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Ovine white-liver disease (OWLD). Pathology
1State Veterinary Research Station for Small Ruminants, Høyland, Sandnes, Norway.
Acta Veterinaria Scandinavica
|January 1, 1990
Summary
Ovine enzootic ataxia (OEA), linked to cobalt/vitamin B12 deficiency, causes liver damage in lambs. Supplementation prevented OEA, suggesting deficiency as the primary cause of liver pathology.
Area of Science:
- Veterinary Pathology
- Animal Nutrition
- Biochemistry
Background:
- Ovine enzootic ataxia (OEA) is a significant disease in lambs grazing pastures.
- The precise pathological mechanisms and contributing factors to OEA require further elucidation.
- Cobalt and vitamin B12 are essential micronutrients for ruminant health.
Purpose of the Study:
- To investigate the microscopic liver changes associated with Ovine enzootic ataxia (OEA) in lambs.
- To determine the role of cobalt/vitamin B12 deficiency in the pathogenesis of OEA.
- To identify potential co-factors or triggers exacerbating liver damage in affected lambs.
Main Methods:
- Histopathological examination of liver tissues from lambs grazing OEA-associated pastures.
- Comparison of pathological findings between supplemented and unsupplemented lambs.
- Assessment of lambs with subclinical deficiencies on control pastures.
Main Results:
- Microscopic liver changes, including fatty change and Councilman bodies, were observed within one month on affected pastures.
- 83% of lambs on OEA pastures exhibited typical or suspect pathological changes.
- Cobalt/vitamin B12 supplementation prevented specific OEA-related liver lesions, while subclinically deficient lambs showed milder features.
Conclusions:
- Ovine enzootic ataxia (OEA) is a manifestation of vitamin B12 deficiency, exacerbated by factors initiating hepatic fatty change.
- Early hepatic fatty change compromises intracellular homeostasis, increasing hepatocyte vulnerability.
- Copper and other elements may play a role in the progression of liver damage in OEA.