Vet Column 7-13-09
Fort Collins, Colo.
Have you ever come across calves that just didn’t act like they knew where they were? Maybe moving around slowly, but unsure of their surroundings. You seem to be able to get a bit closer to them before they move or get out of the way. Polioencephalomalacia (PEM), or polio for short, might be a possibility.
PEM may be acute or subacute. Animals with the acute form manifest blindness, lie down and are reluctant to rise, might display seizures, or be comatose. Animals with the subacute form initially separate from the group, stop eating, and display twitches of the ears and face. The head is held in an elevated position and there is a staggering, sometimes stiff-legged gait. As the disease progresses, there is cortical blindness (blindness due to brain involvement rather than within the eye itself). Affected calves often don’t respond to the movement of a hand or finger near their eye, or a touch with the finger to the inside corner of the eyelids. Some calves might be seen standing with their heads slightly down, somewhat still, pressing their heads against an object such as a wall or post. Grinding of the teeth may be observed.
The subacute form of PEM is frequently followed by recovery with only minor neurologic impairment. However, in a few cases, the subacute form may progress to a more severe form with lying down and seizures. Animals that survive the acute form or advanced subacute form often manifest significant neurologic impairment that necessitates culling. Those with a longer duration of acute signs have poorer responses to therapy and can even die.
PEM has been associated with two types of dietary risks: altered thiamine status and high sulfur intake. Thiamine inadequacy can be caused by such factors as acute dietary deficiency of thiamine or ingestion of plant enzymes that alter or destroy thiamine or form anti-metabolites. Even bacteria within the intestinal tract can produce enzymes that alter thiamine function. The latter microorganisms often proliferate under conditions of high grain intake.
PEM associated with high sulfur intake is recognized with increasing frequency. The basis of sulfur-related PEM appears to be the production of excessive ruminal sulfide due to the microbial reduction of ingested sulfur in the rumen. Hydrogen sulfide (H2S) gas, which has the odor of rotten eggs, accumulates in the rumen gas cap. H2S and its various ionic forms are highly toxic substances that interfere with cellular energy metabolism. The central nervous system, by virtue of its dependence on a high and uninterrupted level of energy production, is likely to be significantly affected by energy deprivation.
Treatment of choice regardless of cause is thiamine. Therapy must be started early in the disease course for benefits to be achieved. If brain lesions are particularly severe or treatment is delayed, full clinical recovery may not be possible. The dosage of thiamine is 5-10, mg/lb, in the muscle or under the skin, three times a day. Initial treatment may best be administered intravenously. Beneficial effects are usually observed within 24 hour and sometimes sooner; however, if there is no initial improvement, treatment should be continued for three days.
Dietary supplementation of thiamine at 3-10 mg/kg in the feed has been recommended for prevention, but the efficacy of this approach has not been carefully evaluated. During a PEM outbreak, sufficient roughage should be provided. When the problem could be associated with high sulfur intake, all possible sources of sulfur, including water, should be analyzed and the total sulfur concentration of the consumed dry matter estimated. Dietary ingredients or water with high sulfur concentration should be avoided; if this is not possible, then more gradual introduction to the new conditions can improve the chances of successful adaptation.
Check with your veterinarian or local county extension personnel for more information should you think it a possibility.
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