Studies on furazolidone-induced cardiotoxicity in ducklings

Dale Merlin Webb, Purdue University

Abstract

Furazolidone is a nitrofuran antibacterial and antiprotozoal drug used routinely in poultry for prevention and treatment of a number of bacterial diseases and coccidiosis. It causes a toxic cardiomyopathy in ducklings when fed at concentrations over 250-300 mg per kg of feed (ppm) characterized by enlargement of all cardiac chambers, thinning of the myocardium, and eventually, congestive heart failure. To investigate the pathogenesis of the cardiotoxicity, three studies were done using male Pekin ducklings. In the first study, cardiomyopathy with accompanying congestive heart failure was induced in groups of ducklings by feeding 650 ppm furazolidone in the ration for 28 days. Ducklings had recovered clinically and gross myocardial alterations, histopathological lesions, and ultrastructural lesions of furazolidone-induced cardiomyopathy were absent within 4 weeks of cessation of furazolidone intake while signs and lesions persisted in ducklings that continued to consume the furazolidone-containing ration. In the second study, ducklings from three strains (small, medium, and large) of commercial birds were fed rations containing 250, 400, 550, or 700 ppm furazolidone for 28 days to determine if the strains differed with respect to their sensitivity to furazolidone intoxication. Ducklings were euthanatized and necropsied on day 28 and the severity of gross alterations in the heart and other organs were assessed. Ducklings of the large strain had more severe lesions and a higher incidence of lesions than those in the medium and small strains. Ducklings from the medium strain generally were intermediate in sensitivity. Cystic testicular tubular dilatation was observed in 16% of the ducklings in the second study. Grossly and histologically, the testicular lesions were similar to those reported in sodium intoxicated cockerels. Ultrastructurally, the seminiferous epithelium was degenerated and became attenuated, but even severely dilated tubules retained a thin, endothelial cell-like lining. In the third study, clinical, gross, and ultrastructural development of furazolidone toxicosis was followed in ducklings fed 700 ppm furazolidone for 3 to 27 days. Mortality and nervous signs (hyperexcitability, incoordination, and seizures) began on day 5 of treatment. Gross myocardial dilatation was present by day 12 and became increasingly severe over the next 2 weeks. Myofibrillar lysis was first present on day 12 of treatment; however, not all dilated hearts had evidence of myofibrillar lysis.

Degree

Ph.D.

Advisors

Vleet, Purdue University.

Subject Area

Veterinary services|Animal diseases

COinS