 Time-Released
Hindgut Buffer for Horses with Subclinical Acidosis
EquiShure is appropriate for horses
suspected of suffering from subclinical acidosis. At-risk
horses often express one or more signs that can derail athletic
performance as well as reduce growth or reproductive potential.
Signs of subclinical acidosis may include:
- Decreased feed intake or complete
inappetence in severe cases
- Mild to moderate colic signs of unexplained
origin
- Poor feed efficiency and subsequent
weight loss
- Loss of performance
- Development of stereotypies such
as wood chewing, weaving, and stall walking
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A diagnosis of subclinical acidosis is often
overlooked initially when one or more of the aforementioned
signs is noticed. EquiShure, a time-released hindgut buffer,
may be beneficial in counteracting the effects of this syndrome.
Cause of Subclinical Acidosis
Subclinical acidosis is thought to result
from overconsumption of either high-starch concentrates
or pasture grasses rich in fructans. The demands placed
on horses—as athletes and as breeding animals—dictate
that substantial quantities of energy-rich feeds be consumed.
When large grain meals are fed to horses,
it is often impossible for the stomach and small intestine
to sufficiently digest and absorb the massive onslaught
of starch. Hence, some starch moves into the hindgut without
being sufficiently digested. As digestion of easily-fermentable
starch progresses in the hindgut, the production of volatile
fatty acids (VFA) and lactic acid increases, causing a significant
decrease in the pH. When the hindgut endures insults such
as this several times a day it teeters on becoming overwhelmed
with acid. Additionally, because lactic acid is a stronger
acid than the VFA, it can cause serious damage to the intestinal
mucosa. In severe cases, lactate may contribute between
50 and 90% of the total acids in the hindgut.
The shift in pH provides an unfavorable environment
for some of the many microorganisms that inhabit the hindgut
and aid in digestion. In particular, fiber-digesting bacteria
such as Ruminococcus albus and Fibrobacter succinogenes
are sensitive to precipitous decreases in pH. For optimal
performance, these bacteria favor an environment with a
pH between 6.5 to 7.0. When pH drops to below 6.0, fiber-digesting
bacteria become less efficient and begin to die off.
In contrast to fiber-digesting bacteria, lactate-producing
and lactate-utilizing bacteria thrive in an environment
with a low pH. Certain microorganisms such as Streptococcus
bovis actually shift their metabolism and produce lactic
acid rather than VFA when exposed to acidic conditions,
serving only to compound the problem.
Changes in the pH of the hindgut due to alterations
in the microbial populations and acid profiles cause a condition
known as subclinical acidosis.
Signs of Subclinical Acidosis
One of the primary signs of subclinical acidosis
is inappetence or decreased appetite. A horse is often reported
to be "off his feed."Because the hindgut is overwhelmed
with lactic acid when a horse is experiencing acidosis,
the intestinal lining becomes inflamed and irritated, causing
the horse discomfort. The irritation may be severe enough
to induce behavior characteristic of colic. Furthermore
and perhaps most detrimental to equine athletes is a reduction
of feed efficiency. Long-term exposure of the intestinal
lining to a low-pH environment may negatively affect the
absorptive capacities of these structures, limiting the
amount of energy available for performance.
In addition to these health concerns, a link
between subclinical acidosis and sterotypies such as wood
chewing, weaving, and stall walking has been suggested by
researchers.
Because of the precarious nature of the hindgut
of a horse afflicted with subclinical acidosis, it is less
able to handle metabolic crises that healthy horses may
be able to fend off. Hence, horses with subclinical acidosis
are more susceptible to colic and laminitis.
Managing Subclinical Acidosis
Subclinical acidosis is not a novel health
risk among domestic animals. Researchers first set out to
solve the problem of subclinical acidosis in dairy cattle.
Cows afflicted with rumen acidosis frequently exhibit abnormal
or erratic eating patterns. More often than not, they eat
less and that leads to decreased milk production and reduced
profit. Therefore, the need to regulate the pH in the rumen
became apparent. Researchers and dairymen successfully accomplished
this by adding a buffer such as sodium bicarbonate to the
feed.
Figure 1. Diagram of how subclinical acidosis
may occur in the hindgut and howit can be attenuated.
With research on dairy cattle as a premise,
the solution for managing horses with subclinical acidosis
seemed simple enough: supply a buffer to the hindgut that
minimizes fluctuations in pH when significant quantities
of easily fermentable carbohydrates are offered.
As researchers delved into this possibility,
they were confronted with a frustrating problem almost immediately.
The site of fermentation in the horse, collectively composed
of the cecum and colon, is located at the end of the digestive
tract rather than near the start like the cow's rumen. Therefore,
in order to reach the horse's hindgut, a buffer must withstand
passage through the stomach and small intestine. Regrettably,
the enzymes secreted in these organs are not particularly
hospitable to buffers. By the time an ordinary buffer reaches
the hindgut, it loses its efficacy. Researchers went back
to the drawing board and found the answer, a time-released
buffer.
Proven Time-Released Buffer
Research supports the use of a hindgut buffer
in cases of high grain and high fructan intake. In 1977,
scientists at the University of Kentucky examined the effects
of a buffer infused directly into the cecum of horses by
analyzing cecal pH. Horses that received hourly cecal infusions
of the buffer maintained consistently higher cecal pH than
horses not infused with the buffer.
Research trials at Kentucky Equine Research
(KER) were designed to test the efficacy of a time-released
hindgut buffer (EquiShure) on hindgut acidosis in horses
fed a high-grain ration. Fecal examination indicated that
nonsupplemented horses had decreased fecal pH after feeding
when compared to horses supplemented with EquiShure hindgut
buffer (Figure 2). In addition, EquiShuresupplemented horses
had significantly lower fecal lactate concentrations, suggesting
that lactatewas being used by lactic-acid-utilizing bacteria
to produceVFA. The VFA are subsequently absorbed by the
intestine and are metabolized as an energy source in the
liver. These significant results suggest that EquiShure
prevented the decrease in pH associated with rapid starch
and sugar fermentation after a large grain meal, enabling
lactate-utilizing bacteria to thrive and convert lactate
into VFA.
Subclinical acidosis can also be caused by
pasture grasses rich in fructan. Microbial digestion of
fructans results in production of VFA and lactic acid similar
to cereal grain digestion in the hindgut. As with large
amounts of grain, high fructan intakes overwhelm the hindgut
resulting in rapid fermentation, accumulation of lactic
acid, and a deleterious decrease in pH. KER therefore tested
the efficacy of EquiShure against a challenge of fructan.
Results showed that EquiShure-supplemented horses had less
fecal lactate when compared to control horses (Figure 3),
which, like in the grain study, indicates that lactate is
being converted into VFA by lactic-acid-utilizing bacteria.
However, both groups of horses exhibited decreased fecal
pH. In control horses, both lactic acid and VFA contributed
to the acidic conditions, whereas in EquiShure-treated horses,
most of the lactic acid was being utilized. Low pH as the
result of VFA is less detrimental to hindgut function compared
with lactate, which is a much stronger acid.
Figure 2. Fecal pH following consumption of
a grain meal.
Figure 3. Percent increase in d-lactate concentration
following a fructan challenge.
Another study conducted at KER demonstrated
the efficacy of a buffer when given to horses that had been
denied access to pasture (perhaps due to injury-related
stall rest). Horses that had not been turned out on pasture
for several weeks were given 24-hour free-choice access
to fall pasture. One group of horses was given a time-released
buffer (EquiShure) for 1 week prior to turnout and another
group served as controls and was given no buffer. Initial
pH readings revealed a moderate decrease in pH despite the
buffer, but an analysis of VFA proved that the drop in pH
was associated with increased VFA production; therefore
more were being produced and available to the horse as energy
sources (Figure 4). Additional analysis demonstrated that
lactic acid was greater in the control group vs. the EquiShure-fed
group, which meant EquiShure was effective and the hindgut
was functioning optimally (Figure 5).
Figure 4. Total VFA from fecal samples after
exposure to pasture.
Figure 5. Change in fecal lactic acid (d-lactate)
after exposure to pasture.
When large grain meals are fed, or high concentrations
of fructans are found in pasture, horses ferment these highly
fermentable carbohydrate "sugars"in the hindgut.
A time-released buffer helps moderate gut conditions by
preventing the drastic drop in pH associated with high lactate
production and supports lactic-acid-utilizing bacteria to
enhance the natural production of VFA from starch and cellulose.
While VFA are weak acids and will reduce pH, the dramatic
effects of lactic acidosis are moderated and the associated
problems attenuated by the time-released buffer EquiShure.
EquiShure Feeding Instructions
Use table below to determine recommended daily
amount based on horse's grain intake, forage source, and
weight. Top-dress EquiShure on daily grain ration. For best
results divide recommended daily amount equally among grain
meals. 1 scoop = 30 g.
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