Subacute Rumenal Acidosis

Description

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. 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.

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. 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

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.