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Sulphide-induced polioencephalomalacia in lambs
M M McAllister1, D H Gould, D W Hamar
1Department of Pathology, Colorado State University, Fort Collins 80523.
Journal of Comparative Pathology
|April 1, 1992
Summary
Polioencephalomalacia (PEM) in lambs can be caused by sulphide toxicosis. This study demonstrates that sulphide administration induces neurological signs and brain lesions characteristic of PEM, independent of thiamine levels.
Area of Science:
- Veterinary Neurology
- Toxicology
- Pathology
Background:
- Polioencephalomalacia (PEM) is a neurological disease in ruminants.
- Previous studies suggested a link between high ruminal sulphide concentrations and PEM.
- The exact mechanism and independent causality of sulphide toxicosis in PEM were not fully established.
Purpose of the Study:
- To experimentally induce Polioencephalomalacia (PEM) in lambs using controlled sulphide administration.
- To characterize the clinical and pathological findings of experimentally induced PEM.
- To determine if sulphide toxicosis can cause PEM independently of thiamine deficiency.
Main Methods:
- Administered sulphide solution via oesophageal infusion to 10 lambs over 40-120 minutes.
- Monitored lambs for clinical signs of neurological dysfunction.
- Examined lambs for gross, autofluorescent, and microscopic brain lesions post-mortem.
Main Results:
- Four out of 10 lambs developed clinical signs consistent with PEM.
- All 10 lambs exhibited neurological dysfunction, including stupor, visual impairment, and seizures.
- Characteristic cerebrocortical lesions, indistinguishable from naturally occurring PEM, were observed as early as 20 hours post-administration.
Conclusions:
- Sulphide toxicosis can experimentally induce Polioencephalomalacia (PEM) in lambs.
- The induced lesions and clinical signs mimic naturally occurring PEM.
- These findings support sulphide toxicosis as a cause of PEM, irrespective of thiamine status.