ูู ู
ุงุชุฑูุฏ ุงู ุชุนุฑูุฉ ุนู ุงูู
ุบุต ูู ุงูุฎููู
Aspiration pneumonia
โEtiology:
Inappropriate administration of therapeutic agents is a common cause of aspiration pneumonia in large animals and less common in dogs and cats. Liquids given by drench or dose syringe should not be delivered faster than the animal can swallow. Drenching is particularly dangerous when the animalโs tongue is drawn out, when the head is held high, or when the animal is coughing or bellowing.
In sheep, poor dipping technique with repeated immersion of the animalโs head may cause aspiration of fluid. Calves and lambs may inhale inflammatory debris if affected with diphtheritic stomatitis/laryngitis. The muscles of deglutition may be affected in lambs with nutritional myopathy. Pigs fed fine particulate food in dry environments may inhale feed granules. Aspiration pneumonia in cattle after treatment for milk fever is usually fatal. Cervids affected with chronic wasting disease may develop aspiration pneumonia due to CNS dysfunction. In dogs and less frequently in cats, aspiration pneumonia is generally associated with inhalation of oral ingesta, regurgitated material, or vomitus. Common risk factors for dogs and cats include pharyngeal abnormalities (cricopharyngeal motor dysfunction), esophageal diseases (megaesophagus, gastroesophageal reflux disease, esophageal obstruction), weakened clinical condition, and anesthesia or heavy sedation. Bacteria in aspirated material may initiate acute infection or secondary infection later in disease.
โ Clinical Findings:
A history suggesting recent foreign body aspiration within the past 1โ2 days is of greatest value for a diagnosis of aspiration pneumonia. Affected animals separate from the rest of the group and present with pyrexia 104ยฐโ105ยฐF (40ยฐโ40.5ยฐC), a painful expression, arched back, inappetance, depression, toxic mucous membranes, and an increased respiratory rate (>40โ60 breaths/min) with a shallow abdominal component. This is often associated with a purulent nasal discharge that sometimes is tinged reddish brown or green. Milk yield is greatly reduced to zero in lactating animals. Thoracic auscultation reveals reduced lung sounds over affected consolidated lung, with increased breath sounds over normal lung. In cows that aspirate ruminal contents as a consequence of becoming cast with hypocalcemia, toxemia is usually fatal within 1โ2 days.
Superficial consolidated lung and overlying lesions of fibrous pleurisy can readily be identified on ultrasound examination using either linear or sector probes connected to 5-MHz machines; pleuritic friction rubs are not audible on auscultation. In dogs and cats, clinical signs may be peracute, acute, or chronic. Cough, dyspnea, tachypnea, or exercise intolerance are seen most frequently. Thoracic radiographs generally show a bronchoalveolar pattern in gravity-dependent ventral lung lobes (right cranial and middle and left cranial lobes); however, radiographic changes may not be seen until 24 hr after acute aspiration.
โ Lesions:
Aspiration pneumonia is usually in the anteroventral parts of the lung; it may be unilateral in animals in which lateral recumbency was the cause of aspiration, or bilateral and centered on airways. In early stages, the lungs are markedly congested with areas of interlobular edema. Bronchi are hyperemic and full of froth. The pneumonic areas tend to be cone-shaped, with the base toward the pleura. Suppuration and necrosis follow. The foci become soft or liquefied, reddish brown, and foul smelling. There usually is an acute fibrinous pleuritis, often with pleural exudate. Animals that survive develop chronic abscesses and fibrous adhesions between the visceral and parietal pleura.
โEtiology:
Inappropriate administration of therapeutic agents is a common cause of aspiration pneumonia in large animals and less common in dogs and cats. Liquids given by drench or dose syringe should not be delivered faster than the animal can swallow. Drenching is particularly dangerous when the animalโs tongue is drawn out, when the head is held high, or when the animal is coughing or bellowing.
In sheep, poor dipping technique with repeated immersion of the animalโs head may cause aspiration of fluid. Calves and lambs may inhale inflammatory debris if affected with diphtheritic stomatitis/laryngitis. The muscles of deglutition may be affected in lambs with nutritional myopathy. Pigs fed fine particulate food in dry environments may inhale feed granules. Aspiration pneumonia in cattle after treatment for milk fever is usually fatal. Cervids affected with chronic wasting disease may develop aspiration pneumonia due to CNS dysfunction. In dogs and less frequently in cats, aspiration pneumonia is generally associated with inhalation of oral ingesta, regurgitated material, or vomitus. Common risk factors for dogs and cats include pharyngeal abnormalities (cricopharyngeal motor dysfunction), esophageal diseases (megaesophagus, gastroesophageal reflux disease, esophageal obstruction), weakened clinical condition, and anesthesia or heavy sedation. Bacteria in aspirated material may initiate acute infection or secondary infection later in disease.
โ Clinical Findings:
A history suggesting recent foreign body aspiration within the past 1โ2 days is of greatest value for a diagnosis of aspiration pneumonia. Affected animals separate from the rest of the group and present with pyrexia 104ยฐโ105ยฐF (40ยฐโ40.5ยฐC), a painful expression, arched back, inappetance, depression, toxic mucous membranes, and an increased respiratory rate (>40โ60 breaths/min) with a shallow abdominal component. This is often associated with a purulent nasal discharge that sometimes is tinged reddish brown or green. Milk yield is greatly reduced to zero in lactating animals. Thoracic auscultation reveals reduced lung sounds over affected consolidated lung, with increased breath sounds over normal lung. In cows that aspirate ruminal contents as a consequence of becoming cast with hypocalcemia, toxemia is usually fatal within 1โ2 days.
Superficial consolidated lung and overlying lesions of fibrous pleurisy can readily be identified on ultrasound examination using either linear or sector probes connected to 5-MHz machines; pleuritic friction rubs are not audible on auscultation. In dogs and cats, clinical signs may be peracute, acute, or chronic. Cough, dyspnea, tachypnea, or exercise intolerance are seen most frequently. Thoracic radiographs generally show a bronchoalveolar pattern in gravity-dependent ventral lung lobes (right cranial and middle and left cranial lobes); however, radiographic changes may not be seen until 24 hr after acute aspiration.
โ Lesions:
Aspiration pneumonia is usually in the anteroventral parts of the lung; it may be unilateral in animals in which lateral recumbency was the cause of aspiration, or bilateral and centered on airways. In early stages, the lungs are markedly congested with areas of interlobular edema. Bronchi are hyperemic and full of froth. The pneumonic areas tend to be cone-shaped, with the base toward the pleura. Suppuration and necrosis follow. The foci become soft or liquefied, reddish brown, and foul smelling. There usually is an acute fibrinous pleuritis, often with pleural exudate. Animals that survive develop chronic abscesses and fibrous adhesions between the visceral and parietal pleura.
โPrevention and Treatment:
Broad-spectrum antibiotics should be used in animals known to have inhaled a foreign substance without waiting for signs of pneumonia to appear; however, this rarely occurs in farm animals presented with severe clinical signs. A transtracheal wash can help identify the causative agent for which an antibiotic sensitivity can be obtained. Care and supportive treatment include NSAIDs such as flunixin meglumine. In small animals, oxygen therapy can be useful. Saline nebulization and coupage may assist with generating a productive cough to facilitate clearance of the aspirated material. Despite all treatments, prognosis is poor, and efforts must be directed at prevention.
Broad-spectrum antibiotics should be used in animals known to have inhaled a foreign substance without waiting for signs of pneumonia to appear; however, this rarely occurs in farm animals presented with severe clinical signs. A transtracheal wash can help identify the causative agent for which an antibiotic sensitivity can be obtained. Care and supportive treatment include NSAIDs such as flunixin meglumine. In small animals, oxygen therapy can be useful. Saline nebulization and coupage may assist with generating a productive cough to facilitate clearance of the aspirated material. Despite all treatments, prognosis is poor, and efforts must be directed at prevention.
ููู
ูุ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
ุดูู ุฑุงููู
ุจูุดุฑ ุงูู
ูุงุถูุน ุจุงููุบุฉ ุงูุฅููููุฒูุฉุ
ูุณุชู ุฑ ุจุงูุงููููุฒู๐
ููุท ุนุฑุจู๐
ุนุฑุจู+ ุงููููุฒู๐
ูุณุชู ุฑ ุจุงูุงููููุฒู๐
ููุท ุนุฑุจู๐
ุนุฑุจู+ ุงููููุฒู๐
ุงุณู
ุฐููุฑ ูุงูุงุซ ูุตุบุงุฑ ุจุนุถ ุงูุญููุงูุงุช