학술논문

An extended outbreak of congenital chondrodysplasia in calves in South East Australia
Document Type
Report
Source
Australian Veterinary Journal. April, 2008, Vol. 86 Issue 4, p130, 6 p.
Subject
Cattle
Genetic disorders
Language
English
ISSN
0005-0423
Abstract
To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1751-0813.2008.00266.x Byline: JG Cave (a), PJ Mclaren (b), SJ Whittaker (c), L Rast (d), A Stephens (e), EM Parker (f) Keywords: Calves; chondrodystrophy; congenital chondrodysplasia; outbreak Abstract: Objective To report an outbreak of congenital chondrodystrophy in calves in South East Australia. Methods District veterinarians investigated reported cases of calf deformities. Owners of affected herds were interviewed using a standard questionnaire to identify potential risk factors. Dams of several affected calves were serologically tested for Akabane virus, Aino virus, pestivirus and bluetongue, and affected calves were tested for pestivirus antigen and serum immunoglobulin concentrations. Gross and histopathological examinations of numerous calves were performed, concentrating on the musculoskeletal system. Results A case definition of distinctive skeletal deformities was established, and 89 property owners reported calves with chondrodystrophy in Spring 2003, 2004 or 2005. Some 14 property owners reported affected calves in more than one year. Prevalence and severity of deformity varied greatly between and within properties. None of breed, sex, age of dam, lineage, pasture type, supplementary feeding, fertiliser use or toxic plants was consistently associated with the disease. All dams experienced hot, dry conditions during the first trimester of pregnancy and were exposed to adverse conditions thereafter. Consistently dams were reported to have been grazing undulating to hilly terrain during early pregnancy. All serological tests were negative for Akabane virus, Aino virus, pestivirus and bluetongue. Histopathology of affected skeletal samples showed chondrodysplasia. Conclusion 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. Author Affiliation: (a)Department of Primary Industries, 1 McKoy St, Wodonga, Vic 3690 (b)Gribbles Veterinary Pathology, 1868 Dandenong Rd, Clayton, Vic 3168 (c)Hume Rural Lands Protection Board, 462 Wagga Rd, Lavington, NSW 2641 (d)Gundagai Rural Lands Protection Board, Box 21, Gundagai, NSW 2722 (e)Cooma Rural Lands Protection Board, Box 29, Cooma, NSW 2630 (f)Department of Primary Industries, 89 Sydney Rd, Benalla, Vic 3672 Article History: (Accepted for publication 30 July 2007)