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Chondrodystrophy in calves associated with manganese deficiency
G Valero1, M R Alley, L M Badcoe
1Departamento de Fisiopatologia, CENID-Microbiologia INIFAP-SARH, Km 15.5 carretera Mexico-Toluca, Mexico D.F. 05100, Mexico.
New Zealand Veterinary Journal
|December 1, 1990
Summary
A congenital chondrodystrophy caused severe skeletal defects in Charolais calves due to poor cartilage development. Low manganese levels in affected calves suggest a dietary link in the dams.
Area of Science:
- Veterinary Pathology
- Animal Genetics
- Nutritional Biochemistry
Background:
- Congenital chondrodystrophy presents as a severe developmental disorder affecting cartilage formation.
- This condition leads to significant skeletal abnormalities in affected newborns.
- Previous cases have been linked to genetic factors or nutritional deficiencies.
Purpose of the Study:
- To describe a severe congenital chondrodystrophy outbreak in Charolais calves.
- To investigate the potential causes, including histological and nutritional factors.
- To characterize the ultrastructural and biochemical changes in cartilage.
Main Methods:
- Clinical examination of 32 affected Charolais calves.
- Histological and ultrastructural analysis of cartilage.
- Biochemical analysis of manganese levels in affected calf liver.
- Evaluation of the dams' diet during gestation.
Main Results:
- Calves exhibited shortened limbs and enlarged joints.
- Histology revealed poor cartilage maturation, rarefied matrix, chondrocyte degeneration, and reduced mucopolysaccharide content.
- Ultrastructural examination showed disorganized fibers and chondrocyte vacuolation.
- Low liver manganese levels were detected in affected calves, correlating with low-manganese maternal diets (apple pulp, corn silage).
Conclusions:
- The findings suggest a manganese deficiency as a likely cause of this chondrodystrophy outbreak.
- Maternal diet during gestation plays a critical role in fetal skeletal development.
- Further research into manganese requirements for pregnant cattle is warranted.