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Many of the ca. 14 million head of cattle in South Africa may be classified as high-producing animals. To people involved with these intensively-fed ruminants the concept of acidosis is not new – most have heard about the menace, some have experienced problems ascribed to it and others have lost animals due to it.

However, as a scientist involved in the study of acidosis I have found it to be somewhat “elusive”. Upon enquiry at a feedlot or dairy farm the answer would often be “I know some people do have acidosis problems but I (we) don’t really have a problem”.

We also did various experiments where we pushed animals beyond generally acceptable feeding levels (both rate of change and final level of concentrate feeding), in a bid to elicit acidosis, and did often not get the anticipated response. There are excellent review papers on acidosis in ruminants (17, 2). The aim of this paper is not to duplicate them but rather to take a closer look at acidosis with a view of shedding some light on the question whether acidosis is a menace or a myth.

Modern day intensive production systems involves feeding high levels of concentrates (mostly non-fibrous carbohydrates such as starch in feed grains) to ruminants. With beef cattle we want to get them from roughage onto high concentrate diets as rapidly as possible (6); With dairy cows we want to feed them even higher concentrate levels to obtain higher energy intake (10, 9). The aim is to maximize performance and efficiency, whilst hopefuly keeping digestive disturbances such as acidosis within acceptable limits through good nutritional management.

Actual data on the incidence and economic impact of acidosis in the South African Beef and Dairy Industries seems scarce. However, USA data shows that digestive disorders (of which acidosis forms the major part) account for approximately 25 to 33% of deaths in feedlot cattle, and likely contribute significantly to decreased performance and efficiency of production (6). Nagaraja et al (15) states that these digestive disorders are of significant economic concern, costing the feedlot industry hundreds of millions of dollars annually. The same situation applies to the dairy industry in the USA (2, 10). Acidosis also costs the Australian feedlot industry approximately $9 million per year (18).


MECHANISM AND SYMPTOMS

Cattle and sheep have a large fore-stomach, the rumen, which contains a stable population of microorganisms. These microorganisms derive energy mainly by fermenting the carbohydrates which the host animal ingests.

The events leading to acidosis occur when the animal’s diet is suddenly changed from forage to concentrate (high in starch or other rapidly fermentable carbohydrates), or when it is fed excessive amounts of such concentrates (14, 6). Introduction of starch into the rumen, or a sudden increase in the starch supply, leads to rapid fermentation and increased production of volatile fatty acids (VFA).

Furthermore glucose, normally found in extremely low concentrations in the rumen, is liberated from starch or other rapidly fermented carbohydrates, resulting in increased ruminal glucose concentrations. This has negative consequences including growth of organisms such as Streptococcus bovis and other lactic acid producing organisms, and increased ruminal osmolality, which further increases ruminal acidity by inhibiting VFA absorption from the rumen (6). As the rate of VFA production exceeds their rate of removal, rumen pH may fall below 6.0.

Streptococcus bovis and other lactic acid producing bacteria (especially the Lactobacilli species) are more tolerant to these acidic (low pH) conditions and they start to replace the other normal rumen microorganisms to become the major components of the microbial population in the rumen (5). At the same time organisms such as Megasphaera elsdenii, which would normally prevent lactate accumulation by metabolizing lactate to VFA’s, are inhibited.

Lactic acid is a 10 times stronger acid than the VFA’s and pH continues to fall further until even the resilient S bovis can no longer grow and Lactobacilli take over, further fermenting the starch to produce even more lactic acid – a self-perpetuating cycle of lactate production leading to ruminal pH values below 5.0. This whole process may be very rapid and overgrowth by lactic acid bacteria can occur within 24 h (5). Lactic acid, which is normally found at very low concentrations in the rumen, can increase to around 100 mM in severe cases of acidosis (14).
Under the above conditions the ciliate protozoa population, which normally has a stabilizing effect on ruminal fermentation, declines because the ruminal pH is below their growth optimum (14). These protozoa have an important role in regulating the production of lactic acid and VFA’s in the rumen. They ingest starch, soluble sugars and bacteria, thereby reducing the rate of fermentation in the rumen. They also appear to be involved in the metabolism of lactic acid. The absence of a stable and active population of ruminal protozoa is therefor likely to increase the severity of lactic acidosis (14).

The general term “acidosis” may often be used to refer to either acute acidosis (also called lactic acidosis) or subacute acidosis, sometimes also refered to as chronic acidosis. This may lead to confusion, and may be part of the reason for asking the question: Acidosis: Myth or menace?

Acidosis is categorized as acute or subacute primarily on the basis of presence or absence of various symptoms (15). Symptoms of acute acidosis include anorexia, rumen stasis, rumenitis, diarrhea, dehydration, laminitis and liver abscesses (14). Rumen lactic acid levels will also be high with a concomitant drop in pH (14). The above-mentioned changes in rumen microbial population, as well as a reduction or complete absence of ciliated protozoa will also be evident.

With subacute acidosis on the other hand decreased and/or erratic feed intake may be the only sign, and this may be difficult to observe for individuals in group-fed cattle. Whereas acute acidosis is easier to detect, and if diagnosed early, can be treated directly, or measures taken to prevent further episodes, subacute acidosis is probably the most prevalent form, and more difficult to detect and treat (15).

A comparison of acute and subacute acidosis is shown in Table 1. It should be clear that ruminal acidosis cannot merely be defined as a condition of low ruminal pH but that it is best described as a syndrome related to a fermentative disorder of the rumen (10).

Another important point is that subacute acidosis does not involve lactate accumulation in the rumen (8), and that the term “lactic acidosis” , if used correctly, can only refer to “acute acidosis”. From the foregoing it is also evident that, although a distinction is often made, subacute and acute acidosis are not two distinct “diseases” but that subacute acidosis can easily develop into acute acidosis if the appropriate circumstances deteriorate.


Table 1. Comparison of acute and subacute acidosis (15)





TRADITIONAL PREVENTATIVE PRACTICES

There are basically two situations where acidosis may occur. One is when changing from a roughage to a concentrate diet. The other is when animals already on a concentrate diet suddenly consume much more concentrates than usual. Traditional preventative practices to reduce the risk of lactic acidosis centre around management strategies aimed at introducing ruminants to grains gradually over a period of time, e.g. stepwise increases in the proportion of grain in the diet (13, 18). This is thought to allow time for the resident populations of bacteria that utilize lactic acid, and others that ferment starch, to keep up with the growth of S bovis, thus preventing acidosis from occuring (13).

However, this gradual adaptation is time-consuming and expensive because it involves numerous changes to the diet, often with frequent feeding, and close monitoring of daily feed intake. It also reduces potential liveweight gain and efficiency of growth – generally the sooner animals can be on the final high-energy diet the more efficient they produce (18). The same applies for dairy cattle, where there are both the challenge to adapt the rumen as rapid as possible to handle high-energy diets and the need to push energy content of the diet as high as possible, in order to obtain high and efficient milk production (9).

The feed management strategy followed will usually dictate a final acceptable dietary roughage content, depending on the kind and physical form of roughage used. From a practical point of view operators would like to get away with as little roughage as possible since it is bulky and relatively expensive and because it takes up space in the diet, which can rather be filled with concentrates for more efficient production. The results of recent experiments with feedlot and dairy cattle, in which KK Animal Nutrition was involved, showed definate advantages in total production and efficiency where concentrate levels were increased above “more traditional” controls (P H Henning, unpublished data).

There are also situations where cattle may consume much greater quantities of concentrate than usual at one time (10). These include dose-feeding of grain (e.g. in the milk parlour); inadequate bunk space / feed provision in which some animals crowd the bunk and gorge themselves whilst others go hungry and then eat even more when they get the chance later; improper mixing in total mixed rations (TMR) allowing selection; other situations of irregular feed provision and changes in intake patterns due to passing weather fronts (10).

Apart from managing the rate of change from roughage to concentrates and retaining sufficient roughage in the final production diet, other traditional preventative practices include the use of ionophores, nonionophore antibiotics and buffers (15, 6). The ionophore monensin has been shown to decrease day-to-day variation in feed intake. This together with direct effects on inhibition of lactate-producing bacteria might decrease the likelihood of high acid production in the rumen. Other ionophores such as lasalocid and salinomycin generally do not affect, or sometimes even increase, feed consumption, and their role in prevention of acidosis is less clear (15).

Dietary inclusion of certain nonionophore antibiotics such as virginiamycin (VM) may also provide protection against acidosis. Results are, however, variable possibly due to the fact that VM inhibits some lactic acid-producing bacteria (S bovis) but not others (e.g. Lactobacillus and Selenomonas spp) (1).

Dietary buffers (e.g. bentonite and bicarbonates) have also been used to control acidosis in ruminants (15), but their role and efficacy is not well defined (6). They also add cost to the diet and take up space at the expense other important ingredients.


VARIABLE INCIDENCES / RESPONSES OBSERVED IN PRACTICE (AND RESEARCH)

As mentioned earlier there appears to be substantial variation in the incidence of acidosis and in the response observed with different remedies. The reason may be the fact that a variety of nutritional, management, genetic, behavioural and environmental factors seem to be involved in the development of acidosis (6). There is e.g. considerable variation in rumen pH among animals fed the same diet (3). Large variation was also evident in the ability of animals to cope with a carbohydrate challenge (4).

Variation in feed intake, and circumstances resulting in erratic feed intake have been suggested to increase the incidence of acidosis, however, the exact nature of the relationship involved seems to be unclear due to its very complexity (6). Other factors such as acids in the diet (e.g. when feeding high levels of silage) and failure to produce sufficient endogenous buffers (e.g. with diets resulting in reduced saliva flow) may also explain variation in the incidence of acidosis (12).

Mackie et al (13) hypothesize that the rapid introduction to a starch-based diet alone is insufficient to trigger an episode of lactic acidosis. They propose that other factors – e.g. a period of feed deprivation – are required to predispose the rumen and allow S bovis to outcompete other, normally dominant bacteria (Figure 1). This may explain those cases where experimental diets designed to induce acidosis appeared unable to give the desired effect – the other management factors were probably just to good so that the rumen was not sufficiently predisposed to acidosis?!




Figure 1. Development of acute ruminal lactic acidosis on high-starch diets (13).



OTHER OPTIONS FOR PREVENTION AND CONTROL

Current practices to reduce the risk of lactic acidosis in livestock centre around management trechniques based on introducing grain gradually to animals. However this procedure is time-consuming and involves numerous changes to the diet, with frequent feeding and close monitoring of daily feed intake. This also reduces potential production and efficiency, and still does not eliminate acidosis. Furthermore, where antibiotics are to some extent effective in preventing lactic acidosis by reducing the populations of S bovis and Lactobacillus, their future use may be restricted due to the potential for emergence of drug-resistance and the risk of antibiotic residues in animal products (18). Immunisation and direct-fed microbials present two alternative options for prevention and control of acidosis.


Immunisation

This was tested in feedlot cattle (18) using an intramuscular immunisation regime to induce the secretion in saliva of antibodies against S bovis and Lactobacillus. Immunisation did reduce numbers of S bovis and Lactobacillus in the rumen, resulting in significantly lower ruminal lactic acid and higher intake – thereby apparently reducing the risk of lactic acidosis. However, the specific immunisation may also still leave other lactate-producers such as Selenomonas ruminantium unscathed and able to produce significant amounts of lactic acid.


Direct-fed microbials

Direct-fed microbials (DFM), also called probiotiocs, refer to microorganisms, generally “live”, usually given to animals in their feed, that improve animal performance in some way or other (11). Their use have come to the forefront lately in response to the increased demand for the use of “natural” performance-promoting substances (11).

Experimentally, there have been several bacteria that have potential as DFM to prevent acidosis in cattle (11). For example various in vitro and in vivo studies have shown that inoculation with the rumen bacterium Megasphaera elsdenii (the major lactate-utilizing organism in the rumen of cattle adapted to high grain diets) helps prevent the accumulation of lactic acid in the rumen during the transition from a low to a high concentrate diet (16, 11). Propionobacterium also have the ability to utilize lactic acid and may be considered as DFM against acidosis.

However, they are probably too slow-growing and acid-intolerant to prevent an acute lactic acidosis challenge (11). A reduced risk of acidosis was reported in dairy cows fed a combination of lactate-producing bacteria, Lactobacillus and Enterococcus, presumably because they caused the rumen microflora to adapt to the presence of lactate within the rumen (7).

Allthough they hold much promise, responses with DFM in ruminants are often small and highly variable (16, 9) and much research are still needed on aspects such as dosage size, mode of application (e.g. a single massive dose vs continuous daily dosing) and addressing viability of oxygen sensitive microorganisms (11, 16).


BOTTOM LINE

From the above discussion it would seem that acidosis is in fact a “menace” rather than merely a “myth”. It is generally agreed by experts that acidosis represents a real threat when ruminants change from a roughage diet to a high-concentrate diet, or when the amount of concentrates being fed is suddenly increased. There are however, reasons why it may sometimes not be observed, or may be judged as “myth rather than menace”.

These include:

The prevalence of the subacute form of acidosis as opposed to the acute form. The latter, which is easily identified, may present only “the tip of the ice berg” in respect of the former, which is not so clearly identifiable.

The complexity of the “syndrome” known as acidosis; It is really a multi-component disorder, with many interactions determining the final outcome that may actually be observed.

The fact that in acidosis research we often “control too well” the other predisposing factors needed, in addition to the mere increase in ruminal starch availability, to precipitate acidosis and ultimately lactic acidosis.

The need thus clearly remains to take the necessary precautions against acidosis in feedlot and dairy cattle, in order to prevent mortalities, to keep treatment costs down and ultimately to prevent a loss of production. It is also clear that further research is required before we will really know all the ins and outs of acidosis. This is even more true in terms of newer measures such as the use of promising DFM.


REFERENCES

1. Al Jassim, R. A. M. and Rowe, J. B. 1999. Better understanding of acidosis and its control. Recent Advances in Animal Nutrition in Australia. 12:91-97.

2. Allen, M. 1996. Causes, detection and prevention of ruminal acidosis in dairy cattle examined. Feedstuffs Sept 1996. p 13.

3. Beauchemin, K. A. 2002. Applying nutritional management to rumen health. Pennsylvania State Dairy Cattle Nutrition Workshop. pp 107-114.

4. Brown, M. S., Krehbiel, C. R., Galyean, M. L., Remmenga, M. D., Peters, J. P., Hibbard, B., Robinson, J. and Moseley, W. M. 2000. Evaluation of models of acute and subacute acidosis on dry matter intake, ruminal fermentation, blood chemistry, and endocrine profiles of beef steers. J. Anim. Sci. 78:3155-3168.

5. Dawson, K. A., Rasmussen, M. A. and Allison, M. J. 1997. Digestive disorders and nutritional toxicity. In: P. N. Hobson and C. S. Stewart (Ed.) The Rumen Microbial Ecosysytem. p 633. Blackie Academic & Professional, London.

6. Galyean, M. L. 2001. Nutritional and metabolic disorders in feedlot cattle. National Beef Science Seminar. pp 105-119.

7. Ghorbani, G. R., Morgavi, D. P., Beauchemin, K. A. and Leedle, J. A. Z. 2002. Effects of bacterial direct-fed microbials on ruminal fermentation, blood variables, and the microbial population of feedlot cattle. J. Anim. Sci. 80:1977-1985.

8. Goad, D. W., Goad, C. L. and Nagaraja, T. G. 1998. Ruminal microbial and fermentative changes associated with experimentally induced subacute acidosis in steers. J. Anim. Sci. 76:234-241.

9. Goff, J. P. and Horst, R. L. 2002. Troubleshooting transition diets for the dairy cow. Southwest Nutrition and Management Conference.

10. Hall, M. B. 2002. Rumen acidosis: Carbohydrate feeding considerations. Proceedings of the 2002 Pennsylvania State Dairy Cattle Nutrition Workshop. pp 1-9.

11. Kung, L. 2001. Direct-fed microbials for dairy cows and enzymes for lactating dairy cows: New theories and applications. Proceedings of the 2001 Pennsylvania State Dairy Cattle Nutrition Workshop. pp 86-103.

12. Lean, I. J., Wade, L. K., Curtis, M. A. and Porter, J. New approaches to control of ruminal acidosis in dairy cattle.

13. Mackie, R. I., McSweeney, C. S. and Klieve, A. V. 2002. Microbial ecology of the ovine rumen. In: M. Freer and H. Dove (Ed.) Sheep Nutrition pp 71-94. CABI Publishing, Wallingford, UK.

14. McSweeney, C. S. and Mackie, R. I. 1997. Gastrointestinal detoxification and digestive disorders in ruminant animals. In: R. I. Mackie and B. A. White (Ed.) Gastrointestinal Microbiology Vol. 1. pp. 583-634.

15. Nagaraja, T. G., Galyean, M. L. and cole, N. A. 1998. Nutrition and disease. Vet. Clin. North Am. Food Anim. Pract. 14:257-277.

16. Newbold, C. J. 2003. Probiotics. Principles for use in ruminant nutrition. In: Proceedings of the 2003 International European Probiotiocs Association Seminar.

17. Owens, F. N., Secrist, D. S., Hill, W. J. and Gill, D. R. 1998. Acidosis in cattle: A review. J. Anim. Sci. 76:275-286.

18. Shu, Q., Gill, H. S., Hennessy, D. W., Leng, R. A., Bird, S. H. and Rowe. J. B. 1999. Immunisation against lactic acidosis in cattle. Res. Vet. Sci. 67:65-71.

Author: Dr Pieter Henning
KK Animal Nutrition, South Africa

The previous article is a special collaboration from AFMA South Africa (Animal Feed Manufacturers Association) and their magazine AFMA Matrix. We thank AFMA for their continuous, kind support!

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06/12/2007

Nozar Farvardin Feed Additive Supplier/afrand Toska Tehran - Iran

Dear Sir, Thanks for a full detail issue about acidosis in ruminants. Its very useful and I appreciate. But you didn't say anything about zeolites especially Clinoptilolite in preventing of acidosis in ruminants. This substance is a natural mineral that may add 2 to 3 percent of feed and because of its special effects, acidosis never occurs in ruminants fed by Clinoptilolite. I will be happy to send to you more details about clinoptilolite and its beneficial effects in animals. Again thanks for the issue. Best Regards, Dr. Nozar Farvardin Answer Checked by Engormix.com

06/12/2007

Víctor Gutiérrez Zootecnista/alenpro S.a. Valle del Cauca - Colombia

Yo también vengo usando la zeolita en vacas de leche en el Eje Cafetero Colombiano y tengo mucho éxito en el control de acidosis, sobre todo porque las suplementaciones deben ser altas en Energía, y usamos mezclas de carbohidratos para balancear las dietas con base en pasturas hiperproteicas. Answer Checked by Engormix.com

06/17/2007

Dr Ram V Patill Qualify this professional Marketing Manager Phone: +919341947152 - Karnataka - India Offered Professional Services (Contact)

Dear Sir, Thank You very much for the nice article on Acidosis. I will request Dr Zohar to e mail the details on Clinoptilotite in acidosis control to me. I will be very thankful for the same. Dr Ram V Patil / India Answer Checked by Engormix.com

06/03/2008

Chong Yulong Shandong [Shantung] - China

Very nice! Answer Checked by Engormix.com