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What is the optimal pH, how is this maintained, and what happens
when the pH goes awry?
• Normal pH of rumen ranges from 6
to 7.5
• If the pH drops below 5, the Gram
negative bacteria begin to die and
the Gram positive bacteria start to
proliferate, especially
Streptoccocus bovis
• As S. bovis proliferates more and
more, the acid drops and the
situation goes from bad to more
bad. At about pH4.5, even the S.
bovis don't do very well and
lactobacilli start replicating like
crazy
• Ruminal mucosa is normally
covered with papillae to help
increase the surface area
• Neonatal animals don't have any
papillae. They don't need them
because the rumen doesn't start
functioning
• As they begin to consume
roughage, these papillae
The rumen on the far left has more leaf-shaped, or tongue- develop
shaped papillae, indicating the ration may have been more
acidic than that consumed by the animal whose rumen is on
the right
• However, if it gets much worse,
these papillae can fuse or clump,
and this decreases the surface
area, which is a definite
disadvantage for the animal
Tympany
• The normal functioning of the
rumen requires that gas be
released periodically
• If this gas can't be released, the
rumen blows up like a balloon
• Besides being incredibly
uncomfortable, this is also life-
threatening
Bloat
• Bloat, also called tympany, is divided into primary and secondary
varieties
• Primary bloat is also referred to as "frothy" bloat. In this type of
bloat, there is no gas to release into the esophagus, because it is all
trapped in little bubbles within the rumen
• instead of having big gas pockets in the dorsal areas, these regions are
filled with foam
Tympany
• Some plants, especially the
legumes, just have too many
soluble proteins, which get mixed
up with the fluid and merge with
the bubbles
• The bubbles are stabilized because
of the excess protein and they
don't burst
• Another reason is the feeding of
high grain diets. This causes less
salivation, and so there isn't as
much saliva to decrease the foam
Primary bloat
There are some ways to avoid or decrease frothy bloat:
• One is to not feed the cattle bloating types of legumes.
• Another is to administer anti-bloating agents which are surfactant-
type materials that help to break down the surface tension of the
foam.
• The third is to increase salivation. Saliva has mucins in it which help to
decrease the foam. Some believe that cattle that are genetically
predisposed to produce minimal saliva are also very susceptible to
developing frothy bloat.
Secondary bloat
Secondary bloat is also called "free gas bloat.“
• it is usually because there is a blockage in the eructation mechanism
so the animal can't belch
• obstruction in the esophagus
• definite obstruction - a tumor, a big old apple that got swallowed
whole, or some adhesions restricting the movement of the rumen
• "vagal indigestion," in which rumen motility is inhibited because of
some vague vagal nerve damage
Why do animals with bloat die? Well, the pressure from the expanding
rumen compresses everything in the thorax and they die of cardiac
arrest. There is extremely poor venous return to the heart because of
the tremendous external pressure on the thorax
This is a photograph of the mucosal surface of the esophagus
from a sheep that came into the postmortem room looking like
a balloon.
Cattle often ingest bits of metal which cause problems Even worse, they can penetrate the reticular wall and
come out the other side, making a nice little track for the
rumen microorganisms to follow.
In decades past, farmers dropped magnets into the
reticulum which helps to keep metal objects anchored
within the reticulum lumen. We don't see many of these
anymore.
disseminated liver abscesses These big red ring-like lesions are due to fungus, so this is
mycotic rumenitis
The ulcers serve as portals of entry for gut organisms to have access to the cow's circulation. Often
what happens after an episode of lactic acidosis is that ruminal flora get into the mucosa, enter the
blood vessels, and get a free ride to the next stop, which is the liver.
Sequela of lactic acidosis