Primary contraction cycle

The primary cyclic activity results in the mixing and circulation of digesta in an organized manner. The primary contraction in cattle begins with a biphasic contraction of the reticulum. The first reticular contraction forces ingesta dorsal and caudad into the rumen, as does the much stronger second reticular contraction. The dorsal ruminal sac then begins to contract as the ventral sac relaxes, thereby causing digesta to move from the dorsal to the ventral sac. Sequential contractions of the caudoventral, caudodorsal and ventral ruminal sacs force digesta back into the reticulum and cranial sac. After a brief pause the contraction sequence is repeated. During each reticular contraction fluid and food particles, particularly heavy grain, pass into the reticulo-omasal orifice and into the omasum and abomasum.

Reticulorumen motility results in stratification of ruminal contents, with firmer fibrous material floating on top of a more fluid layer. Solid matter remains in the rumen until the particle size is sufficiently small (1–2 mm in sheep,2–4 mm in cattle) to pass through the reticulo-omasal orifice. The size of digested plant fragments in ruminant feces can therefore be considered an indirect measurement of forestomach function.

Identification of ruminal contractions requires both auscultation and observation of the left paralumbar fossa. Sound is produced when fibrous material rubs against the rumen during contraction. Only slight sound is produced when the rumen contains small quantities of fibrous material.

External palpation of the rumen is valuable in determining the nature of ruminal contents. The normal rumen feels doughy in the dorsal sac and more fluid ventrally; the difference in consistency is attributable to stratification of ruminal contents. Very liquid ruminal contents that splash and fluctuate on ballottement (fluid-splashing sounds) are suggestive of lactic acidosis, vagal indigestion, ileus or prolonged anorexia.

Rumen hypomotility or hypermotility is usually associated with a change in the type of sounds heard during auscultation, with gurgling, bubbling or distant rustling sounds replacing the normal crescendo– decrescendo crackling sounds. The rumen can be examined and evaluated using a combination of auscultation and simultaneous ballottement or percussion, by palpation through the left flank and by rectal examination. Inspection and laboratory analysis of rumen contents is also possible.

Extrinsic control of primary contractions

Intrinsic control of primary contractions

The contribution of intrinsic smooth muscle tone to forestomach motility is not well understood. Intrinsic contractions are involved in maintaining normal reticulorumen tone, directly influencing the discharge of low-threshold tension receptors to the gastric center. Calcium is required for smooth muscle contraction and hypocalcemia will usually cause ruminal atony. The administration of calcium borogluconate to cattle, sheep and goats with hypocalcemia will restore rumen motility and eructation commonly occurs after the intravenous administration of the calcium.

Treatment of forestomach hypomotility

Anorexia and forestomach hypomotility usually exist together. Reduced feed intake reduces the two primary drives for reticulorumen activity: moderate forestomach distension and chewing activity. A wide variety of drugs have been used for many years to induce forestomach motility with the aim of stimulating anorexic cattle with forestomach hypomotility to begin eating. Most if not all of these drugs have been unsuccessful. Ruminatorics such as nux vomica, ginger, gentian and tartar given orally have not been effective. Parasympathomimetics, such as neostigmine or carbamylcholine, should not be used to treat forestomach atony. Neostigmine requires vagal activity to be effective and therefore cannot incite normal primary contractions in atonic animals. Neostigmine may increase the strength of a primary contraction without altering rhythm or coordination. Carbamylcholine causes hypermotility in sheep but the contractions are uncoordinated, spastic and functionless.

Any effective drug must be able to induce forestomach motility in a coordinated sequence so that the ingesta moves through the reticulo-omasal orifice, into the omasum, out of the omasum, and into the abomasum, and out of the abomasum into the small intestine. This means that there must be a coordinated sequence of contractions and relaxations of sphincters. Experimentally, metoclopramide increases the rate of ruminal contractions and therefore might be beneficial in rumen hypomotility or motility disturbances associated with vagal nerve damage.

Secondary cycle contraction and eructation

Secondary cycles are contractions that involve only the rumen and are associated with the eructation of gas. They occur independently of the primary cycle contractions and usually less frequently, about once every 2 minutes. The contraction rate depends on the gas or fluid pressure in the dorsal sac of the rumen. Secondary cycles can be inhibited by severe distension of the rumen.

Normally, the dorsal sac of the rumen contains a pocket of gas composed of CO_2,, N₂ and CH₄. Gas is produced at a maximum rate of 1 L per minute in cattle, with the rate depending on the speed of microbial degradation of ingesta. Eructation occurs during both primary and secondary contraction cycles but most gas is removed during the latter. Eructation is capable of removing much larger quantities of gas than is produced at the maximum rates of fermentation and therefore free gas bloat does not occur because of excessive gas production but rather from insufficient gas elimination.

Ruminal contractions are essential for eructation. Tension receptors in the medial wall of the dorsal ruminal sac initiate the reflex by means of the dorsal vagus nerve. Contractions begin in the dorsal and caudodorsal ruminal sacs and spread forward to move the gas cap ventrally to the cardia region. Contraction of the reticuloruminal fold is necessary to stop fluid from moving forward to the reticulum and covering the cardia. Receptors in the cardia region detect the presence of gas; the cardia remains firmly closed if fluid or foam (as in frothy bloat) contacts it. Injury to the dorsal vagal nerve decreases the efficiency of eructation but either the ventral or dorsal vagus nerve alone can initiate enough eructation activity to prevent bloat.

Despite the presence of normal secondary contractions, eructation may not occur in recumbent animals when the cardia is covered with fluid. Bloat is often observed in ruminants in lateral recumbency. Eructation occurs after the animal stands or attains sternal recumbency as fluid moves away from the cardia. Bloat can also result from peritonitis, abscesses or masses that distort the normal forestomach anatomy and preventing active removal of fluid from the cardia region. Esophageal obstructions associated with intraluminal, intramural or extraluminal masses are a common cause of free gas bloat. Passage of a stomach tube usually identifies these abnormalities, and forestomach motility is unimpaired unless the vagal nerve is damaged.

Bloat is often observed in cattle with tetanus. Distension of the rumen is usually not severe and can be accompanied by strong and regular ruminal contractions. Because the ruminant esophagus is composed of striated muscle throughout its length, tetanus-associated bloat may be due to spasm of the esophageal musculature.

Persistent mild bloat is often observed in ruminants that have rumen atony or hypomotility secondary to systemic disease. Although the fermentation rate is lower than normal in these cases, ruminal contractions are not strong enough to remove all the gas produced. The bloat usually requires no treatment and resolves with return of normal forestomach motility.

Secondary contractions cannot be distinguished from primary contractions by auscultation of the left paralumbar fossa only, unless a synchronous belch of gas is heard. However, primary contractions can be identified by simultaneous palpation of the left paralumbar fossa and auscultation with the stethoscope over the left costochondral junction between the seventh and eighth ribs. Reticular contractions indicating the beginning of a primary contraction can be heard followed by contraction of the dorsal sac and lifting of the paralumbar fossa.

Secondary contractions are relatively autonomous and are not subject to the same central excitatory and/or inhibitory influences as are primary contractions. Agents that inhibit reticulorumen motility by a central action have a lesser effect on eructation than on primary contraction cycles. However, high doses of xylazine can inhibit secondary contractions and the duration of inhibition is dose-dependent.

No drugs are yet available to improve secondary contractions as a means of treating bloat. Severe bloat usually arises from mechanical or diet-related causes, and therapy should be directed specifically to those causes.

Rumination

Rumination is a complex process and consists of:

Rumination is initiated by the rumination center close to the gastric center in the medulla oblongata. Rumination allows further physical breakdown of feed with the addition of large quantities of saliva and is an integral part of ruminal activity. The time devoted to rumination is determined by the coarseness of ruminal contents and the nature of the diet. Rumination usually commences 30–90 minutes after feeding and proceeds for 10–60 minutes at a time, resulting in up to 7 hours per day spent on this activity.

The epithelial receptors located in the reticulum, esophageal groove area, reticulorumen fold and ruminal pillars detect coarse ingesta and initiate rumination. The receptors can be activated by increases in volatile fatty acid concentration, stretching and mechanical rubbing.

An intact dorsal or ventral vagus nerve is necessary for regurgitation to proceed. Regurgitation is associated with an extra contraction of the reticulum immediately preceding the normal reticular biphasic contraction of the primary cycle. The glottis is closed, and an inspiratory movement lowers the intrathoracic pressure. The cardia then relaxes, and the distal esophagus fills with ingesta. Reverse peristalsis moves the bolus up to the mouth, where it undergoes further mastication.

The usual causes for a reduction or absence of rumination are:

Other less common causes include chronic emphysema (difficulty in creating a negative thoracic pressure) and extensive damage to the epithelial receptors that incite the reflex, as occurs in rumenitis.

Reticulorumen motility is required for rumination to proceed. The extra reticular contraction is not essential for regurgitation because fixation or removal of the reticulum does not prevent rumination from occurring. Rumination can be easily inhibited by higher brain centers, as disturbance of a ruminating cow often stops the process and is absent when animals are stressed or in pain. Milking commonly elicits rumination in cows and goats.

Pharmacologic stimulation of regurgitation is not attempted.

Esophageal groove closure

The esophageal groove reflex allows milk in the sucking preruminant to bypass the forestomach, and directs milk from the esophagus along the reticular groove and omasal canal into the abomasum. Milk initiates the reflex by chemical stimulation of receptors in the oral cavity, pharynx and cranial esophagus. Once the reflex is established in neonatal ruminants, sensory stimuli (visual, auditory, olfactory) can cause esophageal groove closure without milk contacting the chemoreceptors. This occurs in calves teased with milk or given water in an identical manner to which the calf previously received milk. The esophageal groove reflex continues to operate during and after the development of a functional rumen, provided the animal continues to receive milk.

Liquid administered to calves with an esophageal feeder (tube) does not cause groove closure. In calves younger than 3 weeks of age, overflow of liquid from the rumen into the abomasum begins when 400 mL of liquid are given. Thus if the goal of oral feeding is to insure that fluid administration by esophageal tube rapidly enters the abomasum, more than 400 mL of liquid must be given.

Closure of the esophageal groove in cattle younger than 2 years of age can be induced by solutions of sodium chloride, sodium bicarbonate or sugar. From 100–250 mL of 10% solution of sodium bicarbonate induces esophageal groove closure in 93% of cattle immediately and it lasts for 1–2 minutes. Any other oral solution administered during this time is directed into the abomasum to avoid dilution in the rumen. Closure of the groove may be used to treat abomasal ulcers if magnesium hydroxide or kaolin– pectin solutions are given orally immediately after a sodium bicarbonate solution.

Inspection and palpation

The primary and secondary cycle contractions of the reticulorumen are identified by simultaneous auscultation, palpation and observation of the left paralumbar fossa and the left lateral abdominal region. During contractions of the rumen there is an alternate rising and sinking of the left paralumbar fossa in conjunction with abdominal surface ripples. The ripples reflect reticulorumen contractions and occur during both the primary (or mixing) cycle contraction and the secondary (or eructation) cycle contractions.¹ As the left paralumbar fossa rises during the first part of the primary cycle contraction there are two horizontal ripples that move from the lower left abdominal region up to the paralumbar fossa. When the paralumbar fossa sinks, during the second part of the primary cycle, the ripple moves ventrally and fades out at the lower part of the left abdominal region. Similar ripples follow up and down after the rising and sinking of the paralumbar fossa associated with the secondary cycle movements.

In vagus indigestion, there may be three to five vigorous incomplete contractions of the reticulorumen per minute. These contractions may not be audible because the rumen contents are porridge-like and do not cause the normal crackling and rustling sounds of the rumen containing coarse fibrous ingesta. However, the contractions are visible and palpable as waves of undulations of the left flank. If reticulorumen motility is assessed only on the basis of inspection and palpation, the results will be misleading.

Auscultation of the rumen and left flank

In the normal animal on a roughage diet there are two independent contraction sequences of the reticulorumen. The primary cycle recurs approximately every minute and consists of a diphasic contraction of the reticulum followed by a monophasic contraction of the dorsal ruminal sac and then by a monophasic contraction of the ventral ruminal sac. These movements are concerned primarily with ‘mixing’ the rumen contents and with assisting the passage of rumen contents into the omasum.

The secondary cycle movements occur at intervals of about 2 minutes and are confined to the rumen and consist of a contraction of the dorsal sac followed by a contraction of the ventral sac. The former causes the fluid contents of the dorsal sac to be forced ventrally and the gas layer to be forced cranially to the region of the cardia where eructation takes place. Contractions of the dorsal and ventral sacs cause undulations of the left paralumbar fossa and lower flanks that are readily visible and palpable.

The clinical recognition of the presence or absence of either the primary cycle or secondary cycle contractions or both may aid in determining the cause and severity of the disease and the prognosis. These are outlined in Table 6.1.

Mucus

The presence of excessive mucus on the surface of feces suggests increased transit time of the ingesta in the large intestine. The presence of a plug of mucus in the rectum is suggestive of a functional obstruction (paralytic ileus). In enteritis, large quantities of clear, watery mucus may be passed, which sometimes clot to form gelatinous masses.

Fibrin

In fibrinous enteritis, fibrin may be excreted in the form of long strands, which may mold into a print of the intestinal lumen (intestinal fibrinous casts).

Spontaneous recovery

Most cases of simple indigestion recover spontaneously. Small quantities of fresh, good-quality, palatable hay should be provided several times daily to encourage eating and to stimulate reticulorumen motility. Because anorexia and forestomach hypomotility usually exist together the objective is to stimulate both appetite and motility. Reduced feed intake reduces the two primary drives for reticulorumen activity: moderate forestomach distension and chewing activity.

Rumenatorics

A wide variety of oral preparations containing rumenatorics were available for many years and is was conventional to administer these to stimulate reticulorumen motility and to stimulate appetite. These preparations contained nux vomica, ginger and tartar emetic in powder form to be added to water and pumped into the rumen. However, there is no evidence that they are effective and they are not recommended.^1,2 The routine use of magnesium hydroxide for rumen disorders is not recommended unless there is evidence of ruminal acidosis.

Magnesium hydroxide is a potent alkalinizing agent for use in ruminants as an antacid and mild laxative. It can significantly decrease rumen microbial activity and should be used only in cattle with rumen acidosis and not for symptomatic therapy of idiopathic rumen disorders or hypomagnesemia. The oral administration of boluses of magnesium hydroxide (162 g) or a powdered form (450 g) dissolved in 3.5 L of water daily for 3 days resulted in a significant increase in rumen pH after 48 and 24 hours, respectively.³ Both the boluses and the powder forms of magnesium hydroxide decreased rumen protozoal numbers and increased methylene blue reduction times compared with baseline values. There was no change in blood pH, bicarbonate or base excess values.

Parasympathomimetics

These agents have also been used to stimulate reticulorumen activity but have the disadvantage of inducing undesirable side effects and being very transitory in effect. Large doses depress reticulorumen activity but small doses repeated at short intervals increase ruminal activity and promote vigorous emptying of the colon in normal animals. The normal flow of rumen contents from the reticulorumen to the abomasum is the result of a complex of synchronized contractions and relaxations of various parts of the forestomachs, orifices and abomasum occurring simultaneously. One of the major limitations of injectable parasympathomimetics used as rumenatorics is that they do not provide these synchronized movements and therefore little movement of ingesta can occur. Carbamylcholine chloride, physostigmine and neostigmine are most commonly used. Neostigmine is the most effective at a dose of 2.5 mg/45 kg body weight (BW). Carbamylcholine acts on the musculature only and causes uncoordinated and functionless movements. These drugs are not without danger, especially in very sick animals or those with peritonitis, and are specifically contraindicated during late pregnancy.

Experimentally, metoclopramide increases the rate of ruminal contractions and therefore might be beneficial in rumen hypomotility or motility disturbances associated with vagal nerve damage.^1,2

Epsom salts (0.5–1.0 kg per adult cow) and other magnesium salts are reasonably effective and have the merit of simplicity and cheapness.

Alkalinizing and acidifying agents

If an excessive quantity of grain is the cause of the simple indigestion, the use of alkalinizers, such as magnesium hydroxide, at the rate of 400 g per adult cow (450 kg BW), is recommended when the rumen contents are excessively acid. Magnesium oxide or hydroxide should be used only if ruminal acidosis is present. The administration of 400 g of magnesium oxide to normal, mature, nonfasted cattle weighing 450 kg can cause metabolic alkalosis and electrolyte disturbances for up to 24 hours following treatment. A sample of rumen fluid can be readily obtained and the pH determined. If the rumen contents are dry, 15–30 L of water should be administered by stomach tube.

Acetic acid or vinegar, 5–10 L, is used when the rumen contents are alkaline as a result of the ingestion of high-protein concentrates.

Reconstitution of ruminal microflora

In cases of indigestion that have run a course of more than a few days, and in animals that have been anorexic for prolonged periods, there will be significant loss of ruminal microflora, especially if there have been marked changes in pH. Reconstitution of the flora by the use of cud transfers from normal cows is highly effective. An abattoir is the best source of rumen contents (especially rumen fluid) but it can be obtained from live animals by reaching into the mouth during rumination when the bolus is regurgitated. Rumen fluid may also be removed by siphoning from the rumen with a stomach tube or by vacuum withdrawal with a special pump. Best results are obtained if 20–30 L of water is pumped into the rumen and then allowed to siphon by gravity flow (rumen lavage). The rumen fluid to be transferred should be strained and administered as an oral drench or by stomach tube. Repeated dosing is advisable. The infusion will keep for several days at room temperature. Commercial products comprising dried rumen solids are available and provide some bacteria and substrate for their activity.

When affected animals resume eating they are best tempted by good, stalky meadow or cereal hay. Good-quality alfalfa (lucerne) or clover hay, green feed and concentrate may be added to the diet as the appetite improves.

Occurrence

All types of ruminant cattle and sheep are susceptible but the disease occurs most commonly in feedlot cattle and dairy cattle fed on high-level grain diets. The disease also occurs in lamb feedlots and has been recorded in goats, wild deer and farmed ungulates.

Morbidity and case fatality rates

Outbreaks of the disease occur in cattle herds kept on grain farms and in feedlots. Depending on the species of grain, the total amount eaten and the previous experience of the animals, the morbidity will vary from 10–50%. The case fatality rate may be up to 90% in untreated cases, while in treated cases it still may be up to 30–40%.

Types and toxic amounts of feeds

Wheat, barley and corn grains are the most toxic when ingested in large quantities. Oats and grain sorghum are least toxic. All grains are more toxic when ground finely or even crushed or just cracked – processes that expose the starch component of the grain to the ruminal microflora. The experimental feeding of unprocessed barley to cattle did not result in rumenitis, whereas feeding rolled barley was associated with ruminal lesions. An unrestricted supply of stale bread can cause outbreaks.

The amount of a feed required to cause acute illness depends on the species of grain, previous experience of the animal with the grain, its nutritional status and body condition score, and the nature of the ruminal microflora. Dairy cattle accustomed to high-level grain diets may consume 15–20 kg of grain and develop only moderate illness, while beef cows or feedlot cattle may become acutely ill and die after eating 10 kg of grain to which they are unaccustomed. Amounts of feed that are lethal range from 50–60 g of crushed wheat/kg BW in undernourished sheep to 75–80 g/kg BW in well-nourished sheep, and in cattle doses ranging from 25–62 g/kg BW of ground cereal grain or corn produced severe acidosis.

Changes in rumen microflora

The ingestion of excessive quantities of highly fermentable feeds by a ruminant is followed within 2–6 hours by a marked change in the microbial population in the rumen. There is an increase in the number of Streptococcus bovis, which utilize the carbohydrate to produce large quantities of lactic acid. In the presence of a sufficient amount of carbohydrate (a toxic or a lethal amount) the organism will continue to produce lactic acid, which decreases the rumen pH to 5 or less, which results in the destruction of the cellulolytic bacteria and protozoa. When large amounts of starch are added to the diet, growth of S. bovis is no longer restricted by energy source and it multiplies faster than any other species of bacteria.

Volatile fatty acids and lactic acid in the rumen

The concentration of volatile fatty acids increases initially, contributing to the fall in ruminal pH. The low pH allows lactobacilli to use the large quantities of carbohydrate in the rumen to produce excessive quantities of lactic acid, resulting in ruminal lactic acidosis. Both D and L forms of the acid are produced, which markedly increases ruminal osmolality, and water is drawn in from the systemic circulation, causing hemoconcentration and dehydration. Ruminal osmolality increases from a normal of 280 mosmol/L to almost 400 mosmol/L.¹

Some of the lactic acid is buffered by ruminal buffers but large amounts are absorbed by the rumen and some moves into and is absorbed further down the intestinal tract. Lactate is a 10 times stronger acid than the volatile fatty acids, and accumulation of lactate eventually exceeds the buffering capacity of rumen fluid. As the ruminal pH declines, the amplitude and frequency of the rumen contractions are decreased and at about a pH of 5 there is ruminal atony. The increased ruminal levels of unassociated volatile fatty acids may be more important than increased lactic acid or increased hydrogen ion concentration in causing ruminal atony. Experimentally, increased molar concentration of butyrate, not the lactic acid, causes ruminal stasis.¹ Inhibition of ruminal activity may also be due to lactic acid entering the duodenum and exerting a reflex inhibitory action on the rumen. Experimentally, ruminal atony occurs in sheep within 8–12 hours after grain engorgement but the precise pathophysiological mechanism for loss of forestomach motility is uncertain. The diarrhea is considered to be due to the reduction in net absorption of water from the colon.

Systemic lactic acidosis

The absorbed lactic acid is buffered by the plasma bicarbonate buffering system. With nontoxic amounts of lactic acid, the acid–base balance is maintained by utilization of bicarbonate and elimination of carbon dioxide by increased respirations. In those which survive the acute form of the disease, this compensatory mechanism may overcompensate, resulting in alkalosis. In severe cases of lactic acidosis the reserves of plasma bicarbonate are reduced, the blood pH declines steadily, the blood pressure declines, causing a decrease in perfusion pressure and oxygen supply to peripheral tissues and resulting in a further increase in lactic acid from cellular respiration. Lactic acid given intravenously to cattle causes hypertension, increased responses to norepinephrine, slight bradycardia and slight hyperventilation.

Both d- and l-lactic acids are produced. The l-lactic acid is utilized much more rapidly than the d-isomer which accumulates and causes a severe d-lactic acidosis. If the rate of entry of lactic acid into body fluids is not too rapid, compensatory mechanisms are able to maintain the blood pH at a compatible level until the crisis is over, and recovery is usually rapid. This may explain the common observation that feedlot cattle may be ill for a few days after being introduced to a grain ration but quickly recover, while in other cases when the rate of entry is rapid the compensatory mechanisms are overcome and urgent treatment is necessary.

In experimental lactic acidosis using sucrose in sheep, feed intake does not resume until rumen pH has returned to 6.0 or higher and lactic acid is no longer detectable in the rumen. Renal blood flow and glomerular filtration rate are also decreased, resulting in anuria. Eventually there is shock and death. All these events can occur within 24 hours after engorgement of a lethal dose of carbohydrate; with toxic doses the course of events may take 24–48 hours.

Chemical and mycotic rumenitis

The high concentration of lactic acid in the rumen causes chemical rumenitis, which is the precursor for mycotic rumenitis in those that survive; this occurs about 4–6 days later. The low pH of the rumen favors the growth of Mucor, Rhizopus and Absidia spp. which invade the ruminal vessels, causing thrombosis and infarction. Inoculation of Absidia corymbifera orally into sheep with experimental ruminal acidosis produced with barley causes desquamation of the superficial layers of the mucosae and focal necrosis from lamina propria to muscular layers. Severe bacterial rumenitis also occurs. Widespread necrosis and gangrene may affect the entire ventral half of the ruminal walls and lead to the development of an acute peritonitis. The damage to the viscus causes complete atony and this, together with the toxemia resulting from the gangrene, is usually sufficient to cause death. Mycotic omasitis and rumenitis may also occur without a history of grain engorgement in cattle. Anorexia and forestomach atonicity associated with a primary illness in other body systems may predispose the mucosae to fungal infection because of abomasal reflux of acid and the prolonged use of antimicrobials.

Chronic rumenitis and ruminal hyperkeratosis are common in cattle fed for long periods on grain rations, and the lesions are attributed to the chronic acidosis, but it is possible that barley awns and ingested hair may contribute to the severity of the lesions.

Hepatic abscesses

In uncomplicated chemical rumenitis, the ruminal mucosa sloughs and heals with scar tissue and some mucosal regeneration. Hepatic abscesses commonly occur as a complication as a result of a combination of rumenitis caused by lactic acidosis and allowing Fusobacterium necrophorum and Arcanobacter (Corynebacterium) pyogenes to enter directly into ruminal vessels and spread to the liver, which may have also undergone injury from the lactic acidosis. Severe diffuse coagulation necrosis and hyperplasia of the bile duct epithelium and degeneration of renal tubules may also be present histologically.

In cattle being placed on a grain ration, even with control of the daily intake, hepatic cell damage and liver dysfunction occur even though dietary adaptation may have occurred in 2–3 weeks. The biochemical profile indicates that complete metabolic adaptation requires at least 40 days following the start of grain feeding.

Laminitis

Laminitis occurs in acute, subclinical and chronic forms associated with varying degrees of severity of ruminal acidosis. The association between acidosis and laminitis appears to be associated with altered hemodynamics of the peripheral microvasculature. Vasoactive substances (histamine and endotoxins) are released during the decline of rumen pH and the bacteriolysis and tissue degradation. These substances cause vasoconstriction and dilation, which injure the microvasculature of the corium. Ischemia results, which causes a reduction in oxygen and nutrients reaching the extremities of the corium. Ischemia causes physical degradation of junctures between tissues that are structurally critical for locomotion. The insidious rotation of the distal phalanx (pedal bone) can result in permanent anatomical change. Manifestations of subclinical laminitis are sole hemorrhages and yellowish discoloration. Other clinical manifestations include double soles, heel erosion, dorsal wall concavity and ridging of the dorsal wall.²

Other toxic substances produced

Several toxic substances other than lactic acid have been suggested as contributory to the disease. Increased concentrations of histamine have been found in the rumen of experimentally engorged cattle, but its possible role in the disease remains unknown. Histamine is not absorbed from the rumen except at abnormally high pH values, but is absorbed from intestinal loops. Laminitis occurs in some cases of rumen overload but the pathogenesis is unknown.

Other substances that have been recovered from the rumen in grain overload include a suspected endotoxin, ethanol and methanol. In experimental lactic acidosis induced in cattle with 70 g barley/kg BW, endotoxin and arachidonic acid metabolites are produced and may be important. However, the role of the endotoxin is uncertain. Endotoxin administered into the intestine of lactic acidotic sheep is not absorbed. Clostridium perfringens and coliform bacteria have also been found in increased numbers but their significance is uncertain. The electrolyte changes that occur include a mild hypocalcemia due to temporary malabsorption, loss of serum chloride due to sequestration in the rumen, and an increase in serum phosphate due to renal failure.

Experimental lactic acidosis

The disease can be reproduced in cattle and sheep with a variety of grains, fruits, sugars and pure solutions of lactic acid. The oral administration of sucrose at 18 g/kg BW to goats can cause lactic acidosis. In cattle the sucrose is used to induce rumen lactic acidosis experimentally.¹⁴ The severity of the experimental disease and the magnitude of the pathophysiological changes vary depending on the substance used, but changes similar to the natural disease occur.

Lesions in the brain have been recorded in the experimental disease in sheep and naturally occurring cases in cattle, but their pathogenesis and significance are uncertain. There are detectable changes in the cellular and biochemical composition of the cerebrospinal fluid, which suggests that the blood–brain barrier may be affected. Experimentally, sublethal doses of volatile fatty acids, lactate and succinate have an effect on liver function. Toxic and lethal doses of butyrate can cause sudden flaccid paralysis and death from asphyxia.

Adaptation to grain-based diets in beef cattle

The health and ruminal variables during adaptation to grain-based diets in beef cattle have been examined experimentally. Successive diets with forage-to-grain ratios of 75:25 (diet 1), 50:50 (diet 2), 25:75 (diet 3) and 10:90 (diet 4) were each fed for 7 days. The health variables such as rectal temperature, heart rate, respiratory rate, rumen motility rates, fecal consistency, demeanor, blood pH, and blood glucose and L⁺-lactate concentrations remained within reference range limits throughout the adaptation period. Blood pH continually decreased during feeding of the four diets. The pH of the ruminal contents decreased progressively from 6.8 to 5.3. By the end of the period, the ruminal contents were acidic (pH < 5.5) and, on the basis of the amounts of ruminal glucose and dl-lactate, it was concluded that ruminal microbial equilibrium had not yet been achieved. In addition, an increase in the heart and respiratory rates in animals fed diets 2 and 4 indicated stress. During normal fermentation, glucose is not detectable in ruminal fluid because its production is closely linked with its assimilation. In general, changing from a high-roughage to low-roughage diet is stressful for cattle and their resident ruminal microflora.

Subacute ruminal acidosis (dairy cattle)

The pathogenesis of SARA in lactating dairy cows is not as well understood as acute ruminal acidosis associated with the sudden ingestion of large amounts of readily fermentable carbohydrates, for example, most commonly in beef cattle that gain accidental access to large quantities of grain. In early-lactating dairy cows, SARA is usually caused by the consumption of diets with high levels of rapidly fermentable carbohydrates and/or marginal, often deficient, levels of physically active fiber.⁸

The biochemical changes that occur in lactating dairy cows in early lactation that are affected with SARA have not been examined in detail. In SARA, fermentation of nonstructural carbohydrates leads to the production of large quantities of volatile fatty acids and lactate, which accumulate in the rumen and subsequently decrease rumen pH. It has been difficult to reproduce SARA in early-lactation dairy cows even with diets such as high-moisture corn, cracked dried corn grain and rolled barley.⁷ These feeds did not induce SARA, either because of an inability of the feeds to depress the rumen pH rapidly enough or because of the cow’s refusal to consume them.

Wheat/barley pellets were readily consumed by lactating dairy cows and did result in a sustained reduction in rumen pH.⁷ When cows with experimental SARA are given a choice between alfalfa hay and alfalfa pellets, cows will choose the alfalfa hay more strongly, which implies that dairy cows would increase their dietary preference for a feed of longer particle size when given the appropriate choice during a bout of SARA.⁷ As intake of long hay will result in more saliva production and rumen buffering than intake of pelleted alfalfa, this indicates that cows select feeds with high rumen buffering capacity in an attempt to prevent SARA. When cows with SARA were offered sodium bicarbonate ad libitum, they did not select the compound in order to attenuate the ruminal acidosis.¹⁵ When cows with SARA were offered a choice between two test pellets, one containing 4% sodium bicarbonate and the other 4.5% sodium chloride, the intake of the sodium bicarbonate pellets increased over time, but the intake of sodium chloride pellets remained unaltered.¹⁶

There is some evidence that lactic acid is not the causal reason for the prolonged reduction in pH of the ruminal contents. Studies have shown only low lactate levels between 0.45 mmol/L and 0.74 mmol/L in cows with suspected SARA. Excessive volatile fatty acid production may be a more important contributor to SARA in lactating dairy cows.

The induction of SARA by excess feeding of wheat/barley pellets reduces the rumen digestion of neutral detergent fiber from grass hay, legume hay and corn silage.¹⁷ It is thought that SARA affects the productivity of dairy cows by reducing the fiber digestion, because low pH negatively affects cellulolytic bacteria. The induction of SARA in lactating dairy cows by replacing 25% of the total mixed ration intake with pellets consisting of 50% wheat and 50% barley reduced the in-situ dry matter and neutral detergent fiber digestion of mixed hay. Disappearance of neutral detergent fiber was reduced from 39.5% to 30.9%.¹⁸

In experimentally induced SARA, lipopolysaccharide concentration in the rumen increases during periods of grain feeding compared with times when only hay is fed.¹⁹ The concentration of serum amyloid-A and serum haptoglobin indicate a systemic inflammatory response.

Rumen pH drops considerably in dairy cows after calving when the diet is changed. Monitoring rumen pH throughout the transition period of dairy cows in which the concentrate to forage ration was changed from 70:30 to 55:45 at calving found that 1 week prior to calving the average daily pH was 6.83, average daily time with rumen pH below 6 was 25.5 minutes and average daily time with rumen pH below 5.6 was 5.6 minutes. During the first week after calving, average daily pH was 6.51, and average daily time with rumen pH below 6 and 5.6 were 312 and 59.6 minutes respectively.¹⁸ The drop in rumen pH is associated with an increase in the rate of production of volatile fatty acids, which temporarily increases the concentration of volatile fatty acids in the rumen, until the absorptive capacity of the rumen mucosa for volatile fatty acids has been increased.

The pathogenesis of rumenitis, hepatic abnormalities and laminitis associated with SARA is considered to be similar to those described above for acute ruminal acidosis.

Speed of onset and severity

The speed of onset of the illness varies with the nature of the feed, being more rapid with ground feed than with whole grain. The severity increases with the amount of feed eaten. If cattle are examined clinically within a few hours after engorgement, the only abnormalities that may be detectable are a distended rumen and abdomen, and occasionally some abdominal discomfort, evidenced by kicking at the belly. In the mild form, affected cattle are anorexic and still fairly bright and alert, and the feces may be softer than normal. Rumen movements are reduced but not entirely absent. Affected cattle do not ruminate for a few days but usually begin to eat on the third or fourth day without any specific treatment.

In outbreaks of the severe form, within 24–48 hours some animals will be recumbent, some staggering and others standing quietly alone. Most affected cattle are anorexic, apathetic and depressed. Teeth grinding may occur in about 25% of affected sheep and goats. Once they are ill they usually do not drink water, but cattle may engorge themselves on water if it is readily available immediately after consuming large quantities of dry grain. In an outbreak, inspection of the feces on the ground will usually reveal many spots of soft to watery feces.

Individual animals

Depression, dehydration, inactivity, weakness, abdominal distension, diarrhea and anorexia are typical. The temperature is usually below normal, 36.5–38.5°C (98–101°F), but animals exposed to the sun may have temperatures up to 41°C (106°F). In sheep and goats, the rectal temperatures may be slightly higher than normal. The heart rate in cattle is usually increased and continues to increase with the severity of the acidosis and circulatory failure. In general, the prognosis is better in those with heart rates below 100/min than those with rates up to 120–140/min. In sheep and goats, the heart rate may be higher than 100/min. The respirations are usually shallow and increased up to 60–90/min. A mucopurulent discharge is common because animals fail to lick their nares.

Diarrhea is almost always present and usually profuse, and the feces are light-colored with an obvious sweet–sour odor. The feces commonly contain an excessive quantity of kernels of grain in grain overload, and pips and skins when grapes or apples have been eaten. An absence of feces is considered by some veterinarians as a grave prognostic sign but diarrhea is much more common. The dehydration is severe and progressive. In mild cases, the dehydration is about 4–6% BW, and with severe involvement up to 10–12% BW. Anuria is a common finding in acute cases and diuresis following fluid therapy is a good prognostic sign.

Careful examination of the rumen is important. The rumen contents palpated through the left paralumbar fossa may feel firm and doughy in cattle that were previously on a roughage diet and have consumed a large amount of grain. In cattle that have become ill on smaller amounts of grain, the rumen will not necessarily feel full but rather resilient because the excessive fluid contents are being palpated. Therefore, the findings on palpation of the rumen may be deceptive and a source of error. The primary contractions of the reticulorumen are usually totally absent, although low-pitched tinkling and gurgling sounds associated with the excessive quantity of fluid in the rumen are commonly audible on auscultation of the rumen. The ruminal fluid is a milky green to olive brown color and has a pungent acid smell. Collection of a sample of ruminal fluid in a glass beaker will reveal an absence of foam. The pH of the rumen fluid is usually below 5.

Severely affected animals have a staggery, drunken gait and their eyesight is impaired. They bump into objects and their palpebral eye preservation reflex is sluggish or absent. The pupillary light reflex is usually present but slower than normal. Acute laminitis may be present and is most common in cases that are not severely affected and appear to be good treatment risks. Affected animals are lame in all four feet, shuffle while they walk slowly and may be reluctant to stand. The lameness commonly resolves if the animals recover from the acute acidosis. Evidence of chronic laminitis may develop several weeks later.

Recumbency usually follows after about 48 hours but may occur earlier. Affected animals lie quietly, often with their heads turned into the flank, and their response to any stimulus is much decreased so that they resemble parturient paresis. A rapid onset of recumbency suggests an unfavorable prognosis and the necessity for urgent treatment, because death may occur in 24–72 hours after the ingestion of the feed. Evidence of improvement during this time includes a fall in heart rate, rise in temperature, return of ruminal movement and passage of large amounts of soft feces.

The clinical findings described above are most common but when a group of animals have been exposed to overfeeding there are all degrees of severity from simple indigestion, cases of which recover spontaneously, to the severe cases that need intensive therapy. The prognosis varies with the severity, and the clinical variables that are useful in deciding on a course of treatment or action are summarized in Table 6.8.

Table 6.8 Guidelines for the use of clinical findings in assessing the severity of grain overload in cattle for the selection of the treatment of choice

Mycotic rumenitis

Some animals appear to recover following treatment but become severely ill again on the third or fourth day. Mycotic rumenitis is common in these animals and is characterized by a fluid-filled atonic rumen, dehydration in spite of fluid therapy, diarrhea, anorexia, weakness leading to recumbency and death in 2–3 days due to acute diffuse peritonitis.

Complications

Chronic laminitis may occur several weeks or months later. This is particularly important in dairy cattle herds affected with subacute acidosis.⁵

Abortions may occur 10 days to 2 weeks later in pregnant cattle that survive the severe form of the disease.

Subacute ruminal acidosis in dairy cattle

Subacute ruminal acidosis (SARA) is being recognized with increased frequency in dairy herds.^3-5 However, the case definition is not yet well described. Clinical findings include laminitis, intermittent diarrhea, suboptimal appetite or cyclic feed intake, a high herd culling rate, loss of body condition in spite of adequate energy intake, liver abscesses, and hemoptysis and epistaxis associated with venal caval thrombosis and pulmonary hemorrhage. Milk-fat depression and suboptimal milk production in the second- and subsequent-lactation cows compared to the first-lactation cows may occur.³

A decrease in dry matter intake is commonly reported in herds with SARA.⁴ The causes of a lowered dry matter intake are uncertain but may be related to weaker rumen motility during low pH phases, bacterial endotoxins and changes in the osmolarity of the rumen contents.

The laminitis is characterized by ridges in the dorsal hoof wall, sole ulceration, white line lesions, sole hemorrhages and misshapen hooves.²⁰ It is suggested that when the incidence of laminitis exceeds 10% of the herd, it should be considered a herd problem related to the feeding program.

Ruminal fluid pH

The pH of the ruminal fluid obtained by stomach tube or by rumenocentesis through the left paralumbar fossa can be measured in the field using wide-range pH (2–12) indicator paper. The ruminal fluid must be examined immediately because the pH will increase upon exposure to air. Cattle that have been fed a roughage diet will have a ruminal pH of 6–7; for those on a grain diet it will be 5.5–6. A ruminal pH of 5–6 in roughage-fed cattle suggests a moderate degree of abnormality but a pH of less than 5 suggests severe grain overload and the need for energetic treatment. Feedlot cattle that have been on grain for several days or weeks and are affected with grain overload usually have a pH below 5.

Rumenocentesis has become a commonly used diagnostic test for subacute ruminal acidosis.^13,20 A hypodermic needle of 1.6 (outer diameter) × 130 mm (length) is inserted into the ventral rumen and rumen contents aspirated with a syringe. Landmarks for the puncture site are the left side, on a horizontal line level with the top of the patella about 15–20 cm posterior to the last rib. The hair of the site is clipped and prepared using a standard scrub. The cow is restrained in a stanchion or head-gate and one assistant elevates the tail of the cow while another assistant inserts a ‘nose leader’ and pulls the cow’s head to the right side. The needle will usually become obstructed by ingesta, which is cleared by forcing a small amount of air or fluid back through the needle. When the needle becomes obstructed it is important to avoid creating a negative pressure within the syringe, as carbon dioxide will leave the fluid and increase the pH. Typically, 3–5 mL of rumen fluid can be collected with minimal difficulty.

The pH is measured immediately using a pH meter with a digital readout. Samples should be collected when the pH is likely to be near the lowest point of the day. If the ration is fed as separate components, rumenocentesis should be performed 2–4 hours after the cows are fed the primary concentrate of the day. If the ration is fed as a total mixed ration, the samples should be collected 4–8 hours later. A pH of 5.5 is recommended as the cut-point between normal and abnormal.²⁰ At least 12 or more cows should be sampled from any group in which acidosis is suspected. If 30% of 10 or more sampled cows are below 5.5, the group is classified as in a state of ruminal acidosis. A subsample of 12 cows from a herd or diet group and a critical number of three cows with a ruminal pH less than or equal to 5.5 may effectively differentiate between herds with 15% or less or greater than 30% prevalence of cows with a low ruminal pH.¹³

Ruminal protozoa

Microscopic examination of a few drops of ruminal fluid on a glass slide (with a coverslip) at low power will reveal the absence of ruminal protozoa, which is a reliable indicator of an abnormal state of the rumen, usually acidosis. The predominantly Gram-negative bacterial flora of the rumen is replaced by a Gram-positive one.

Serum biochemistry

The degree of hemoconcentration, as indicated by hematocrit, increases with the amount of fluid withdrawn from the extracellular fluid space into the rumen. The hematocrit rises from a normal of 30–32% to 50–60% in the terminal stages and is accompanied by a fall in blood pressure. Blood lactate and inorganic phosphate levels rise and blood pH and bicarbonate fall markedly. In almost all cases there is a mild hypocalcemia, which is presumably due to a temporary malabsorption. Serum levels may drop to between 6–8 mg/dL (1.5–2 mmol/L).

The serum enzyme activities of cattle fed on barley for several months has been measured and suggest that hepatocellular damage occurs during the early stages of feeding grain but that recovery occurs after about 1 month.

Urine pH

The urine pH falls to about 5 and becomes progressively more concentrated; terminally there is anuria.

Triage

The recommendations for treatment given in Table 6.8 are guidelines. In an outbreak, some animals will not require any treatment while severely affected cases will obviously need a rumenotomy. For those that are not severely affected, it is often difficult to decide whether to treat them only medically with antacids orally and systemically or to do a rumenotomy. Each case must be examined clinically and the most appropriate treatment selected. The degree of mental depression, muscular strength, degree of dehydration, heart rate, body temperature, and rumen pH are clinical parameters that can be used to assess severity and to determine the treatment likely to be most successful.

Rumenotomy

In severe cases, in which there is recumbency, severe depression, hypothermia, prominent ruminal distension with fluid, a heart rate of 110–130/min and a rumen pH of 5 or below, a rumenotomy is the best course of action. The rumen is emptied, washed out with a siphon and examined for evidence of and the extent of chemical rumenitis, and a cud transfer (10–20 L of rumen juice) is placed in the rumen along with a few handfuls of hay. The rumenotomy will usually correct the ruminal acidosis and an alkalinizing agent in the rumen is not necessary. A large quantity of the lactic acid and its substrate can be removed. The oral or intraruminal administration of compounds such as magnesium oxide or magnesium hydroxide to cattle following complete evacuation of the rumen may cause metabolic alkalosis for up to 24–36 hours. Not all of the feed consumed will be removed because considerable quantities may have moved into the omasum and abomasum, where fermentation may also occur. The major disadvantages of a rumenotomy are time and cost, particularly when many animals are involved.

Intravenous sodium bicarbonate and fluid therapy

The systemic acidosis and the dehydration are treated with intravenous solutions of 5% sodium bicarbonate at the rate of 5 L for a 450 kg animal given initially over a period of about 30 minutes. This will usually correct the systemic acidosis. This is followed by isotonic sodium bicarbonate (1.3%) at 150 mL/kg BW intravenously over the next 6–12 hours. Cattle that respond favorably to the rumenotomy and fluid therapy will show improved muscular strength, begin to urinate within 1 hour and attempt to stand within 6–12 hours.

Rumen lavage

In less severe cases, in which affected cattle are still standing but are depressed, their heart rate is 90–100/min, there is moderate ruminal distension and the rumen pH is between 5 and 6, an alternative to a rumenotomy is rumen lavage if the necessary facilities are available. A large 25–28 mm inside-diameter rubber tube is passed into the rumen and warm water is pumped in until there is an obvious distension of the left paralumbar fossa; the rumen is then allowed to empty by gravity flow. The rumen can be almost completely emptied by 10–15 irrigations. With successful gastric lavage, alkalinizing agents are not placed in the rumen but the systemic acidosis is treated as described above.

Intraruminal alkalinizing agents

In moderately affected cases, the use of 500 g of magnesium hydroxide per 450 kg BW, or magnesium oxide in 10 L of warm water pumped into the rumen and followed by kneading of the rumen to promote mixing will usually suffice.

Magnesium hydroxide is a potent alkalinizing agent for use in ruminants as an antacid and mild laxative. It can significantly decrease rumen microbial activity and should be used only in cattle with rumen acidosis and not for symptomatic therapy of idiopathic rumen disorders or hypomagnesemia.²² The oral administration of boluses of magnesium hydroxide (162 g) or a powdered form (450 g) dissolved in 3.5 L of water daily for 3 days resulted in a significant increase in rumen pH after 48 and 24 hours, respectively. Both the boluses and the powder forms of magnesium hydroxide decreased rumen protozoal numbers and increased methylene blue reduction times compared with baseline values. There was no change in blood pH, bicarbonate or base excess values. Serum magnesium values were significantly increased in cows receiving the powder.

Ancillary therapy

Ancillary treatment has included antihistamines for laminitis, NSAIDs for shock therapy, thiamin or brewer’s yeast to promote the metabolism of lactic acid, and parasympathomimetics to stimulate gut motility. Their efficacy has been difficult to evaluate and it is unlikely that any of them would be of much value. Calcium borogluconate is used widely because there is a mild hypocalcemia and a beneficial but temporary response does occur, but it is of doubtful value.

Orally administered antimicrobials including penicillin and the tetracyclines have been used to control growth of the bacteria that produce lactic acid, but appear to be of limited value.

Monitor response to therapy

Regardless of the treatment used, all cases must be monitored several times daily until recovery is obvious, for evidence of unexpected deterioration. Following treatment, cattle should begin eating hay by the third day, some ruminal movements should be present, large quantities of soft feces should be passed and they should maintain hydration. In those that become worse, the heart rate increases, depression is marked, the rumen fills with fluid and weakness and recumbency occur. During treatment, the water supply should be restricted because some cattle, either immediately after they have engorged themselves or once they become ill, appear to have an intense thirst and will drink excessive quantities of water and die precipitously within a few hours.

The fungal rumenitis that may occur about 3–5 days after engorgement is best prevented by early effective treatment of the ruminal acidosis.

Total mixed rations

One of the safest procedures is to feed a milled mixed ration, consisting of 50–60% roughage and 40–50% grain, as the starting ration for 7–10 days and monitor the response. If results are satisfactory, the level of roughage is decreased by 10% every 2–4 days down to a level of 10–15% roughage, with the remainder grain and vitamins–mineral–salt supplement. The use of roughage–grain mixtures insures that cattle do not engorge themselves on grain, and adaptation can occur in about 21 days.

Small incremental increases in concentrate

Another method is to begin with small amounts of concentrate 8–10 g/kg BW, which is increased every 2–4 days by increments of 10–12%. A source of roughage is supplied separately. The disadvantages of this system are that hungry or dominant cattle may eat much more than their calculated share and there is no assurance that sufficient roughage will be consumed. In this system, on a practical basis, the cattle are usually fed twice daily and brought up to a daily intake of concentrate that satisfies their appetite and then the concentrate ration is offered free-choice from self-feeders. Unless there is sufficient feeding space in the self-feeders, competitive and dominant animals will often overeat and careful monitoring is necessary.

Feedlot starter rations

Feedlot starter rations consisting of a mixture of roughage and grain, offered free-choice along with hay and gradually replaced by a finishing ration have successfully adapted cattle in 10 days. The starter ration contains about 2500 kcal (10 460 kJ) DE (digestible energy) per kg of feed. The finishing ration contains about 3100 kcal (12 970 kJ), and controlling the rate of increase of DE concentration of the ration was a major factor in getting cattle on feed.

A comparison of the effect of rapid or gradual grain adaptation on subacute acidosis and feed intake by feedlot cattle indicates a range of individual responses to grain challenge and current management strategies for preventing acidosis in pens of cattle are based on responses of the most susceptible individuals.²³ Using this approach requires consideration of individual animal responses. The data suggest that most cattle can be rapidly adapted to high-grain diets in few incremental steps; minimizing acidosis in the most susceptible individuals requires decreasing the pace of grain adaptation for the entire group.

Dietary buffers

The incorporation of buffers, such as sodium bicarbonate, into the ration of feedlot cattle has been studied extensively but to date the results are inconclusive and reliable recommendations cannot be made. A level of 2% dietary sodium bicarbonate, sodium bentonite or limestone provided some protection from acidosis during the early adaptation phase of high-concentrate feeding; but they were no more effective than 10% alfalfa hay. Buffers have been most effective in reducing acidosis early in the feeding period and have little or no effect later. They may be associated with an increased incidence of urinary calculi, bloat and vitamin deficiencies. The experimental results to date are conflicting. Some trials indicate that buffers maintain a Gram-negative rumen flora in sheep fed grain compared to a shift to Gram-positive rumen flora in animals not fed buffers. Liveweight performance is also improved in some trials but not in others fed 0.75, 1.0 or 2.25% of diet as sodium bicarbonate.

The potential efficiency of products for the control of ruminal acidosis has been examined through the measurement of the increase in buffer capacity and acid-consuming capacity.²⁴ Sodium bicarbonate provided the highest increment in buffering capacity and acid-consuming capacity compared to calcium carbonate. Magnesium oxide provided higher acid-consuming capacity but had no effect on buffer capacity.

Dietary supplementation of sodium bicarbonate at a level of 1.5% for 90 days in high-concentrate diets fed to lambs improved cellulose digestibility, ciliate protozoal number, ruminal pH and total nitrogen concentration, resulting in improved growth of lambs maintained on a high-concentrate diet.²⁵

Ionophores

The ionophores salinomycin, monensin and lasalocid have been compared for their protective effects, and salinomycin is more effective than the other two; monensin also shows some promise. Laidlomycin propionate does not prevent ruminal acidosis but may reduce the severity of ruminal acidosis during adaptation to a 100% concentrated diet. Monensin supplementation did not affect dry matter intake, milk yield and composition, and ruminal pH characteristics in experimentally induced SARA.¹⁶ The rates of ruminal forage fiber degradability were similar between control and monensin-treated cows; however, monensin supplementation increased total digestive tract fiber digestion, especially at postruminal sites. Thus monensin could be used for the improvement of nutrient digestion during grain-induced SARA in dairy cows.²⁶

Subacute ruminal acidosis in dairy cattle

The basic principles of preventing SARA in dairy herds include:

Prevention of subacute ruminal acidosis includes proper adaptation of rumen papillae during the prepartum period, adequate intake of forage in early lactation, and adequate fiber nutrition throughout lactation. Successful management of energy balance through the periparturient transition period depends on providing adequate energy density in the prepartum diet. Increasing energy density of the prepartum diet also promotes dry matter intake before and after calving. The energy density in the prepartum diet should be 1.54–1.63 Mcal/kg NE_l.

Dry cows should be fed according to their needs; cows in the early and middle portion of the dry period (far-off cows) and cows in the final 3 weeks prior to calving (pre-fresh cows) have different nutritional requirements in order to achieve optimal milk production and maintain the health and fertility of early-lactation cows.

Prepartum diets should be offered, starting at least 3 weeks prior to calving. Because of the different calving dates of dry cows fed in groups, the use of a prepartum diet over a prepartum feeding period of 21 days will usually allow each cow to consume the diet for a minimum of 5 days. The nutrient requirements for pre-fresh dry cows is controversial. The National Research Council does not provide recommendations for pre-fresh cows and it is recommended that a dairy cattle nutritionist be consulted for formulation of such rations. In general, a pre-fresh diet will provide about 0.50–0.75% BW per day as concentrates. Pre-fresh diets should be similar to early lactation diets so that the transition occurs effectively. The forages fed in the pre-fresh diet should be similar to those fed in early lactation.

Dairy cows are usually fed total mixed rations, where the concentrates and forages are mixed and fed as a total ration, or separate component rations in which the concentrates and forage are fed independently. In herds using separate component diets, the concentrates in the pre-fresh diet should be gradually introduced over a period of 3–5 days, and preferably fed individually. Forages should also be fed individually so that intake can be evaluated.

Vaccination against lactic acidosis

Some preliminary research has investigated the immunization of cattle against lactic-acid-producing bacteria, S. bovis and Lactobacillus. Immunization induced high levels of persistent saliva antibody responses against S. bovis and Lactobacillus, which reduced the risk of lactic acidosis in cattle.²⁹