Abstract
Acute acidosis problems in ruminants is the result of excessive consumption of fermentable carbohydrates which causes a non-physiological reduction in pH and the production of a toxic factor(s). The low ruminal pH is the result of the production of large quantities of volatile fatty acids as well as other acids (such as lactic, which has a pK of 3.7) and the weaker buffering power of concentrates compared with that of forages (in the pH range of six to four in the rumen). It is most likely to occur if glucose accumulates in conjunction with ruminal pH reductions to 5.0 or less. Acidosis problems should occur in the absence of ruminal glucose accumulation if ruminal pH is sufficiently low and if other readily fermentable carbohydrates which aciduric bacteria can utilize are available in excess. Wheat seems more prone to cause acidosis than other farm grains. Once the lower ruminal pH's (between five and six) are attained, free amylase of the ruminal ingesta may increase and microbial glucose utilization rates decrease. The increased rate of glucose production and decreased rate of its utilization leads to glucose accumulation in the rumen and to an increased number of lactic acid forming bacteria. Also, free glucose inhibits lactic acid metabolism (at least by pure cultures of Selenomonas ruminantium), and the slower rate of lactic utilization is likely to cause even greater initial ruminal lactic accumulation and absorption. Compounds other than lactic acid are also responsible for digestive disturbances. For instance, cattle have been noted to reduce feed intake or to have diarrhea, or both, when ruminal pH was maintained at 5.5 or above, and lactic acid did not accumulate in the rumen. In general, ruminants in poorer condition are more prone to acidosis problems. The importance of cellulose digesting bacteria and protozoa for cattle in feedlots is not clear. These organisms have been suggested to be important in giving stability to the ruminal populations. They disappear or are reduced to fewer numbers in cattle with acidosis. The protozoa may serve a useful role by slowing down ruminal fermentation of carbohydrates to fatty acids. Other consequences of acidosis in cattle include reduced salivation, reduced intestinal motility, reduced intestinal ingesta turnover, redistribution of water in the body, change in removal rates of toxic compounds from the body, and damage to rumen, liver and other tissues. The time required for the ruminant's intestinal microbes to be restablized after a digestive disturbance (once conditions favor such stabilization) has not been clearly established. A week or more is required for cattle not inoculated with ruminal ingesta (but changed from a forage to a concentrate diet) to attain the diet intake levels of cattle treated similarily except for being inoculated with 2 liters of ruminal ingesta. Results from in vitro studies have shown that 10 to 15 volume turnovers or about 6 to 10 days may be required to bring a rumen microbial population receiving glucose in a chemostat to steady state conditions. Reduced rumen turnover caused by digestive disturbances is likely to result in less microbe synthesis in the rumen per unit of energy utilized. Consequently, less protein will be made available to the host animal for the productive purposes. Copyright © 1976. American Society of Animal Science . Copyright 1976 by American Society of Animal Science