Thank you!
Read it through and it confirmed my concerns. However – Is very unclear which concentration they have used. In the abstract and from chapter 2.4 they use mg/ml which is 1000 time weaker than mg/l – however in chapter 2,2 and 2.3 they use mg/l, further in the appendix they use ppm – which is equal to mg/l in this case. I have written to the main author and ask about this – if there is something I miss or if it is a typo. If they mean mg/l – all should probably stop dosing 10 ppm to our salt watyer fish and that protocol should not be used IMO. The histological damage is huge in this test run and in that case - if the real concentration is 3.2 ppm during 35 days. Thats we do not know for the moment - but I suspect that mg/ml is wrong and a typo
The tested animal
Cyprinus carpio is among one of the must toughest fish I have handled - only the African catfish
Clarias gariepinus is tougher IMO. That fish you can´t even kill with a hammer – believe me – I have tried
But it does not matter (the concentrations) in the long run - the drug is lipophilic and together with time – it will concentrate in the body of the fish – it means that even a low water concentration will bioaccumulate into the fish and mostly in the fatty parts of the body. It is not a matter of plain equilibrium – the fat in the fish will “suck” up every lipophilic substance with time in the water. What I understand – the sensitivity among the wrasses is depended of the length of the exposure period with the commonly used concentrations. Of course – the concentration in the water of lipophilic drugs have an importance – but only if you take with a timeframe. Let us say that you want x nanogram/l in the bloodstream of a fish. You can achieve this with two different strategies – high water concentration – short exposure time or low water concentrations – long exposure time.
The article
@MnFish1 dig up show that the drug will be transported into the fish from the surrounding water and will be able to reach concentrations that will damage certain organs inside the fish. When it finally in the fish – it will be broken down and the normal pathway for this is by a cascade enzyme system known as MFO (Mixed Function Oxidase). The main goal for this system is to transfer lipophilic substances into smaller substances and preparing for other system to make them more hydrophilic - hence be able to further transport out from the body. These processes take mainly place in the liver and kidney. The MFO system is fascinating – it has an ability to change its active enzymes in order to manage new compounds and old enzymes can act against new compounds – but the result – the metabolite - can be a more toxic substance.
Now we will come to a rather interesting thing – the excretion time. As I can see in the article, I linked to in #4 – the excretion is mainly through the kidneys and through the pee. Because of osmotic reasons – saltwater fish does not pee so much and if they do – it is vey concentrated. IMO – there is a reason to believe that QP (and its metabolites) will have a longer residence time in saltwater fish compared with other animals. I.e. – if there is a therapeutic concentration of QP in the body fluids against the ich parasite it can be enough with a dip in a certain concentration of QP to maintain that concentration for a prolonged period.
Is there a therapeutic concentration of QP in the body fluids against ich parasite (and maybe velvet) – with other words – can QP be active against the Trophont stage?
I think that you can just get an idea from these descriptions of this stage:
A short note on the sensitivity of the wrasses. I think that the gills is the main pathway for uptake of lipophilic substances but fishes with small scales or non, maybe will take up these substances faster than other fish, hence get lethal blood concentrations faster.
Sincerely Lasse
