With the intent to use this blog to answer questions I also wanted to share firsthand experiences as they occurred. I’m also going to start sharing more scenarios like these due to our local vet not seeing livestock and I now have shepherds without easy vet access. Whenever possible CONSULT WITH YOUR VET. This is my experience, that is all.
In this case, it was a sad experience. We’ve grown accustomed to losing very few lambs. So when I suddenly (within 24 hours) found myself with three healthy 6 month old lambs all moving slowly, with vacant expressions, I knew I had a problem. The initial onset of neurological symptoms can be subtle, but if you can learn to spot them quickly it can help to narrow in on a diagnosis. These symptoms can present differently but vacant expressions, slow uncoordinated movement, staggering, not getting up to run for food, muscle tremors, head nodding, lose their appetite or don’t drink, blindness, a crooked neck are common. They progress in severeness.
The three most common causes of neurological symptoms are listeriosis, PEM, or Meningeal worms (M-worm). Each of these deserve a long description, but I’ll be focusing on this incident. Listeria is a bacteria that is usually contracted from moldy hay and attacks the brain. Meningeal worm is a parasite that does the same and is usually contracted from deer or wildlife scat as well as snails. The last, Polioencephalomalacia, is often referred to as polio which I find very confusing! It is in no way related to polio. It is a disease of the central nervous system caused by a thiamine (Vitamin B1) deficiency. To be very specific it is a disorder that effects the metabolism of carbohydrates and ultimately the availability of glucose in the body. The brain is one of the first organs to suffer from a shortage of glucose. This is why we see neurological symptoms. I’m going to refer to it as PEM, many call it polio.
As Icelandic sheep owners, you are probably like me and hear the word ‘deficiency’ and run to your multiple bags of supplements looking for thiamine. How did I forget the thiamine? Or you think, it can’t be PEM my sheep have all their supplements, it must be something terrible like Listeria or M-worm. In the case of PEM, neither applies.
Thiamine is produced naturally in the rumen of sheep. With the rumen producing B vitamins, PEM is actually caused when the rumen cannot synthesize it properly.
The next thought is, can it be a thiamine deficiency if only a couple of my lambs are affected? Wouldn’t they all be ‘deficient’? In my case I had three lambs out of twenty-six. Their feed and environments were nearly identical. I hadn’t had a case of PEM in ten years, but there was little doubt in mine or my vet’s mind. I will discuss treatment in this post, but it is important to know that I’m not a vet and it is best to always get a vet’s assessment before starting treatment. I will also discuss possible causes for PEM arising in my flock. This is the area I spent most of my time researching and I thought might help others.
Last question that always lingers, is it contagious? No, PEM is not an infectious disease. Due to the multitude of factors that can cause it you may have more then one sheep present symptoms, but it is due to external circumstances not contracting it from one another.
Thiamine deficiency can develop very quickly in otherwise healthy lambs when certain factors are in place:
Stress. This can include transport, weaning or change of environment.
Sudden change in diet. Feeding high-grain diets to ruminants can predispose them to PEM.
Onset of acidosis.
Elevated chlorine levels in drinking water
Giving sulfa drugs and/or corid usually to treat or prevent coccocidia.
High-sulfur intake. This can include natural sources ie certain plants.
Advanced cases of PEM can run a fever as high as 104. If you detect it early, the afflicted lamb may not yet have a fever. If PEM goes untreated most will die within 48 hours. If treatment is given early, recovery can often be quick, but prepared for some lambs to require Vitamin B Complex or thiamine support for weeks. These sheep will survive but they will refuse to thrive. They will be slower moving and not as interested in food. If turned out with the flock, without extra support, they may not survive due to this.
The symptoms of PEM are subtle and can easily be confused with more then listeriosis and M-worm, such as rabies, over- eating, tetanus, pregnancy toxemia, black leg and others. A lab diagnosis is preferable, but because PEM kills so quickly there is seldom time to even get a vet to the barn. In this case, I feel that understanding your treatment choices can make all the difference. In my case, the onset was rapid, the majority of the lambs were fine, and it was fall which is a common time for PEM.
Treatment is simple if you are working with a vet. They will prescribe you thiamine. If a vet is involved then the first dose should be given by IV which drastically increases the speed and effectiveness of treatment. Otherwise you will be begin treatment by giving injections of thiamine yourself (my route).
The bottles are either 200 mg/ml or 500 mg/ml of thiamine. 200 mg/ml is common, but my bottle was 500 mg so definitely check that.
At 200 mg/ml the dose would equate to 1⁄2 cc per 20 lbs, or 2.5cc per 100 lbs. Make the adjustment if your bottle is 500 mg/ml or better yet ask your vet for her recommended dosage. Follow-up doses can be given every 6-12 hours for a couple days. These can be given either SM or SQ.
So let’s say you don’t have thiamine and you need to treat immediately. Or better yet, you’re running out to get thiamine but want to treat with something immediately. You can substitute Vitamin B Complex. Be certain it’s the Complex. Many feed stores sell B12 by itself. This will not help. You need B1. Because you are trying to provide 200-500 mg of thiamine you will need to give a higher dose of B Complex. Deep breath, it is water soluble which means the sheep will excrete the extra. Use common sense, but you won’t overdose an animal on Vit B Complex. In this situation I dose high. I give 1.5 cc for 20 lbs or 7.5 cc for 100 lbs.
Dexamethasone can also be given to reduce inflammation in the brain, but be cautious. First, never give to an animal that may be pregnant. Second, Dexamethasone is a steroid and can repress the immune system. I try to only use it in a life threatening situation where you have limited choices. Fluxion/Banamine can also be used to address inflammation.
Most of the symptoms can be reversed if treatment is prompt, although blindness can be permanent. Support the animal by providing easily accessible fresh water, high quality forage/hay. Abrupt changes in feed should be avoided, but forage is essential to correcting the low PH in the rumen. Avoid sweet grains and molasses. The lower the PH drops the more the healthy microbes in the rumen, that produce thiamine, struggle. This leads to a decrease of available glucose. Without glucose, the cells in the brain begin to starve and die. The low PH leads to an overgrowth of bad microbes that produce byproducts that inhibit the bodies ability to absorb the thiamine it needs.
Okay, so what caused my sudden onset of PEM. But first, how did my three lambs fare. The first to come down with symptoms did not get immediate attention. Far from it. He was a nice sized 6 month old ram lamb who was a part of our meat program. He was in with a large group of ram lambs with the same purpose. They had been separated from the ewes (their mothers) a couple weeks earlier. Could it have been the weaning? Maybe. It wasn’t until day 4 I really noticed that this lamb had slowed down. It was a weekend, no vet. I started giving large doses of Vit B Complex. On Monday I got thiamine. This lamb lived but it took weeks for him to return to thriving. By this time his weight daily gains had been significantly impacted. The second ewe lamb came down with symptoms the same weekend I noticed the ram lamb. I treated her with Vit B Complex. In 16 hours, she was struggling to stand and her neck was crooking backwards. I was able to get a dose of thiamine from a neighbor, but it was too late. 28 hours after initial onset of symptoms she was gone. The quick onset was staggering. She’d been fine the evening before, running over to get black sunflower seeds and jostling with the other ewe lambs. The last ewe lamb showed symptoms a few days later. I treated immediately and aggressively with thiamine (first doses 6 hours apart, followed by two days of 12 hours apart). She recovered.
So why? Feed hadn’t changed other then adding a small amount of high quality hay in the beginning of October. Water was the same. Some weaning had occurred (the ram only), but they had not progressed to not sharing a fence line. No coccidia and definitely no Corid or medication. Everything appeared fine. The lambs didn’t appear unduly stressed and everyone was healthy.
The only difference had been the use of electronetting to let the flock spend more time foraging in the woods rather then grazing the pasture. The increase in plant diversity when implementing Silvio-pasture methods had made a big difference in our flock. I had seen stronger parasite resistance and improvement in body scores without the need for hay. Yet I wondered if there could be any connection between PEM and the diversity of plants. I had never heard of one but thought it was worth investigating. The first result was bracken. It’s a fern like plant and it’s a thiamine blocker. From this point on I’m going to include inserts from studies on thiamine blocking plants. It gets technical and I don’t want to risk making a mistake in paraphrasing. I will include all the sources for the information included so you can go digging deeper if you’d like.
“Local agronomist was contacted to identify any weeds or plants within the paddock that could be implicated with PEM, in particular Nardoo fern, Bracken and Rock fern, which contain high levels of thiaminase I enzyme. This plant had not been identified by the farmer previously. Chenopodium spp have been linked to high sulphur intake PEM in sheep as they accumulate sulphate in high concentrations (Kahn, 2011 and Burgess, 2008).”
“PEM because of sulphur toxicity has been reported to cause clinical signs from a few hours to 32 days following exposure (Aitken, 2007 & Kahn, 201 1).”
High sulphur intake
“High sulphur sources include lucerne, molasses-urea supplements, plants such as Kochia (Kochia scoparia) and Chenopodium spp, turnips, rape mustard, oil seed meals, by-products of com, sugar cane, sugar beet and within the water in some areas (Kahn 2011 & Burgess, 2008). Excess sulphur may decrease the levels of thiamine either directly or via thiaminase production. The sulphite ion is a strong nucleophile and it readily binds to thiamine and may cause secondary deficits in vitamin B1. Alternatively it is hypothesised that high sulphur intake results in the production of excessive ruminal sulphide due to ruminal microbial reduction of ingested sulphur. The hydrogen sulphide gas accumulates and on eructation the gas is inhaled (refer to Figure I). High concentrations of hydrogen sulphide have been associated with energy deprivation to the central nervous system (CNS) through interference with cellular energy metabolism (Kahn 2011).”
Altered thiamine status:
”i. Acute dietary deficiency of thiamine: This is usually only prevalent in pre-ruminants .e. young animals with an underdeveloped rumen (Burgess, 2008).
ii. Thiaminases; can be produced by gut bacteria or ingested as preformed plant products. They can either destroy thiamine or form anti-metabolites that interfere with thiamine function (Kahn, 201 1). Thiaminase I is produced by Bacillus thiaminolyticus and Clostridium sporogenes. High amounts of thiaminase I enzyme is found in Nardoo fern (Mars ilea drummondii), Rockfern (Cheilanthes sieberi) and Bracken fern (Pteridium aquilinum). Anthelmintics such as levamisole or thiabendazole can act as co-substrates for thiaminase I (Burgess, 2008). Thiaminase II is produced by B aneurinolyticus, which proliferates under high grain intake and catalyses the cleavage of thiamine (Kahn, 2011).
iii. Thiamine analogs; competitively inhibit glycolytic reactions. Bacteria, plants (bracken) and drugs such as amprolium, pyrithiamine and oxythiamine (Burgess, 2008) can produce them.”
REFERENCES
Aitken ID, 2007, Diseases of Sheep 4th0 Edition, Blackwell Publishing, Singapore
Burgess BA, 2008, Polioencephalomalacia, Large Animal Veterinary Rounds, vol 8, 3
Clark, G, 2011, Diseases of sheep, cattle and deer, Ministry for Culture and Heritage, New Zealand Government, www.teara.govt.nz
Drewnoski, M, 2010, Sulfate induced polioencephalomalacia (PEM) in feedlot cattle, lecture
Kahn CM, 2011, Polioencephalomalacia: introduction, The Merck Veterinary Manual,
Merck & Co., Inc, Whitehouse Station USA
Smith BP, 2009, Large Animal Internal Medicine 4th0 Edition, Mosby Elsevier, Missouri
Lévy, M. (2015, March). Overview of Polioencephalomalacia. Retrieved May 16, 2020, from Merck Manual Veterinary Manual: https://www.merckvetmanual.com/nervous-system/polioencephalomalacia/overview-of-polioencephalomalacia
In conclusion, I feel the benefits of Silvio-pasture and increasing the consumption of diverse forage far outweigh the risk of thiamine blocking plants. I will continue to increase the time our flock is in the woods, but I’m grateful to be aware of this risk. It will make me more diligent in observing the flock, especially the lambs for early symptoms. I won’t hesitate to treat with Vit B Complex or Thiamine.
Testing the feed/forage and water is always a good idea when PEM appears in many animals in a short period of time, but also being aware of the many causes of PEM can help you make educated choices.
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