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  • Kendra R. Shatswell

Goat Polio

Firstly, NO, the goat on the cover photo of this blog did NOT have polio. Rogue was just a very proficient "death napper" - it was quite the disconcerting sight! Silly girl.


Polioencephalomalacia. More commonly called “goat polio” or simply “thiamine deficiency,” polioencephalomalacia is a neurological disease characterized by brain swelling and tissue death – the word literally means “softening of the brain.” Ruminants harbor beneficial bacteria and protozoa that produce Vitamin B12 (cobalamin) and Vitamin B1 (thiamine) under normal environmental conditions. If this production is interrupted, thiamine deficiency can occur.


Thiamine production can also be hindered by thiaminases, "enzymes that catalyze the break down of thiamine" - Webster Merriam. Some bacteria that produce thiaminases are usually present in the the rumen but overgrowth is the issue; thiaminases inactivate or degrade thiamine molecules, leaving the goat thiamine-deficient.


To put it simply, the rumen must be kept happy to produce thiamine; thiamine is necessary for proper nerve conduction, and negative neurological symptoms present when thiamine is lacking.


Pre-ruminant goat kids rely on dietary thiamine – goat milk and colostrum contains B vitamins.

Low-quality colostrums or milk replacers or whole milk recipes can lack the essential B vitamins for optimal kid health.


Many factors can contribute to reduced or cessation of normal thiamine production in adult ruminants, including dietary issues or certain medications.


Dietary Causes

Dietary causes include too much grain and not enough roughage, consumption of moldy

feedstuffs, diets high in sulfur, cobalt-deficient diets, or consuming certain certain plants.


Sudden changes in the diet, especially increased or excessive grain or carbohydrate consumption, can decrease the PH in the rumen and disturb the thiamine production of the microorganisms there. In this case study, sheep ate far too much cracked barely at once, for instance - https://onlinelibrary.wiley.com/doi/full/10.1111/j.1939-1676.2008.0094.x

Moldy feedstuffs can contain certain enzymes that produce thiaminases, as well.


Plants such as bracken ferns are problematic – while toxicity symptoms vary widely based on dose, duration, and species of affected animals – these plants contain thiaminases, and thiamine deficiency has been noted in sheep grazing on the plants in Australia.


Diets high in sulfur – foodstuffs or water or a combination of the two – can also lead to thiamine

deficiency. According to “Digestive System and Nutrient Needs of Meat Goats” by Purdue

Extension, “Sulfur produces thiamine-like compounds called analogs that decrease the

absorption of thiamine in the rumen.” There are many possible sources of excessive sulfur,

including: water sources, alfalfa*, brassicas, distillers grains, molasses, and corn, sugar beet, and sugar cane byproducts. According to Goat Medicine by Mary C. Smith and David M. Sherman,

“Extrapolating from recommendations based on cattle and sheep, the maximum total dietary

sulfur in high concentrate diets is 0.30% and 0.05% if the diet consists of at least 40% forage.

Drinking water should contain less that 600mg/L sulfate/L for high concentrate diets, whereas

2,500 mg sulfate/L is acceptable with higher forage intake (NRC 2005.)” Generally speaking,

sulfur should not exceed 0.3% total diet dry matter.


Cobalt-deficient diets are also precursors to goat polio. The trace mineral is essential for the

microorganisms to manufacture and utilize Vitamin B12. Vitamin B12 is essential to maintain

nervous system integrity and promote red blood cell synthesis. Certain areas in the U.S. are

known to be cobalt-deficient – a map can be found at http://www2.luresext.edu/goats/training/nutrition.html. Sandy soils and alkaline soils are more

likely to be cobalt-deficient. Though not much research has been conducted on goats specifically, it has been established that goats require a very small amount of cobalt and are less

sensitive to cobalt deficiencies than sheep. Sufficient daily cobalt intake is estimated to be between 0.1ppm and 0.3ppm. Toxicity can occur at 10ppm.


Additional Causes

Infectious and parasitic diseases increase thiamine requirements and can lead to goat polio if

those requirements are not met. Since antibiotics do not distinguish between beneficial or

harmful organisms, antibiotics can diminish the beneficial gut flora responsible for thiamine

production.


Amprolium – the active ingredient in some coccidiostats such as CORID® – works by blocking

thiamine uptake of certain coccidian protozoa that require more than the host. Misuse or long-

term use can result in thiamine deficiency in the goat, especially if the goat experienced dietary

thiamine deficiencies already. Ammonium Sulphate - sometimes used instead of ammonium chloride for the prevention of urinary calculi. However, this is less effective for its intended purpose and has been shown to cause thiamine deficiency in both sheep and cattle.


Symptoms of Goat Polio

  •  Off feed/water

  •  Disorientation

  •  Staggering

  •  Circling

  •  Stargazing

  •  Convulsions

  •  Involuntary eye movements

  •  Blindness

  •  Sudden death


Stargazing is characterized by the goat’s head thrown backwards due to rigid neck muscles. Temporary blindness may last as long as 2-3 weeks. Diarrhea, while not a neurological symptom, can present because the rumen is not functioning properly.


Treatment

Severe thiamine deficiency can possibly kill a goat in 24 hours to a few days if left untreated.

Affected goats can also die from poor rumen function or inability to eat. Correct treatment usually results in quick improvement. The only effective therapy is supplementing thiamine. Very severe cases might require an intravenous treatment performed by a veterinarian.


Thiamine dosage is recommended at 10mg/kg bodyweight. Fortified Vitamin B or thiamine subcutaneous injections are more commonly used, though thiamine is prescription only. Oral vitamin B/thiamine supplements are not effective.


The dosage will depend on the concentration of thiamine. For instance, Fortified Vitamin B contains 100mg/kg thiamine/B1 while thiamine from the veterinarian might be 200mg/kg or 500mg/kg thiamine/B1. Some B complexes found over the counter contain very very little thiamine, as little as 12.5mg/kg, so these would be such a massive volume they should be avoided unless there's no other option. So let's take my two options below, if I were dosing the 500mg thiamine, it would be 1cc per 100lb. If the high level Vitamin B complex which is 100mg, it would be 5cc per 100lb (or 1cc per 20lb if that is easier to calculate for a smaller animal). (If you are on Facebook, Noodleville Farm has a wonderful post on thiamine as well - just go to her page and search "thiamine.")




B Vitamins are water-soluble and excess is excreted through the urine so it is better to guess a bit higher on weight than lower.


Injections should be given every six hours as needed. Taper off treatments gradually, lengthening

time between injections, to monitor for potential relapse. If the goat is truly experiencing goat

polio, vast improvements can be seen in as little as minutes or hours if caught early. More severe cases might take longer and full recovery might not be possible. Since goat polio and listeriosis symptoms are so similar, many producers choose to treat the condition as listeriosis, with antibiotics and/or anti-inflammatories as well.


*alfalfa fields are often heavily fertilized with sulfur and a couple sources showed alfalfa usually had a higher % dry matter sulfur than grass hay - one said .28% for beef cattle, but I cannot find any more elaboration on this in relation to potential thiamine deficiency or specific to goats.



Sources

Article reviewed by Dr. Ken Brown DVM

  1. “Animal Sciences Common Diseases and Health Problems in Sheep and Goats” - Purdue

  2. “Digestive System and Nutrient Needs of Meat Goats” - Purdue Extensions.

  3. “Dietary Sulphur in Ruminant Diets” – Westway Feed Products

  4. “Polioencephalomalacia (Goat Polio)” Alabama and Auburn Universities UNP-65 – Maria Leite-Browning, DVM, MS Extension Anima Scientist Alabama A&M University.

  5. “Ramifications of Thiamine Deficiency” – Department of Natural Resources, Cornell University, 2017.

  6. Smith, Mary C., and David M. Sherman. Goat Medicine. 2nd ed., Wiley-Blackwell, 2009.

  7. H. R. Crookshank, Effect of Ammonium Salts on the Production of Ovine Urinary Calculi, Journal of Animal Science, Volume 30, Issue 6, June 1970, Pages 1002–1004, https://doi.org/10.2527/jas1970.3061002x

  8. Jeffrey M, Duff JP, Higgins RJ, Simpson VR, Jackman R, Jones TO, Mechie SC, Livesey CT. Polioencephalomalacia associated with the ingestion of ammonium sulphate by sheep and cattle. Vet Rec. 1994 Apr 2;134(14):343-8. doi: 10.1136/vr.134.14.343. PMID: 8017015.

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