If your entire flock of sheep are chronically anemic, it could be a cobalt deficiency. Not too long ago, our entire flock of sheep had severe anemia, as in they could drop dead any moment FAMACHA scores. Yet fecal egg counts repeatedly came back with low to no worm count. We dewormed our sheep anyways because we thought it must be barber pole worms. No change in their anemia. So we did fecal egg count reduction tests to verify the efficacy of our dewormer when deworming didn’t help, and we found out the dewormer we used IS highly effective. So then what?
99% of the time anemia in small ruminants is caused by parasitism by the barber pole worm. You should always start looking at anemia as if it is caused by parasites. Always. Before you even consider anything else, thoroughly rule out all kinds of internal parasites first.
After thoroughly ruling out parasites, we recently found ourselves in that 1% of anemia that isn’t parasite caused. It was a frustrating, nerve-wracking summer. And the question was:
Where do you go from there?
Our lambs, and in particular our ram lambs, had FAMACHA scores of 5. That summer a score of 3 was GREAT for any of our animals. (if you are unfamiliar with what FAMACHA is, please take a minute to check out our article explaining it and why it is so important for small rumiants) We did fecal egg count after fecal egg count, and multiple fecal egg count reduction tests. We dewormed, we didn’t deworm, we tried putting them on drylot with hay, we tried leaving them on pasture. Absolutely nothing worked.
Nothing we did budged their anemia scores AT ALL. What was worse, we bought in a new Katahdin ram who was supposed to have excellent parasite resistance. He arrived with the richest red mucus membranes we have ever seen. Within a month his mucus membranes were no different than those of the rest of the flock.
Our flock of sheep displayed no other symptoms, none.
Needless to say, we spent the majority of the summer on knife edge. We were worrying that one of these lambs with white mucus membranes was going to drop dead and there wasn’t a single sorry thing we could do for them.
In between collecting fecal samples, checking FAMACHA scores obsessively, and asking everyone we possibly could think of to interrogate, there was a flurry of research. No one seems to have had this problem before, nor did they have any ideas or solutions. So, what could the problem be?
As we mentioned before anemia is most often parasites, and almost everything online regarding anemia points to barber pole worms. However, we were very convinced before the end of the summer that we were not dealing with worm problems. We also knew from a local farmer that he historically had the same unsolved anemia problem in their goats, but never in their cattle.
So we dug deeper and started researching individual minerals one by one.
There are 3 main minerals required to make blood that are typically associated with anemia. Iron, copper, and Vitamin B12 which rumen bacteria manufacture from cobalt.
Even though in humans iron deficiency is a very common cause of anemia, we immediately ruled our iron as extremely unlikely. There has never been a documented case of a direct iron deficiency in ruminants. Not ever. Typically grazing animals diets are extremely high in iron because they are accidentally eating a lot of dirt with their grass. It is far more likely for iron to be present in toxic amounts negatively impacting the absorption of other nutrients.
Next we ruled out copper as also unlikely. Not because it isn’t possible for a sheep to be copper deficient, but because our new ram got anemic within a few weeks of being here. Because sheep are so good at storing copper, and they have such a minimal requirement for it, the likelihood of our new ram becoming so copper deficient as to be extremely anemic in under a month seemed low.
After crossing iron and copper off our list, we again researched all sorts of other common deficiencies to see if we missed any mention in the literature of common deficiencies, like zinc or selenium, causing anemia. Nada.
Eventually we decided that it must be cobalt even though cobalt was a seemingly unlikely culprit, and is not often mentioned. Cobalt is the ruminant precursor for Vitamin B12. Without sufficient cobalt, ruminants cannot make the B12 their bodies require.
In the United States cobalt deficiency in ruminants is quite rare.
The majority of the soils, and thus forages, in this country have plenty of cobalt in them. Cobalt deficiency is much more commonly seen in other countries than it is here. However, there is one place in the United States where we historically could not keep ruminants because they would always waste away and die. This area was the coastal plains of the southeast. When we learned about the ruminant requirement for cobalt we were able to cure this coastal wasting disease.
Cobalt maps of the USA show that our location here in Virginia technically should have sufficient cobalt. However, slightly south of this location is where severe deficiency starts to be noted, so it seemed highly likely that our sandy soils could be deficient.
The only problem was that our sheep did not have any of the other normal symptoms of cobalt deficiency. Plus, their trace mineral mix contained what should have been enough cobalt to meet their needs. We rushed down the cobalt deficiency rabbit hole anyways trying to learn everything we could possibly learn about cobalt.
What we learned about cobalt and sheep
As it would turn out sheep have a very high cobalt requirement, much higher than cattle, and probably higher than goats. This is possibly why our neighbor never experiences problems with his cattle, but did when he had goats.
Also, sheep have no ability to store cobalt as they do not actually absorb the cobalt, but rather the rumen bacteria use cobalt to manufacture vitamin B12. This means that if their diet does not consistently contain cobalt, they cannot manufacture Vitamin B12. Additionally, as you might know B12 is a water-soluble vitamin, meaning that our bodies have a very limited ability to store it. Thus, a deficiency can develop rapidly—within a months time.
Symptoms of cobalt deficiency are typically mainly that sheep lose their appetite, have a poor wool coat and lack body condition. They also say that weeping eyes, scabby ears and anemia can also be signs of cobalt deficiency. Lambs may fail to thrive and ewes may have poor fertility or be poor mothers.
As we mentioned before, the only symptom our sheep had was chronic anemia. Our sheep showed none of these other symptoms which are typically seen before anemia. Nonetheless, it is inexpensive and easy to test the cobalt deficiency theory. So we did.
Cobalt deficiency is actually a vitamin B12 deficiency, therefore B12 injections will rapidly improve symptoms.
Anemia however takes time to recover from because it takes time to make red blood cells. It can take a month or more for anemia to be completely cured. So we gave B vitamin injections to our lambs with the worst FAMACHA scores and waited.
Sure enough, in a few week’s time, we were quite sure that cobalt was the problem. So we promptly got cobalt boluses and dosed our flock. For those of you who don’t know what a bolus is, it is just a large pill that in this case contained a chunk of cobalt designed to sit in their rumen and slowly dissolve over time.
Over the course of the next couple months the anemia in our flock drastically improved. And then it stopped improving. Unfortunately, it did not improve as much as we would have liked. Nor did it improve uniformly across our flock.
This leads to so many more questions that we are still working on solving.
Resolving nutrient deficiencies can be very difficult and complex. There are many interactions between various minerals that occur in the rumen, many of which we do not fully understand yet. This often makes determining exactly what an animal actually needs very difficult and time consuming to do when a problem arises.
One of the biggest questions we have is why is our flock so cobalt deficient? On paper their diet is more than sufficient. During this whole process we got a forage analysis done. The cobalt levels in our feed and mineral mix combined should be sufficient to meet the sheep’s needs. And yet they were severely anemic. Boluses helped significantly, but have not completely resolved the anemia even though they should be getting well more cobalt than their requirements at this point.
So do they somehow still need more cobalt?
The answer is yes, for some reason they seem to. After seeing a significant improvement and then a plateau from adding cobalt boluses we eventually increased the cobalt level in their mineral mix significantly. Because cobalt is needed in such small amounts, we were hesitant to do so initially. However, we are glad we did. This drastically improved our FAMACHA scores, particularly in our lambs who started FAMACHA scores of dead. They now all have scores of about 2.
We are still busy working out the perfect dosage of cobalt to keep them from being anemic. We also still have many questions such as why do they need yet more cobalt? What about their diet is preventing them from being able to utilize the cobalt present? We gave cobalt boluses and more than quadrupled the level of cobalt in their mineral mix before we saw the anemia start to clear up, and its something that is reoccurring. Their anemia levels fluctuate (we are guessing) depending on how much mineral mix they have been consuming.
Dietary requirements for many mineral nutrients are complicated because they can interact and interfere with each other. However, most everything indicates that cobalt has little to no interaction with other nutrients in the rumen. So is there some yet unknown factor involved?
What complicates the matter even more is that we have two different breeds of sheep. The cobalt boluses affected them differently even though they are living in the same pasture and eating the same diet and mineral mix.
We have a mixed flock of black and white Katahdins (hair sheep), and white East Friesian x Finns (wool sheep). The Katahdins had a marginal anemia improvement to be a 2-3 FAMACHA whereas the East Friesian had an improvement to be a 1-2 FAMACHA. Why did they respond differently? Is it due to the size difference between the two breeds, or different nutrient requirements?
Is copper somehow also coming into play?
Copper deficiency can also cause anemia. We have been supplementing our flock with copper for several years for other reasons, and did not think we had any copper deficiency problems. However, one marked difference between the two breeds is that they have significantly different copper requirements. Katahdins, particularly our heavily pigmented ones, have a much higher copper requirement than East Friesians, who happen to be highly sensitive to copper toxicity. (Please keep in mind copper is a mineral you have to experiment with very carefully under a vet’s guidance so that you don’t poison your sheep.)
At this point, we just don’t know. We hope to be able to come back with answers in the future. Until then we will keep up our search. There is so much that we (as a farm, and also as a scientific community) just don’t know about nutrition yet. So if you happen to be in a situation similar to ours where you are chasing trace mineral deficiencies, don’t be discouraged. We are right there with you!
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