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4.5.6. Acidosis - Grain Poisoning
Acidosis, or grain poisoning, is a debilitating nutritional condition that results from the accumulation of large
quantities of lactic acid arising from the fermentation of grains that are high in rapidly fermentable carbohydrates.
Wheat, triticale, rye, barley and oats are in that order the most likely grains to cause acidosis. It can also occur
in high quality diets that are low in efective ibre.
Although it is not strictly a disease, it can have signiicant impacts on the herd, particularly where breeding cows
and weaner cattle are fed grain diets during winter, calves are fed grain as a weaning supplement, or cattle
are fed inishing diets with very high levels of grain.
Acidosis commonly occurs when cattle that are not adapted to grain diets are irst given access to the
grain. During the fermentation of grain by rumen microorganisms, lactic acid is produced. An excess of
lactic acid afects the animal by;
• Decreasing the numbers of useful bacteria in the rumen and increasing the amount of acid-producing
bacteria causing further build-up of acid in the rumen
• Causing rumen contractions to cease • Causing dehydration by drawing luid into the rumen
from the tissues and blood • Causing the blood to become more acidic, resulting
in heart failure, kidney failure and death • Damaging the rumen wall and enabling fungal or
bacterial invasion of the body. This can result in peritonitis or liver abscess even up to a week after
grain poisoning
• Laminitis; a painful inlammation of the hoof, may occur, resulting in severe lameness.
Fortunately, some species of bacteria that are normally resident in the rumen are able to utilise lactic acid and
prevent excess lactic acid build-up, but unless grain is present in the diet, they remain only a minor component
of the rumen micro-lora. Consequently, grain needs to be introduced gradually over a period of time to allow
the lactic acid utilising bacteria to build up in numbers to a level where they can cope with the rapid production
of lactic acid by other microbes in the rumen. Other instances where acidosis may occur include
when a sudden increase in the quantity of grain is fed and excessive quantities are consumed, where a change
in grain type or concentrate is fed, and as a result of an inadequate consumption of efective ibre. It has also
been observed where animals have had accidental access to grain storage areas, or split grains.
Cattle may sufer either of two forms of acidosis; acute rapid onset and chronic Table 4.5. Where cattle sufer
acute acidosis, unless intervention is applied immediately upon observing afected animals, they will die from the
efects of the condition. Chronic sub-acute acidosis may persist for an extended period, and although may
not cause the death of the animals, they will sufer production losses by going ‘of-feed’ for periods of time
when they are afected. Prevention
Prevention of acidosis requires a multi-factorial approach to manage the inherent risk of high grain, low-ibre diets.
1. The gradual introduction of high risk feeds to cattle over a period of at least 14 days or longer is
the most efective way to ensure that the rumen microorganisms adapt to the grain in the diet
2. Supplementary feeding with neutralising agents rumen bufers can also be used to further reduce
the risk of acidosis. However, using bufers alone and without other preventative measures is not an
efective way to prevent the condition. Commonly used rumen bufers include;
• Sodium bicarbonate at 0.75 to 1.5 ww • Magnesium oxide at 0.5 to 0.975 ww plus sodium
bicarbonate • Calcium carbonate at 1-2 ww, barley or triticale
or 3 ww wheat 3. Adding ibre to the diet to promote rumination and
salivabicarbonate production by the animal 4. Feeding cattle on a daily basis, or twice daily
particularly during very cold weather see Section 3.7.1 will help cattle perform better than those fed
irregularly, as it further limits the chances of grain poisoning
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5. Total mixed rations can assist in the prevention of acidosis by providing a balanced ration containing
ibre and grain. Faecal consistency should be monitored daily to identify
potential problems as they develop. Treatment
Cattle afected by grain poisoning should be removed from the herd and placed on a ‘recovery’ diet. This
involves removing access to grain and providing good quality hay until the animal recovers and is usually
efective for animals with mild cases. Feedlot animals that are scouring can be temporarily
changed to a ration 20–25 lower in grain content for 2 to 3 days to see if their condition improves.
In severe cases, where the animals are unable to stand and have abnormal body temperature, urgent veterinary
assistance should be sought, and if unavailable, consideration should be given to humane destruction
of the individual see Section 4.2.6.
Table 4.5. Symptoms of cattle with acidosis grain poisoning.
Acute Acidosis Chronic Acidosis
Rumen contents become acidic, falling below 5.0
Reduction in rumen pH, and motility Excessive luid build-up within rumen
and intestinal contents lead to a distension of the abdomen
Faeces may appear as diarrhea Fig. 4.5, foamy, with gas bubbles, and contain
undigested ibre or grain Loss of appetite, depression,
isolation, panting, dehydration Reduction in rumination cud chewing
Laminitis lameness Reduced feed eiciency
Diarrhea Daily variation in feed intake is high
Death Reduction in average daily growth rates
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4.5.7. Bloat