Understanding dilated cardiomyopathy in poultry: The Guinea fowl model.

摘要

Cardiomyopathy, a form of heart failure, is a naturally occurring disease in poultry and has few identifiable causes. This condition has not been reported in guinea fowl. The purpose of this study was to induce cardiomyopathy in guinea fowl and to elucidate possible physiological changes that lead to the condition. In three replications five week old Pearl Gray Guinea fowl Keets were fed corn-soy diets containing 800, 600, 400 and 0 parts per million (ppm) Furazolidone for four weeks. The experimental diets were fed in mash form and contained 3,000 kcal of metabolizable energy (ME)/kg diet and 24% crude protein (CP) at 0-5 weeks of age (WOA) and 3,100 ME kcal/kg and 24% CP at 5-9 WOA. After nine WOA, experimental birds were selected at random, blood samples were collected, the birds were then euthanized and liver and heart tissue samples were collected and immediately frozen in liquid nitrogen. Total RNA was extracted from the tissues, reverse transcribed and quantified to evaluate the expression of the cardiac Troponin (cTNT) and Phospholamban (PLN) genes which serve as markers for Dilated Cardiomyopathy. Feeding guinea fowl keets 800 and 600 ppm furazolidone successfully induced cardiomyopathy in guinea fowl. The induction of the condition was associated with a significant decrease in feed consumption and body weight gain and a significant reduction in feed efficiency. Feeding the 600 ppm and 800 ppm Furazolidone, had a notable reduction in the expression of cTNT and PLN in the heart muscle and liver. Liver hyperplasia and severe ascites were also observed.