I’m super sorry about that platinum ogon butterfly. Suuuuuuuuuccckkkkkkkssssss when that happens.
Since literally everything I’ve used has failed in the past – (pretty much) I’ll say that we can certainly do Baytril shots – peas, salt, blah blah blah…..but I always wonder if “this or that” would work. If you’re ever interested in “this or that” – let me know.
In particular I’m wondering if intracoelomic DMSO in NaCl would benefit these fish.
Reason: Dropsy is the unchecked ontake of water in the tissues. Everything from muscle to fat, to third space: All take on water.
There are four fundamental reasons for Dropsy, Ascites, Pinecone:
1) BIG defect in the skin (giant ulcer) where water has no impediment by mucus, scale or skin to get into the fish and it’s beyond the fishes’ metabolism to dismiss that water. Because these are related to a defect in the skin, sometimes they can be saved by closing the osmotic gap, and then closing the defect in the skin. The “defect” in the skin can be a million tiny defects, or one or two giant defects. Both are “gigantic” in their own way as far as surface area breach.
2) Kidney failure: The kidney in freshwater fish is engineered to retain salts and expel water. Not a little water. A LOT of water all the time. And if the kidney fails, (Using Amikacin for infections, or kidney-damaging germs, or tuberculosis or fungus, or toxins, or cancer) then the kidney can’t dismiss that much water = Dropsy. In all but a VERY few cases, saving the kidney is just stopping progression in a “moment in time” and while the infection and kidney damage are ‘checked’ – it’s seldom enough to re-start the kidney to the extent that the Dropsy is “cured”. Mitraspora cyprini: Causes #2. A transmissible infection.
3) Liver failure: The liver makes proteins that make the blood thick. When the blood is nice and thick, it doesn’t run out of the veins (extravasate) and it stays where it belongs. When these proteins are missing (proteins: albumin, globulin) the blood is thin, and gets out of the veins and Dropsy is the result. In all but a VERY few cases, saving the liver is just stopping progression in a “moment in time” and while the infection and liver damage are ‘checked’ – it’s seldom enough to re-start the liver to the extent that the Dropsy is “cured”.
4) Abdominal tumors / growths or egg impactions / resorbtions. Sometimes a Koi goldfish gets an abdominal tumor or mass that eventually gets so large that it:
- Crushes the intestines and starves the fish while it gets “fatter and fatter”.
- Or impacts and shuts down other organs that needed the space.
- Or the mass just gets so huge that the body of the fish gets SO round, that the scales simply stand up for that. These can be assessed on a case by case basis.
- In some of THESE types of “pinecone” you don’t actually get the wet “jelly scales” squishiness in the skin even as the scales are poking out. It’s a clue.
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“Koi bellies are like a bawx of chawcolates. You never know what you’re gonna get.”
Why do some treatments work?
- On occasion, if the fish can close the skin defect, for example a wound, or chlorine-removal of ALL the slime coat – the fish can (with normal kidney function) finally “catch up” and recover.
- On occasion, a fish may get a salt bath for a week or two and by closing the osmotic-gap between fish and water, it may show recovery. As soon as it resumes pure freshwater, it regresses. But this is after the person has gotten on Facebook and proclaimed “I cured Dropsy!” and they never go back on and say “But it’s died now, a month later.”
- On occasion a fish may get a few injections of antibiotic or some medicated food and it may show recovery. As soon as it resumes life without antibiotics and injections, it declines and eventually regresses. But this is after the person has gotten on Facebook and proclaimed “I cured Dropsy!” and they never go back on and say “But it’s died now, two months later.”
Treatments for Dropsy include:
If a mass, eggbinding, resorption, or other pathology is suspected, that should be examined and corrected if possible. Sadly, this is usually “fail” because usually the fish is “too far gone” and not a surgical candidate. It’s disappointing when gently handling the fish dispatches it to heaven. The thought of surgery in a case as frail as that is in retrospect, preposterous.
Balance Water Ontake
Increase salinity to 0.3% – 0.6% or even 0.9% – The more salt you deploy, the less water they’ll take on. In fact, theoretically, at 0.9% salinity the fish should be taking on little if any water. This is a band aid.
- 0.3% = 3 tsp salt per gallon of water (Will kill a few species of plants.)
- 0.6% = 6 tsp salt per gallon (Do not add “all at once”) (Will kill some plants.)
- 0.9% = 9 tsp salt per gallon (Do not add “all at once”) (Will kill tf out of plants.)
Feed, bathe in, or give injections of antibiotics safe for Koi, goldfish or the target species. Antibiotics like Amikacin are “aminoglycosides” and help shut kidneys down. Don’t use them.
Minn Finn strips the slime coat and coagulates gill tips, INCREASING the permeability of the fish to the influx of water. Don’t use it.
I rather prefer an injection of something like Baytril, Nuflor, (Florfenicol) for antimicrobial therapy.
Increase salinity and give antibiotics and say a prayer promising to be good for the remainder of your years. Maybe….just maybe…..
One theoretical idea: DMSO internally 1.2% solution IP
So, how would DMSO make any difference?
In the first place, it will probably kill the fish in 5 minutes. If you’re not ready for that possibility, let’s not do it. This is entirely theoretical, and
1. DMSO is a powerful antioxidant and as such, antioxidants give almost every species of animal a boost fighting infections, and sheer survival.
2. DMSO destroys amyloid (protein deposits) in the kidneys
3. DMSO is extremely beneficial in liver disease, and supports hepatocytes when given IV. (We would be going IP)
Things we don’t know at all: Do fish get “congestive heart failure and develop ascites? Do fish kidneys ‘age out’ like extremely elderly mammalian kidneys? Would a blood thickener (Hetastarch or transfusion) make any difference if the fish had ascites from hypoproteinemia? How tf would a regular person know the fish had a hypoproteinemia?
We probably need to toddle over to some British message board for those answers, elderly pundits there can piece together bits of information from human medical journals, apply these bits to fish-metabolism and physiology, and pronounce their answer, and the rest will swear to it. A fact is born.