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.

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.