कुक्कुट, मत्स्य पालन और वन्यजीव विज्ञान
खुला एक्सेस

अमूर्त

Growth and Metabolic Indices of Furazolidone-induced Cardiomyopathy in the Pearl Grey Guinea Fowl

Collins N Khwatenge, Kellee N Hill and Samuel N Nahashon

Dilated cardiomyopathy (DCM) is a naturally occurring heart disease associated with high mortality in rapidly
growing poultry. The disease is common in broilers and its causes are least understood. This condition has not
been reported in guinea fowl hence, the purpose of this study was to induce DCM in guinea fowl and elucidate
physiological changes associated with onset of DCM. In three replications 5 week-old Pearl gray guinea fowl keets
were fed corn-soy diets containing 0 (control), 400, 600 and 800 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 cardiac and liver troponin (TNT) and phospholamban (PLN)
genes which serve as markers for DCM. Feeding 800 and 600 ppm furazolidone successfully induced DCM in
Pearl gray guinea fowl. Induction of DCM was associated with a significant decrease in feed consumption and body
weight gain and a significant reduction in feed efficiency. Increasing furazolidone concentration from 0-800 ppm
significantly down regulated both TNT and PLN in the heart and liver. Liver hyperplasia, severe ascites, a decrease in
serum creatinine, bilirubin, glucose, protein, and alkaline phosphatase, and an increase in serum glutamic pyruvate
transaminase were observed. For the first time we report induction of DCM in the guinea fowl by feeding either 600
or 800 ppm furazolidone. DCM was characterized by metabolic changes and down regulation of heart and liver TNT
and PLN.