Abstract

Abstract The movement to price an increasing percentage of fed cattle on carcass merit grids has renewed interest in the effect of cattle disease on carcass traits. There is growing evidence that disease has the potential to affect not only carcass weight, but also the quantity, location, and ratio of muscle, fat, and water. A clear mechanistic pathway linking disease to changes in carcass traits has not been made. Three theories considered in this review are 1) a change in metabolic signals, such as cytokines and cortisol, could affect carcass composition through modification of hypothalamic secretions of thyrotropin-releasing hormone, by inhibition of IGF-I and insulin actions on muscle and fat tissues, and by direct protein catabolism and lipolysis; 2) disease-induced anorexia causing a decrease in serum IGF-I and an increase in serum GH, which induces a change in the partitioning of nutrients for tissue deposition; and 3) an indirect (and reversible) effect of anorexia, whereby sick cattle are on feed for fewer effective days than pen mates that do not become sick. Other pathogen or immune-mediated responses to disease, as well as interactions among hormones and cytokines, may influence nutrient partitioning and body composition but have yet to be described. The use of carcass merit to determine the value of fed cattle provides an improved economic signal of the cost of cattle disease. The value of disease avoidance as well as rapid diagnosis and treatment of disease increases when cattle are sold on carcass merit basis because of the negative effects of disease on carcass traits.

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