Subacute Rumenal Acidosis

Also known as: subacute ruminal acidosis, SARA, subclinical acidosis, low milk fat syndrome.

Description

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. The results in a fall in rumen pH below the optimum range of 6-7. This is known as subacute rumenal acidosis. 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 ominvores, 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 in 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 absorbedinto the portal circulation. This bacteraemia can seed infection to many tissues and can result in, for example, liver abscesses, pneumonia, endocarditis, pyelonephritis, or arthritis if the liver, lunds, heart valves, kidneys or joints become infected. Any of these conditions are therefore potential complications of SARA.

Subacute ruminal acidosis has also been associated with coriosis (lamintis), 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 the diet contains sufficient fibre, but of the wrong lenght, this will also give suboptimal rumen function. 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 difficult 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 ME) silage rather than that of good fibre quality; this contributes to a lack of sufficient long fibre in the feed.

Inaccurate fodder dry matter estimation: If the dry matter content of fodder is overestimated, insufficient fodder may be provided, thereby leading to SARA. Excessive mixing of a TMR diet If a diet is overmixed in the TMR mixer wagon, long fibre will become less effective. The long fibre (forages) should always be placed in the mixer wagon last to ensure minimal degradation. Excessive feeding of starches and sugars Excessive feeding of starches and sugars is a common problem, especially soon after calving. Maize silage is a rich source of starches and sugars and this property, together with its lack of effective fibre, means that it is frequently implicated as a factor in the development of SARA. A common scenario is for a farmer and his advisors to counter poor yields or an excessive loss of body condition score during early lactation by feeding additional concentrates in order to supply additional energy. However, often the problem is one of SARA, and feeding additional energy actually makes the situation worse - although a temporary increase in milk yield may be observed, probably as a result of small intestinal carbohydrate digestion.

Poor dry cow management: As mentioned earlier, feeding a suitable transition diet is essential for rumen papillar development and the acquisition of a suitable rumen microflora capable of dealing with the lactation diet.

Feeding post-calving: While most farmers appreciate the need for a pre-calving transition diet, they frequently fail to appreciate the fact that the transition period is properly defined as three to four weeks pre-calving to three to four weeks post-calving. The rumen is not capable of handling high energy density diets until this period is complete. Cows should be fed a relatively low energy diet during this postcalving period. Ideally, the energy density of the diet during this time should be no more than 10 per cent greater than the transition diet. In practice, this means that freshly calved cows should remain on a diet suitable for M+25 to M+28 litres during this period. This will encourage a maximal dry matter intake and avoid SARA. All too often, post-calving cows are fed a diet with too high an energy density in the mistaken belief that they would otherwise develop negative energy balance. Many cows and their lactations are ruined during this critical period. The objective during the post-calving period is to maximise dry matter intake rather than keep up with the daily energy requirements of the cow.

Sorting of long fibre: If the fibre in a TMR is longer than 10 cm, cows are likely to sort the food and only consume small particles and short fibres, leaving the long fibre alone (Lammers and others 1996). Cows which sort food in this manner will be at risk of developing SARA. If feed barrier space is restricted, dominant cows may sort the food and thus develop SARA. Subordinate animals, such as heifers and lame animals, will then consume the sorted diet and so obtain a diet of lower energy but greater fibre content than is intended. The net result is that both groups are at risk of negative energy balance, although for different reasons. Ensuring that fibre length in a TMR is adequate to prevent SARA, but not too long such that sorting occurs, is problematic. Many mixer wagons will not cut f0o1age to an appropri ate leng-Ith (25 to 10() cm1) and thet e is eur-r-elItIx no suitaSlic for-age choppei- on the UK miarket, althouLgh sonic. but 1ot 1all, stli\ax clioppers Wxill Cut to a suLitahble length. OneoCptioll is to nSe a stationiarx foIagce hair-\cstel fromil xxhich blades cani he reni-oved it' reqUoired to enlsui e the conICCt Chop leingth. Hoxxcxeri, the nise ot' suLICh miachineiv inI this 1manIler is not xxithout risk to the oper-atoi- a1njid appr-oprialtc safectV guLardl-CIs illust be eni1ployed.

Slug feeding of concentrates in the milking parlour: It' giealtei- th.an 3 to 4 kg-, of co-ceniiti ates arc fed at a timlie. I-Lillmen IpH is likelx to tall anid i-emiiain loxW fol- mnLIchI of the time. The pi-ohlemi is comI)pounided if cox\x7 aIre receCixinc a TMR at the Itcd bhai-i iei- that is hiTh inI en-erx coni-pari-ed to gri-ass silalc. It mIulst he remicemicber-ed that suIbstitution effects xvill also he oCCurlrine so that, the miore cake is fed, the less foraoc xxill be coIlsumLIed. In the conitext ol' 1K ag1i cuIltuIre, tIlC aIthor- considers this pr-actice of hxhl-id TMR feedii-Ig to bc a miajoi factoIr iII thIe dex elopmenlet o(fSARA.

Food deprivation and irregular feeding: InI oidel- to naiilalisc dr- illattei intake, a TMR should be axllablc at all times. It is gen1erall recomimiiciided that 5 to 11) pei cenit of the ationi should be left ox er each daxl anid remiosved befoi-c t'frcshi food is ot't'ered. It is comImIIIonto ftind situation-s xxheci ther-c is 0o f'ood in frouit of the coW s. su(estinSt it ian out )A thin the last fcxx flurs. AlteiratxVcly f(oodI ilay he Pliscilt, but unlax ailable to the cox s since it Ilas not benCI puLshed uip to tile barl--icr SO that thex cani eat it. Peliods ot' food deprixvatioil mia disrLipt the riLiIeillniicrobial pOpu-lation. aIld tencd to caulse coxs to oxvercat xvhleu food is cintioduced. Both of thesc factol S ilneealse the i-isk of SARA dcx eloping. Most tfaric- s tccd a TMIR oil-ce daIilvx, elerallx, iil the illoiilillg t im.av be adxaitagLeouLs to feedl the TMR ii the afterilooni, tllerbhy CilsuIr-lgtl tilat fooCd is il tfr(lilt of the cox S aIt iiglit (XxV1lCl tilexC arC ilMatteilded). DuLingt the dax!' food cain casily bhc psiledC uIP to tile barrier as tai-ll staff arec ceilerallN, illiattendalnlce.

Poor cow comfort: Pooi covx coilltort xxi -Csuilt in lcss tinle beint spceit 1uillila.1til-L xxith ani associated r-eduLctioll in saliaa produLIctionI anIdi runlinaiial hbfl't'clrilng Miscellaneous factors Lailileiless. pooi tfeedl hbianci-s. aildtc so olil. ill.a all play a Phart il tlic dcx\cloPi-ille-it of'SARA.

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 occure in these ruminants.

Diagnosis

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. 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.

Clinical Signs

Clinically, SARA is characterised by:

• Variable faccal coinsistenicy, with many cows within a

gTroup having loose faeces. This occurs following the development of osmIlotic diarrhoea due to colonic fermentation of foodstuff's. However, if colonic pH falls excessively. the colonic flora is killed off and hind gut fermentation ceases, reSsulting in the production of coarse, firmer faeces which are rathei- sticky to the touch (probably due to the preseince of undigested, short chain polysaccharides in the t'aeces):

• Fibrin casts in the faeces. This is indicative of severe

acid-induced damage to the colonic mucosa fArgenLio aind Meuten 199 1);

• Excessive faecal soiling, especially of the tail, udder

and rump;Cow's swishing their tails in the absence of flies. This is likely to be associated with irritation caLused by the production ot' acidic urine and faeces. Tail swishing leads to rump faecal soiling, a common finding in affected herds;

• Rumlleni hypomotility and hypophagia. Individual cows

will be seen to be 'off their food' with no other clear presentinr sig'ns. The condition usually resolxes spontaneously within 24 to 48 hours; this is attributable to a reduction in appetite, accompanied by a tendency to select and consume forage rather than smaller high energy particles;

• Cows 'dropping the cud' while ruminatincy;
• Reduced feed efficiency (Krajcarski-Hunt and others

2002). This is caused by reduced rumeni digestive efficiency with the subsequent passag-e of undigested foodstuLffs in the t'aeces. It is common in such situations for blame to be attributed to the feedstuff quality rather than suboptimal rumen function;

• Reduced milk yield (albeit this may not be recognised

on farms where the problem is continuously present);

• Reduced milk butterfat. There is some debate on the

precise aetiology of reduced milk butterfat. Traditionally, butterfat yield was thought to be dependent on acetate production from dietary neutral detergent fibre (NDF), although recent work suggests that interference with ruminal biohydrogenation of fatty acids may be the underlying mechanism behind reduced milk fat (Bauman and Griinari 2001). However, since rumen pH is dependent on the amount of long fibre (physically effective NDF or peNDF) in the diet, and milk fat is dependent on the amount of NDF in the diet, it is possible to have a situation where butterfat levels are acceptable in the face of a ruminal acidosis if the fibre being fed is too short to be effective;

• Increased numbers of cases of digestive disease,

including displacement of the abomasum;

• Laminitis. SARA predisposes to laminitis (Nordlund

2000). Affected herds may have a high prevalence of foot lameness. However, there is a time lag between the period of nutritional insult and the resultant lameness. While the exact mechanism by which SARA predisposes animals to laminitis has not been elucidated, it may involve the products of colonic fermentation rather than SARA per se;

• Reduced dry matter intake (Garrett and others 1999);
• Excessive weight loss in early lactation. This can

occur as cows affected by SARA fail to increase their dry matter intake as a coping strategy for negative energy balance;

• Increased incidence of ketosis;
• Poor reproductive performance. This is a reflection

of both reduced conception rates and a reduction in the intensity and duration of oestrous behaviour;

• Environmental mastitis. Levels may be increased due

to poor hygiene and a reduction in the cow's immune function. Negative energy balance occurring secondarily to SARA is recognised as impacting

Treatment

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. Back to top Prevention: 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. 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. 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. 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. 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. 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

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.