our normally used vitamin and mineral supplements contain very low levels of both folic acid and vitamin E, I suggest that some form of supplementation may be necessary, though a considerable amount of work will be needed to ascertain dosages. It may be that, in the first instance, a simple addition to the usual vitamin/mineral supplements, might be tried.
The next text is from Brander G. C. & Pugh D. 11 1977 Veterinary Applied Pharmacology and Therapeutics: Folic acid, folinic acid, vitamin C and cyanocobalamin are connected with nucleic acid synthesis. The acid is also involved in ansmethylating actions along with cyanocobalamin, both in nucleoprotein formation and in fat metabolism through methylation in the synthesis of choline and methionine. Through this latter action folic acid and cyanocobalamin reduce nutritional requirements of choline and methionine. Clinically the symptoms shown in experimentally induced deficiencies are unlikely to occur. These symptoms include macrocytic anaemias with reduction in the numbers of all cellular elements of the blood, diarrhoea, skin lesions, reduced growth rates in experimental animals and birds. It should be noted, however, that, as with paraaminobenzoic acid, which is a precursor of folic acid, small quantities of the gut 'active' sulphonamides will promote a deficiency, probably by reducing bacterial numbers and therefore the synthesis of this and other vitamins.
Therapy when an outbreak of (vitamin E) deficiency disease is suspected usually consists of immediate administration of vitamin E and/or selenium in whatever form is appropriate and convenient. Nutritional requirements are not defined. This is possibly because the availability of the vitamin is conditioned by the composition of the diet. Where the level of unsaturated fatty acids in the diet is high, the vitamin requirements will also be high, but it should be remembered that other compounds and conditions besides these acids will depress absorption of vitamin E, including triorthocresylphosphate (in. some species), possibly sulphaguanidine and gastroenteritis. It must also be borne in mind that variations in mineral and carbohydrate concentrations in a diet will modify the symptoms resulting from a vitamin E deficiency or insufficiency. Deficiencies other vitamins such as choline may predispose muscles to the effects of vitamin E deficiencies.
Conclusions: Many people are, trying to solve the problems of spindly leg and, whilst not suggesting that my ideas are the answer, I feel that they are worthy of further investigations. Hugo Claessen Antwerp Belgian Herpetological Society
Editor's note:
Whilst some of Hugo's article above is conjecture, it is well thought out and would form an excellent basis for further research. If there are any members currently producing froglets with spindle leg it would be worth adding vitamin E and folic acid to the usual vitamin and mineral supplements to see if this alleviates the problem. Please let the rest of us know your results.
Here is one more item from the BD about SLS, (it's a long one, but worth reading) not to confuse the issue, it just gives us very good ideas to think about...
[/quote]DEVELOPMENTS IN THE STUDY OF SPINDLE LEG SYNDROME
Spindle leg syndrome, a condition that was identified as a problem many years ago, affects the front legs of metamorphosing tadpoles. The result is froglets which have weak, deformed limbs and which are seldom able to feed effectively and thus die. Last year I attended the "Anuren Taggung 1998" in Germany where I gained further information about Spindle Legs which I have investigated and now produce my conclusions.
A German vet, Dr. Thomas Wohrmann, from the University of Aachen, has examined, by histology, hundreds of affected Dendrobatids and has found the following:
1) The thyroid gland is always normal
2) The fore-legs always have muscular atrophy
3) The spinal column has subtotal dystrophy
4) The medulla oblongata is not closed
Because I am an amateur, but wanted to fully understand what this meant, I spoke with veterinary professors in Belgium and the Netherlands and these are the conclusions:
1. Whilst the thyroid is histologically normal this does not confirm normal secretion of hormones which requires further investigation.
2. This muscular atrophy is the histological examination of the visible effect of spindle leg. The 'elbows' are fixed and the musculature has too few fibres, which are also small (Gouda & Hak, University of Utrecht, 1995).
3. The spinal column has subtotal dystrophy, it is not completely closed.
4. The medulla oblongata is not closed at all (this is the section of the brain that connects with the spinal chord).
THE BIOLOGY:
(Development stages are the standard stages of early development of anurans according to Gosner, 1960)
In the development of frogs eggs the closing of the spinal column starts at stage 13, when the neural plate is formed. This closing is complete at stage 15 when a neural tube is completely formed. The medulla oblongata stays open which is normal for amphibians. The closing of the spinal column and the formation of the forelegs are controlled by a gene, the homeobox gene XLHBox 1. If there is a disturbance of this gene, the frogs develop spindly legs. The German investigators were able to generate this in the laboratory and each time they introduced a disrupter the frogs developed spindly legs. The external influences on that gene are not known, but it is possible that the disrupter is introduced by the parents, by high temperature or radiation (perhaps UV?), after the eggs have been laid, but prior to the tadpoles becoming free swimming at Stage 25.
If this is true, it means that it is too late to change the process once tadpoles have formed as the genetic information to produce spindly legs is set in the egg. Only the influences of temperature or radiation can generate a further disruption of the gene making it impossible to repair a disruption that has existed from stages 13 to 15. Therefore, in my opinion, if we wish to find the reasons for spindly leg, and its cure, we must look at the parents, not the tadpoles.
The human condition, spina bifida, in which babies are born with a spinal column not completely closed is also caused by the XLHBox 1 gene. The incidence of the condition has been demonstrated to be reduced by giving, the mother large quantities of folic acid, and often vitamin E, as a prophylactic. Both spindly legs and spina bifida are conditions generated by a disruption of the same gene making it feasible that the same prophylactic could work, a possibility which must be worth trying with frog parents.
The Question:
It is questionable how the frogs obtain these substances in the wild but it should be possible to give the frogs fruit flies dusted with folic Acid and vitamin E powders but how, and in what quantities, as there is no information on dosage for amphibians? Pregnant women are frequently given a medication called OMNIBIOTA Prenatal which gives a dose of folic acid of 5mg and 12mg of vitamin E for a woman of 55kg body weight. This equates to 0.lmg and 0.22mg/kg respectively.
Folic Acid: Because folic acid is one of the vitamins from the B complex, there is little risk of hypervitaminosis (overdosing). Information for fish and poultry gives a dosage of about 10 to 20 mg folic acid /kg food. Daily
doses of 20 mg/kg body weight would seem to be sufficient for fish and poultry but this is over 100 times the level indicated for humans.
Vitamin E: In a professional fish food for Tillapia and Trout, a dosage of 50-100mg/kg bodyweight of fish is given. This is again, at least, 200 times the level indicated for humans. Vitamin E prevents the formation of free radicals that can initiate the disruption of the relevant gene.
As our normally used vitamin and mineral supplements contain very low levels of both folic acid and vitamin E, I suggest that some form of supplementation may be necessary, though a considerable amount of work will be needed to ascertain dosages. It may be that, in the first instance, a simple addition to the usual vitamin/mineral supplements, might be tried.
The next text is from Brander G. C. & Pugh D. 11 1977 Veterinary Applied Pharmacology and Therapeutics: Folic acid, folinic acid, vitamin C and cyanocobalamin are connected with nucleic acid synthesis. The acid is also involved in ansmethylating actions along with cyanocobalamin, both in nucleoprotein formation and in fat metabolism through methylation in the synthesis of choline and methionine. Through this latter action folic acid and cyanocobalamin reduce nutritional requirements of choline and methionine. Clinically the symptoms shown in experimentally induced deficiencies are unlikely to occur. These symptoms include macrocytic anaemias with reduction in the numbers of all cellular elements of the blood, diarrhoea, skin lesions, reduced growth rates in experimental animals and birds. It should be noted, however, that, as with paraaminobenzoic acid, which is a precursor of folic acid, small quantities of the gut 'active' sulphonamides will promote a deficiency, probably by reducing bacterial numbers and therefore the synthesis of this and other vitamins.
Therapy when an outbreak of (vitamin E) deficiency disease is suspected usually consists of immediate administration of vitamin E and/or selenium in whatever form is appropriate and convenient. Nutritional requirements are not defined. This is possibly because the availability of the vitamin is conditioned by the composition of the diet. Where the level of unsaturated fatty acids in the diet is high, the vitamin requirements will also be high, but it should be remembered that other compounds and conditions besides these acids will depress absorption of vitamin E, including triorthocresylphosphate (in. some species), possibly sulphaguanidine and gastroenteritis. It must also be borne in mind that variations in mineral and carbohydrate concentrations in a diet will modify the symptoms resulting from a vitamin E deficiency or insufficiency. Deficiencies other vitamins such as choline may predispose muscles to the effects of vitamin E deficiencies.
Conclusions: Many people are, trying to solve the problems of spindly leg and, whilst not suggesting that my ideas are the answer, I feel that they are worthy of further investigations. Hugo Claessen Antwerp Belgian Herpetological Society
Editor's note:
Whilst some of Hugo's article above is conjecture, it is well thought out and would form an excellent basis for further research. If there are any members currently producing froglets with spindle leg it would be worth adding vitamin E and folic acid to the usual vitamin and mineral supplements to see if this alleviates the problem. Please let the rest of us know your results.
Interesting reading. Thanks to all who have posted material.
Alan
Alan
before people begin adhoc additions of vitamin E please keep in mind that this is a fat soluable vitamin that can be overdosed. Not only can it be over dosed but it also competes for uptake with vitamin A and D3 so if the ratio of supplementation of A: D3: E exceeds 10:1:0.1 conditional deficiencies can also develop.
In practice deficiencies in vitamin E are very rarely seen in captive animals unless they have been fed foods in which the fatty acids have begun to degrade.
Yes the development of the limbs can be disrupted early assuring SLS but there are also indications that it can be disrupted later in development.
After installing a carbon prefilter set on the water supply for the amphibians we went from 0% SLS to 100% SLS in multiple genera of anurans (Smilesca, Epidobates and Dendrobates). This was tested with several controls ( Artificial Pond Water made with RO, Carbon filtered and aged tap water) and at the end of study all surviving tadpoles were placed back into aged tap water. The resulting metamorphs demonstrated a range of SLS from no legs to usable but thin front legs to totally normal legs depending on the age of the tadpole when it was switched back to aged tap water. All of the tadpoles were well after Gosner stage 25.
Some more comments
Ed
In practice deficiencies in vitamin E are very rarely seen in captive animals unless they have been fed foods in which the fatty acids have begun to degrade.
Yes the development of the limbs can be disrupted early assuring SLS but there are also indications that it can be disrupted later in development.
After installing a carbon prefilter set on the water supply for the amphibians we went from 0% SLS to 100% SLS in multiple genera of anurans (Smilesca, Epidobates and Dendrobates). This was tested with several controls ( Artificial Pond Water made with RO, Carbon filtered and aged tap water) and at the end of study all surviving tadpoles were placed back into aged tap water. The resulting metamorphs demonstrated a range of SLS from no legs to usable but thin front legs to totally normal legs depending on the age of the tadpole when it was switched back to aged tap water. All of the tadpoles were well after Gosner stage 25.
Some more comments
Ed
Hi Ed,
I dont understand the correlation between the carbon filtered water and the occurance of SLS. Are you saying that using carbon filters will cause SLS? Is it because of the removal of certain other"nutrients"(for lack of a better term) or that the chlorine was not all removed or something else?
I dont understand the correlation between the carbon filtered water and the occurance of SLS. Are you saying that using carbon filters will cause SLS? Is it because of the removal of certain other"nutrients"(for lack of a better term) or that the chlorine was not all removed or something else?
I am not and will not say carbon filtered water WILL cause SLS. I will say in once instance it has caused SLS as this was the only parameter changed in the husbandry resulting in 100% SLS in several genera and that when the husbandry was changed back to tap water the incidence of SLS went from 100% back to 0%.
I was using this to illustrate that disruption of the development can occur later in the tadpole's development. (This is the link to SLS and artificial pond water mentioned in Amphibian Medicine and Captive Husbandry)...
Ed
I was using this to illustrate that disruption of the development can occur later in the tadpole's development. (This is the link to SLS and artificial pond water mentioned in Amphibian Medicine and Captive Husbandry)...
Ed
who knows what they put in that jersey water. i just wanted to clarify that i use carbon in both whole house filtration and my fluval 404 and havent had a problem w/ sls since i started using them. it mustve been a water additive that evaporates over time or a buildup of chlorine in the filter and some slow release from breakdown or something. i have no experience to relate it to as ive never used carbon filtered tap water.
i was wondering how long this went on for. do you use jars of vit and calcium and fish food like we do? i was just wondering if the time period this happened could have been synonymous with the amount of time it takes for you to go thru a jar of vitamins or fish food and there was some possibility of a spoiled product.
if i understand correctly, the only tads that exhibited sls were the ones that were placed in carbon filtered water(not set out for 24hrs) and the pond water and aged tap water tads didnt have spindly?
sorry, i just want to understand this correctly. i have found that tads can get sls from heat, cold, bad tad nutrients(although this is unlikely given a good diet to the parents) and mostly from the shape the breeders are in(heat stress, cold, sufficient vit and minerals etc) and i imagined it could be caused by hormone disruptors and other chemicals in the environment. i had never heard of carbon filters being a culprit and can only surmise that there was a chemical that would evaporate but not be filtered by the carbon. i`m not saying you didnt see what you saw, i`m just trying to deduce a cause between our 2 experiences w/ carbon prefilters. i imagine there is also a difference between my modest carbon house filters and the system installed for a zoo. did you do a chemistry workup on strait tap, carbon filtered tap and aged tap water? this is interesting as we may be able to figure out why some people are having problems if they are using carbon pre filters on municipal water systems. you didnt have a group of aged carbon filtered water tads did you? this may tell if it was something the water had which would evaporate or if it was a byproduct of the system. if the aged filtered tads showd no spidly it was just that the water system wasnt removing all the chlorine or the re was something else that wasnt removed and needed time to evaporate.
i was wondering how long this went on for. do you use jars of vit and calcium and fish food like we do? i was just wondering if the time period this happened could have been synonymous with the amount of time it takes for you to go thru a jar of vitamins or fish food and there was some possibility of a spoiled product.
if i understand correctly, the only tads that exhibited sls were the ones that were placed in carbon filtered water(not set out for 24hrs) and the pond water and aged tap water tads didnt have spindly?
sorry, i just want to understand this correctly. i have found that tads can get sls from heat, cold, bad tad nutrients(although this is unlikely given a good diet to the parents) and mostly from the shape the breeders are in(heat stress, cold, sufficient vit and minerals etc) and i imagined it could be caused by hormone disruptors and other chemicals in the environment. i had never heard of carbon filters being a culprit and can only surmise that there was a chemical that would evaporate but not be filtered by the carbon. i`m not saying you didnt see what you saw, i`m just trying to deduce a cause between our 2 experiences w/ carbon prefilters. i imagine there is also a difference between my modest carbon house filters and the system installed for a zoo. did you do a chemistry workup on strait tap, carbon filtered tap and aged tap water? this is interesting as we may be able to figure out why some people are having problems if they are using carbon pre filters on municipal water systems. you didnt have a group of aged carbon filtered water tads did you? this may tell if it was something the water had which would evaporate or if it was a byproduct of the system. if the aged filtered tads showd no spidly it was just that the water system wasnt removing all the chlorine or the re was something else that wasnt removed and needed time to evaporate.
Maybe we should start a poll about SLS...
We could have people post their raising protocol and their rates of SLS and importantly their location and type of water used.
If we get enough posts and enough people from one area (say, Idaho) that use the same type of water (say, well water) and they all have similarly high (or low) rates of SLS, maybe we can tease out some of the details of what contaminants may contribute to sls...
Just a thought.
Great thread.
~B
We could have people post their raising protocol and their rates of SLS and importantly their location and type of water used.
If we get enough posts and enough people from one area (say, Idaho) that use the same type of water (say, well water) and they all have similarly high (or low) rates of SLS, maybe we can tease out some of the details of what contaminants may contribute to sls...
Just a thought.
Great thread.
~B
i tried that when i got my well. i asked what kind of water people used and how it worked. no one responded.
Okay I'll go over the break down and you can see how we narrowed it down to the filter.
There was a 0% incidence of SLS in any anuran here at work with the earlier exception of some Smilesca phaeota that were heavily parasitized with nematodes until the incidence of the carbon filtration of incoming water. After SLS started up (we went from 0% in those species to 100%, there were no exceptions), there were multiple changes to both the supplements for the adults as well as the tadpoles as well as foods used with no change in the incidence of SLS (still 100%).
Three groups of tinct tadpoles were setup and reared in the following manner (same food and supplements between all groups)
1) clutches were split amoung the three test groups to reduce/eliminate any genetic influences on the development
2) tadpoles were reared in labeled dannon pint yogurt containers filled to the same volume
3) containers were maintained in mixed groups in the exact same locations to prevent thermal differences from skewing the results
4) tadpoles were kept in three different locations to eliminate temperature difference as a potential cause
5) test groups were maintained in one of the following
a) artificial pond water made with RO water (aged 48 hours)
b) carbon treated aged tap water (aged for 48 hours)
c) tapwater aged for 48 hours
6) tadpoles were fed and cleaned on the same schedules
7) necropsied SLS affected metamorphs were not parasitized like the earlier mentioned Smilesca phaeota.
In the test the following results developed
artificial pond water had 100 %SLS
carbon filtered tapwater has 100% SLS
aged tapwater had 0% SLS.
After about 15-20 tads metamorphed out in each group the experiment was halted and all tadpoles were placed into aged tapwater with the varying metamorphosis described in the previous post.
The conclusion I drew from this is that there was some micronutrient that was being pulled from the tapwater by both the carbon and the RO filter. As far as I know this is the only incidence of carbon filtered induced SLS.
Ed
There was a 0% incidence of SLS in any anuran here at work with the earlier exception of some Smilesca phaeota that were heavily parasitized with nematodes until the incidence of the carbon filtration of incoming water. After SLS started up (we went from 0% in those species to 100%, there were no exceptions), there were multiple changes to both the supplements for the adults as well as the tadpoles as well as foods used with no change in the incidence of SLS (still 100%).
Three groups of tinct tadpoles were setup and reared in the following manner (same food and supplements between all groups)
1) clutches were split amoung the three test groups to reduce/eliminate any genetic influences on the development
2) tadpoles were reared in labeled dannon pint yogurt containers filled to the same volume
3) containers were maintained in mixed groups in the exact same locations to prevent thermal differences from skewing the results
4) tadpoles were kept in three different locations to eliminate temperature difference as a potential cause
5) test groups were maintained in one of the following
a) artificial pond water made with RO water (aged 48 hours)
b) carbon treated aged tap water (aged for 48 hours)
c) tapwater aged for 48 hours
6) tadpoles were fed and cleaned on the same schedules
7) necropsied SLS affected metamorphs were not parasitized like the earlier mentioned Smilesca phaeota.
In the test the following results developed
artificial pond water had 100 %SLS
carbon filtered tapwater has 100% SLS
aged tapwater had 0% SLS.
After about 15-20 tads metamorphed out in each group the experiment was halted and all tadpoles were placed into aged tapwater with the varying metamorphosis described in the previous post.
The conclusion I drew from this is that there was some micronutrient that was being pulled from the tapwater by both the carbon and the RO filter. As far as I know this is the only incidence of carbon filtered induced SLS.
Ed
Awesome information Ed.
Thanks
Ed, you obviously know a lot about frogs (amphibians in general) so I must ask, where do you work? My guess is a zoo.Okay I'll go over the break down and you can see how we narrowed it down to the filter.
Thanks
Just a minor note I did run some very small tests 5-10 tads in RO and did not have any issues. I have since switched to reconstituted RO (RO Right) and have had great results.
Ed,
Could this be a micronutrient or something else that made it through the filters? I for get the name at the moment of the chlorine like additive, but im sure there are some things not blocked by RO units. Most RO units also have carbon filters.
Ed,
Could this be a micronutrient or something else that made it through the filters? I for get the name at the moment of the chlorine like additive, but im sure there are some things not blocked by RO units. Most RO units also have carbon filters.
I think its the other way around, its a micronutrient that didn't get through the filters.
Carbon is an indiscriminate absorber that pulls all different kinds of things from the water while RO systems (depending on the system) (especially when combined with an absorbtion column) result in water that is equivalent to distilled.
As I noted before this is the only case that I am aware of where this occured.
Ed
PS: I am the lead keeper in a Dept of Herpetology at a Zoo..
Ed
Carbon is an indiscriminate absorber that pulls all different kinds of things from the water while RO systems (depending on the system) (especially when combined with an absorbtion column) result in water that is equivalent to distilled.
As I noted before this is the only case that I am aware of where this occured.
Ed
PS: I am the lead keeper in a Dept of Herpetology at a Zoo..
Ed
Thank you Ed, I knew your intelligence came from somewhere!!
Kyle, where do you get your RO Right?I have since switched to reconstituted RO (RO Right) and have had great results.
http://www.marinedepot.com/md_viewItem.asp?idproduct=KM5333
I mix 1/8th of a teaspoon per gallon.
I mix 1/8th of a teaspoon per gallon.
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