L15. Sulfur-Associated Polioencephalomalacia Flashcards
Polioencephalomalacia (PEM)
- brain lesion lacking etiologicla specificity
- A neurologic disease syndrome traditionally blamed on disturbed thiamine status
Many etiologies can cause the characteristic brian lesion
- salt poisoning / water deprivation
- lead poisoning
- Sulfer intoxication / thiamine deficiency
Sulfur (S) and Sulfate (SO42-)
- Sulfur is ubiquitous in nature
- necessary for most biological structures and processes
- Sulfate is a sulfur ion
- common in great plains ground water
- rotten egg smell
- In many feed supplements
- High in manure wastes
- common in great plains ground water
- Large excesses of S and (SO42-) are hazardous
Risk factors
Water conamination with high sulfur industrial waste
Naturally high sulfate levels in drinking water
sulfur-contianing fertilizers
Excessive use of sulfur compounds as feed additives
Feedion ammonium sulfate to prevent urinary calculi
Dosing sulfur as a tonic to horses
Algal blooms
Ethanol Co Products
- why are we concerned wtih ethanol co products?
- What does this have ot do with animal health and veterinary medicine?
- What is the relationship between ethanol co products and PEM or sulfur toxicosis
- Does this impact animals other than food animals?
What are the co-products form corn ethanol production?
Distilers Dry grian and Solubles (DDGS)
very safe normally
Produced by the newer dry mills plants
Less variation
a high percentage is shipped out of iowa
Includes high moisture DDGS products like modified wet DDGS, WDGS, MDGS, corn syrup
THere are no standards for DDGS, WDGS, or corn syrup
WDGS ~65% moisture
Sulfer and Sulfate toxicity
Sulfur and sulfate are converted to sulfide (S2-) by rumen and cecum microbes
It is hypothesized that sulfide
blocks neuronal energy metabolism
Interferes with cerebrum blood flow
Generates reactive oxygen species
Induces polioencephalomalacia (PEM)
Clinical Picture:
Signs
weight loss, roteen egg smell on breath, diarrhea, rumen stasis, dehydration, tachycardia, lethargy, apparent blindness, head pressing, ataxia, recumbency, convulsions, death
Clinical Picture:
Clinical pathology
metabolic acidosis
Hypokalemia
Hypochloremia
Sulfur Toxicosis
Casue PEM
thaimain deficiency used to be thought of as the primary cause fo PEM, not now with waht we know of high sulfer feeds
THiamine is a general neruoprotectant and traditional polio cases are thiamine-responsive
Clinicla signs of PEM
the brian is the target organ
SIgns can vary widely from mild blindness to grand mal seizures and death
head pressing
muscle tremors
Hyper salivation
Convulsions may be sporadic
Treatment
Thaimine injection is a non-specific treatment for neuronal injury
There is no effective treatment for the cerebral necorsis
Remove suspected sulfur sources
Corticosteroids, oral fluids and good nutrition may reduce the incidence of further cases
Postmortem
There mayd be gray/black sulfide deposits int eh GI tract
Swelling, flattening and shortening of cerebral gyri
Focal malacia or caviation in the midbrain and thalamus
There areas may fluoresce under UV light, especially if fixed in formalin
Rarely: cerebral herniation into the foramen magnum
Diagnosis
On a live animla we evaluate response to treatment
On a dead aniaml we look at brian pahtology
Only 3-% of PEM cases will have the diagnostic laminar necrosis
Evaluate total dietary Sulfur consumption
Dietary sulfur/sulfate levels >0.4%
hydrogen sulfide int her umen contents >10,000ppm
histological confirmation fo PEM changes in brian tissues
Sulfur Toxicity
Adult cattle seem to tolerate high sulfate diets
Cows have been fed free choise CCDS without problems
