Sulfur-Associated Polioenephalomalacia Flashcards
1
Q
What is Polioencephalomalacia?
A
- Term used in 2 ways:
- Brain lesion lacking etiological specificity
- Neurologic disease syndrome traditionally blamed on disturbed thiamine status
2
Q
What are the etiologies for the characteristic brain lesion in PEM?
A
- Salt poisoning / water deprivation
- Lead poisoning
- Sulfur intoxication/thiamine deficiency
3
Q
How does Sulfur/Sulfate cause toxicity?
A
- Sulfur/sulfate converted to sulfide by rumen and cecum microbes
- Hypothesized that sulfide:
- blocks neuronal energy metabolism
- interferes with cerebrum blood flow
- generates reactive oxygen species
- Induces PEM
4
Q
What are the signs of Sulfur poisoning?
A
- Weight loss
- rotten egg smell on breath
- diarrhea
- rumen stasis
- dehydration
- tachycardia
- lethargy
- apparent blindness
- head pressing
- ataxia
- recumbency
- convulsions
- death
5
Q
What clinical pathology can sulfur toxicity cause?
A
- Metabolic acidosis
- Hypokalemia
- hypochloremia
6
Q
What are the clinical signs of PEM
A
- Mild blindness to grand mal seizures and death
- Head pressing
- muscle tremors
- hypersalivation
- convulsions may be sporadic
7
Q
What is the treatment for PEM?
A
- Thiamine injection - nonspecific for neuronal injury
- No effective treatment for cerebral necrosis
- Remove suspected sulfur sources
- Corticosteroids, oral fluids, good nutrition may reduce incidence of further cases
8
Q
What does the brain of sulfur-associated PEM look like postmortem?
A
- Swelling, flattening, and shortening of cerebral gyri
- focal malacia or cavitation in the midbrain/thalamus
- may fluoresce under UV light - especially if fixed in formalin
- Rarely: cerebral herniation into the foramen magnum
9
Q
How is Sulfur-associate PEM diagnosed?
A
- Response to treatment
- Total dietary S consumption - >0.4%
- Hydrogen sulfide in the rumen contents > 10,000 ppm
- Histological confirmation of PEM changes in brain tissue
