Grain overload is an acute disease of ruminants that is characterized by rumen hypomotility to atony, dehydration, acidemia, diarrhea, depression, incoordination, collapse, and in severe cases, death.
Etiology and Pathogenesis
The disease is most common in cattle that accidentally gain access to large quantities of readily digestible carbohydrates, particularly grain. Grain overload also is common in feedlot cattle when they are introduced to heavy grain diets too quickly. Wheat, barley, and corn are the most readily digestible grains; oats are less digestible. Less common causes include engorgement with apples, grapes, bread, batter's dough, sugar beets, potatoes, mangels, or sour wet brewer's grain that was incompletely fermented in the brewery. The amount of feed required to produce acute illness depends on the kind of grain, previous experience of the animal with that grain, the nutritional status and condition of the animal, and the nature of the ruminal microflora. Adult cattle accustomed to heavy grain diets may consume 30–45 lb (15–20 kg) of grain and develop only moderate illness, whereas others may become acutely ill and die after eating 20 lb (10 kg) of grain.
Ingestion of toxic amounts of highly fermentable carbohydrates is followed within 2–6 hr by a change in the microbial population in the rumen. The number of gram-positive bacteria (such as Streptococcus bovis) increases markedly, which results in the production of large quantities of lactic acid. The rumen pH falls to ≤5, which destroys protozoa, cellulolytic organisms, and lactate-utilizing organisms, and impairs rumen motility. The low pH allows the lactobacilli to utilize the carbohydrate and to produce excessive quantities of lactic acid. The superimposition of lactic acid and its salts, l-lactate and d-lactate, on the existing solutes in the rumen liquid causes osmotic pressure to rise substantially, which results in the movement of excessive quantities of fluid into the rumen, causing fluid ruminal contents and dehydration.
The low ruminal pH causes a chemical rumenitis, and the absorption of lactate, particularly d-lactate, results in lactic acidosis and acidemia. In addition to metabolic (strong ion) acidosis and dehydration, the pathophysiologic consequences are hemoconcentration, cardiovascular collapse, renal failure, muscular weakness, shock, and death. Animals that survive may develop mycotic rumenitis in several days and hepatic abscesses several weeks or months later. They may have evidence of ruminal epithelial damage at slaughter. The relation between grain overload and chronic laminitis in cattle is unclear.
Carbohydrate engorgement results in conditions ranging from simple indigestion (see Simple Indigestion in Ruminants) to a rapidly fatal acidemia and strong ion (metabolic) acidosis. The interval between overeating and onset of signs is shorter with ground feed than with whole grain, and severity increases with the amount eaten. A few hours after engorgement, the only detectable abnormality may be an enlarged rumen and possibly some abdominal pain (manifest by belly kicking or treading of the hindlimbs). In the mild form, the rumen movements are reduced but not entirely absent, the cattle are anorectic but bright and alert, and diarrhea is common. The animals usually begin eating again 3–4 days later without any specific treatment.
Within 24–48 hr of the onset of severe overload, some animals will be recumbent, some will be staggering, and others will be standing quietly; all will be completely off feed. Immediately after consuming large quantities of dry grain, cattle may gorge themselves on water, but once ill they usually do not drink at all.
Body temperature is usually below normal, 98°–101°F (36.5°–38.5°C); however, in animals exposed to the sun in hot weather, it may be increased to 106°F (41°C). Respirations tend to be shallow and rapid, up to 60–90/min. The heart rate usually is increased in accordance with severity of the acidemia; the prognosis is poor for cattle with heart rates >120 bpm. Diarrhea is common and usually profuse and malodorous. The feces are soft to liquid, yellow or tan, and have an obvious sweet-sour odor. The feces frequently contain undigested kernels of the feed that has induced the overload. In mild cases, dehydration equals 4%–6% body wt, but losses may reach 10%–12% in severe cases.
In severe grain overload, the primary contractions of the rumen are completely absent, although the gurgling sounds of gas rising through the large quantity of fluid are usually audible on auscultation. Ballottement and auscultation of the left flank may elicit fluid-splashing sounds in the rumen. The contents of the rumen, as 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 feel not necessarily full, but rather resilient because of the excessive fluid. Severely affected animals stagger and may bump into objects; their palpebral reflex is sluggish or absent, and the pupillary light reflex is usually present but slower than normal. The extent of depression of the palpebral reflex is associated with the plasma d-lactate concentration and provides a useful clinical method to categorize severity of lactic acidosis and monitor response to treatment. Affected animals commonly lie quietly, often with the head turned into the flank, and their response to any stimulus is much decreased so that they resemble cases of parturient paresis.
Acute laminitis may be present and is most common in those animals not severely affected; chronic laminitis may develop weeks or months later. Anuria is a common finding in acute cases, and diuresis after fluid therapy is a good prognostic sign.
Death may occur in 24–72 hr, and rapid development of acute signs, particularly recumbency, indicates a need for aggressive treatment. A decrease in heart rate, increase in temperature, return of ruminal movement, and passage of large amounts of soft feces are more favorable signs. However, some animals appear to improve temporarily but become severely ill again 3–4 days later, probably because of severe bacterial and fungal rumenitis; death from acute, diffuse peritonitis usually follows in 2–3 days. In pregnant cattle that survive the severe form of the disease, abortion may occur 10–14 days later.
The diagnosis is usually obvious if the history is available and multiple animals are affected. The diagnosis can be confirmed by the clinical findings, a low ruminal pH (<5.5 in cattle unaccustomed to a high grain diet), and examination of the microflora of the rumen for presence of live protozoa. When only one animal is involved and there is no history of engorgement, the diagnosis is less obvious, but the clinical signs—a static rumen with gurgling fluid sounds, diarrhea, ataxia, and a normal temperature—are characteristic. Rumen fluid analysis in these animals is required to confirm the diagnosis of grain overload.
Although parturient paresis (see Parturient Paresis in Cows) may resemble rumen overload, diarrhea and dehydration are not typical, the intensity of heart sounds is reduced, and the response to calcium injection is usually dramatic. Peracute coliform mastitis and acute diffuse peritonitis may also resemble overload, but usually a careful examination will reveal the cause of the toxemia.
To avoid an increase in pH on exposure to air, the pH of rumen fluid obtained by ororuminal stomach tube or ruminal paracentesis should be checked promptly. Normally, the pH in cattle on roughage is 6–7; in those on a high grain diet, 5.5–6. Values <5.5 are strongly suggestive of grain overload, and a rumen pH <5 indicates severe acidemia and metabolic acidosis. Wide-range (2–11) pH indicator paper is suitable for field use. Ruminal fluid should also be examined microscopically if access to a laboratory is available; fluid from affected cattle will have decreased numbers of protozoa (particularly large and medium-sized protozoa). In grain overload, a Gram stain of ruminal fluid will reveal a change from predominantly gram-negative bacteria (normal) to predominantly gram-positive bacteria, with a concomitant loss in bacterial diversity.
Increased blood d-lactate and l-lactate and inorganic phosphate concentrations, mild hypocalcemia, and reduced urinary pH are also seen, but it is seldom necessary to check such values to make a firm diagnosis. The diagnostic problem is to properly assess which animals require vigorous therapy (or slaughter), which require supportive therapy, which have only a mild indigestion that will correct itself if water and grain intake are restricted and hay and exercise are provided, and which need nothing beyond their routine care and ration. In an outbreak of overload involving several animals, it is necessary to identify those animals that need the most intensive therapy and those that will recover with minimal medical therapy.
If the cattle are found while still eating, it is possible that some of the group will fall into each category, and close monitoring is necessary to minimize losses. Cattle found while engorging or shortly thereafter should be allowed no more concentrate but plenty of good hay for up to 24 hr and should be forced to walk periodically. Cattle that appear normal at the end of the first day are probably in good health, although if even one is ill, all should be monitored closely for 48 hr. Most of those that have eaten enough concentrate to be affected seriously show signs within 6–8 hr.
For all cattle suspected of having eaten large quantities of concentrate, it is believed that restricting water intake for the first 18–24 hr is helpful, although this has not been proved. If overload is serious, slaughter for salvage should be considered; in feeders nearing the end of their feeding period, it may well be the most economic choice. Mortality is high in severely affected animals unless aggressive therapeutic measures are started early. In such animals, removal of rumen contents and replacement with ingesta taken from healthy animals is necessary. In animals still standing, rumenotomy is preferred to rumen lavage, because animals may aspirate during the lavage procedure and only rumenotomy ensures that all ingested grain has been removed. Rumen lavage may be accomplished with a large stomach tube if sufficient water is available. A large-bore tube (2.5 cm inside diameter, 3 m long) should be used, and enough water added to distend the left paralumbar fossa; gravity flow is then allowed to empty out what it will. Repeating this 15–20 times achieves the same results (and requires about as much time) as using rumenotomy to empty and wash out the rumen with a siphon.
Emptying the rumen should be followed by rumen inoculation (see Drugs for Specific Purposes in the Ruminant Digestive System) and, if not accomplished before signs of severe illness are evident, by rigorous fluid therapy to correct the metabolic acidosis and dehydration and to restore renal function. Initially, over a period of ~30 min, 5% sodium bicarbonate solution should be given IV (5 L/450 kg). During the next 6–12 hr, a balanced electrolyte solution, or a 1.3% solution of sodium bicarbonate in saline, may be given IV, up to as much as 60 L/450 kg body wt. Urination should resume during this period. Usually, it is unnecessary and even undesirable to also administer antacids PO (or intraruminally), particularly if IV sodium bicarbonate has been administered. Procaine penicillin G (22,000 U/kg/day) should be administered IM to all affected animals for at least 5 days to minimize development of bacterial rumenitis and liver abscesses. Thiamine should also be administered IM to facilitate metabolism of l-lactate via pyruvate and oxidative phosphorylation; animals with grain overload also have low concentrations of thiamine in rumen fluid because of increased production of thiaminase by ruminal bacteria. There is no effective preventive treatment for mycotic rumenitis.
Emptying the rumen is unnecessary in less severe cases. In these cattle, magnesium hydroxide (500 g/450 kg body wt) should be added to warm water, pumped into the rumen, and mixed therein via kneading the flank. This may be all that is necessary if the rumen pH is >5 and the animal is still standing and reasonably alert several hours after the engorgement. A heart rate of 70–85 bpm, weak ruminal contractions, normal body temperature, and especially willingness to eat are additional reassurances that this therapy will suffice. If any question remains, additional fluids should be given. During the convalescent period, which may last 2–4 days, good-quality hay and no grain should be given, and the grain then reintroduced gradually. If good appetite returns within 3 days, the prognosis is good. However, if treatment was not started early enough to prevent acidification of the ruminal contents, and mycotic infection of the rumen wall ensues, relapse is likely within 3–5 days and the prognosis is grave.
Accidental access to concentrates for which cattle have developed an appetite, in quantities to which they are unaccustomed, should be avoided. Feedlot cattle should be introduced gradually to concentrate rations over a period of 2–3 wk, beginning with a mixture of ≤50% concentrate in the milled feed containing roughage.
Last full review/revision May 2015 by Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM