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This article was published in 1994
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A Case of Monensin Toxicity in Steers and Heifers on a Grain Ration
James Godwin
Introduction
This paper describes a case in which eight of one hundred cattle of mixed breeds died as a result of monensin toxicity when Rumensin® was fed at 20mg/kg of a triticale grain ration.
Background
Monensin is a carboxylic ionophore. It is used in cattle to increase feed conversion efficiency by both increasing the relative numbers of propionic acid producing bacteria in the rumen and the amount of propionic acid they produce. (1)
Monensin is able to transport cations across cell membranes and it prefers to transport calcium over other ions. In essence this breaches the cellular and intracellular membrane integrity causing swelling of the cell. It also causes increased contractility of muscle cells including the myocardium. The effects on the myocardium progress from this increase in contractility to tonic contractions to degenerative changes. (1)
It is surmised that the changes seen in cases of monensin toxicity in the gut are due to changes in the gut flora which leads to diarrhoea. (1)
The recorded clinical signs of toxicosis in cattle are anorexia, sudden death without struggle, dark coloured diarrhoea, stiffness, weakness, dyspnea, depression, jugular pulse and non responsiveness to visual stimuli. (1,2)
History
The owner of the cattle was experienced in the feeding of concentrates to cattle. At the time of the toxicity two grades of animals were being fed from steel troughs (converted sheep footbaths) in a 35 acre paddock. There were beasts of 500kgs or more that had been on the feed for 100 to 120 days (seventy in number) and beasts of 260 to 270 kgs (thirty in number) that had been on the feed for 4 to 5 days. Only cattle in the second group of thirty were affected.
The ration consisted of
1% urea
1% salt
1% bentonite (pellet form)
2% peas (uncrushed)
20gm/tonne Rumensin®
Balance Triticale.
This was fed at the rate of 5 to 6 kg per head per day. Oaten or pasture hay was available ad lib. There was green pasture in the paddock equivalent to more than 3000kg/hectare dry matter.
The group of animals that were affected had been grazing a green crop of triticale up to the time they were moved and introduced to the grain. In this instance the thirty cattle when introduced to the grain had not been fed grain before in their lives.
The owner relies on the pecking order amongst the cattle to prevent gorging by the younger/smaller animals when they are first introduced to the grain.
Grain was mixed with Rumensin® and the other additives via a hopper that was especially designed for the purpose. It was situated mid-way along a pencil auger. Further mixing occurred as the feed was transferred from a small chaser bin to the metal troughs on a daily basis.
The troughs are cleaned out only in wet weather.
Approximately 4 to 5 days after the younger animals had been introduced to the grain the entire mob was yarded to draft off some of the larger animals for sale. At this stage one of the younger beasts was noticed to be lethargic. Upon release from the yards it was noticed to go down in lateral recumbency. By the time the owner walked over to the beast it was dead.
The next week a further animal was found dead in the paddock. The owner dragged the animal into a rubbish tip and did not contact me until 24 hrs after the death. Due to the degree of decomposition only a limited post-mortem was conducted. Diarrhoea was of normal colour but having a strong odour was noticed. Hyperaemia of the rumen wall was seen and a section submitted for histopathology. A moderate amount of grain was seen in the rumen. A provisional diagnosis of acidosis was made.
The next day two further animals were noticed to be lethargic and with diarrhoea. The animals were removed from the paddock with the troughs.
Histopathology of the rumen revealed only,'a mild to moderate degree of congestion of the propria submucosa'. (Histology performed at Wagga Wagga Regional Veterinary Laboratory)
A further four animals died in the next two to three days. The owner informed me 12 hrs after the death of the last of these animals. A post-mortem revealed; 1/ hyperaemia of the abomasum, small intestine, lungs and kidneys, 2/ a large amount of serous fluid in the thoracic cavity and pericardial sac and 3/ a small excess of serous fluid in the abdominal cavity. At the same time a further sick animal was examined in a crush. This animal was very weak and walked with a slow unsteady gait. It had a pronounced jugular pulse, normal gut sounds and a rapid heart rate. The animal exhibited signs of abdominal pain and had moderate diarrhoea. Magnesium sulphate was recommended as a purgative. At this stage I was concerned that urea toxicity was the cause, based upon the signs of abdominal pain. The jugular pulse was dismissed as being related to the high heart rate and stress associated with the pain of urea toxicity.
A diagnosis of monensin toxicity was made when histopathology of the second animal post-mortemed revealed severe sub-acute diffuse degenerative myocardiopathy. (Histology performed at Wagga Wagga Regional Veterinary Laboratory)
Following the diagnosis and appropriate action a further 2 animals died in the ensuing 14 days. One animal was lethargic and anorexic for 10 days before it eventually died. Conclusions At the time that the diagnosis of Rumensin® toxicity was made from histopathology the owner stated that it was probably due to the settling out of the Rumensin® in the base of the troughs. He felt that the younger animals would be most likely to lick up this residue for two reasons, 1/ the younger animals could only access the trough when the older animals had had their fill and 2/ these animals would be more interested in the salty residue than the grain when first introduced to the ration.
However when I revisited the owner to collect further details for this paper he showed me that there was virtually no settling out of any of the feed additives, at least not visibly.
According to the label instructions for Rumensin® the premix should be added at 10 to 33gms per tonne. The owner had taken an average of 20gms per tonne as a safe choice. Given that he had calculated 5 to 6 kgs of grain per head, this would work out to be 120mgs per 260 kg beast or roughly 5mg/kg body weight. Deaths are reported at 12.5mg/kg body weight(3). To reach this level animals would have needed to ingest 162 kgs of grain mixed at 20gms per tonne.
Possible reasons for the toxicity could include; (a)concentration of the Rumensin® at some stage of the mixing, (b)Rumensin® settling out and concentrating at the bottom of the troughs or (c) the actual toxicity is higher than that recorded or previously encountered in such circumstances.
References
(1) V C Langston et al. 'Toxicity and therapeutics of monensin: A review', Veterinary medicine, pp 75 - 84, October 1985
(2)M N Novilla and T M Folkerts 'Ionophores: Monensin Lasolocid, Salinomycin, Narasin'
(3) Rumensin Technical Manual, pp 67 - 78