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ARS Home » Southeast Area » Fayetteville, Arkansas » Poultry Production and Product Safety Research » Research » Publications at this Location » Publication #155394
Title: MECHANISM OF THIRAM-INDUCED TIBIAL DYSCHONDROPLASIA IN CHICKENS.

Author
item Rath, Narayan
item Huff, William
item Huff, Geraldine
item Balog, Janice

Submitted to: World Poultry Congress Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 12/1/2003
Publication Date: 6/8/2004
Citation: Rath, N.C., Huff, W.E., Huff, G.R., Balog, J.M. 2004. Mechanism of thiram-induced tibial dyschondroplasia in chickens. In: Proceedings of the World Poultry Congress, June 6-14, 2004, Istanbul, Turkey. Paper No. 798. 2004 CDROM.

Interpretive Summary:

Technical Abstract: Tibial dyschondroplasia (TD) is a leading cause of lameness in poultry where the proximal growth plate of the tibia fails to form bone. To understand the mechanisms of TD we fed young broiler chicks with feed containing 100 ppm of thiram for 2 days which induces severe TD lesions in > 90% of birds. Using this model, we tested whether the onset of TD was the consequences of the suppression of chondrocyte maturation-related gene expression or whether it is related to cell death induced by thiram. The growth plate tissues from 11-day-old chickens that were given thiram in the feed for 48 h between days 7-9 were excised and used. RNA from these tissues was subjected to RT-PCR using primers for genes related to cartilage growth and maturation, and the amplicons were analyzed with capillary electrophoresis. The expression of aggrecan, type II and X collagen, bone morphogenetic protein (BMP), and matrix metalloproteinase (MMP) genes were analyzed relative to glyceraldehyde phosphatedehydrogenase using peak ratios of the amplicons. Cell death related changes were examined using terminal deoxyribonucleotide transferase mediated fluorescein-dUTP nick end labeling of growth plate tissues from birds at days 11 and 15. Compared to controls, the relative expression of none of aggrecan, type II collagen, BMP, and MMP-2, or type X collagen genes was affected but there was cellular apoptosis which affected mostly endothelial cells and some chondrocytes on day 11 which increased by day 15 to include evidence of DNA fragmentation in tissues of day 15 tissues. The TD-related changes were largely limited to the distal growth plate. These data were also supported by histological changes observed on different days following thiram treatment. Our results demonstrate that TD does may result from premature cell death of both endothelial cells and chondrocytes.