ACIDOSIS EXPLAINED
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Acidosis is a condition of fatal, or potentially fatal, high acidity of the blood. This is systemic acidosis. In ruminant animals (cattle, sheep, deer, etc.) the term also refers to acidity in the rumen (rumen acidosis or lactic acidosis). Development of acid conditions within the rumen is diet-related and is caused by an abrupt increase in consumption of readily fermentable carbohydrates (concentrates). The source of these carbohydrates is usually cereal grains, but other sources include tubers or root crops, as well as immature rapidly growing forages. Rumen acidosis is commonly brought about by a sudden increase in grain consumption or a rapid change from an all-forage or high-forage diet, hence the term grain overload. Acidosis can be acute and life-threatening, or chronic (subacute), causing reduced feed intake and weight gain.
Development of acidosis has 2 major phases. The first phase involves the sudden increased ingestion of concentrates followed by their rapid fermentation within the rumen. This produces acids that alter the population mix of rumen microbes. The second phase is the absorption of these acids into the blood stream, resulting in systemic acidosis.
Fermentation of carbohydrates by rumen microbes produces volatile fatty acids (VFA's) and lactate (lactic acid). However, some rumen microbes consume lactate and convert it into VFA's as well, such that there is normally very little lactic acid present in rumen liquid. VFA's are absorbed into the blood through the rumen wall and transported to the liver and kidneys where they are converted to glucose for use as energy by body tissues. Abrupt changes in diet destabilize the population mix of rumen microbes, especially with the sudden introduction of high-concentrate feeds. Rapid fermentation of carbohydrates within the rumen quickly increases production of VFA's and lactic acid. Increased acidity in the rumen favours bacteria that produce lactic acid over those that consume it, making conditions within the rumen even more acidic. Lactic acid begins to accumulate and can constitute 50-90% of rumen acids. Lactate produced in the rumen can be absorbed through the rumen wall, passed from the rumen with ingested food, or provide substrate for bacteria. Lactic acid accumulated in the rumen or passed through it into the lower intestinal tract is readily absorbed into the bloodstream. There, increased acidity disrupts electrolyte balance, kidney function, and oxygen transport. Persistence of these conditions can result in death.
In non-fatal cases of acidosis, acidic conditions within the rumen reduce its function and interrupt normal digestion. The rumen wall can also be damaged, giving rise to potential systemic bacterial invasion of the kind responsible for liver abscesses. The lower intestinal tract can also be adversely affected by acidic conditions. The small intestine can become inflamed and alteration of its bacterial population can occur, contributing to diarrhea and loss of electrolytes.
Symptoms of acidosis include reduction or cessation of feed intake, diarrhea, depressed or distressed appearance, intoxication, founder, and death. Other less obvious symptoms are poor weight gain or feed efficiency. Symptoms observable post-mortem include liver abscesses, rumenitis, or altered blood metabolic profiles. Immediate treatment for acidosis would be to remove the source of readily fermentable carbohydrate and replace it with a good quality forage diet. Where only one or a few animals are acutely affected, it may be practical to supply electrolytes or bicarbonate buffers intravenously. Antibiotics may also be useful to treat bacterial infections arising from acidosis.
The most effective treatment of course, is to prevent acidosis from occurring in the first place. Prevention centres around gradual introduction of feeds high in readily fermentable carbohydrates and close monitoring of daily intakes of such diets. Populations of lactate consuming bacteria begin to rise within the rumen immediately upon ingestion of readily fermentable carbohydrates and will increase 6 to 8 times their original numbers within 4 weeks. Gradually introducing concentrate feeds allows the lactate-consuming bacterial populations time to grow at a rate more consistent with lactate production, such that lactic acid is not allowed to accumulate in the rumen. Four weeks is the recommended time over which ruminants should be adjusted from primarily forage to high-concentrate diets. Observation of animal condition and provision of fresh feed and water daily are also important. Providing roughage in the form of good quality forage when feeding concentrates is useful in preventing acidosis for several reasons. First, acid production is reduced when diets contain adequate roughage. Second, roughage increases chewing and rumination activity, thereby increasing saliva production. Increased saliva will dilute and buffer the acidic products of fermentation. Finally, forages themselves provide some buffering ability. Providing adequate roughage is particularly important when feeding processed (rolled, ground, pelleted) feeds. While processing high roughage diets may improve animal performance, processed feeds that are low in roughage and high in concentrates reduce chewing activity, saliva production, and rumen motility. The rumen's ability to properly digest material and buffer acidic conditions is thereby reduced. Weanling animals are particularly susceptible to grain overload because of the stress of weaning as well as possible unfamiliarity with their feed. It is therefore important to provide good quality forage with which fawns are already familiar to help prevent acidosis at weaning time.
Terry Osko
Waskwei Creek
Whitetails
Vegreville, AB
References:
Church, D.C. 1988. The ruminant animal: digestive physiology and nutrition. Prentice Hall, New Jersey 07632, USA.
Frandson, R.D. 1986. Anatomy and physiology of farm animals, 4th edition. Lea & Febiger, Philadelphia 19109-4198, USA.
Van Soest, P.J. 1982. Nutritional ecology of the ruminant. Cornell University Press, Ithaca 14850, USA.
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