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Rumen Dysfunction

Rumen Dysfunction

Our previous blogs have already discussed some situations where the processes of rumen function are likely to be less than optimal. There are many feeding situations where the efficiency of ruminal utilisation of dietary proteins is compromised, due principally to the nature as well as the amount of protein being consumed. An imbalance between protein supply and the ability of the microbes to utilise that protein can result in significant losses of dietary protein as ammonia prior to the small intestines. High levels of protein in freshly grazed forages is one such situation, especially when levels of water soluble carbohydrates in the forage are compromised, possibly due to low levels of sunshine affecting overall photosynthetic activity of the plant. It is on this basis of providing an improved balance of protein and ruminal degradable carbohydrate that the concept of high sugar grasses was developed through plant breeding. However, the responses in terms of improved animal performance have been unpredictable, possibly due to variable effects on total sugar content being reported.

Excess production of rumen ammonia leads to increased urea production in the liver. It is crucial that the animal removes most of this ammonia to prevent it from entering peripheral circulation where it can have toxic effects. In most situations this can be achieved by the condensation of two molecules of ammonia to form one molecule of urea. When ammonia load in the liver is high however, an alternative pathway will operate where one of the two NH2 groups is provided by the catabolism of specific free amino acids, the net outcome being a reduction in the quantity of amino acids that are available to the animal. At the same time, it is often reported that the production of urea from excess rumen ammonia may have a significant energy cost. In reality this is not likely to be the case, certainly not to the level that is frequently suggested.

It is also pertinent to note that high rumen ammonia levels can arise when high levels of non-protein nitrogen (eg urea) are included in the ration, and in extreme cases may result in animals dying from ammonia toxicity. In such situations, the load of ammonia is too high to allow efficient capture by the rumen microbes, and when liver capacity to remove this excess ammonia is exceeded, a pronounced rise in plasma ammonia level is inevitable. Research has shown that with increasing plasma ammonia levels, animals’ first show reluctance to consume feed. This can be quickly followed by the animals becoming recumbent and if the condition continues, coma followed by death can occur.

It has already been mentioned that when the supply of ruminal degradable carbohydrate is high, especially when a significant amount is being derived from non-fibre carbohydrates (eg starch), there may be a pronounced increase in rumen lactate levels with a concomitant reduction in rumen pH. This can lead to subclinical rumen acidosis, defined as rumen pH levels below 6.0, leading in some cases to acute rumen acidosis when rumen pH levels rumen fall below 5.5. The impact of this on rumen function can be quite severe. At consistently low rumen pH, the functionality of the rumen papillae will be compromised, often noted by thickening or clumping of the papillae (rumen parakeratosis) which inevitably compromises the absorptive capacity of the rumen epithelium. In turn this will exacerbate the already low rumen pH conditions. Further damage of the rumen epithelium may seriously compromise its integrity and allow microbial toxins, produced by the rumen microbes which are now under considerable metabolic stress, to pass through into peripheral circulation. If the condition is not treated rapidly these toxins can ultimately result in the death of the animal.

Sub-clinical or clinical rumen acidosis must be avoided in all situations through appropriate dietary management. Feeding large amounts of starch-rich feeds in single meals is not advisable whilst balancing the nature of the starch in the ration to provide a balanced supply of rapidly and slowly degradable starch is recommended. Contrary to general opinion however, low rumen pH levels are not only caused by high starch feeding, and when formulating rations it is important to take account of the levels of water soluble carbohydrates being consumed by the animal. Whilst sugars tend to be fermented more to acetate and butyrate than to propionate and lactate, they are an almost instantaneously available source of carbohydrate which can seriously impact on rumen pH. This has been demonstrated recently in research from Australia where cattle grazing lush irrigated pastures where found to have rumen pH levels below 6.0 for up to 16hrs during each 24hr period and on occasions, pH levels approached 5.5 where the condition could be considered to be on the border of becoming acute. At the same time, rumen ammonia-N levels exceeded 30mg/100 ml for over 12hrs during the day, adding a further burden to the animal in terms of excreting this as urea, whilst indicating considerable loss of valuable plant protein.

When rumen pH falls below 6.0, one further consequence is the effect on rumen fibre digestion. Fibre degrading microbes are relatively slow growing compared with starch utilising microbes and most importantly are sensitive to rumen pH level. At or below pH 6.0, the fibrolytic microbes are affected, with reduced production of fibrolytic enzymes leading to impaired fibre digestion. This will immediately impact on the overall nutritional value of the feed being consumed, as any reduction in the digestibility of dietary fibre will reduce total dietary ME value. Given that fibre generally constitutes between 30 and 40% of total ration DM intake, this can be quite significant. Compromised digestion of fibre in the rumen will reduce the production of acetate and butyrate which are important precursors of milk fat synthesis and as a consequence milk fat levels and total milk fat production are likely to be reduced. Finally, in response to compromised fibre digestion in the rumen, feed intake will decline, simply due to a reduced rate of clearance of feed by digestion in or passage out of the rumen.