Protein meal toxicity

Caution is required when feeding high protein content, highly degradable, palatable meals to cattle, particularly those on low energy diets.

In late 2002 and early 2003 a number of cases of severe sheep and cattle losses occurred in groups fed straight soybean meal. Deaths have typically occurred within 12-24 hours of feeding and continue for up to three days.

Protein metabolism

A proportion of all protein is degraded to ammonia in the rumen and rumen microbes use ammonia as their source of nitrogen with digestible carbohydrate from feed for their growth. This process converts low quality roughages to microbial protein that the animal can use.

Excess ammonia passes into the blood stream and is converted to urea in the liver. The urea can then be excreted or recycled through the rumen. If ammonia levels get too high, the liver cannot convert it all to urea and toxic levels may be reached.

Although ammonia toxicity is generally a result of excessive urea intake, a similar result can occur with highly degradable protein meals if they are very palatable and eaten quickly in sufficient quantity (Table 1).

* Protein content on 'as fed' basis

Drought conditions increase the risk of ammonia toxicity because:

1. The combination of poor quality forage and low intakes reduces the amount of carbohydrate available to rumen microbes and consequently their ablity to utilise ammonia.
2. The slower rate of digestion, which results from poor quality forage, provides more opportunity for porteins to degrade in the rumen and release ammonia.

Feeding strategy

Deaths in animals fed soybean meal indicate that offering two to four days intake at one feeding, as generally done with cottonseed meal and copra meal to reduce bullying, is hazardous. To date, no problems have been reported where the feeding methods restricts soybean meal intake i.e. fortified molasses, urea and salt dry licks or mixed with dicalcium phosphate.

Symptoms of toxicity

Post mortem examination has shown little of significance. A conculsive diagnosis has been difficult, but acute ammonia toxicity appears the most likely cause.

Predominately nervous signs have been observed. These may include:

• head tremor with side to side twitching
• weight shifted off front feet with circling on hind feet in the one spot
• tail flicking
• eye lid twitching
• high stepping in front
• apparent blindness
• slight bloating
• licking at flank
• depression
• sternal recumbency with death often occurring in this position.

Treatment

The antidote for ammonia toxicity (urea poisoning) is oral dosing with vinegar if treated in the early stages of poisoning. Dosage for cattle is 600ml; sheep 120ml diluted with water.

Minimising risk of toxicity

Recommendations to avoid potentially hazardous intakes are:

• do not offer more than one day's intake at a feeding (Table 2)
• ensure there is adequate trough space (20cm/hd) so 'bullies' have less chance to over eat
• ensure animals have adequate roughage
• gradually introduce animals to highly palatable feeds. This is particularly important if animals have previously been fed less palatable feeds
• add products, which are known to control intakes in a particular area. Possibilities are salt and dicalcium phosphate or as a fortified molasses mix.

All stock fed high protein rations following periods of poor quality feed, should be vaccinated to protect against enterotoxaemia.

Recommendation

Closely monitor animals when introducing or changing to a high protein content meal, and contact the Customer Service Centre or your local veterinarian if sickness or deaths occur.