Agriculture Reference
In-Depth Information
physiological changes allowing the newborn and prerumi-
nant to becomes a functional ruminant.
hydrates (starches and sugars) to the diet. When an animal
is fed a high concentrate feed without being adapted, rapid
fermentation by facultative bacteria produces lactic acid
and reduces the rumen pH into a range favorable for amy-
lolytic bacteria. Under normal circumstances, secondary
rumen bacteria convert lactic acid or other acids to propio-
nate. But secondary fermenters have lower metabolic rates,
higher generation intervals (16 hours), and a higher
optimum pH (6.2-6.8) than amylolytic bacteria. Therefore,
hydrogen disposal is hindered, acids accumulate, and
rumen acids accumulate. Rumen pH may drop as low as 4
and cause rumenitis and rumen parakeratosis, a condition
where the rumen epithelium is sloughed from the basal
membrane. Lactic acid may be absorbed through the rumen
wall into the blood and carried to the liver where the
natural L (+) lactate form can be metabolized, but the
bacterial form of lactate (the D [−] isomer) may accumu-
late in the blood causing systemic acidosis and death from
a reduced oxygen carrying capacity of hemoglobin.
Treatment often involved dosing with bicarbonate buffers
while prevention involved feeding more roughage, particu-
larly long hay that induces rumination and saliva produc-
tion. In severe cases, the rumen may be partially or fully
evacuated and replaced with fresh rumen fl uid from a
healthy animal.
RUMEN DYSFUNCTION
The major digestive disorders common to ruminants will
be discussed briefl y. Readers are referred to a more detailed
discussion of these problems in textbooks on veterinary
physiology (Reece, 2004). Because most dysfunctions
refl ect specifi c aberrations in normal rumen function, such
discussion helps to reinforce the reader's knowledge about
normal rumen function.
Bloat
Bloat is defi ned as the distension of the reticulo-rumen
associated with accumulation of gases produced by fer-
mentation of certain feeds with failure in gas removal by
eructation. Bloat is not common in free ranging ruminants
consuming grasses but is manifested by mismanagement
of the animal and the diet. Van Soest (1994) divided bloat
into two types: legume or frothy bloat, and grain bloat that
may be either acute or chronic. Legume or frothy bloat
usually is associated with animals grazing rapidly growing
legume (alfalfa or white clover) pastures grown in temper-
ate climates. Proteins involved with carbon dioxide fi xa-
tion apparently uncoil and fl oat to the top of the rumen,
and this leads to a foam or froth that traps gas in a form
that cannot be eructed. Tropical legumes, temperate trefoil,
vetch, or sanfoin contain higher amounts of tannins that
precipitate proteins. This prevents formation of stable
foam. Grain bloat usually is the result of feeding high grain
diets (typically wheat and barley) and pelleted feeds. High
concentrate diets that have a very small particle size from
grinding and pelleting are often implicated. Such feeds are
associated with less saliva production per unit of feed and
less salivary mucin that helps protect animals from bloat.
High amylolytic activity that produces rumen acids (lactic
acid) also may reduce rumen motility to promote bloat.
Grain bloat is commonly chronic while legume bloat
usually is acute. Acute bloat causes death by placing pres-
sure on the heart or blood vessels preventing fl ow that
results in cardiovascular collapse. Oils or detergents that
reduce surface tension help to suppress foam formation. In
severe cases the rumen can be punctured to release gases
as a last resort. Goats, being intermediate food selectors,
have relatively larger salivary glands and their habit of
browsing helps makes them more resistant to bloat.
Displaced Abomasum
Ruminants fed fi nely ground, very high concentrate diets
tend to have highly acidic and fl uid ruminal digesta with
little fi brous material. High acidity and low fi ber content
of digesta reaching the abomasums is associated with
reduced motility and altered gastric function. Impaired
motility causes abomasal distension. The abomasum may
become engorged with fl uids and gas and become dis-
placed laterally. Left displacement is associated with a
chronic condition, whereas right displacement is associ-
ated with blockage of digesta fl ow and may prove fatal.
The actual cause of this symptom is not clearly understood,
but its association with high starch, fi ne particle diets has
been documented.
Urea/Ammonia Toxicity
Urea or ammonia toxicity usually occurs when an exces-
sive amounts of urea is consumed by an animal. Animals
grazing lush forage pastures with highly soluble proteins
also may be at risk. Bacterial urease rapidly hydrolyzes
urea-forming ammonia. In the presence of an adequate
supply of readily available carbohydrates such as starch
and sugars that are rapidly fermented (amylolytic fermen-
tation), rumen microbes will use available ammonia to
Acidosis
Acidosis is defi ned as an imbalance in rumen fermentation
elicited by abrupt introduction of rapidly fermented carbo-
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