Mineral workshop Flashcards
Sole and Sons are a 200 cow dairy unit on the Somerset-Dorset border. They have recent had a sudden cow death. The cow had anaemia and a jaundiced appearance with elevated GGT, AST and GLDH.
The herd is in an area described as ‘teart’, please explain what this means?
- soil or herbage: containing excessive quantities of molybdenum
- high molybdenum in an area
Sole and Sons are a 200 cow dairy unit on the Somerset-Dorset border. They have recent had a sudden cow death. The cow had anaemia and a jaundiced appearance with elevated GGT, AST and GLDH.
The herd is in an area described as ‘teart’, please explain what this means?
soil or herbage: containing excessive quantities of molybdenum
high molybdenum in an area
The herd is fed a high level of copper (1.8 g/day), mainly a mixture of copper sulphate and an ‘organic’ copper supplement added to bypass the rumen and any potential interaction.
What are the potential mineral - antagonist issues?
Copper is a cumulative poison
Copper toxicity is mainly a problem of over or inappropriate copper supplementation
Feeding high copper as we think we have a high molybdenum problem, so trying to get around that…
molybdenum, copper and Sulphur potentially interact
Iron, copper and sulphur potentially interact – but we have no idea what it forms at the moment
If really high sulphur – direct Sulphur interactions
Sole and Sons are a 200 cow dairy unit on the Somerset-Dorset border. They have recent had a sudden cow death. The cow had anaemia and a jaundiced appearance with elevated GGT, AST and GLDH.
The herd is in an area described as ‘teart’, please explain what this means?
soil or herbage: containing excessive quantities of molybdenum
high molybdenum in an area
The herd is fed a high level of copper (1.8 g/day), mainly a mixture of copper sulphate and an ‘organic’ copper supplement added to bypass the rumen and any potential interaction.
What are the potential mineral - antagonist issues?
Copper is a cumulative poison
Copper toxicity is mainly a problem of over or inappropriate copper supplementation
Feeding high copper as we think we have a high molybdenum problem, so trying to get around that…
molybdenum, copper and Sulphur potentially interact
Iron, copper and sulphur potentially interact – but we have no idea what it forms at the moment
If really high sulphur – direct Sulphur interactions
The plasma and liver samples of this cow came back with copper concentrations of 38.7 µmol/l and 32000 µmol/kg DM respectively. In addition, some cull cows also had liver samples analysed which were found to be 17564, 24050, 23240 µmol/kg DM.
- All really high
- Liver Cu concentrations are over double what they should be
- Plasma Cu just under double what they should be
Sole and Sons are a 200 cow dairy unit on the Somerset-Dorset border. They have recent had a sudden cow death. The cow had anaemia and a jaundiced appearance with elevated GGT, AST and GLDH.
The herd is in an area described as ‘teart’, please explain what this means?
soil or herbage: containing excessive quantities of molybdenum
high molybdenum in an area
The herd is fed a high level of copper (1.8 g/day), mainly a mixture of copper sulphate and an ‘organic’ copper supplement added to bypass the rumen and any potential interaction.
What are the potential mineral - antagonist issues?
Copper is a cumulative poison
Copper toxicity is mainly a problem of over or inappropriate copper supplementation
Feeding high copper as we think we have a high molybdenum problem, so trying to get around that…
molybdenum, copper and Sulphur potentially interact
Iron, copper and sulphur potentially interact – but we have no idea what it forms at the moment
If really high sulphur – direct Sulphur interactions
The plasma and liver samples of this cow came back with copper concentrations of 38.7 µmol/l and 32000 µmol/kg DM respectively. In addition, some cull cows also had liver samples analysed which were found to be 17564, 24050, 23240 µmol/kg DM.
What does this indicate, given a APHA reference range for plasma copper of 9.4-19 µmol/l and for liver copper of 300-8000 µmol/kg DM?
Diagnosis: liver enzymes AST, GGT – but liver already damaged when these rise and the enzymes are detected: damage is already done
As it has jaundice and anaemia already – gone into copper toxicity. Can be due to either a large acute dose of copper or the release of elevated copper from the liver
Results indicate they are high – toxic doses high! Cow that is probably dead from copper toxicity, but supplemented lots of copper as we think we have a molybdenum issue
Reference range based on distribution
Sole and Sons are a 200 cow dairy unit on the Somerset-Dorset border. They have recent had a sudden cow death. The cow had anaemia and a jaundiced appearance with elevated GGT, AST and GLDH.
The herd is in an area described as ‘teart’, please explain what this means?
soil or herbage: containing excessive quantities of molybdenum
high molybdenum in an area
The herd is fed a high level of copper (1.8 g/day), mainly a mixture of copper sulphate and an ‘organic’ copper supplement added to bypass the rumen and any potential interaction.
What are the potential mineral - antagonist issues?
Copper is a cumulative poison
Copper toxicity is mainly a problem of over or inappropriate copper supplementation
Feeding high copper as we think we have a high molybdenum problem, so trying to get around that…
molybdenum, copper and Sulphur potentially interact
Iron, copper and sulphur potentially interact – but we have no idea what it forms at the moment
If really high sulphur – direct Sulphur interactions
The plasma and liver samples of this cow came back with copper concentrations of 38.7 µmol/l and 32000 µmol/kg DM respectively. In addition, some cull cows also had liver samples analysed which were found to be 17564, 24050, 23240 µmol/kg DM.
What does this indicate, given a APHA reference range for plasma copper of 9.4-19 µmol/l and for liver copper of 300-8000 µmol/kg DM?
Diagnosis: liver enzymes AST, GGT – but liver already damaged when these rises in the enzymes are detected – damage is already done
As it has jaundice and anaemia already – gone into copper toxicity. Can be due to either a large acute dose of copper or the release of elevated copper from the liver
Results indicate they are high – toxic doses high! Cow that is probably dead from copper toxicity, but supplemented lots of copper as we think we have a molybdenum issue
Reference range based on distribution
And at what concentration does this become a Food standards agency issue (it is the same for sheep)?
- 500 parts per million wet way – 2400 micromole/kg DM – issue for FSA reporting
- Means the farm needs investigating
- Issue with milk and also meat?
The herd still has poor hair quality, with a brownish tinge and apparent hair loss/depigmentation around the eyes (see above), giving a spectacle appearance and they had recently sent samples to NUVetNA at Nottingham and the results are below.
CP mg/dl 20 20.2 25.6 17.4
Pl Cu µmol/l 15.9 13.1 17.7 13.2
CP/PlCu 1.3 1.5 1.5 1.3
SOD U/g Hb 2324 1894 2303 2481
What do these results indicate (interpretation sheet provided)?
- CP – all above minimum (15), not into an acute phase response or stress raising this artificially
- Pl Cu – WNL
- CP/PlCu – less plasma inactivity given the copper there – we have got a loss of inactivity of an enzyme even though we have the copper there – indicating we have thiomolybdate in the blood
- SOD – one is a big marginal
The herd still has poor hair quality, with a brownish tinge and apparent hair loss/depigmentation around the eyes (see above), giving a spectacle appearance and they had recently sent samples to NUVetNA at Nottingham and the results are below.
CP mg/dl 20 20.2 25.6 17.4
Pl Cu µmol/l 15.9 13.1 17.7 13.2
CP/PlCu 1.3 1.5 1.5 1.3
SOD U/g Hb 2324 1894 2303 2481
What do these results indicate (interpretation sheet provided)?
CP – all above minimum (15), not into an acute phase response or stress raising this artificially
Pl Cu – WNL
CP/PlCu – less plasma inactivity given the copper there – we have got a loss of inactivity of an enzyme even though we have the copper there – indicating we have thiomolybdate in the blood
SOD – one is a big marginal
How is it possible to have a co-occurrence of these two apparently opposite conditions?
Results indicate and suggest:
- Thiomolybdate is affecting copper activity – think of it as a TOXIN – trying to poison copper metabolism, doesn’t mean copper isn’t there?
- Rumen – have copper, sulphate and molybdenum. Sulphur can come in as sulphides. In the rumen, microflora will turn a lot of sulphates into sulphides, which are more reactive and will react with molybdenum to form thiomolybdate – all have an affinity for copper )this happens in solid liquid phase of rumen levels). All we doing at the moment is bringing copper to thiomolybdate – but once with copper, its then insoluble – so we have COPPER LOCK UP – have bound it all to thiomolybdate. If we are just doing this, then how do we get copper toxicity? As its bound up? Other thing we have got – iron copper and sulphur interact but this occurs in liquid phase of rumen, so possibly binding some here before it goes to solid phase.
- If thiomolybdate forms and no copper available In rumen to detoxify – the thiomolybdate can be absorbed in the body, will find copper, bind it and affect the activity
- Bypass copper they are feeding – are they unavailable in the rumen? We aren’t quite sure – they may well be available! But if they are truly bypass, we have not got them available in the rumen - so will get formation of thiomolybdate, so not preventing it going into the body
- Intestine – lots coming in from rumen, iron copper sulphur complex stays together, Cu thiomolybdate stays together – lost this also. Copper can be absorbed and molybdate can be absorbed (rest of complex is lost) – so copper and molybdate in the body – nothing happens in body as it ISNT THE MOLYBDATE THAT BINDS TO THE COPPER!! IT IS THE THIOMOLYBDATE!!
- Lots of copper absorbed, this goes to the liver – to try to excrete it, but probably too fast for it to happen – so end up with increased risk of toxicity
- High liver copper and give more copper – hugely increased risk of getting toxicity
- High copper and thiomolybdate – inappropriate copper use – getting out this, you strip all copper from the diet and then nit takes a long time for liver Cu to come down, at least 18 months sometimes! Takes a while to deplete copper. Strip copper out and don’t seem to get the problem anymore?
Mr Kerswell has a flock of 200 ewes, kept on his mainly arable farm in Yorkshire. He lambs at Easter to make use of vet students to assist with his lambing. It is now August and the sheep are in a permanent pasture paddock next to the lambing shed and sheep handling facility. The best lambs were approaching slaughter weight when weighed 2 weeks ago. However, the lambs when weighed the subsequent week had not put as much weight as expected, and this week there seems to be no weight gain at all.
Please consider possible differential diagnoses for this cessation of growth?
- Trace element deficiency – includes cobalt, copper, vitamin E and selenium
- Considerable interplay between parasitic gastroenteritis and trace element deficiency
- Poor food intake due to overstocking and not enough food in front of them! First thing to look at – is there enough food at all?!
- Decent water source available?
- Enough protein and energy available?
- Trace element deficiency
- Parasites
- Clostridia
Mr Kerswell has a flock of 200 ewes, kept on his mainly arable farm in Yorkshire. He lambs at Easter to make use of vet students to assist with his lambing. It is now August and the sheep are in a permanent pasture paddock next to the lambing shed and sheep handling facility. The best lambs were approaching slaughter weight when weighed 2 weeks ago. However, the lambs when weighed the subsequent week had not put as much weight as expected, and this week there seems to be no weight gain at all.
Mr Kerswell had noticed that the lambs seemed to be spending quite a lot of time in the gateway, licking/nibbling the gate and the bare hard soil on the ground.
How might you explain this?
- Sheep who don’t get enough ‘salt’ and minerals will lick this and eat soil – not enough cobalt?
- Pica behaviour – abnormal appetite
Mr Kerswell has a flock of 200 ewes, kept on his mainly arable farm in Yorkshire. He lambs at Easter to make use of vet students to assist with his lambing. It is now August and the sheep are in a permanent pasture paddock next to the lambing shed and sheep handling facility. The best lambs were approaching slaughter weight when weighed 2 weeks ago. However, the lambs when weighed the subsequent week had not put as much weight as expected, and this week there seems to be no weight gain at all.
Mr Kerswell had noticed that the lambs seemed to be spending quite a lot of time in the gateway, licking/nibbling the gate and the bare hard soil on the ground.
How might you explain this?
Sheep who don’t get enough ‘salt’ and minerals will lick this and eat soil – not enough cobalt?
Pica behaviour – abnormal appetite
Given this information what nutritional condition might you expect?
Late summer/autumn cobalt deficiency – poor BCS despite adequate nutrition
Cobalt deficient animals have low vitamin B12, therefore following reaction blocked and build-up of methylmalonic acid, making them feel unwell
Suspect comes down to cobalt and phosphorus – classic pica minerals – SUSPECT COBALT DEFICIENCY
What test(s) would you do to confirm cobalt deficiency diagnosis?
- Clinicals signs in areas with known cobalt deficient soils
- Specific diagnostic – low plasma and/or liver Vitamin B12 concentrations – minimum of 10 blood samples is recommended
- Vet might advise supplementation trial whereby the growth rates are measured over 8-10 weeks
- Blood test for vitamin B12
What treatment options are there and what would you recommend in this case of cobalt deficiency?
- Combination of IM injection of B12 and drenching with up to 1mg/kg bodyweight of cobalt sulphate – thereafter, monthly drenching with cobalt sulphate – often in combination with an anthelmintic, should ensure live weight gain
- B12 injections long acting – probably lasts for about a month – 3 months
- Drench with cobalt – drenching every week in research at the moment
- Cobalt boluses - but they off for slaughter in 2 weeks! Don’t want to waste all that money if it is only for 2 weeks?!
- B12 drenches
- Put into feed
- Spread cobalt on the pasture
- Where do we need cobalt?? Needs to be delivered to the RUMEN – this is the site of action, injections wouldn’t work
- Sulphate – usually soluble
- If not soluble – not necessarily available in the rumen
- Basically – lots of treatment options! Lambs have already stopped growing, already got production loss – want to get them back growing as soon as possible – more how can we avoid the problem, so we don’t get the loss next time – don’t wait until lambs stop growing, get ahead to keep them growing, now we know they might get this issue – so maybe put bolus in earlier so it is worth a lot more – PREVENTION IS BETTER THAN CURE! Takes a lot to get the lambs back growing that fast again, so don’t let it get to this stage
Mr Kerswell also found that the day after weighing the lambs, one or two were found dead with pasteurella. Why might the nutritional condition and handling predispose the lambs to this secondary problem?
- Cobalt deficient sheep are more susceptible to pasterullosis
- Cobalt deficiency affects immune system, compromised, more likely to have other conditions – more likely to take hold than in a cobalt sufficient lamb!
If cobalt deficiency is left untreated why does this problem, disappear as the autumn progresses into winter?
- Lambs have a higher requirement than ewes
- In June July august and September – deficit. But cobalt increases in grass in autumn
- 2 reasons we get this problem – later into autumn, grass increases in cobalt content to fulfil requirements and requirement of lambs is likely to drop off in autumn as grass drops off, so growing drops off, so less B12 requirement to keep up with the growth, as it has slowed down.
B Potter runs a sheep farm on the edge of the North York Moors. They keep a flock of Swaledale ewes, which graze common land on the moor during the summer. They mate a proportion of these with a Bluefaced Leicester tup to get North Country Mules, many of which are sold for breeding, although a small proportion are retained and mated with some Texel tups. Mr Potter shows his pedigree Texel sheep very successfully.
It is mid March and he has just started lambing the first of the Swaledales. Due to the poor weather conditions in February the Swaledales had been brought in to the in-bye land earlier than usual and were fed some big bale silage harvested from this improved grassland in June, he has had a few lambs born that have an ataxic condition (see picture below). Mr Potter thinks it may be swayback.
What is swayback?
- Copper deficiency
- Physiologically – demyelination of myelin sheath resulting in ataxia – neonate ataxia
