A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin

• Published in: Avian diseases Vol. 41; no. 1; p. 20
• Main Authors: Reams, R Y, Thacker, H L, Harrington, D D, Novilla, M N, Rottinghaus, G E, Bennett, G A, Horn, J
• Format: Journal Article
• Language: English
• Published: United States 01.01.1997
• Subjects: acide pyruvique; acido piruvico; animales jovenes; Animals; Antifungal Agents - therapeutic use; blood serum; body parts; Body Weight; Chickens; chicks; coeur; corazon; Cyclobutanes - administration & dosage; Cyclobutanes - toxicity; death; Death, Sudden, Cardiac - etiology; Death, Sudden, Cardiac - prevention & control; Death, Sudden, Cardiac - veterinary; Diet; dindon; electrocardiografia; electrocardiographie; Electrocardiography; Fusarium; gibberella fujikuroi; heart; Heart - drug effects; Heart - physiopathology; jeune animal; lesion; lesiones; lesions; micotoxinas; monensin; Monensin - therapeutic use; monensina; mort; muerte; mycotoxine; mycotoxins; Mycotoxins - administration & dosage; Mycotoxins - toxicity; Myocardium - pathology; Myocardium - ultrastructure; Organ Size; partes del cuerpo; partie du corps; pavo; peso; poids; pollito; poussin; Pyruvates - blood; pyruvic acid; serum sanguin; sintomas; suero sanguineo; symptome; symptoms; toxicidad; toxicite; toxicity; turkeys; weight; young animals
• ISSN: 0005-2086; 1938-4351
• DOI: 10.2307/1592440

A sudden death syndrome was induced in chicks and poults fed diets containing Fusarium fujikuroi, formulated to contain 0-330 mg/kg moniliformin (M) with or without the maximum recommended therapeutic concentration of monensin. Lesions of monensin toxicosis were not observed. Clinical signs were referable to cardiac dysfunction (sudden death, dyspnea, cyanosis, depression). Poults and chicks dying early in the study had no gross lesions or had lesions of right ventricular dilation. Treated poults and chicks dying late in the study or euthanatized at termination of the study had lesions of bilateral myocardial hypertrophy, usually concentric. Absolute heart weights and relative heart weights, expressed as a percentage of body weight, were significantly greater in treated birds than controls (P < 0.05), whereas body weights were significantly less (P < 0.05). Microscopically, lesions progressed from acute myocardial degeneration to necrosis, fibrosis, and hypertrophy. Ultrastructural findings were consistent with the gross and microscopic lesions. Serum pyruvate concentrations were a useful indicator of M-induced cardiotoxicosis. Concentrations of serum pyruvate increased with increased concentration of dietary M, but were not affected by addition of monensin to the diet. In chicks ingesting 40-300 mg/kg M, serum pyruvate concentrations were significantly greater (P < 0.05) than those in controls (controls, 0.28 +/- 0.08 mmol/liter; exposed 0.38 +/-0.11-0.55 +/- 0.13 mmol/liter). Poults ingesting 80-330 mg/kg M had significantly greater serum pyruvate concentrations than controls (controls 0.33 +/- 0.09 mmol/liter; exposed 0.43 +/- 0.13-1.00 +/- 0.06 mmol/liter). The Vetronics System was used to evaluate electrocardiographic alterations in a limited number of chicks and poults surviving to the end of the feeding trial.