ููู
ูุงุก ุญูุงุชูู ุจุงููุบุฉ ุงูุนุฑุจูุฉ
Acute lactic acidosis
โDefinition:
It is an over production of ruminal lactic acid due to
excessive consumption of highly fermented carbohydrates. It
is lethal in less than 24 hours in severe cases.
โ Etiology:
Sudden exposure to the feeds without prior adaptation, or
because of accidental access, unrestricted access to
concentrates or engorging with cereal grains as well as with
fruits, root crops, starch, soluble sugars and molasses.
โ Pathophysiology:
(1) The severity of rumen acidosis and clinical signs depend
on the amount and type of carbohydrate rich feed
consumed and the degree of prior rumen microbial
adaptation to the carbohydrate substrate. The disease may
be a mild form of indigestion or be a toxemic form, which
is difficult to be distinguished from other acute toxicities
or various diseases with endotoxemia.
(2) The first clinical signs occur 4 - 8 hours or shorter in case
of grinded grain engorgement, as rumen pH fell rapidly
under normal limit at 2-4 hours due to production of
lactic acid and thus induce more acid, ingestion and
fermentation.
(3) As the amount of concentrates or highly fermentable feed
increases, It is followed within 2-6 hours by a marked
increase in the gram positive streptococcus bovis which
multiply rapidly utilizing starch or glucose to produce
lactic acid decreasing the rumen pH and increasing rumen
fluid osmalality.
(4) As more and more lactic acid and volatile fatty acids are
produced and if sufficient substrate is available, the
rumen pH may drop to 5-5.
(5)The increased lactic acid production and rumen fluid
osmolality, inhibit or kill rumen protozoa, which normally use starch and sugar and limits the increase in lactic acid production.
(6)Lactic acid concentration usually reaches its peak within 7-24 hours after acute overeating. Thus decreased rumen pH during the first 6-8 hours of acidosis is not caused by lactic acidosis, but by an increased production of other
organic acids.
(7)Additional microbial changes include increased proportion
of coliforms and clostridium perfemgens in the rumen,
elaborating enterotoxins. The Streptococcous bovis
organisms began the lactic acid production are inhibited
below pH 4.5, leaving the Lactobacilli as the most acidresistant species, to generate more lactic acid (equal
mixture of L & D isomers of lactate).
(8)The rumen pH is lowered, the amplitude and frequency of
rumen movements are decreased and complete ruminal stasis occurs at pH of 5.
(9)The changes of rumen microflora are associated with
production of toxins, especially histamine, tyramine,
tryptamine, alcohol and endotoxins, all of these toxins
may result in further cardiac, hepatic and renal damage
and development of laminitis (due to releasing of
histamine and endotoxins as a result of bacteriolysis and
tissue degradation).
(10) The increase lactic acid and break down products of the
starch increase the rumen fluid osmolality. This inhibits
and kills some microflora and osmotically draws
extracellular fluid into the rumen causing rumen
distention and severe dehydration which leads to
circulatory impairment, decrease renal blood flow and
glomerular filtration or even anuria as well as production
of more lactic acid from cellular anaerobic metabolism.
Furthermore, lactic acid is converted to sodium lactate,
which is absorbed directly from the rumen or is passed
down the intestinal tract producing an osmotic gradient
and draws water into small intestine, contributing to the
diarrhea.
(11) Clostridium sporogenes or Bacillus thiaminolyticus are
capable o f producing thiaminase, thiaminase I and II
which breakdown thiamin, in addition, streptococci also
consume thiamin, causing a subsequent neurologic signs
of central nervous system.
(12) Ruminal buffers treat some of lactic acid but considerable
amount are absorbed through the wall of the rumen and
some are moved and absorbed from gastrointestinal tract
as a result of acidemia.
(13) Lactic acid is a strong corrosive agent and its high
concentration in the rumen destroy the rumen epithelium
โDefinition:
It is an over production of ruminal lactic acid due to
excessive consumption of highly fermented carbohydrates. It
is lethal in less than 24 hours in severe cases.
โ Etiology:
Sudden exposure to the feeds without prior adaptation, or
because of accidental access, unrestricted access to
concentrates or engorging with cereal grains as well as with
fruits, root crops, starch, soluble sugars and molasses.
โ Pathophysiology:
(1) The severity of rumen acidosis and clinical signs depend
on the amount and type of carbohydrate rich feed
consumed and the degree of prior rumen microbial
adaptation to the carbohydrate substrate. The disease may
be a mild form of indigestion or be a toxemic form, which
is difficult to be distinguished from other acute toxicities
or various diseases with endotoxemia.
(2) The first clinical signs occur 4 - 8 hours or shorter in case
of grinded grain engorgement, as rumen pH fell rapidly
under normal limit at 2-4 hours due to production of
lactic acid and thus induce more acid, ingestion and
fermentation.
(3) As the amount of concentrates or highly fermentable feed
increases, It is followed within 2-6 hours by a marked
increase in the gram positive streptococcus bovis which
multiply rapidly utilizing starch or glucose to produce
lactic acid decreasing the rumen pH and increasing rumen
fluid osmalality.
(4) As more and more lactic acid and volatile fatty acids are
produced and if sufficient substrate is available, the
rumen pH may drop to 5-5.
(5)The increased lactic acid production and rumen fluid
osmolality, inhibit or kill rumen protozoa, which normally use starch and sugar and limits the increase in lactic acid production.
(6)Lactic acid concentration usually reaches its peak within 7-24 hours after acute overeating. Thus decreased rumen pH during the first 6-8 hours of acidosis is not caused by lactic acidosis, but by an increased production of other
organic acids.
(7)Additional microbial changes include increased proportion
of coliforms and clostridium perfemgens in the rumen,
elaborating enterotoxins. The Streptococcous bovis
organisms began the lactic acid production are inhibited
below pH 4.5, leaving the Lactobacilli as the most acidresistant species, to generate more lactic acid (equal
mixture of L & D isomers of lactate).
(8)The rumen pH is lowered, the amplitude and frequency of
rumen movements are decreased and complete ruminal stasis occurs at pH of 5.
(9)The changes of rumen microflora are associated with
production of toxins, especially histamine, tyramine,
tryptamine, alcohol and endotoxins, all of these toxins
may result in further cardiac, hepatic and renal damage
and development of laminitis (due to releasing of
histamine and endotoxins as a result of bacteriolysis and
tissue degradation).
(10) The increase lactic acid and break down products of the
starch increase the rumen fluid osmolality. This inhibits
and kills some microflora and osmotically draws
extracellular fluid into the rumen causing rumen
distention and severe dehydration which leads to
circulatory impairment, decrease renal blood flow and
glomerular filtration or even anuria as well as production
of more lactic acid from cellular anaerobic metabolism.
Furthermore, lactic acid is converted to sodium lactate,
which is absorbed directly from the rumen or is passed
down the intestinal tract producing an osmotic gradient
and draws water into small intestine, contributing to the
diarrhea.
(11) Clostridium sporogenes or Bacillus thiaminolyticus are
capable o f producing thiaminase, thiaminase I and II
which breakdown thiamin, in addition, streptococci also
consume thiamin, causing a subsequent neurologic signs
of central nervous system.
(12) Ruminal buffers treat some of lactic acid but considerable
amount are absorbed through the wall of the rumen and
some are moved and absorbed from gastrointestinal tract
as a result of acidemia.
(13) Lactic acid is a strong corrosive agent and its high
concentration in the rumen destroy the rumen epithelium
giving rise to chemical rumenitis that set the stage for the development of mycotic and bacterial ruminitis in those
which survive and even diarrhea.
(14) The low rumen pH favors the growth of some yeast, fungi
and bacteria that are resistant to the high acidity. They
readily colonize the damaged sites, invade the vasculature
and causes thrombosis or spread to the liver and other
organs. Bacterial ruminitis can also results from chemical
damage and may lead to local abscess formation; diffuse
cellulitis and the access of bacteria to the portal
circulation which may lead to liver abscess.
(15) Severe acidosis and electrolyte disturbance lead to
respiratopy and circulatory disorder and even death.
Pathogenesis o f ruminal acidosis:
โClinical findings:
(1) General depression anorexia, labored breathing, cessation of rumination and ruminal movements, ruminal distension and mild bloat with presence of gurgling or splaching sound.
(2) Abdominal pain and prostration.
(3) Increase in heartbeats (100/minute) and respiratory rates
(60-90/minute)
(4) Wet pasty feces that contain undigested food and profuse
yellowish green, foamy diarrhea may be evidenced.
(5) Acute laminitis may be occur, in about 1-10% of affected cases and most common in mild and moderate cases.
(6) Nervous signs such as dropping of the head and marked depression followed by muscular tremors, incoordination.
(7) Severe dehydration cause sunken, glassy eyes with scleral
congestion dry muzzle and cold extremities.
(8) Sternal recumbency and the head may be turned into flank
with coma.
(9) In pregnant cattle, abortion may occur 10-15 days after
survive the acute phase of the disease.
(10) Some animals appear to make improvement but become
severely ill again in the 3rd or 4th day, these animals
probably have previous fungal rumenitis and death occur
3-5 days latter due to diffuse peritonitis.
(11) Rapid development of recumbency reveals unfavorable
prognosis and death may occur 24 -72 hours and
improvement during this time is best measured by fall in
heart rate, return of ruminal movement and passage of
large amount soft feces.
which survive and even diarrhea.
(14) The low rumen pH favors the growth of some yeast, fungi
and bacteria that are resistant to the high acidity. They
readily colonize the damaged sites, invade the vasculature
and causes thrombosis or spread to the liver and other
organs. Bacterial ruminitis can also results from chemical
damage and may lead to local abscess formation; diffuse
cellulitis and the access of bacteria to the portal
circulation which may lead to liver abscess.
(15) Severe acidosis and electrolyte disturbance lead to
respiratopy and circulatory disorder and even death.
Pathogenesis o f ruminal acidosis:
โClinical findings:
(1) General depression anorexia, labored breathing, cessation of rumination and ruminal movements, ruminal distension and mild bloat with presence of gurgling or splaching sound.
(2) Abdominal pain and prostration.
(3) Increase in heartbeats (100/minute) and respiratory rates
(60-90/minute)
(4) Wet pasty feces that contain undigested food and profuse
yellowish green, foamy diarrhea may be evidenced.
(5) Acute laminitis may be occur, in about 1-10% of affected cases and most common in mild and moderate cases.
(6) Nervous signs such as dropping of the head and marked depression followed by muscular tremors, incoordination.
(7) Severe dehydration cause sunken, glassy eyes with scleral
congestion dry muzzle and cold extremities.
(8) Sternal recumbency and the head may be turned into flank
with coma.
(9) In pregnant cattle, abortion may occur 10-15 days after
survive the acute phase of the disease.
(10) Some animals appear to make improvement but become
severely ill again in the 3rd or 4th day, these animals
probably have previous fungal rumenitis and death occur
3-5 days latter due to diffuse peritonitis.
(11) Rapid development of recumbency reveals unfavorable
prognosis and death may occur 24 -72 hours and
improvement during this time is best measured by fall in
heart rate, return of ruminal movement and passage of
large amount soft feces.
โTreatment:
The principle goal of therapy for acute lactic acidosis in
ruminants is to correct ruminal and systemic acidosis,
evacuation of ruminal fermented material, restore the blood
volume and electrolyte loss and to restore forestomach and
intestinal motility.
(1) Water supply should be restricted due to distension and atony of the rumen.
(2) Avoid further access to feed but use a good quality
palatable hay.
(3) IV fluid therapy with balanced electrolyte solution.
(4) Rumen lavage or purgatives in moderate cases if animals
are still standing, but are depressed with heart rate of 90 -100 beats / minute, moderate rumen distention and rumen
pH between 5.0 - 6.0
A) Rumen lavage with warm water using a stomach tube.
Water is pumped (until there is an obvious distention
of left paralumber fossa) and siphoned, 10 irrigationโs
may be required for complete rumen evacuation.
B) Purgatives: Back racking then rectal enema then 1-5
liters liquid paraffin per os and rectum, then (after 3-6
hours) 500-1000 gm magnesium sulphate (insufficient quantity of water per os) or carbcoal 1-2 ml (SC).
Avoid Mg sulphate or carbcoal in pregnancy.
(5) Oral antacids as sodium bicarbonate or magnesium
hydroxide mixed with sufficient quantity of water (to treat
local acidosis) and or IV solution of 5% sodium bicarbonate at rate of 2-5 litter for a 450 kg animals, this is
followed by I/V administration of 1.3% sodium
bicarbonates at 150 ml/kg given over the next 6 -1 2 hours
(to treat acidemia) and also oral sodium bicarbonates
(maximum oral and or IV dose of sodium bicarbonate is
Igm/KgBW).
(6) Rumenotomy and evacuation of rumen content (rinsing of
rumen with water for several times and rumen juice
transplantation of 10 - 20 litter placed in the rumen) in
severely affected cases (Animals have rumen pH of 5.0,
heart rate of more than 100 beat/minute, dehydration of 8
%, rumen distention and recumbence).
(7) Antihistaminic, thiamin and calcium borogluconate and
dextrose solution was recommended.
(8) Ionophors such as monensin, tetronasin, lasalocid & salinomycin are recently used for treatment and prevention
of rumen acidosis and increase ruminal microbial population.
The principle goal of therapy for acute lactic acidosis in
ruminants is to correct ruminal and systemic acidosis,
evacuation of ruminal fermented material, restore the blood
volume and electrolyte loss and to restore forestomach and
intestinal motility.
(1) Water supply should be restricted due to distension and atony of the rumen.
(2) Avoid further access to feed but use a good quality
palatable hay.
(3) IV fluid therapy with balanced electrolyte solution.
(4) Rumen lavage or purgatives in moderate cases if animals
are still standing, but are depressed with heart rate of 90 -100 beats / minute, moderate rumen distention and rumen
pH between 5.0 - 6.0
A) Rumen lavage with warm water using a stomach tube.
Water is pumped (until there is an obvious distention
of left paralumber fossa) and siphoned, 10 irrigationโs
may be required for complete rumen evacuation.
B) Purgatives: Back racking then rectal enema then 1-5
liters liquid paraffin per os and rectum, then (after 3-6
hours) 500-1000 gm magnesium sulphate (insufficient quantity of water per os) or carbcoal 1-2 ml (SC).
Avoid Mg sulphate or carbcoal in pregnancy.
(5) Oral antacids as sodium bicarbonate or magnesium
hydroxide mixed with sufficient quantity of water (to treat
local acidosis) and or IV solution of 5% sodium bicarbonate at rate of 2-5 litter for a 450 kg animals, this is
followed by I/V administration of 1.3% sodium
bicarbonates at 150 ml/kg given over the next 6 -1 2 hours
(to treat acidemia) and also oral sodium bicarbonates
(maximum oral and or IV dose of sodium bicarbonate is
Igm/KgBW).
(6) Rumenotomy and evacuation of rumen content (rinsing of
rumen with water for several times and rumen juice
transplantation of 10 - 20 litter placed in the rumen) in
severely affected cases (Animals have rumen pH of 5.0,
heart rate of more than 100 beat/minute, dehydration of 8
%, rumen distention and recumbence).
(7) Antihistaminic, thiamin and calcium borogluconate and
dextrose solution was recommended.
(8) Ionophors such as monensin, tetronasin, lasalocid & salinomycin are recently used for treatment and prevention
of rumen acidosis and increase ruminal microbial population.
๐1
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ูุงุถูุน ุจุงููุบุฉ ุงูุฅููููุฒูุฉุ
ูุณุชู ุฑ ุจุงูุงููููุฒู๐
ููุท ุนุฑุจู๐
ุนุฑุจู+ ุงููููุฒู๐
ูุณุชู ุฑ ุจุงูุงููููุฒู๐
ููุท ุนุฑุจู๐
ุนุฑุจู+ ุงููููุฒู๐
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ุฐููุฑ ูุงูุงุซ ูุตุบุงุฑ ุจุนุถ ุงูุญููุงูุงุช
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ููุฐุงูู ูุญุต ุงูุทููููุงุช ุงูุฎุงุฑุฌูู ูุงููุซูุฑ...
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