monensin and Anorexia

Monensin has been tested to determine its toxicity and safety in cattle. Single dose acute toxicity and signs associated with toxicity were determined by oral gavage, 7-d oral gavage and feeding experiments with high concentrations of monensin in feed. Oral feeding studies indicated a near complete anorexia resulting from intake of sublethal amounts of monensin. In these cases, cattle recovered from the insulting dose and resumed growth and feed intake. In long-term chronic feedlot, pasture supplement, and reproduction safety studies conducted with monensin administered in the feed, the high concentrations caused cattle to show signs of mild monensin intoxication. Mortality resulted from feeding groups of cattle large quantities of monensin in small quantities of feed. Furthermore, these studies have demonstrated no detrimental effects upon reproduction. Collectively, these studies indicate that the greatest risk of intoxication occurs when cattle first receive a feed containing monensin. Mixing errors and misuse situations under actual use conditions have resulted in cases of cattle mortality. In most cases the mortality was predictable based upon the exposure in controlled studies.

Topics: Animals; Anorexia; Body Weight; Cattle; Cattle Diseases; Eating; Female; Food, Fortified; Furans; Male; Monensin; Reproduction

Six adult horses were administered sodium monensin, 1.0-1.5 mg/kg, via gastric gavage. Anorexia and/or diarrhea occurred within 24 hr after monensin administration in all 6 horses. Cardiac disease and dysfunction were evaluated by both elevations in heart rate, echocardiography, and an increase in serum concentrations of cardiac troponin I (cTnI), occurred in 4 horses. The development and severity of cardiac disease was likely affected by the monensin dose, vehicle (water or corn oil) mixed with monensin, and/or whether the monensin was administered to fed or fasted horses. Initial increases in cTnI concentrations occurred between 24 and 72 hr after monensin administration. The 2 horses with the highest cTnI concentrations died or were euthanized within 5 days after monensin administration and had severe cardiac disease. One horse had increased cTnI concentrations from day 2 to day 16, but no apparent change in ventricular contractile function was evident on echocardiography. The fourth diseased horse did not return to cTnI reference intervals until day 27 after monensin administration, and the ventricular function was still abnormal just before euthanasia 9 months later. Cardiac troponin I measurements could be useful in managing farm outbreaks of accidental monensin feeding by the early identification of horses with cardiac disease.

Topics: Administration, Oral; Animals; Anorexia; Diarrhea; Heart Failure; Horse Diseases; Horses; Monensin; Myocardium; Troponin I

The consumption of monensin-containing feed resulted in deaths of water buffaloes from a feedlot in which cattle and buffaloes were kept together. The monensin formulation was recommended only for use in cattle. Anorexia, muscular weakness, dyspnea, and recumbency were the major clinical findings. The most significant gross lesions were focal pale areas in semitendinosus and semimembranosus muscles, in which segmental necrosis of myofibers was seen microscopically. To compare susceptibilities of species to monensin, 3 bovine calves and 3 buffalo calves were orally dosed. At 5, 7.5, and 10 mg/kg of monensin, only the buffaloes became ill and died. Clinical signs initiated 18-20 h postdosing and were comparable to those from field cases. Gross changes consisted of ascites, hydrothorax, hydropericardium, hepatomegaly, and focal pale areas in the myocardium and to a lesser degree in semitendinosus and semimembranosus muscles. Histopathological changes also resembled those from the field cases, but were especially pronounced in the myocardial cells. The hypothesis that buffaloes could have a lower tolerance to monensin than cattle has been supported by experimental cases.

Topics: Animals; Anorexia; Buffaloes; Histocytochemistry; Ionophores; Monensin; Muscular Diseases