Ruminant animals are adapted to digest and metabolize predominantly forage diets; however, growth rates and milk production are increased substantially when ruminants 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, which is characterized by periods of low ruminal pH that resolve without treatment and is rarely diagnosed. Dairy cows, feedlot cattle, and feedlot sheep are at risk of developing this condition.
Ruminal pH fluctuates considerably during a 24–hr period (typically between 0.5–1 pH units) and is determined by the dynamic balance between the intake of fermentable carbohydrates, buffering capacity of the rumen, and rate of acid absorption from the rumen. In general, subacute ruminal acidosis is caused by ingestion of diets high in rapidly fermentable carbohydrates and/or deficient in physically active fiber. Subacute ruminal acidosis is most commonly defined as repeatedly occurring prolonged periods of depression of the ruminal pH to values between 5.6 and 5.2. The low ruminal pH is caused by excessive accumulation of volatile fatty acids (VFAs) without persistent lactic acid accumulation and is restored to normal by the animal’s own physiologic responses.
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 VFAs already absorbed from the rumen; however, absorption of these VFAs from the rumen can be an important bottleneck.
Ruminal VFAs are absorbed passively across the rumen wall. This passive absorption is enhanced by finger-like papillae, which project away from the rumen wall and provide massive surface area for absorption. 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. Dairy cows are especially at risk in the transition period, because the ruminal mucosa needs several weeks to adjust to high-grain diets, and in peak lactation, when high levels of easily fermentable carbohydrates are fed to avoid excessive negative energy balance.
One mechanism by which affected animals resolve ruminal acidosis and return ruminal pH to normal is by selecting long forage particles, either by choosing to preferentially consume long dry hay or by sorting a mixed ration in favor of longer forage particles. Another mechanism is by reducing overall feed intake. Depressed dry-matter intake becomes especially evident if ruminal pH falls below ~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 also contribute to intake depression during subacute ruminal acidosis.
Absorption of VFA inherently increases as ruminal pH drops. These acids are absorbed only in the protonated state. Because they have a pKa of ~4.8, the proportion of these acids that is protonated increases dramatically as ruminal pH decreases below 5.5. Lactate levels in the ruminal fluid of cattle with subacute ruminal acidosis, if measured, are usually not increased; however, the pathogenesis of excessive lactate production in the rumen is well described. Ruminal carbohydrate fermentation shifts to lactate production at lower ruminal pH (mostly due to Streptococcus bovis proliferating and shifting to lactate instead of VFA production); this can offset gains from VFA absorption. Ruminal lactate production is undesirable, because lactate has a much lower pKa than VFAs (3.9 vs. 4.8). For example, lactate is 5.2 times less protonated than VFAs at pH 5. 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 VFAs, 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 followed by overconsumption greatly increase the risk of 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 particularly limited at lower ruminal pH; the absence of ciliated protozoa in ruminal fluid is often observed during bouts of subacute ruminal acidosis. 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, periods of subacute ruminal acidosis leave animals more susceptible to future episodes of ruminal acidosis.
The pathophysiologic consequences of ruminal acidosis have mainly been described in feedlot cattle and in cattle surviving acute ruminal acidosis. Low ruminal pH may lead 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.
Caudal vena cava syndrome is caused by the release of septic emboli from liver abscesses; this septic material then travels via the caudal vena cava to the lungs. These bacteria proliferate in lung tissue and may ultimately invade pulmonary vessels, causing them to rupture. This is observed clinically as hemoptysis and even peracute deaths due to massive pulmonary hemorrhage.
Subacute ruminal acidosis has traditionally been associated with claw horn lesions, assumed to be caused by subacute laminitis. However, this pathophysiologic mechanism has not been experimentally characterized or reproduced. In recent years, alternative explanations for the development of claw horn lesions have been suggested.
The main clinical signs attributed to subacute ruminal acidosis are reduced or cyclic feed intake, decreased milk production, reduced fat, poor body condition score despite adequate feed intake, and unexplained diarrhea. High rates of culling or unexplained deaths may be noted in the herd. Sporadic cases of caudal vena cava syndrome may also be seen. 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 inconsistent and may be related to other dietary factors as well.
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 help make the diagnosis of subacute ruminal acidosis in dairy herds. Animal selection should be from highest-risk groups: cows between ~15–30 days in milk in component-fed herds and cows between ~50–150 days in milk in herds fed total mixed rations. Ruminal fluid is collected by rumenocentesis, and its pH is determined on a pH meter. 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 feeding of a total mixed ration. 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.
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.
The key to prevention of subacute ruminal acidosis is allowing for ruminal adaption to high-grain diets, as well as limiting intake of readily fermentable carbohydrates. 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 of this condition if they tend to eat large meals because of excessive competition for bunk space or after periods of feed deprivation.
Field recommendations to feed 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 concentrates instead of forage 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 Nutritional Requirements of Beef 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. The provision of adequate long-fiber particles reduces the risk of ruminal acidosis but cannot eliminate it. If a total mixed ration is fed, it is important that the long-fiber particles 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. Sorting can be prevented by providing long-fiber particles less than ~5 cm in length, by having adequate (~50%–55%) moisture in the mixed ration, and by including ingredients such as liquid molasses that help ration ingredients stick together.
Ruminant diets should also be formulated to provide adequate buffering. This can be accomplished by feedstuff selection and/or by addition of dietary buffers such as sodium bicarbonate or potassium carbonate. The dietary cation-anion difference (DCAD) is used to quantify the buffering capacity of a diet; diets for animals at high risk of ruminal acidosis should be formulated to provide a DCAD of >250 mEq/kg of diet dry matter, using the formula (Na + K) – (CI + S) to calculate DCAD.
Supplementing the diet with direct-fed microbials that enhance lactate utilization 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 and by reducing meal size.