Grain Overload in Ruminants , Ruminal Acidosis

   Grain Overload in Ruminants / Ruminal Acidosis 

Grain overload is an acute disease of ruminants that is characterized by rumen hypomotility to atony, dehydration, acidemia, diarrhoea, toxaemia, incoordination, collapse, and in severe cases, death.

Aetiology 

—  All types of ruminant cattle and sheep are susceptible but  more common in feedlot cattle and feedlot lambs 

—  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.

—   The case fatality rate may be up to 90% in untreated cases, while in treated cases it still may be up to 30-40 %.

—  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 (Streptococcus Bovis) increases markedly, - 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 dehydration

—  The low ruminal pH causes chemical rumenitis, and the absorption of lactate, particularly d-lactate, results in lactic acidosis and academia. 

—   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.

Clinical Findings

—  Carbohydrate engorgement results in conditions ranging from simple indigestion 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 diarrhoea 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 engorge themselves on water, but once ill they usually do not drink at all.

—  Body temperature is usually below normal, 98–101F

—  Respirations tend to be shallow and rapid, up to 60–90/min.

—  The heart rate usually is increased by the severity of the acidemia;

•      the prognosis is poor for cattle with heart rates >120 bpm.

•      Diarrhea is common and usually profuse and malodorous.

—  The faeces are soft to liquid, yellow or tan, and have an obvious sweet-sour odour.

—  The faeces commonly contain an excessive quantity of kernels of grain in grain overload.

—  In mild cases, dehydration equals 4–6% body wt, but losses may reach 10–12% in severe cases.

—  In severe cases, the primary contractions of the rumen are completely absent, although the gurgling sounds of gas rising through the large quantity of fluid on auscultation.

—  The contents of the rumen, as palpated may feel firm and doughy in cattle that were previously on a roughage diet and have consumed a large amount of grain.

—  Severely affected animals have a staggering, drunken gait and their eyesight is impaired

—  may bump into objects; their palpebral reflex is sluggish or absent,  the pupillary light reflex is usually present but slower than normal.

—  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.

—  Anuria is a common finding in acute cases, and diuresis after fluid therapy is a good prognostic sign.

Laminitis

—  Laminitis occurs in acute, subclinical and chronic forms associated with varying degrees of severity of ruminal acidosis.

—  Vasoactive substances (histamine and endotoxins) are released during the decline of rumen pH and the bacteriolysis and tissue degradation.

Diagnosis

—  usually obvious if the history is available. Can be confirmed by the clinical findings, a low ruminal pH (<5.5 in cattle unaccustomed to a high grain diet), and examining the microflora of the rumen for the presence of live protozoa. 

—  Differential diagnosis list: Simple indigestion, parturient hypocalcemia, peracute coliform mastitis, acute diffuse peritonitis

TREATMENT

—  The PRINCIPLES OF TREATMENT are:

—   Correct the ruminal and systemic acidosis and prevent further production of lactic acid

—   Restore fluid and electrolyte losses and maintain circulating blood volumes

—   Restore forestomach and intestinal motility to normal.

—  Initially, over 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.

—  Procaine penicillin G should be administered IM to all affected animals for at least 5 days to minimize the development of bacterial rumenitis and liver abscesses. 

—  Emptying the rumen (Rumen lavage) is unnecessary in less severe cases.

—  Alkalinizing agents: 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 be sufficient.

—  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 is 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.

—  Ancillary therapy

—  Antihistamines for laminitis, NSAIDs for shock therapy, thiamin or brewer's yeast to promote the metabolism of lactic acid,

—  parasympathomimetics to stimulate gut motility.

—  Calcium borogluconate is used widely because there is a mild hypocalcemia

Prevention

 Accidental access to concentrates for which the cattle have developed an appetite, in quantities to which they are unaccustomed, should be avoided. Feedlot cattle should be introduced gradually to concentrate rations throughout 2–3 wk, beginning with a mixture of ≤50% concentrate in the milled feed containing roughage.

TOTAL MIXED RATIONS:

is to feed, consisting of 50-60% roughage and 40-50% grain, as the starting ratio for 7-10 days, 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 micro£lora.