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 generally to a lesser degree as they are raised more extensively and their energy demands are considerably lower.

Pathogenesis

The normal physiologic nadir for rumen pH is 5.5. 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.

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. 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. 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. 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. 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. 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. 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.

Pathogenesis: 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. 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. 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.

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

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. 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.

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.

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.