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Title:   Author  item
                                            GRESSLEY, TANYA - University Of Delawareitem
                                            Hall, Mary Bethitem
                                            ARMENTANO, LOUIS - University Of Wisconsin
  Submitted to: American Dairy Science Association Abstracts
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 3/10/2010
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary:
                                Technical Abstract: Microbial fermentation of carbohydrates in the large intestine of dairy cattle is responsible for 5 to 10% of total tract carbohydrate digestion. When dietary, animal, and/or environmental factors contribute to abnormal, excessive flow of fermentable carbohydrates to the large intestine, hind-gut acidosis can occur. Hind-gut acidosis is characterized by increased rates of production of volatile fatty acids (VFA) including lactic acid, decreased digesta pH, and damage to gut epithelium as evidenced by the appearance of mucin casts in feces. In parallel to ruminal disorders, it is possible that hindgut acidosis can also be classified as acute or sub-acute. In the more severe situations, hind-gut acidosis is characterized by an inflammatory response; the resulting breach of the barrier between animal and digesta may contribute to laminitis and other disorders. In a research setting, hind-gut acidosis has been evaluated using pulse-dose or continuous abomasal infusions of varying amounts of fermentable carbohydrates. Continuous low dose infusions of pectin or fructans (1 kg/d) into lactating cows resulted in decreased diet digestibility, increased intake variation, decreased milk fat percentage, decreased milk urea N concentration, and increased fecal N output, without affecting fecal pH or VFA. Pulse dose fructan infusions (1 g/kg body weight) into steers resulted in watery feces, decreased fecal pH, and increased fecal VFA, without causing an inflammatory response. Daily 12 h abomasal infusions of a high dose of starch (~4 kg/d) have also induced hind-gut acidosis as indicated by decreased fecal pH and watery feces. Evidence of hind-gut acidosis has also been noted on farms as detected by fecal signs of excessive fermentation (watery or foamy appearance) or of epithelial damage (presence of mucin casts). In summary, hind-gut acidosis occurs as a result of relatively high rates of large intestinal fermentation, likely as a result of digestive dysfunction in other parts of the gut. A better understanding of the relationship of this disorder to other animal health disorders is needed.


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