compound stomach
some anatomical aspects of compound stomach.
In ruminant animals , stomach is consists of four chambers :reticulum , omasum , rumen , abomasum.
The first three chambers known as fore stomach or proventriculus while the forth called true stomach.
The last chamber (abomasum) is like simple stomach of dogs ,so called true or glandular stomach .
In large ruminants
The rumen occupies 80% of the whole size of stomach , the reticulum occupies 5% , omasum occupies 8% while the abomasum occupies 7% .
In small ruminants
The rumen occupies 75% of the whole size of stomach , the reticulum 8%, omasum 4% and the abomasum 13% .
In newly born ruminant
At the time of birth , the ruminant stomach is prepared for digestion milk.
The abomasum predominates and is remarkable in size and structure (about 60% of the whole size of stomach .
Esophageal groove = reticular groove 
There is a prominent gutter that descends form the cardia over the right surface of the reticulum towards the fundus , the groove is bounded by spiral fleshy lips .
In un-weaned animals, this groove might be converted into a closed tube forming a channel that coneys milk directly from the esophagus to the omasal canal , hence it drops into the abomasum .
The contraction of this tube in reflexly
stimulated by sucking from the dam or by the presentation of suitable bucket feeding .
Motor activity of the compound stomach
a)Motility of the Reticulo-rumen
Forestomach
motor function comprises a well- coordinated and carefully regulated series of
events, which accomplish the following criteria:
1- Mixing of
fluid and solid ingesta, which include:
- Maceration of the fibrous foodstuffs.
- Circulation of ruminal fluid in order to
bring the fluid in contact with epithelial surface, thus aiding absorption of VFAs(volatile fatty acids).
- Filtering or
sorting of fine particulate materials for presentation at the reticulo-omasal opening and passage to the lower GIT.
2- Removal
of excessive gas by eructation.
3-
Regurgitation of fibrous ingesta for remastication .
1) Mixing
cycle (primary contraction cycle)
The primary cyclic activity results in
mixing and circulation of digesta in an organized manner.
The primary contraction in cattle begins
with a biphasic contraction of the reticulum .
- The first reticular contraction forces
ingesta dorsal and caudal in to the rimen .
-The second reticular contraction as the
first, but much stronger.
The dorsal ruminal sac then begins to
contract as the ventral sac relaxes, thereby causing digesta to
move from the
dorsal to the ventral sac.
Sequential contractions of the
caudo-ventral, caudo-dorsal and ventral ruminal sacs force digesta
back into the
reticulum and cranial sac.
After a brief pause, the contraction sequence
is repeated.
During each reticular contraction fluid and
food particles, particularly heavy grain, pass into the
reticulo-omasal orifice
and into the omasum and abomasum.
Reticulo-rumen motility results in
stratification of ruminal contents, with firmer fibrous material
floating on
top of a more fluid layer. Solid matter remains in the rumen until the particle
size is
sufficiently small to pass through the reticulo- omasal orifice.
2)
Eructation cycle (Secondary contraction cycle)
Secondary cycles are contractions that
involve only the rumen and are associated with the eructation
of gas.
They occur independently of the primary
cycle contractions and usually less frequently, about once
every 2 minutes.
The contraction rate depends on the gas or
fluid pressure in the dorsal sac of the rumen.
Secondary cycles can be inhibited by severe
distension of the rumen.
Contractions begin in the dorsal and
caudo-dorsal ruminal sacs and spread forward to move the gas
cap ventrally to
the cardia region.
Contraction of the reticulo-ruminal fold is
necessary to stop fluid from moving forward
to the reticulum and covering the
cardia.
Despite the presence of normal secondary
contractions, eructation may not occur in recumbent animals when the cardia is
covered with fluid.
Bloat is often observed in ruminants in
lateral recumbency.
3) Rumination cycle = Regurgitation for
re-mastication
Rumination is a complex process and consists of
Regurgitation.
Re-mastication.
Insalivation.
Deglutition
Rumination is initiated by the rumination
center close to the gastric center in the
medulla oblongata.
Rumination allows further physical breakdown
of feed with the addition of large quantities of saliva
and is an integral part
of ruminal activity.
1- Reticulo-rumen hypo-motility or atony.
2- Central nervous system depression.
3- Excitement, pain or both
4- Liquid ruminal contents such as a
high-concentrate diet with no coarse fiber.
5- Mechanical injury to the reticulum
(peritonitis).
Other less common causes include chronic
emphysema (difficulty in creating a negative thoracic
pressure) and extensive
damage to the epithelial receptors that incite the reflex,
as occurs in rumenitis.
b) Motility of Omasum
Contractions of omasum are biphasic.
The first one acts to squeeze the contents
from omasal recesses between the lamina.
While, the second phase is a mass
contraction of the whole omasum, and its function is to squeeze
the fluid ingesta from the material in recesses to the abomasum.
c) Motility
of Abomasum
The movements of abomasum are sluggish. They
consist of general contractions of the proximal limb
and more forceful
peristalsis confined to the pyloric part.
Decomposition and splitting of cellulose and
hydrolysis of starch and simple sugars resulting in
formation of volatile fatty
acids [Acetic (body fat), butyric (milk fat), propionic (glucose synthesis)] +
Energy supply.
Decomposition of protein and formation of
amino acids and ammonia with subsequent formation of
microbial protein from
nitrogenous and non-nitrogenous substances.
Vitamin biosynthesis, especially vitamin - B
complex in the presence of cobalt and source of vitamin A.
Degradation of fat materials and formation
of long & short chain fatty acids.
The clinical
findings which suggest primary ruminant gastrointestinal dysfunction include
the following
Inappetence to anorexia, failure to
ruminate.
Dropping regurgitated cuds occurs in straw
impaction of the rumen,
vagus indigestion, esophageal dilatation and rumenitis.
Visible distension of the abdomen
The abdomen may appear gaunt or empty
The rumen may feel abnormal on palpation
through the left para-lumbar fossa
Ruminal atony or hyper-motility
Abdominal pain
Abnormal feces
Diseases Of The Compound Stomach
INDIGESTION
It is the impairment of the process of
digestion as a result of either changes or disturbances in the
microbial
digestion or motor activity of the compound stomach.
Indigestion in ruminants could be
categorized into two main categories:
1) Primary Indigestion
This type of
indigestion includes those diseases in which the reticulo-rumen is directly affected
A. Diseases
of the motor function of the reticulo-rumen (Motor Indigestion(
- Diseases of
the reticulo-rumen wall.
- Disorders of
the nervous regulation of the stomach.
-Impedance or physical obstruction to the
passage of ingesta from the reticulo-rumen into omasum
and subsequently to
abomasum.
-Such as
ruminal bloat, vagus indigestion, traumatic reticulitis, abomasal displacement
and volvulus
and Diaphragmatic hernia.
B. Abnormalities
of the contents of reticulo-rumen, with dysfunction of microbial and biochemical fermentation and known as (Microbial Indigestion(
This group
of diseases may be accompanied with
Low pH value of reticulo rumen contents e.g.
Ruminal Acidosis.
High pH
value of reticulo rumen contents e.g. Ruminal alkalosis & Ruminal
putrefaction .
Normal or slightly low pH value of rumen
contents e.g. simple inactivity o ruminal flora & fauna.
2) Secondary Indigestion
Which is the
sequel of diseases in other organ system or of systemic problems
Those diseases may affect the motor activity
or the microbial digestion
within the compound stomach.
Simple indigestion
Simple
indigestion is the most common sequel of abrupt changes in the ration which occurs more
commonly in hand–fed ruminants. Such changes present the rumen
microbiota with nutrient
substrates:
To which
they are not metabolically adapted.
To which
they are adapted but in lesser quantities.
To which
contain inhibitory substances or produce an inhibitory substances upon
fermentation.
The result is an imbalance in the microbial
ecosystem and its fermentation products. It is clinically characterized by:
Disturbances in appetite (in-appetence or
anorexia).
Depressed ruminal movements
Scanty, dry feces or voluminous feces with
diarrhea.
Causes
Primary
causes:
_ Dietary
abnormalities such as
Indigestible
roughage.
Moldy,
overheated or frosty food.
Decomposed
or spoiled food.
Increased
concentrates in the diet.
Insufficient water intake especially in
summer season.
Increased protein content in the diet
causing putrefaction.
Oral administration of antibiotics or
sulphonamides.
Secondary
causes:
Systemic
diseases.
Traumatic
reticulo-peritonitis .
Post-parturient
paresis.
Advanced stage of pregnancy.
Pathogenesis
__Changes in the pH of its contents markedly
affect the motility of the rumen and in cases caused by
overeating on grain an
increase in acidity is probably of importance
_High protein diets, including
the feeding of excessively large quantities of legumes or
urea also depress
motility because of the sharp increase in alkalinity that results.
_ The simple accumulation of indigestible food
may physically impede ruminal activity.
_ The toxic amides and amines produced may
include histamine, which is known to cause ruminal
atony when given
intravenously and to be reversed by the administration of antihistamine drugs.
_ Histamine may contribute to the ruminal
atony that occurs in allergy, or after heavy grain feeding,
but the absorption
of histamine from the fore-stomachs in any circumstances is probably very
limited.
_ A marked fall in milk yield occurs, caused
probably by the sharp decrease in volatile fatty acid
production in a hypotonic
reticulo-rumen.
_ Rumen contractions appear to play the same
role as hunger contractions in simple stomachs and the
decreased food intake is
probably due to the ruminal atony.
_ Reduction in appetite, varied from
in-appetence to anorexia.
_ Mild depression and dullness.
_ Reduced milk production in dairy animals.
_ Suppression of rumination, depressed ruminal
movements in frequency and amplitude and sometimes
are almost absent.
_ The rumen may be larger than normal if the
cause is sudden access to an un-limited supply
of palatable feed.
_ Some cases may show tympany, but the usual
finding is a firm, doughy rumen without obvious
distension.
_ The feces are usually reduced in quantity
and are drier than normal on the first day. However, 24-48
hours later the
animal is commonly diarrheic; the feces are softer than normal, voluminous and
commonly malodorous.
_ There is no systemic reaction and the heart
rate, temperature and respirations are usually within
normal ranges.
_ Pain cannot be elicited by deep palpation of
the ventral abdominal wall, although cows that have
consumed an excessive
quantity of a highly palatable feed such as silage will have a grossly
distended rumen, and mild abdominal discomfort may be present for several
hours.
_ The discomfort usually resolves when the
rumen movements return to normal and the rumen returns
to its normal size.
_ Most cases recover spontaneously or with
simple treatments in about 48 hours.
Diagnosis
Physical examination
Clinical pathology findings; blood samples,
ruminal fluid samples (physical + biochemical) and
urine samples.
Differential diagnosis
_ Acetonemia or pregnancy toxemia
The appetite
and milk production decrease over a few days, there is ketonuria and the rumen
contractions are present but weaker than normal.
_ Traumatic reticulo-peritonitis
There is a
sudden onset of anorexia and agalactia, a mild fever, a painful grunt on deep palpation of
the. Xiphoid sternum, and the rumen is static with an increase in the size of the gas cap.
Characterized
by depression, dehydration, tachycardia, staggering, recumbency,
diarrhea and
ruminal stasis with the presence of fluid-splashing sounds, and the pH of the ruminal
fluid is usually below 6 and commonly down to 5 .
_ Abomasal displacement
It is
usually related to parturition, acetonuria, in-appetence, reduced feces, ruminal atony, reduced
milk production dehydration and tachycardia.
There is ping sound on the flank areas
_ Vagus indigestion:
Characterized
by gradual distension of the abdomen due to distension of the rumen over a period of
several days, progressive dehydration and scant feces. Initially,
there is hyper-motility of the rumen
and the development of secondary frothy bloat. This is commonly followed by ruminal atony.
Treatment
Spontaneous
recovery
_ Most cases of simple indigestion recover
spontaneously.
_ Small quantities of fresh, good-quality,
palatable hay should be provided several times daily to
encourage eating and to
stimulate reticulo-rumen motility.
_ Because anorexia and forestomach
hypo-motility usually exist together, stimulate both
appetite and
motility.
_ Reduced feed intake reduces the two primary
drives for reticulo-rumen activity: moderate
forestomach distension and chewing
activity.
Treatment
trials
Because of lack of knowledge about the
specific etiology, the main objectives of the treatment are:
Correction of ruminal pH.
Re-establishment of ruminal motility.
Evacuation of the stomach content
Correction
of ruminal pH
Magnesium. Hydroxide = milk of monesia which acts
as laxative, antacid, anti-ferment.
Lactic Acid 50-70 mL in 8-10 Liters water.
Kitchen vinegar 2 liter orally.
Glacial acetic acid 10 mL X 500mL water.
It is acute digestive disorders of the fore-stomach due to ingestion of large quantities of carbohydrates rich diet and resulting in acute acidosis , or ingestion protein rich diet and results in rumen alkalosis or putrefaction .
Acute rumen acidosis = carbohydrate engorgement (founder)
It is an acute disorder (most dramtic form of rumen microbial fermentative disorders ) produced by ingestion of toxic amount of highly fermentable carbohydrate ricg diet which leads to produuction of large quantities of lactic acid in the rumen causing ruminal acidosis and achemical ruminitis , it is clinically characterized by :
1- ruminal stasis
2- staggering and blindness
3- weakness and recumbency
4- high mortality rate
5- sever dehydration
Etiology
1- abrupt change in the diet without prior adaptation.
2- accidental ingestion of toxic doses of carbohydrates rich diet such as grain which is the most common cause of acute ruminal acidosis.
3- feeding on excessive amount of carbohydrates after a period of anorexia or fasting.
4- excessive consumption of concentrates such as molasses , sugar beets , wheat , corn , barely , apples , grapes , bread and baker’s dough .
Pathogenesis
hours by a marked change in the microbial population in the rumen.
large quantities of lactic acid.
destruction of the cellulolytic bacteria and protozoa.
When large amounts of starch are added to the diet, growth of some bacteria is no longer restricted by
energy source and it multiplies faster .
_The low pH allows lactobacilli to use the large quantities of carbohydrate in the rumen to produce
excessive quantities of lactic acid, resulting in ruminal lactic acidosis.
_ Both D and L forms of the acid are produced, which markedly increases ruminal osmolality, and
water is drawn from the systemic circulation, causing hemo-concentration and dehydration.
_ Lactate is a 10 times stronger acid than the volatile fatty acids, and accumulation of lactate
eventually exceeds the buffering capacity of rumen fluid.
_ As the ruminal pH declines, the amplitude and frequency of the rumen contractions are decreased
and at about a pH of 5 there is ruminal atony.
_ The absorbed lactic acid is buffered by the plasma bicarbonate buffering system.
_With nontoxic amounts of lactic acid, the acid-base balance is maintained by utilization
of bicarbonate and elimination of carbon dioxide by increased respiration.
_ In severe cases of lactic acidosis the reserves of plasma bicarbonate are reduced, the blood pH
declines steadily, the blood pressure declines, causing a decrease in perfusion pressure and oxygen
supply to peripheral tissues and resulting in a further increase in lactic acid from cellular respiration.
ruminal vessels, causing thrombosis and infarction.
_ Widespread necrosis and gangrene may affect the entire ventral half of the ruminal walls and lead to the development of an acute peritonitis.
the gangrene, is usually sufficient to cause death.
rations, and the lesions are attributed to the chronic acidosis
_Hepatic abscesses commonly occur as a complication as a result of a combination of rumenitis
caused by lactic acidosis and allowing Fusobacterium necrophorum and Arcanobacter
(Corynebacterium) pyogenes to enter directly into ruminal vessels and spread to the liver, which may
have also undergone injury from the lactic acidosis.
_In cattle being placed on a grain ration, even with control of the daily intake, hepatic cell damage
and liver dysfunction occur even though dietary adaptation may have occurred in 2-3 weeks.
_The biochemical profile indicates that complete metabolic adaptation requires at least 40 days
following the start of grain feeding.
Laminitis occurs in acute, subclinical and chronic forms associated with varying degrees of severity of
ruminal acidosis
The association between acidosis and laminitis appears to be associated with altered hemodynamics
of the peripheral microvasculature.
Vasoactive substances (histamine and endotoxins) are released during the decline of rumen pH and the bacteriolysis and tissue degradation.
These substances cause vasoconstriction, which injure the microvasculature of the corium.
Ischemia results, which causes a reduction in oxygen and nutrients reaching the extremities of the
corium. Ischemia causes physical degradation of junctures between tissues that are structurally critical
for locomotion.
Several toxic substances other than lactic acid have been suggested as contributory to the disease.
Increased concentrations of histamine have been found in the rumen of experimentally engorged
cattle, but its possible role in the disease remains unknown.
Histamine is not absorbed from the rumen except at abnormally high pH values, but is absorbed from
intestinal loops.
Other substances that have been recovered from the rumen in grain overload include a suspected
endotoxin, ethanol and methanol.
The temperature is usually below normal, 36.5-38.5 o C.
The heart rate in cattle is usually increased and continues to increase with the severity of the acidosis and circulatory failure.
The respirations are usually shallow and increased.
Acute abdominal pain, manifested by kicking at the belly.
Diarrhea is almost always present and usually profuse, and the feces are light-colored with an obvious sweet-sour odor.
The dehydration is severe and progressive. In mild cases, the dehydration is about 4-6%
Anuria is a common finding in acute cases and diuresis following fluid therapy is a good
prognostic sign.
_ Staggering, drunken gait with impairment of eye sight, loss of palpebral reflex
_ Recumbency usually follows after about 48 hours but may occur earlier.
_ Careful examination of the rumen is important. The rumen contents palpated through
_ The primary contractions of the reticulo-rumen are usuallytotally absent, although low pitched tinkling and gurgling sounds associated with the excessive quantity of fluid in the rumen are commonly audible on auscultation of the rumen.
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