Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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Acute Carbohydrate Engorgement Of Ruminants
(Ruminal Lactic Acidosis, Rumen Overload)
Etiology
1- The sudden ingestion of toxic doses of carbohydrate-rich
feed, such as grain, is the most common cause of the acute
form.
2- engorgement with apples, grapes, bread, baker's dough, sugar
beet, mangels.
3- sour wet brewers' grain that was incompletely fermented in
the brewery.
4- concentrated sucrose solutions used in apiculture.
EPIDEMIOLOGY:
1- All types of ruminant cattle and sheep are susceptible
2- Most commonly in feedlot cattle and dairy cattle fed on high-
level grain diets.
3- a change from one ration to
4- another requires a period of microbial adaptation.
5- Animals being fed a low-energy ration are most susceptible
to a rapid change to a high energy ration because satisfactory
adaptation cannot occur quickly enough
6- Accidental consumption of excess carbohydrates
7- The adaptation of the ruminal microflora and papillae from a
requires a gradual change during a period of 3-5 weeks.
8- Morbidity will vary from 10-50%.
9- case fatality rate may be up to 90% in untreated cases, while
in treated cases it still may be up to 30-40 %.
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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10-
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 microflora.
11-
Amounts of feed that are lethal range from 50-60 g of
crushed wheat/kg BW in undernourished sheep
12-
75-80 g/kg BW in well-nourished sheep.
13-
in cattle doses ranging from 25-62 g/kg BW of ground
cereal grain or corn produced severe acidosis.
PATHOGENESIS:
1. The ingestion of excessive quantities of highly fermentable
feeds by a ruminant
2. followed within 2-6 hours by a marked change in the
microbial population in the rumen.
3. increase in the number of Streptococcus bovis
4. utilize the carbohydrate to produce large quantities of lactic
acid.
5. In the presence of a sufficient amount of carbohydrate the
organism will continue to produce lactic acid
6. decreases the rumen pH to 5 or less
7. destruction of the cellulolytic bacteria and protozoa.
8. The concentration of volatile fatty acids increases initially,
contributing to the fall in ruminal pH.
9. 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.
10. increases ruminal osmolality, and water is drawn in from the
systemic circulation, causing hemoconcentration and
dehydration.
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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11. As the ruminal pH declines, the amplitude and frequency of
the rumen contractions are decreased
12. The absorbed lactic acid is buffered by the plasma
bicarbonate buffering system.
13. With nontoxic amounts of lactic acid, the acid-base balance
is maintained by utilization of bicarbonate and elimination of
carbon dioxide by increased respirations
14. 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.
Sequels of ruminal acidosis:
1. Chemical and mycotic rumenitis
The low pH of the rumen favors the growth of Mucor,
Rhizopus and Absidia spp. which invade the ruminal vessels,
causing thrombosis and infarction
2. Hepatic abscesses
Fusobacterium
necrophorum
and
Arcanobacter
(Corynebacterium) pyogenes enter directly into ruminal
vessels as a result of a combination of rumenitis
3. Laminitis
Vasoactive substances (histamine and endotoxins) are
released during the decline of rumen pH and the
bacteriolysis and tissue degradation. These substances cause
vasoconstriction
and
dilation,
which
injure
the
microvasculature of the corium.
Ischemia causes physical
degradation of junctures between tissues that are structurally
critical for locomotion.
4. Mild hypocalcemia due to temporary malabsorption.
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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CLINICAL FINDINGS:
1) Cattle suffered from distended rumen and abdomen
2) abdominal discomfort, evidenced by kicking at the belly
3) anorexic and still fairly bright and alert, and the feces may be
softer than normal
4) Rumen movements are reduced but not entirely absent.
5) Affected cattle do not ruminate for a few days but usually
begin to eat on the third or fourth day without any specific
treatment.
6) In severe form, within 24-48 hours some animals will be
recumbent,
7) some staggering and others standing quietly alone.
8) Teeth grinding may occur in about 25 % of affected sheep
and goats.
9) Once they are ill they usually do not drink water
10)
Cattle may engorge themselves on water if it is readily
available immediately after consuming large quantities of dry
grain.
11)
inspection of the feces on the ground will usually reveal
Depression, dehydration, inactivity,
12)
The temperature is usually below normal, 36.5-38SC
(98-101°F), but animals exposed to the sun may have
temperatures up to 41°C (106°F).
13)
In sheep and goats, the rectal temperatures may be
slightly higher than normal.
14)
The heart rate in cattle is usually increased and
continues to increase with the severity of the acidosis and
circulatory failure.
15)
In general, the prognosis is better in those with heart
rates below 100/min than those with rates up to 120-140/min.
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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16)
In sheep and goats, the heart rate may be higher than
100/min.
17)
The respirations are usually shallow and increased up to
18)
60-90/min.
19)
A mucopurulent discharge is common because animals
fail to lick their nares.
20)
dehydration is severe and progressive.
21)
The rumen contents palpated through the left
paralumbar fossa may feel firm and doughy
22)
pH of the rumen fluid is usually below 5.
23)
Severely affected animals have a staggery, drunken gait
and their eye sight is impaired.
CLINICAL PATHOLOGY:
1) Ruminal fluid pH
a) A ruminal pH of 5-6 in roughage fed cattle suggests a
moderate degree of abnormality
b) a pH of less than 5 suggests severe grain overload and
the need for energetic treatment.
c) Feedlot cattle that have been on grain for several days
or weeks and are affected with grain overload usually
have a pH below 5.
2) Ruminal protozoa
3) Serum biochemistry
1- Blood lactate and inorganic phosphate levels rise
2- blood pH and bicarbonate fall markedly
3- mild hypocalcemia
4) Urine pH
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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a) The urine pH falls to about 5 and becomes
progressively more concentrated; terminally there is
anuria.
NECROPSY FINDINGS:
1- the contents of the rumen and reticulum are thin and
porridge-like and have a typical odor suggestive of
fermentation.
2- The cornified epithelium may be mushy and easily wiped off,
leaving a dark, hemorrhagic surface beneath
DIFFERENTIAL DIAGNOSIS:
1) Simple indigestion
2) Parturient paresis
3) Toxemias
TREATMENT
The principles of treatment are:
1- Correct the ruminal and systemic acidosis
2- prevent further production of lactic acid
3- Restore fluid and electrolyte losses
4- maintain circulating blood volumes
5- Restore forestomach and intestinal motility to normal
6- Prevent further access to feed
7- Do not provide any water for 12-24 hours
8- Offer a supply of good-quality palatable hay equal to one-
half of the daily allowance per head
9- Exercise all animals every hour for 12-24 hours to encourage
movement of the ingesta through the digestive tract
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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A. Rumenotomy in severe cases
B. Intravenous sodium bicarbonate and fluid therapy
1- 5% sodium bicarbonate at the rate of 5 L for a 450 kg
animal given initially over a period of about 30
minutes
2- followed by isotonic sodium bicarbonate (1.3%) at 150
mL/kg BW intravenously over the next 6-12 hours.
C. Rumen lavage in less severe cases
D. Intraruminal alkalinizing agents in moderately affected cases,
the use of 500 g of magnesium hydroxide per 450 kg/BW
E. NSAIDs for shock therapy
F. thiamin or brewer's yeast to promote the metabolism of lactic
acid
G. parasympathomimetics to stimulate gut motility.
H. Calcium borogluconate
RUMINAL TYMPANY (BLOAT)
Ruminal tympany is abnormal distension of the rumen and
reticulum caused by excessive retention of the gases of
fermentation, either in the form of a persistent foam mixed with the
rumen contents or as free gas separated from the ingesta.
Normally, gas bubbles produced in the rumen coalesce, separate
from the rumen contents t o form pockets o f free gas above the
level of the contents and finally are eliminated by eructation.
ETIOLOGY
A. Primary ruminal tympany (frothy bloat)
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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1- Leguminous, is due to the foaming qualities of the
soluble leaf proteins
2- cattle that graze pastures consisting of bloating forages
(alfalfa, clover)
3- lush pasture.
4- Spring and autumn are the most dangerous seasons,
when the pastures are lush and young
5- the leaves of the plants contain a high concentration of
soluble proteins
B. Secondary ruminal tympany (free-gas bloat):
Physical obstruction to eructation occurs in esophageal
obstruction caused by a foreign body, by stenosis of the
esophagus, by pressure from enlargements outside the
esophagus
PATHOGENESIS:
1. Normally, gas bubbles produced in the rumen fluid
coalesce, separate from the rumen contents to form
pockets of free gas above the level of the contents, and
are finally eliminated by eructation
2. In frothy bloat, the gas bubbles remain dispersed
throughout the rumen contents
3. Most of the gas is mixed with the solid and fluid
ruminal contents to form a dense, stable froth
4. producing an abnormal increase in the volume of the
ruminoreticular contents and, consequently, inhibiting
eructation.
5. In free-gas bloat the gas bubbles coalesce and separate
from the rumen fluid but the animals cannot eructate
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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the pockets of free gas because of abnormalities of the
reticulorumen or esophagus.
CLINICAL FINDINGS:
1. Bloat is a common cause of sudden death (or found dead) in
cattle.
2. Obvious distension of the rumen occurs quickly, sometimes
as soon as 15 minutes after going on to bloat-producing
pasture
3. the animal stops grazing.
4. The distension is usually more obvious in the upper left
paralumbar fossa but the entire abdomen is enlarged.
5. There is discomfort and the animal may stand and lie down
frequently, kick at its abdomen and even roll.
6. Frequent defecation and urination are common.
7. Dyspnea is marked
8. mouth breathing, protrusion of the tongue, salivation and
extension of the head.
9. Ruminal contractions are usually increased in strength and
frequency in the early stages
10. Trocarization or the passage of a stomach tube, only small
amounts of gas are released before froth blocks the cannula
or tube.
11. In Secondary bloat Passage of a stomach tube or
Trocarization results in the release of large quantities of gas
and subsidence of the ruminal distension
DIFFERENTIAL DIAGNOSIS:
1. vagus indigestion
Medicine Lecture 4th Year 6-11-2016 Dr.Osamah Muwafk
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2. Carcinoma and papillomata of the esophageal groove and
reticulum and actinobacillosis of the reticulum
3. Animals found dead (Blackleg, lightning strike, anthrax and
snakebite)
TREATM ENT:
1) Emergency Rumenotomy
2) Trocar and cannula
3) Promote salivation (tie a stick in the mouth)
4) Stomach tube
5) Antifoaming agents
1. Poloxalene synthetic surfactants at a dose of 25-50 g
2. Any nontoxic oil, doses of up to 500 mL