Abstract. Outbreaks of chondrodysplasia in calves occur sporadically every 10-15 years, particularly following prolonged drought conditions, throughout Northeastern Victoria and the Southern Table-lands of New South Wales, Australia. An outbreak spanning 2 calving seasons (2003)(2004) involving numerous losses through stillbirth, perinatal loss, and poor growth was investigated. Investigations of 4 representative cases are presented here with a definition of the gross and histopathologic defects and an overview of epidemiologic data gathered from affected farms. Calves showed variable disproportionate dwarfism without arthrogryposis. Long bones were shortened and showed axial rotation. Articular surfaces were distorted with misshapen weight-bearing surfaces associated with variable thickness of articular cartilage. Physes were distorted and variable in thickness with occasional foci of complete closure. The major histologic abnormality in the physes was disorderly development of the zones of cartilage hypertrophy, with reduced number and irregular arrangement of hypertrophic chondrocytes; similar less severe changes were present in the zones of cartilage proliferation. Histochemical staining of the cartilage matrix was variable in intensity, and there was evidence of abnormal resorption of cartilage matrix at the level of the primary spongiosa. Osteoid formation and subsequent bone remodelling seemed unaffected, and diaphyseal cortical bone appeared normal at the gross and light microscopic level. No infectious agents were identified, and other known causes for chondrodysplasia in calves were excluded. The most likely cause for the syndrome was considered to be congenital manganese deficiency. Further surveys of tissue and blood manganese levels from cows and calves with and without clinical signs from the region are planned.

The outbreak had similarities with previous outbreaks reported in the region. No specific aetiology could be determined. There is some evidence that the cause of the deformities could be a manganese deficiency during foetal development. Ongoing work to test this hypothesis is therefore warranted.