Holstein suckling calves on a farm manifested severe emaciation, generalized alopecia, dome-like cranial deformation, and high mortality (Case 1). Metaphyseal growth plates of the femur were achondroplastic; segmented, partially resorped, and replaced with immature bony trabeculae containing degenerated chondrocytes. The skull was thin and partially replaced with connective tissue. Diffuse and severe fatty degeneration was observed in the hepatic stellate (Ito') cells. After 6 mo, surviving calves manifested unthrifty with short and irregular hindquarters (Case 2). The metaphyseal growth plates were poorly formed, irregular, partially disappeared centrally, and often sealed with thin bony trabeculae. The cartilage matrix was not homogeneous but was finely fibrous, and chondrocytes were flat and degenerated. The bone lesion was diagnosed as chondrodysplasia due to premature physeal closure. These calves had been administered excessive amounts of vitamins A, D3 and E, and blood chemistry of acute case showed hypervitaminosis A and E. Case I demonstrated acute disease, while Case 2 demonstrated chronic sequelae. Hypervitaminosis A was the suspected cause.