Sulfur Toxicity


Polio in Cattle can be Caused by Sulfur Toxicity

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Polioencephalomalacia (PEM) was first reported in 1956 and was described as a neurologic disorder of cattle characterized by blindness, ataxia, recumbancy and seizures.  The micropathologic description was a laminar cortical necrosis.  This description of PEM is still accurate 50 years later, but several additional causes have been identified.

Polioencephalomalacia in cattle was thought at one time to be caused exclusively by a thiamine deficiency.  The deficiency was thought to develop because the rumen did not produce enough thiamine or products such as amprolium inhibited thiamine production. Some of the confusion surrounding the cause of PEM is because there is no method to accurately evaluate thiamine status in animals.  It is now known that the laminar cortical necrosis observed in the brain can be caused by sulfur toxicity in addition to lead toxicity, salt toxicity, hypoxia, thiamine deficiency and vascular damage in general.  Sulfur toxicity is still responsive to thiamine treatment but is not caused by a thiamine deficiency.  At one time, blind staggers or PEM observed in Wyoming was thought to be caused by selenium toxicity.  This theory has now been discounted and the condition is known to be caused by sulfur toxicity.

When sulfur is ingested in excess, rumen microbes produce too much hydrogen sulfide.  The soluble hydrosulfide anions stay in the rumen fluid phase and hydrogen sulfide gas accumulates in the rumen gas cap.  The hydrogen sulfide is absorbed across the rumen wall into the blood stream.  This elevated level of sulfide in the blood interferes with cellular energy production. Since the brain has a high requirement for energy production it is one of the most affected body systems.  Sulfide interferes with energy production much in the same way that cyanide does.  It is thought that sulfur and cyanide interfere with cytochrome oxidases, the terminal enzymes of respiratory chains in mitochondria.

Sulfur intake can occur in the feed or water so the total dietary intake of sulfur is needed in order to evaluate the risk of developing PEM.  This is especially pertinent in Iowa now because of ethanol byproducts, especially dried distillers grain with solubles (DDGS).  Ethanol byproducts may contain a high concentration of sulfur.  When cattle are transitioning to high sulfate intake conditions, the ruminal sulfide concentration peaks 1 to 3 weeks after the change.

The maximum tolerable dietary concentration of sulfur is 0.4% of the ration on a dry matter basis. Not all cattle consuming 0.4% or more will develop clinical PEM.  Other factors such as ruminal microbial populations, trace element concentration or ruminal pH can affect sulfur production and absorption.  Insoluble metal sulfides of copper, iron or zinc could decrease the availability of sulfide.  As the pH decreases, the amount of hydrogen sulfide in the gas cap increases.

Sulfur associated PEM occurs in 2 forms. The acute form is characterized by blindness, recumbancy, seizures and death.  The subacute form is characterized by visual impairment and ataxia.  Twitching of the ears or facial muscles is frequently observed.  The subacute form is frequently followed by recovery with minor neurologic impairment.

The best diagnostic specimen at this time is fixed brain.  We are currently investigating analysis of fresh brain and possible additional tissues for sulfide content. In PEM cases, it is also important to analyze water and feed for sulfur levels. There is much variability in the sulfur content from ethanol byproducts, both within an ethanol plant and between plants, so periodic sampling may have to be done to have an accurate idea of the dietary intake of sulfur. Please contact the diagnostic laboratory for the latest information on submission of samples from PEM cases.

There is no specific treatment for PEM, treatment is supportive.  Parenteral thiamine and glucocorticoids may have nonspecific beneficial effects.  When animals go off feed with PEM, production of sulfide ceases and this is one of the reasons subacutely affected animals recover without treatment.  Removal of animals from sulfur sources is the most important control measure.