Difference between revisions of "Subacute Rumenal Acidosis"

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Also known as: '''''Subacute Ruminal Acidosis — SARA — Subclinical Acidosis — Low Milk Fat Syndrome
  
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Also known as: subacute ruminal acidosis, SARA, subclinical acidosis, low milk fat syndrome.
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Do not confuse with: fulminant ruminal acidosis, grain overload
  
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==Description==
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==Introduction==
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In the last 20 years, selective breeding and improved genetics have dramatically increased the individual dairy cow's milk yield and hence the energy requirements for lactation. In order to meet these increased energy demands and avoid prolonged negative energy balance in early lactation, the energy density of the ration has also been increased. This has been achieved by feeding high levels of concentrate feed and energy-rich maize silage. Although these are effective in helping to meet energy requirements, they also contain large quantities of rapidly fermentable carbohydrates that cause increased production of acid in the rumen. This results in a fall in rumen pH below the optimum range of 6-7, known as subacute rumenal acidosis (SARA). Subacute rumenal acidosis is a herd problem that is often never recognised, let alone controlled. However, it can contribute to many aspects of ill-health in cattle, and reduces productivity, and so management of the condition makes good economic sense.
  
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In the last 20 years, selective breeding and improved genetics have dramatically increased the individual cow's milk yield and hence the energy requirements for lactation. In order to meet these increased energy demands and avoid prolonged negative energy balance in early lactation, the energy density of the ration has also been increased. This has been achieved by feeding high levels of concentrate feed and energy-rich maize silage. Although these are effective in helping to meet energy requirements, they also contain large quantities of rapidly fermentable carbohydrates that cause increased production of acid in the rumen. The results in a fall in rumen pH below the optimum range of 6-7. This is known as subacute rumenal acidosis.  
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Beef cattle and sheep may also face this problem, but this is less common as they are raised more extensively and their energy demands are considerably lower.
  
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It is
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===Pathogenesis===
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insidious and, in many cases is never recognised or
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Excessive quantities of rapidly fermentable carbohydrates in the ruminant diet results in overproduction of [[Volatile Fatty Acids|volatile fatty acids]] by the rumen microflora, lowering rumen pH below its ideal range of pH 6-7. Volatile fatty acids are a normal product of rumen fermentation and are readily used by tissues as an energy source. Tissues are capable of utilising the excess volatile fatty acids (VFAs) produced from the fermentation of high levels of carbohydrate; however, the instability in rumen pH makes it difficult for these to be absorbed properly and hence put to good use. VFA are normally passively absorbed across the rumen wall via finger-like papillae. These papillae increase in length when ruminants are fed high-carbohydrate diets, presumably to enhance absorption and protect the animal from accumulation of acids in the rumen. Despite this, a diet too high in concentrates will actually impair the absorptive capacity of the rumen, and VFAs will acumulate without effective utilisation by tissues.  
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diagnosed. let alone prevented. It is a group problem and
 
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is best described as a fermentative disorder character-ised
 
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bv a number of the g)rOup members having suboptimal
 
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ruIllenl pH values. The deflinitioni applied in the USA is at
 
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least 30 per cent of animials having rumen pH values of
 
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5 5 or less when saimipled by ruIlmenlocentesis (Nordlund
 
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2001). However, the author su,(ests that, under UK conditions,
 
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a more sensitive threshold mnay be pH <5 7. This
 
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is based on1 production anld intake responses seen after
 
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dietary intervention in herds diag,nosed as suffering from
 
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SARA using this threshold.
 
  
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Unlike in the glandular stomachs of carnivore and omnivores, the epithelium of the rumen is not protected by a layer of mucus. This means that ruminal epithelial cells are sensitive to chemical damage, for example by increased acidity. Low ruminal pH therefore leads to rumenitis, with erosion and ulceration of the ruminal epithelium. Bacteria can then colonise the ruminal papillae and be absorbed into the portal circulation. This bacteraemia can seed infection to many tissues and can result in, for example, liver abscesses, pneumonia, endocarditis, pyelonephritis, or arthritis. Any of these conditions are therefore potential complications of SARA. Subacute ruminal acidosis has also been associated with coriosis (laminitis), hoof overgrowth and solar abscesses/ulcers, which may occur weeks to months following the inciting acidotic event. The mechanism of coriosis is currently poorly understood.
  
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Ruminant animals are adapted to digest and metabolize predominantly forage diets; however, growth rates and milk production are increased substantially when they consume high-grain diets. One consequence of feeding excessive amounts of rapidly fermentable carbohydrates in conjunction with inadequate fiber to ruminants is subacute ruminal acidosis, characterized by periods of low ruminal pH, depressed feed intake, and subsequent health problems. Chronic disease conditions secondary to subacute ruminal acidosis can negate the production gains accomplished by high grain feeding. Dairy cattle, feedlot cattle, and feedlot sheep are all at high risk for developing this condition. Although dairy cattle are typically fed diets that are higher in forage and fiber compared with feedlot animals, this advantage is offset by their much higher dry-matter intakes.
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===Risk Factors===
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Field observations suggest that periparturient cows are at risk of subacute ruminal acidosis because of the time required for the rumen microflora and papillae to adapt to increased intakes of concentrates immediately before parturition and during early lactation when feed intake increases rapidly to meet the energy needs of high-producing dairy cows. The adaptation of the ruminal microflora and papillae from a system appropriate for forage to a system capable of utilizing high-energy lactation rations requires a gradual change over a period of 3-5 wk.
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'''Insufficient long fibre in the diet''': It is essential that the diet contains adequate fibre of 2-5cm in length, as it stimulates rumination and forms the rumen mat, where much fermentation occurs. Insufficient long dietary fibre can therefore be detrimental to rumen health. If sufficient fibre of the wrong length is contained within the ration, rumen function will also be suboptimal rumen. Fibre that is chopped too short will not stimulate rumination, and fibre greater than 10cm in length can be selectively sorted out of the diet by the cows themselves. Because the difficulty of feeding dairy cattle lies in providing sufficient metabolisable energy, there is a tendency for farmers to focus on making highly digestible (and therefore high metabolisable energy(ME)) silage rather than that of good fibre quality; this contributes to a lack of sufficient long fibre in the feed.
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[[Image:Cows Eating TMR.jpg|thumb|200px|right|Cows eating a total mixed ration. Source: Wikimedia Commons; Author: Tractorboy60 (2007)]]
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'''Overmixing the total mixed ration''': If the total mixed ration is mixed too much in the mixer wagon, the long fibre will be broken into shorter pieces and hence become less effective. This can be overcome by adding the forage into the mixer wagon last, ensuring minimal degradation.
  
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Ruminal pH drops below ~5.5 (the normal physiologic nadir) when ruminants consume excessive amounts of rapidly fermentable carbohydrates. Any additional intake puts the ruminant at risk of subacute ruminal acidosis because it results in the fermentation of carbohydrates into volatile fatty acids (VFA). Ruminal pH typically drops 0.5-1.0 pH units after the major meal of the day.
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'''Sorting of long fibre''': When the fibre in a total mixed ration is longer than 10cm, cows tend to sift through the diet and consume smaller, more palatable particles and the pieces of forage too small to sort out. This alters the concentrate-to-forage dry matter ratio which is actually eaten by the cow (even if it is correct in the diet presented to the animals), which increases the risk of developing subacute rumenal acidosis. In this situation there is the additional problem that animals lower down the hierarchy, such as heifers, will eat the remainder of the sorted diet and thus not receive the energy they require. Both groups of animals are therefore likely to be in negative energy balance, but for different reasons.
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The ability of the rumen to rapidly absorb organic acids contributes greatly to the stability of ruminal pH. It is rarely difficult for peripheral tissues to utilize VFA already absorbed from the rumen; however, absorption of these VFA from the rumen can be an important bottleneck.
 
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VFA from the rumen are absorbed passively across the rumen wall. This passive absorption is enhanced by finger-like papillae, which project away from the rumen wall. Ruminal papillae increase in length when cattle are fed higher-grain diets; this presumably increases ruminal surface area and absorptive capacity, which protects the animal from acid accumulation in the rumen. If the absorptive capacity of these cells is impaired (eg, chronic rumenitis with fibrosis), it becomes much more difficult for the animal to maintain a stable ruminal pH following a meal.
 
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Intake depression is the ruminant’s last resort for regulating ruminal pH. Depressed dry-matter intake becomes especially evident if ruminal pH falls to <~5.5. Intake depression may be mediated by pH receptors and/or osmolality receptors in the rumen. Inflammation of the ruminal epithelium (rumenitis) could cause pain and contribute to intake depression during subacute ruminal acidosis.
 
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Unfortunately, lactate production at low ruminal pH can offset gains from VFA absorption. As pH drops, lactate-synthesizing bacteria such as Streptococcus bovis begin to ferment glucose to lactate instead of VFA. This is a dangerous situation, since lactate has a much lower pKa than VFA (3.9 vs 4.8) and lactate is 5.2 times less dissociated than VFA at pH 5.0. As a result, lactate stays in the rumen longer and contributes to the downward spiral in ruminal pH.
 
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Additional adaptive responses are invoked if lactate production begins. Lactate-utilizing bacteria, such as Megasphaera elsdenii and Selenomonas ruminantium , begin to proliferate. These beneficial bacteria convert lactate to other VFA, which are then easily protonated and absorbed. However, the turnover time of lactate utilizers is much slower than that of lactate synthesizers. Thus, this mechanism may not be invoked quickly enough to fully stabilize ruminal pH. Periods of very high ruminal pH, as during feed deprivation, may inhibit populations of lactate utilizers (which are sensitive to higher ruminal pH) and leave them more susceptible to severe ruminal acidosis.
 
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Besides disrupting microbial balance, feed deprivation causes cattle to overeat when feed is reintroduced. This creates a double effect in lowering ruminal pH. Cycles of feed deprivation and refeeding are critical risk factors for subacute ruminal acidosis.
 
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Low ruminal pH during subacute ruminal acidosis also reduces the number of species of bacteria in the rumen, although the metabolic activity of the bacteria that remain is very high. Protozoal populations are limited as ruminal pH approaches 5.0. When fewer species of bacteria and protozoa are present, the ruminal microflora are less stable and less able to maintain normal ruminal pH during periods of sudden dietary change. Thus, pre-existing subacute ruminal acidosis increases the risk of acute ruminal acidosis in the event of accidental ingestion of excessive amounts of grain.
 
  
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Pathogenesis:
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'''Overestimation of forage dry matter content''': The dry matter of forage must be estimated in order to calculate how much of it should be included in the diet. The cut of for healthy rumen function is a concentrate-to-forage dry matter ration of 60:40; if this is exceeded then SARA can develop. Therefore, if the dry matter content of forage is overestimated, a relatively smaller quantity of the fodder will be included in the diet, tilting the ratio to potentially detrimental proportions.
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Ruminal epithelial cells are not protected by mucus, so they are vulnerable to chemical damage by acids. Low ruminal pH leads to rumenitis, erosion, and ulceration of the ruminal epithelium. Once the ruminal epithelium is inflamed, bacteria may colonize the papillae and leak into the portal circulation. These bacteria may cause liver abscesses, which may eventually lead to peritonitis around the site of the abscess. If the ruminal bacteria clear the liver (or if bacteria from liver infections are released into circulation), they may colonize the lungs, heart valves, kidneys, or joints. The resulting pneumonia, endocarditis, pyelonephritis, and arthritis are often difficult to diagnose antemortem. Postmortem evaluation of these conditions in animals that are slaughtered, culled, or that died on the farm can be very beneficial.
 
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Caudal vena cava syndrome can cause hemoptysis and peracute deaths due to massive pulmonary hemorrhage in affected cows. In these cases, septic emboli from liver abscesses can lead to lung infections, which ultimately invade pulmonary vessels and cause them to rupture.
 
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Subacute ruminal acidosis has also been associated with laminitis and subsequent hoof overgrowth, sole abscesses, and sole ulcers. The severity of laminitis depends on the duration and frequency of metabolic insult. These foot problems generally do not appear until weeks or months after the initiating event. The mechanism by which subacute ruminal acidosis increases the risk of laminitis has not been fully characterized.
 
  
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Risk factors: inadequate effective long fibre in the ration: overall lack of fibre (concentrat:forage DM ratio more than 60:40), lack of effective on fibre (short chop length, overmixing of TMR diets), cow chooses not to eat fibre(sorting of ration; poor/no mixing of TMR diet).
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'''High proportions of starches and sugars in the diet''': Dairy farmers often include large amounts of rapidly fermentable carbohydrates in the diet in order to meet energy requirements to maintain body condition score and milk production. These carbohydrates can take the form of concentrates or maize silage. However, rapid fermentation leads to over-production of volatile fatty acids, and thus subacute rumenal acidosis. This actually makes digestion less effective, so the cattle do not benefit as much as they should do from the increased supply of metabolisable energy. A vicious cycle can ensue of poor performance and supplementary feeding of concentrates.
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'''Slug-feeding of concentrates in the milking parlour''': If relatively large quantities of concentrates are supplied over a short period of time, rapid fermentation occurs and the rumen pH fluctuates more widely than if a less carbohydrate-rich diet is consumed more steadily. The pH also remains low for longer. Substitution effects may also take place as the consumption of more concentrate can reduce the subsequent intake of forage. These factors combined can lead to the development of SARA.
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'''Food deprivation''': Food should always be available to a dairy cow, and it is recommended that slight over-feeding, with 5-10% of the ration left over at the time of the next feed, can be implemented to achieve this. If a cow goes without food for any period of time, the population of microbes in the rumen can be disrupted and the animal is likely to gorge when next presented with the ration. Both of these factors encourage subacute rumenal acidosis.
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'''Inadequate dry cow diet''': the diet fed immediately before calving (the transitional cow diet) should be formulated to stimulate the development of rumen papillae and the acquisition of an appropriate colony of microflora. This should ensure that cattle can adequately ferment the post-calving diet and effectively absorb the nutrients it provides. Therefore, if the dry cow diet does not encourage these processes, volatile fatty acids can accumulate in the rumen when the lactation diet is introduced, leading to SARA. This is a particularly common problem, since dry cows are "non-milkers" and so tend to be the forgotten members of a herd.
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'''Post-calving nutrition''': The "transitional period" for a dairy cow is defined as the period four weeks pre-calving, to four weeks-post calving. Often, farmers will provide a transition diet before calving, but introduce the lactating cow diet immediately afterwards. In the first four weeks after calving, the rumen cannot properly handle diets that are dense in energy: the ration fed in this period ideally should contain 10% more energy than the transition diet fed before calving. The rationale to this is that dry matter intake will be increased, and will then remain at high levels throughout lactation. Animals do not achieve their peak milk yield in the first few weeks post-calving, and so optimising dry matter intake rather than energy consumption should not cause problems.
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'''Poor cow comfort''': The optimum daily routine of a dairy cow includes 12-14 hours lying down and 10 hours of rumination. If cow comfort is poor, the time spent performing these activities will be reduced, and less saliva will be produced to buffer the pH of the rumen.
  
 
==Signalment==
 
==Signalment==
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SARA is a common condition of dairy cattle, owing to the diet required to meet their high energy demands. Beef cattle and sheep are reared more extensively and are therefore fed less concentrate, but the condition does sometimes occur in these ruminants.
  
 
==Diagnosis==
 
==Diagnosis==
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Subacute ruminal acidosis is diagnosed on a group rather than individual basis. Measurement of pH in the ruminal fluid of a representative portion of apparently healthy animals in a group has been used to assist in making the diagnosis of subacute ruminal acidosis in dairy herds. Animal selection should be from high-risk groups, eg, in the first 60 days of lactation. Ruminal fluid is collected by rumenocentesis or stomach tube and can be measured in the field using wide-range pH (2-12) indicator paper, although a pH meter yields more accurate results. Twelve or more animals are typically sampled at ~2-4 hr after a grain feeding (in component-fed herds) or 6-10 hr after the first daily total mixed ration feeding. If >25% of the animals tested have a ruminal pH <5.5, then the group is considered to be at high risk of subacute ruminal acidosis. This type of diagnostic tool should be used in conjunction with other factors such as ration evaluation, evaluation of management practices, and identification of health problems on a herd basis.
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Subacute ruminal acidosis is diagnosed on a group rather than an individual basis. Certain clinical signs may be suggestive, and there are a number of procedures that can be preformed to help make the diagnosis.  
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Milk fat depression is a poor and insensitive indicator of subacute ruminal acidosis in dairy herds. Cows and herds with severe subacute ruminal acidosis may have normal milk fat tests. Thus, it is vitally important not to exclude the diagnosis in a dairy herd that has a normal milk-fat test.  
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===Clinical Signs===
 
===Clinical Signs===
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The nature of the faeces can give clues to the existence of SARA within a herd. Suboptimal rumen function means that some feed passes to the colon before digestion. Therefore, many animals in a group of cows with subacute rumenal acidosis will have a looser faecal consistency, due to osmotic diarrhoea caused by colonic fermentation of feed. In turn, the udder, tail and rump will have large amounts of faecal staining. In some animals, the colonic pH falls to such a degree that the microflora are killed and no hind-gut fermentation occurs. This leads to firmer, sticky faeces that contain undigested sugars. There may be other abnormalities to faecal appearance, for example cows may excrete undigested grain. Fibrin casts, indicative of colonic mucosal damage induced by an excess of acid, may also be seen. A low rumen pH can lead to the production of acidic urine and faeces. Cows may therefore be seen to swish their tails in the absence of flies due to the irritation this causes. When tail-swishing occurs frequently, faecal staining of the rump can be seen and may be an indicator of SARA in many herds.
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Feeding behaviour can also be affected. Individual cows may show inappetance for 24-48h, with no other clinical signs and spontaneous resolution. A chronic, overall increase in dry matter intake is a common finding. This depression in intake may be mediated via pH or osmolality receptors in the rumen, or by pain caused by rumenitis. Animals may also fail to increase their food intakes in response to negative energy balance, and excessive weight may be lost in early lactation. Cows may be seen to "drop the cud" while ruminating, and feed efficiency is reduced. This reduced efficiency may not be noticed in the field situation, but has been demonstrated experimentally and is associated with the passage of undigested food in the faeces.
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SARA can impact production parameters. Milk yield is lowered, although on farms where subacute rumenal acidosis is an ongoing, chronic problem, this may not be recognised. Milk butterfat levels are also reduced, which may be due to two factors. Firstly, milk fat is produced from acetate and butyrate, which in turn are produced from fibre in the diet. Dietary fibre is often reduced in SARA and so butterfat levels are, in turn, decreased. Alternatively, the changes in the rumen environment in subacute rumenal acidosis could interfere with the biohydrogenation of fatty acids. Reproductive performance is also poor; bulling behaviour and the duration of oestrus are negatively affected, and suboptimal nutrition reduces conception rates.
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The incidence of a number of diseases is increased by concurrent subacute rumenal acidosis. For example, cases of clinical acetonaemia and [[Displaced Abomasum|left displacement of the abomasum]] occur more frequently with herds where SARA is an issue. Loose faeces gives contamination of the environment and the udder, and in combination with the detrimental effects of SARA on the immune system, this can give a rise in levels of environmental mastitis. Subacute rumenal acidosis also predisposes to coriosis (the bovine equivalent of laminitis), so affected herds may have a high prevalence of foot lameness, with solar abscesses and ulcers frequently seen. Knowledge of the mechanism for induction of coriosis by SARA is limited.
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When investigating a case of potential subacute rumenal acidosis, the cows should be closely examined. The condition score of animals in early lactation should be recorded, as well as rumen fill and the percentage of cows ruminating at any time. This latter value should be at least 60% in a normal herd. A cow comfort quotient can be calculated by dividing the number of cows lying correctly in cubicles by the total number of cows in the cubicles. This figure should be in the region of 80-90%. The cows should also be examined for cleanliness, and the consistency of their faeces scored. The production and records should be viewed and interpreted and the overall appearance and vigor of the animals appreciated.
  
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Loose faeces with excessive faecal soiling of hindquarters. Closer examination of the faeces may revela fibrin casts, undigested cereal grains and long fibres. Cows swishing their tails when there are no flies due to gut and or urine irritation. Reduction in milk butterfat. Reduction in milk yoeld. with cows not milking to expectation. REduction in DMI. Individual animals variably go off their food with a consequent reduction in milk yeild. Cows spilling their cud whilts ruminating. Increased incidence of nutritional-related diseases, such as NEB/acetonaemia, LDAs, poor fertility, lameness and other peri-parturient diseases e.g. mastitis.
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===Laboratory Tests===
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The major clinical manifestation is reduced or cyclic feed intake, or both. Other associated signs include decreased efficiency of milk production, reduced fat test, poor body condition score despite adequate energy intake, unexplained diarrhea, and episodes of laminitis. High rates of culling or unexplained deaths may be noted in the herd. Sporadic nosebleeds due to caudal vena cava syndrome may also be observed. The clinical signs are delayed and insidious. Actual episodes of low ruminal pH are not identified; in fact, by the time an animal is observed to be off-feed, its ruminal pH has probably been restored to normal. Diarrhea may follow periods of low ruminal pH; however, this finding is subtle and difficult to evaluate.
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The diagnosis of subacute rumenal acidosis is aided by the measurement of the pH of rumenal fluid in a sample of animals. Cattle with the highest risk of SARA, i.e. those in early lactation, are selected and rumen fluid is obtained by rumenocentesis or, less commonly, stomach tube. Indicator paper or a pH meter is then used to measure the pH of the samples. In general twelve animals per group should be sampled, and if greater than 25-30% of the group have a pH less than 5.5 a diagnosis of SARA can be made. In a herd fed a total mixed ration as a single group, it might be useful to sample twelve recently (14-21 days) calved cows and twelve animals with the maximal dry matter intake (60-80 days calved) in order to evaluate the adequacy of the diet for all animals and to identify at what stage the feeding is problematic. Samples should be taken 6-10 hours after access to fresh TMR, or 2-4 hours after grain feeding in component-fed herds. The amount of concentrate fed in component-fed herds can be varied before sampling to determine what level of feeding is associated with SARA.
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Previously, measurement of milk fat depression has been advocated in the diagnosis of SARA. However, this is an insensitive indicator as some animals with severe SARA can have normal milk fat tests. It is therefore important not to exclude a diagnosis of SARA in an underperforming dairy herd that has a normal milk butterfat levels.
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===Other Tests===
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Cow management and nutrition should be assessed on the farm. The adequacy of effective long fibre can be determined by visual inspection of the diet, or by use of the Penn State Forage Particle Seperator. This is a set of sieves designed to separate the ration by particle size to facilitate the evaluation of effective long fibre. It cannot be used for diets containing large amounts of wet grass silage, as this clogs the sieve, but can be useful for evaluating separate forage components and total mixed rations. Sequential analysis of the ration throughout the day will identify whether the ration is being sorted. It is also important to determine the availability of food to cattle at all times, and a detailed management history should be obtained.  
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Sieving of faeces can provide useful information. Between 6 and 12 faecal samples per group of cows are collected from the ground and seived in a kitchen sieve under running water. Fibre length and the presence of undigested food can then be visually assessed. Fibres of greater than 1.25cm in the faeces is suggestive of SARA, and undigested grains indicate either SARA or poor grain preparation. Fibrin casts may also be visualised in this way.
  
 
===Pathology===
 
===Pathology===
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Pathological findings are generally unremarkable but erosions and ulcerations of the rumenal mucosa may be seen.
  
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==Treatment==
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==Treatment and Prevention==
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Because subacute ruminal acidosis is not detected at the time of depressed ruminal pH, there is no specific treatment for it. Secondary conditions may be treated as needed.
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There is no specific treatment for subacute rumenal acidosis, because it is not normally detected at the time of subobtimal rumen pH. Correcting the diet and managing the feeding regime should however bring the pH back into the ideal range. Conditions occurring secondary to SARA, such as mastitis, lameness and LDAs, should be treated as necessary.
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Back to top
 
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Prevention:
 
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The key to prevention is reducing the amount of readily fermentable carbohydrate consumed at each meal. This requires both good diet formulation (proper balance of fiber and nonfiber carbohydrates) and excellent feed bunk management. Animals consuming well-formulated diets remain at high risk for this condition if they tend to eat large meals because of excessive competition for bunk space or following periods of feed deprivation.
 
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Field recommendations for feeding component-fed concentrates to dairy cattle during the first 3 wk of lactation are usually excessive. Feeding excessive quantities of concentrate and insufficient forage results in a fiber-deficient ration likely to cause subacute ruminal acidosis. The same situation may be seen during the last few days before parturition if the ration is fed in separate components; as dry-matter intake drops before calving, dry cows preferentially consume concentrate over fiber and develop acidosis.
 
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Subacute ruminal acidosis may also be caused by errors in delivery of the rations or by formulation of rations that contain excessive amounts of rapidly fermentable carbohydrates or a deficiency of fiber. Recommendations for the fiber content of dairy rations are available in the National Research Council report, Nutrient Requirements of Dairy Cattle (see nutrition: dairy cattle, ). Dry-matter content errors in total mixed rations are commonly related to a lack of adjustment for changes in moisture content of forages.
 
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Including long-fiber particles in the diet reduces the risk of subacute ruminal acidosis by encouraging saliva production during chewing and by increasing rumination after feeding. However, long-fiber particles should not be easily sorted away from the rest of the diet; this could delay their consumption until later in the day or cause them to be refused completely.
 
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Ruminant diets should also be formulated to provide adequate buffering. This can be accomplished by feedstuff selection and/or by the addition of dietary buffers such as sodium bicarbonate or potassium carbonate. Dietary anion-cation difference is used to quantify the buffering capacity of a diet.
 
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Supplementing the diet with direct-fed microbials that enhance lactate utilizers in the rumen may reduce the risk of subacute ruminal acidosis. Yeasts, propionobacteria, lactobacilli, and enterococci have been used for this purpose. Ionophore (eg, monensin sodium) supplementation may also reduce the risk by selectively inhibiting ruminal lactate producers; however, ionophores are not currently approved for use in lactating dairy cows in North America
 
  
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==Prognosis==
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SARA can be prevented by considering the risk factors already described. The amount of rapidly fermentable carbohydrate consumed at each meal should be limited; this can be achieved by accurate diet formulation relative to the needs of the animal, and by proper management of the feeding regime. The dry matter content of forage should be realistically estimated to ensure that its contribution is adequate, and sufficient effective long fibre must be included in the diet. However, forage particles should not be long enough to facilitate separation from the consumed ration by the cows. Transitional diets must be carefully implemented, and animals should be fed a diet appropriate to their level of production. The dietary cation-anion balance can be manipulated to improve the buffering capacity of a ration.
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==Literature Search==
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[[File:CABI logo.jpg|left|90px]]
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Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
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<br><br><br>
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[http://www.cabdirect.org/search.html?q=title%3A%28Subacute+Rumenal+Acidosis%29+OR+title%3A%28Subacute+Ruminal+Acidosis%29+OR+title%3A%28Subclinical+Acidosis%29+OR+title%3A%28Low+Milk+Fat+Syndrome%29 Subacute Ruminal Acidosis publication]
  
 
==Links==
 
==Links==
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*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/21704.htm The Merck Veterinary Manual - Subacute Ruminal Acidosis]
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*[http://www.wcds.afns.ualberta.ca/Proceedings/2003/PDFs/Manuscripts/Chapter%2024%20Oetzel%20.pdf Subacute Ruminal Acidosis in Dairy Cows (Garrett R. Oetzel)]
  
 
==References==
 
==References==
  
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#Grove-White, D (2004) Rumen healthcare in the dairy cow. ''In Practice'', '''26(2)'', 88-95.
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#Grove-White, D (2004) Rumen healthcare in the dairy cow. ''In Practice'', '''26(2)''', 88-95.
 
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
 
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
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#Agnew, R E and Newbold, J R (2002) Butritional standards for dairy cattle. ''Report of the British Society of Animal Science Nutritional Standards Working Group: Dairy Cows''.
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#Divers, T J and Peek, S F (2008) Rebhun's diseases of dairy cattle. ''Elsevier Health Sciences''.
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#Nordlund, K (2003) [http://www.vetmed.wisc.edu/dms/fapm/fapmtools/2nutr/sara2aabp.pdf Herd-based diagnosis of subacute ruminal acidosis.] ''Proceedings of the American Association of Bovine Practitioners 36th Annual Conference''.
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[[Category:Forestomach_-_Nutritional_Pathology]][[Category:Cattle]][[Category:Sheep]][[Category:Goat]][[Category:To_Do_-_Lizzie]]
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{{review}}
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[[Category:Forestomach_-_Nutritional_Pathology]][[Category:Gastric Diseases - Cattle]][[Category:Brian Aldridge reviewing]]

Latest revision as of 22:51, 5 May 2011

Also known as: Subacute Ruminal Acidosis — SARA — Subclinical Acidosis — Low Milk Fat Syndrome

Do not confuse with: fulminant ruminal acidosis, grain overload

Introduction

In the last 20 years, selective breeding and improved genetics have dramatically increased the individual dairy cow's milk yield and hence the energy requirements for lactation. In order to meet these increased energy demands and avoid prolonged negative energy balance in early lactation, the energy density of the ration has also been increased. This has been achieved by feeding high levels of concentrate feed and energy-rich maize silage. Although these are effective in helping to meet energy requirements, they also contain large quantities of rapidly fermentable carbohydrates that cause increased production of acid in the rumen. This results in a fall in rumen pH below the optimum range of 6-7, known as subacute rumenal acidosis (SARA). Subacute rumenal acidosis is a herd problem that is often never recognised, let alone controlled. However, it can contribute to many aspects of ill-health in cattle, and reduces productivity, and so management of the condition makes good economic sense.

Beef cattle and sheep may also face this problem, but this is less common as they are raised more extensively and their energy demands are considerably lower.

Pathogenesis

Excessive quantities of rapidly fermentable carbohydrates in the ruminant diet results in overproduction of volatile fatty acids by the rumen microflora, lowering rumen pH below its ideal range of pH 6-7. Volatile fatty acids are a normal product of rumen fermentation and are readily used by tissues as an energy source. Tissues are capable of utilising the excess volatile fatty acids (VFAs) produced from the fermentation of high levels of carbohydrate; however, the instability in rumen pH makes it difficult for these to be absorbed properly and hence put to good use. VFA are normally passively absorbed across the rumen wall via finger-like papillae. These papillae increase in length when ruminants are fed high-carbohydrate diets, presumably to enhance absorption and protect the animal from accumulation of acids in the rumen. Despite this, a diet too high in concentrates will actually impair the absorptive capacity of the rumen, and VFAs will acumulate without effective utilisation by tissues.

Unlike in the glandular stomachs of carnivore and omnivores, the epithelium of the rumen is not protected by a layer of mucus. This means that ruminal epithelial cells are sensitive to chemical damage, for example by increased acidity. Low ruminal pH therefore leads to rumenitis, with erosion and ulceration of the ruminal epithelium. Bacteria can then colonise the ruminal papillae and be absorbed into the portal circulation. This bacteraemia can seed infection to many tissues and can result in, for example, liver abscesses, pneumonia, endocarditis, pyelonephritis, or arthritis. Any of these conditions are therefore potential complications of SARA. Subacute ruminal acidosis has also been associated with coriosis (laminitis), hoof overgrowth and solar abscesses/ulcers, which may occur weeks to months following the inciting acidotic event. The mechanism of coriosis is currently poorly understood.

Risk Factors

Insufficient long fibre in the diet: It is essential that the diet contains adequate fibre of 2-5cm in length, as it stimulates rumination and forms the rumen mat, where much fermentation occurs. Insufficient long dietary fibre can therefore be detrimental to rumen health. If sufficient fibre of the wrong length is contained within the ration, rumen function will also be suboptimal rumen. Fibre that is chopped too short will not stimulate rumination, and fibre greater than 10cm in length can be selectively sorted out of the diet by the cows themselves. Because the difficulty of feeding dairy cattle lies in providing sufficient metabolisable energy, there is a tendency for farmers to focus on making highly digestible (and therefore high metabolisable energy(ME)) silage rather than that of good fibre quality; this contributes to a lack of sufficient long fibre in the feed.

Cows eating a total mixed ration. Source: Wikimedia Commons; Author: Tractorboy60 (2007)

Overmixing the total mixed ration: If the total mixed ration is mixed too much in the mixer wagon, the long fibre will be broken into shorter pieces and hence become less effective. This can be overcome by adding the forage into the mixer wagon last, ensuring minimal degradation.

Sorting of long fibre: When the fibre in a total mixed ration is longer than 10cm, cows tend to sift through the diet and consume smaller, more palatable particles and the pieces of forage too small to sort out. This alters the concentrate-to-forage dry matter ratio which is actually eaten by the cow (even if it is correct in the diet presented to the animals), which increases the risk of developing subacute rumenal acidosis. In this situation there is the additional problem that animals lower down the hierarchy, such as heifers, will eat the remainder of the sorted diet and thus not receive the energy they require. Both groups of animals are therefore likely to be in negative energy balance, but for different reasons.

Overestimation of forage dry matter content: The dry matter of forage must be estimated in order to calculate how much of it should be included in the diet. The cut of for healthy rumen function is a concentrate-to-forage dry matter ration of 60:40; if this is exceeded then SARA can develop. Therefore, if the dry matter content of forage is overestimated, a relatively smaller quantity of the fodder will be included in the diet, tilting the ratio to potentially detrimental proportions.

High proportions of starches and sugars in the diet: Dairy farmers often include large amounts of rapidly fermentable carbohydrates in the diet in order to meet energy requirements to maintain body condition score and milk production. These carbohydrates can take the form of concentrates or maize silage. However, rapid fermentation leads to over-production of volatile fatty acids, and thus subacute rumenal acidosis. This actually makes digestion less effective, so the cattle do not benefit as much as they should do from the increased supply of metabolisable energy. A vicious cycle can ensue of poor performance and supplementary feeding of concentrates.

Slug-feeding of concentrates in the milking parlour: If relatively large quantities of concentrates are supplied over a short period of time, rapid fermentation occurs and the rumen pH fluctuates more widely than if a less carbohydrate-rich diet is consumed more steadily. The pH also remains low for longer. Substitution effects may also take place as the consumption of more concentrate can reduce the subsequent intake of forage. These factors combined can lead to the development of SARA.

Food deprivation: Food should always be available to a dairy cow, and it is recommended that slight over-feeding, with 5-10% of the ration left over at the time of the next feed, can be implemented to achieve this. If a cow goes without food for any period of time, the population of microbes in the rumen can be disrupted and the animal is likely to gorge when next presented with the ration. Both of these factors encourage subacute rumenal acidosis.

Inadequate dry cow diet: the diet fed immediately before calving (the transitional cow diet) should be formulated to stimulate the development of rumen papillae and the acquisition of an appropriate colony of microflora. This should ensure that cattle can adequately ferment the post-calving diet and effectively absorb the nutrients it provides. Therefore, if the dry cow diet does not encourage these processes, volatile fatty acids can accumulate in the rumen when the lactation diet is introduced, leading to SARA. This is a particularly common problem, since dry cows are "non-milkers" and so tend to be the forgotten members of a herd.

Post-calving nutrition: The "transitional period" for a dairy cow is defined as the period four weeks pre-calving, to four weeks-post calving. Often, farmers will provide a transition diet before calving, but introduce the lactating cow diet immediately afterwards. In the first four weeks after calving, the rumen cannot properly handle diets that are dense in energy: the ration fed in this period ideally should contain 10% more energy than the transition diet fed before calving. The rationale to this is that dry matter intake will be increased, and will then remain at high levels throughout lactation. Animals do not achieve their peak milk yield in the first few weeks post-calving, and so optimising dry matter intake rather than energy consumption should not cause problems.

Poor cow comfort: The optimum daily routine of a dairy cow includes 12-14 hours lying down and 10 hours of rumination. If cow comfort is poor, the time spent performing these activities will be reduced, and less saliva will be produced to buffer the pH of the rumen.

Signalment

SARA is a common condition of dairy cattle, owing to the diet required to meet their high energy demands. Beef cattle and sheep are reared more extensively and are therefore fed less concentrate, but the condition does sometimes occur in these ruminants.

Diagnosis

Subacute ruminal acidosis is diagnosed on a group rather than an individual basis. Certain clinical signs may be suggestive, and there are a number of procedures that can be preformed to help make the diagnosis.

Clinical Signs

The nature of the faeces can give clues to the existence of SARA within a herd. Suboptimal rumen function means that some feed passes to the colon before digestion. Therefore, many animals in a group of cows with subacute rumenal acidosis will have a looser faecal consistency, due to osmotic diarrhoea caused by colonic fermentation of feed. In turn, the udder, tail and rump will have large amounts of faecal staining. In some animals, the colonic pH falls to such a degree that the microflora are killed and no hind-gut fermentation occurs. This leads to firmer, sticky faeces that contain undigested sugars. There may be other abnormalities to faecal appearance, for example cows may excrete undigested grain. Fibrin casts, indicative of colonic mucosal damage induced by an excess of acid, may also be seen. A low rumen pH can lead to the production of acidic urine and faeces. Cows may therefore be seen to swish their tails in the absence of flies due to the irritation this causes. When tail-swishing occurs frequently, faecal staining of the rump can be seen and may be an indicator of SARA in many herds.

Feeding behaviour can also be affected. Individual cows may show inappetance for 24-48h, with no other clinical signs and spontaneous resolution. A chronic, overall increase in dry matter intake is a common finding. This depression in intake may be mediated via pH or osmolality receptors in the rumen, or by pain caused by rumenitis. Animals may also fail to increase their food intakes in response to negative energy balance, and excessive weight may be lost in early lactation. Cows may be seen to "drop the cud" while ruminating, and feed efficiency is reduced. This reduced efficiency may not be noticed in the field situation, but has been demonstrated experimentally and is associated with the passage of undigested food in the faeces.

SARA can impact production parameters. Milk yield is lowered, although on farms where subacute rumenal acidosis is an ongoing, chronic problem, this may not be recognised. Milk butterfat levels are also reduced, which may be due to two factors. Firstly, milk fat is produced from acetate and butyrate, which in turn are produced from fibre in the diet. Dietary fibre is often reduced in SARA and so butterfat levels are, in turn, decreased. Alternatively, the changes in the rumen environment in subacute rumenal acidosis could interfere with the biohydrogenation of fatty acids. Reproductive performance is also poor; bulling behaviour and the duration of oestrus are negatively affected, and suboptimal nutrition reduces conception rates.

The incidence of a number of diseases is increased by concurrent subacute rumenal acidosis. For example, cases of clinical acetonaemia and left displacement of the abomasum occur more frequently with herds where SARA is an issue. Loose faeces gives contamination of the environment and the udder, and in combination with the detrimental effects of SARA on the immune system, this can give a rise in levels of environmental mastitis. Subacute rumenal acidosis also predisposes to coriosis (the bovine equivalent of laminitis), so affected herds may have a high prevalence of foot lameness, with solar abscesses and ulcers frequently seen. Knowledge of the mechanism for induction of coriosis by SARA is limited.

When investigating a case of potential subacute rumenal acidosis, the cows should be closely examined. The condition score of animals in early lactation should be recorded, as well as rumen fill and the percentage of cows ruminating at any time. This latter value should be at least 60% in a normal herd. A cow comfort quotient can be calculated by dividing the number of cows lying correctly in cubicles by the total number of cows in the cubicles. This figure should be in the region of 80-90%. The cows should also be examined for cleanliness, and the consistency of their faeces scored. The production and records should be viewed and interpreted and the overall appearance and vigor of the animals appreciated.

Laboratory Tests

The diagnosis of subacute rumenal acidosis is aided by the measurement of the pH of rumenal fluid in a sample of animals. Cattle with the highest risk of SARA, i.e. those in early lactation, are selected and rumen fluid is obtained by rumenocentesis or, less commonly, stomach tube. Indicator paper or a pH meter is then used to measure the pH of the samples. In general twelve animals per group should be sampled, and if greater than 25-30% of the group have a pH less than 5.5 a diagnosis of SARA can be made. In a herd fed a total mixed ration as a single group, it might be useful to sample twelve recently (14-21 days) calved cows and twelve animals with the maximal dry matter intake (60-80 days calved) in order to evaluate the adequacy of the diet for all animals and to identify at what stage the feeding is problematic. Samples should be taken 6-10 hours after access to fresh TMR, or 2-4 hours after grain feeding in component-fed herds. The amount of concentrate fed in component-fed herds can be varied before sampling to determine what level of feeding is associated with SARA.

Previously, measurement of milk fat depression has been advocated in the diagnosis of SARA. However, this is an insensitive indicator as some animals with severe SARA can have normal milk fat tests. It is therefore important not to exclude a diagnosis of SARA in an underperforming dairy herd that has a normal milk butterfat levels.

Other Tests

Cow management and nutrition should be assessed on the farm. The adequacy of effective long fibre can be determined by visual inspection of the diet, or by use of the Penn State Forage Particle Seperator. This is a set of sieves designed to separate the ration by particle size to facilitate the evaluation of effective long fibre. It cannot be used for diets containing large amounts of wet grass silage, as this clogs the sieve, but can be useful for evaluating separate forage components and total mixed rations. Sequential analysis of the ration throughout the day will identify whether the ration is being sorted. It is also important to determine the availability of food to cattle at all times, and a detailed management history should be obtained.

Sieving of faeces can provide useful information. Between 6 and 12 faecal samples per group of cows are collected from the ground and seived in a kitchen sieve under running water. Fibre length and the presence of undigested food can then be visually assessed. Fibres of greater than 1.25cm in the faeces is suggestive of SARA, and undigested grains indicate either SARA or poor grain preparation. Fibrin casts may also be visualised in this way.

Pathology

Pathological findings are generally unremarkable but erosions and ulcerations of the rumenal mucosa may be seen.

Treatment and Prevention

There is no specific treatment for subacute rumenal acidosis, because it is not normally detected at the time of subobtimal rumen pH. Correcting the diet and managing the feeding regime should however bring the pH back into the ideal range. Conditions occurring secondary to SARA, such as mastitis, lameness and LDAs, should be treated as necessary.

SARA can be prevented by considering the risk factors already described. The amount of rapidly fermentable carbohydrate consumed at each meal should be limited; this can be achieved by accurate diet formulation relative to the needs of the animal, and by proper management of the feeding regime. The dry matter content of forage should be realistically estimated to ensure that its contribution is adequate, and sufficient effective long fibre must be included in the diet. However, forage particles should not be long enough to facilitate separation from the consumed ration by the cows. Transitional diets must be carefully implemented, and animals should be fed a diet appropriate to their level of production. The dietary cation-anion balance can be manipulated to improve the buffering capacity of a ration.

Literature Search

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References

  1. Grove-White, D (2004) Rumen healthcare in the dairy cow. In Practice, 26(2), 88-95.
  2. Merck & Co (2008) The Merck Veterinary Manual (Eight Edition), Merial.
  3. Agnew, R E and Newbold, J R (2002) Butritional standards for dairy cattle. Report of the British Society of Animal Science Nutritional Standards Working Group: Dairy Cows.
  4. Divers, T J and Peek, S F (2008) Rebhun's diseases of dairy cattle. Elsevier Health Sciences.
  5. Nordlund, K (2003) Herd-based diagnosis of subacute ruminal acidosis. Proceedings of the American Association of Bovine Practitioners 36th Annual Conference.


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