Diseases of the Alimentary Tract

• The primary functions of the alimentary tract

are the
– prehension, mastication, digestion and
absorption of food and water and
– the maintenance of the internal environment by
modification of the amount and nature of the
materials absorbed.
• there are four major modes of alimentary
dysfunction.
• abnormality of
– motility,
– secretion,
– digestion or
– absorption
• The procedure in diagnosis should be to determine which
mode or modes of function are disturbed before
proceeding to the determination of the site and nature of
the lesion and ultimately of the specific cause.
HYPERMOTILITY AND HYPOMOTILITY
• The peristaltic movements that move ingesta
from the esophagus to the rectum,
• The segmentation movements that churn and
mix the ingesta,
• Important in
– Prehension, mastication and swallowing
– move ingesta from the esophagus to the rectum
– Churning of ingesta,
– Eructation of ruminal gases
• Abnormal motor function may take the form
of increased or decreased motility.
• Motility depends upon stimulation via the
sympathetic and parasympathetic nervous
systems
• Autonomic imbalance,
• Debility, accompanied by weakness of the
musculature, or severe inflammation (e.g.
peritonitis, after trauma) or infarction, results in
atony of the intestinal wall.
• Less severe inflammation (gastritis, enteritis) may
result in an increase in muscular activity and
increased propulsive activity.
• Increased motility causes diarrhea, decreased
motility causes constipation, and both have
deleterious effects on digestion and absorption.
DISTENSION
• result of abnormality of motility
• the rapid accumulation or inefficient expulsion of
gas,
• complete occlusion of the lumen by intestinal
accident or pyloric or ileocecal valve obstruction,
• engorgement on solid or liquid feeds.
• Fluids, and to a lesser extent gas, accumulate
because of their failure to pass along the tract.
• Much of the accumulated fluid represents saliva
and gastric and intestinal juices secreted during
normal digestion.
Distension cont’d

• causes pain and, reflexly, increased spasm and

motility of adjoining gut segments.
• stimulates further secretion of fluid into the
lumen of the intestine and this exaggerates
the distension.
• If the distension gets severe, the initial pain
disappears, and a state of paralytic ileus
develops in which all muscle tone is lost.
DIARRHEA
• the increased frequency of defecation
accompanied by feces that contain an increased
concentration of water and decrease in dry
matter content.
• the total amount of feces passed and frequency
of defecation per day is increased.
• The consistency of the feces varies from soft to
liquid.
• when there is a general increase in peristaltic
activity there is increased caudal flow, resulting
in a decrease in intestinal transit time and
diarrhea.
Common causes of diarrhea are:
• Enteritis, including secretory enteropathy
• Malabsorption,
• Neurogenic diarrhea as in excitement
• Local structural lesions of the stomach or
intestine, including:
– ulcer, e.g. of the abomasum or stomach
– tumor, e.g. intestinal adenocarcinoma
Causes of diarrhea cont’d
• Indigestible diet, e.g. lactose intolerance in
foals
• Carbohydrate engorgement in cattle
• Terminal stages of congestive heart failure
(visceral edema)
 Principles of treatment in alimentary tract disease

• Removal of the primary cause of the disease is

essential
• supportive and symptomatic treatment.
– relieving pain and distension,
– replacement of fluids and electrolytes,
– correcting abnormal motility and-relieving
tenesmus and
– reconstitution of the digestive flora if necessary.
RELIEF OF ABDOMINAL PAIN

• of prime importance from the humane aspect,

• to prevent the animal from self-injury,
• Non-narcotic and narcotic analgesics are in
general use.
RELIEF OF DISTENSION
• a critical principle in order to minimize shock and
to prevent rupture of the viscus.
• Relief of distension of the stomach of the horse
with colic is accomplished by nasogastric
intubation.
• Distension due to bloat in cattle can be relieved
by stomach tube or trocarization of the rumen.
• with the use of laxatives and purgatives when
there is accumulation of ingesta without a
physical obstruction.
Relief of distension cont’d
• intestinal or gastric accidents require surgical
correction

• In functional distension (paralytic ileus), relief

of the atony or spasm can be effected by the
use of drugs such as metoclopramide.
REPLACEMENT OF FLUIDS AND ELECTROLYTES
• it is necessary to replace lost fluids and
electrolytes by the parenteral
administration of large quantities of
isotonic glucose-saline or other
physiologically normal electrolyte solutions.
– In gastric or intestinal obstruction, or
– when diarrhea is severe,
CORRECTION OF ABNORMAL MOTILITY
• INCREASED MOTILITY
• Administration of atropine or other
spasmolytics such as dipyrone or
proquamezine
– disappearance of the abdominal pain and a
diminution of fluid loss
• Meperidine, butorphanol and pentazocine
inhibit regular cyclic myoelectric activity in the
jejunum
Correction of abnormal motility cont’d
• DECREASED MOTILITY
• parasympathomimetic drugs or purgatives,
usually combined with an analgesic.
• Prokinetic drugs such as metoclopramide
hydrochloride and cisapride monohydrate
increase the movement of ingesta through the
gastrointestinal tract.
– They are useful because they induce coordinated
motility patterns.
Correction of abnormal motility cont’d
• RELIEF OF TENESMUS
• Tenesmus can be difficult to treat effectively.
• Long-acting epidural anesthesia and sedation
are in common use.
• Combinations of xylazine and lidocaine may
be used.
• Irrigation of the rectum with water and the
application of topical anesthetic in a jelly-like
base are also used.
RECONSTITUTION OF RUMEN FLORA AND CORRECTION OF
ACIDITY OR ALKALINITY
• When prolonged anorexia or acute indigestion
occurs in ruminants, the rumen flora may be
seriously reduced.
• the reconstitution of the flora can be
hastened by the oral administration of a
suspension of ruminal contents from a normal
cow, or of dried ruminal contents, which
contain viable bacteria and yeasts and the
substances necessary for growth of the
organisms.
• hyperacidity or hyperalkalinity, should be
corrected by the administration of alkalinizing
or acidifying drugs
 STOMATITIS
• Stomatitis is inflammation of the oral mucosa
– includes glossitis (inflammation of the tongue),
palatitis (lampas)(inflammation of the palate) and
gingivitis (inflammation of the mucosa of the gums).
• Clinically it is characterized by
– partial or complete loss of appetite,
– smacking of the lips and
– profuse salivation
• It is commonly an accompaniment of systemic
disease.
• ETIOLOGY
– Stomatitis may be caused by physical, chemical or
infectious agents
 Etiology of stomatitis
• Infectious agents
• Cattle
• Oral necrobacillosis associated with
Fusobacterium necrophorus
• Actinobacillosis of the bovine tongue
• Stomatitis with vesicles occurs in foot-and-mouth
disease and in vesicular stomatitis
• Erosive, with some secondary ulcerative,
stomatitis occurs in bovine viral diarrhea (mucosal
disease), bovine malignant catarrh, rinderpest and
rarely in bluetongue.
Etiology of stomatitis cont’d
• Sheep
– Erosive lesions in bluetongue, rinderpest and
peste de petits ruminantes (PPR)
– Vesicular lesions rarely in foot and mouth disease
– contagious ecthyma especially in young lambs.
Etiology of stomatitis cont’d
• Horses
• Cheilitis and gingivitis (inflammatory nodules of
the lips and gums caused by plant awns)
• Vesicular lesions in vesicular stomatitis
• Herpesvirus infections
• Lingual abscess associated with Actinobacillus spp.
• Pigs
• The vesicular diseases: foot and mouth disease,
vesicular stomatitis, vesicular exanthema of swine
and swine vesicular disease.
PATHOGENESIS

• The clinical signs of stomatitis are caused by

the inflammation or erosion of the mucosa
and the signs vary in severity with the degree
of inflammation.
CLINICAL FINDINGS
• Partial or complete anorexia and
• Slow, painful mastication.
• Chewing movements and smacking of the lips are
accompanied by salivation,
– either frothy and in small amounts, or profuse and
drooling if the animal does not swallow normally.
• A fetid odor is present on the breath
– only if bacterial invasion of the lesion has occurred.
• Enlargement of local lymph nodes
• Swelling of the face
CLINICAL PATHOLOGY

• Examination for Bacteria and fungi

TREATMENT
• frequent application of a mild antiseptic
– such as a 2% solution of copper sulfate, a 2 % suspension
of borax or a 1 % suspension of a sulfonamide in glycerin.
• In all cases, soft, appetizing food should be
offered and
• feeding by stomach tube or IV alimentation
may be resorted to in severe, prolonged
cases.
 PHARYNGITIS
• inflammation of the pharynx
• characterized clinically by
– coughing
– painful swallowing
– a variable appetite
– Regurgitation through the nostrils and drooling of
saliva may occur in severe cases
ETIOLOGY
• in farm animals is usually traumatic
• Infectious pharyngitis is often part of a
syndrome with other more obvious signs
• Physical causes
• Injury
• irritant or hot or cold substances
• Foreign bodies,
– including grass and cereal awns, wire, bones
Etiology cont’d
• Infectious causes
• Cattle
– Oral necrobacillosis,
– Actinobacillosis as a granuloma
– Infectious bovine rhinotracheitis
Etiology cont’d
• Horses
• As part of strangles or anthrax
• Viral infections of the upper respiratory tract,
including equine herpesvirus-I, parainfluenza
virus, adenovirus, rhinovirus, viral arteritis,
influenza 1A/E1 and 1A/E2
• Chronic follicular pharyngitis
• Pigs
• As part of anthrax and in some outbreaks of
Aujeszky's disease
PATHOGENESIS
• Painful swallowing and disinclination to eat
• If the swelling of the mucosa and wall is
severe, there may be virtual obstruction of
the pharynx.
– especially so if the retropharyngeal lymph node is
enlarged.
CLINICAL FINDINGS
• The animal may refuse to eat or drink or
• it may swallow reluctantly and with evident pain.
• Opening of the jaws to examine the mouth is
resented and
• manual compression of the throat from the
exterior causes paroxysmal coughing.
• There may be a mucopurulent nasal discharge,
sometimes containing blood,
• spontaneous cough and, in severe cases,
regurgitation of fluid and food through the
nostrils.
Clinical findings cont’d
• Extended head, drooling of saliva and frequent
tentative jaw movements
• Severe toxemia may accompany the local lesions
• there may be obstruction of respiration and
visible swelling of the throat
• The retropharyngeal and parotid lymph nodes
are commonly enlarged
• a purulent exudate may be seen on the
pharyngeal mucosa and in the nostrils.
• Affected horses cough persistently, especially
during exercise, are dyspneic and tire easily.
• Guttural pouch infections may occur secondarily
TREATMENT

• The primary disease must be treated, usually

parenterally, by the use of antimicrobials.
 ESOPHAGITIS

• Inflammation of the esophagus

• accompanied initially by
– spasm and obstruction,
– pain on swallowing and palpation, and
– regurgitation of bloodstained, slimy
material
ETIOLOGY
• Primary esophagitis
– caused by the ingestion of chemical or physical
irritants
– usually accompanied by stomatitis and pharyngitis.
– Laceration of the mucosa by a foreign body or
complications of nasogastric intubation may occur.
• occurs commonly in many specific diseases,
particularly those that cause stomatitis,
– clinical signs of the diseases dominate those of
esophagitis.
PATHOGENESIS
• a functional obstruction and difficulty in
swallowing.
• Perforation of the thoracic esophagus can
result in severe and fatal pleuritis.
CLINICAL FINDINGS
• Salivation and attempts to swallow
• Severe pain, particularly in horses
• In some cases, attempts at swallowing are
followed by regurgitation and coughing, pain,
retching activities and vigorous contractions
of the cervical and abdominal muscles
• Marked drooling of saliva, grinding of the
teeth
• Coughing and profuse nasal discharge
Clinical findings cont’d

• Regurgitation may occur and the regurgitus

contains mucus and some fresh blood
• If the esophagitis is in the cervical region,
palpation in the jugular furrow causes pain
and edematous tissues around the esophagus
may be palpable
• If perforation has occurred, there is local pain
and swelling and often crepitus
• CLINICAL PATHOLOGY
– a marked neutrophilia may occur,
suggesting active inflammation

• NECROPSY FINDINGS
– Pathological findings pertaining to the
various specific diseases
– In traumatic lesions
• gross edema, inflammation and, in some cases,
perforation
TREATMENT
• Feed should be withheld for 2-3 days and
• Fluid and electrolyte therapy may be
necessary for several days
• Parenteral antimicrobials
• Reintroduction to feed should be monitored
carefully and all feed should be moistened
 ESOPHAGEAL OBSTRUCTION
• may be acute or chronic
• characterized clinically by:
– inability to swallow
– regurgitation of feed and water
– continuous drooling of saliva, and
– bloat in ruminants
ETIOLOGY
• May be intraluminal by swallowed material or
• Extraluminal due to pressure on the
esophagus by surrounding organs or tissues

– Esophageal paralysis may also result in

obstruction.
Intraluminal obstructions
• due to ingestion of materials:
– Solid obstructions, especially in cattle by
mangoes, potatoes, peaches, apples, oranges,
corncob etc.
• The most common type of esophageal
obstruction in horses is simple obstruction
due to impaction of ingesta
• Extraluminal obstructions
– Tuberculous or neoplastic lymph nodes in the
mediastinum or at the base of lung
– Cervical or mediastinal abscess
– Persistent right aortic arch
• Esophageal paralysis
– This may be due to congenital or acquired
abnormalities of the esophagus
• Megaesophagus
– dilatation and atony of the body of the esophagus
• Esophageal strictures
– as a result of cicatricial or granulation tissue
deposition
• Other causes of obstruction include
– Carcinoma of stomach and squamous cell
carcinoma of the esophagus of a horse
PATHOGENESIS
• a physical inability to swallow
• in cattle, inability to eructate with resulting
bloat
• Complications of esophageal obstruction
include laceration and rupture of the
esophagus, esophagitis, stricture and stenosis,
and the development of a diverticulum.
CLINICAL FINDINGS
• Acute obstruction or choke
– Cattle
• The animal suddenly stops eating
• shows anxiety and restlessness
• forceful attempts to swallow and regurgitate,
• salivation
• coughing
• continuous chewing movements
• If obstruction is complete, bloating occurs
rapidly
Clinical findings, cattle cont’d
• Ruminal movements are continuous and
forceful
• Passage of a nasogastric tube is impossible
• Persistent obstruction causes pressure
necrosis of the mucosa and may result in
perforation or subsequent stenosis due to
fibrous tissue
Clinical findings cont’d
• Horse
– Vary with the location, nature, extent and
duration of the obstruction.
– dysphagia with nasal reflux of saliva, feed and
water.
– Stop further eating but will drink and attempt to
swallow water
Clinical findings cont’d
• External palpation of the cervical esophagus
may reveal a firm cylindrical swelling along the
course of the neck on the left side when the
esophagus is obstructed with feed
• Horses are commonly difficult to handle
because they are panicky and make forceful
attempts to swallow or retch
• They may vigorously extend and flex their
necks and stamp their front feet
Clinical findings cont’d
• May sweat profusely,
• tachycardia may be present and
• they may appear to be in abdominal pain.
• attempted passage of a nasogastric tube as
part of the examination of a horse with colic
reveals the obstruction
• The level of obstruction can be approximated
by the amount of tube that has been passed.
Clinical findings cont’d
• In foals the clinical findings include
– nasal reflux of saliva, feed and milk,
– reluctance to eat solid feed and
– dyspnea if aspiration pneumonia has
occurred
• Chronic obstruction
• In cattle
– Chronic bloat,
– Rumen contractions may be within the
normal range
– Swallowing movements are usually normal
until the bolus reaches the obstruction,
when they are replaced by more forceful
movements
Complications following esophageal obstruction

• most common in the horse and include

– esophagitis,
– mucosal ulceration in long-standing cases,
– esophageal perforation and
– aspiration pneumonia
CLINICAL PATHOLOGY
• radiographic examination
• endoscopy
TREATMENT
Conservative approach
• Many obstructions will resolve spontaneously
and a careful conservative approach is
recommended.
– Sedation
• In acute obstruction, if there is marked
anxiety and distress, the animal should
be sedated before proceeding with
specific treatment
• Acepromazine
• Xylazine
• Detomidine
• Romifidine
• Pass a stomach tube and allow object to move
into stomach.
• in the horse it is suggested that conservative
measures, principally sedation, waiting and
lavaging the esophagus, be continued for
several hours before attempting radical
procedures.
• Manual removal through oral cavity in cattle
• Solid obstructions in the upper esophagus of
cattle may be reached by passing the hand
into the pharynx with the aid of a speculum
and having an assistant press the foreign body
up towards to the mouth. In cattle it may be
necessary to trocarize the rumen and leave
the cannula in place until the obstruction is
relieved.
• General anesthesia in the horse
• In horses, attempts to manually remove solid
obstructions from the cranial portion of the
esophagus require a general anesthetic, a
speculum in the mouth and a manipulator
with a small hand.
• The fauces are much narrower in the horse
than in the cow and it is only with difficulty
that the hand can be advanced through the
pharynx to the beginning of the esophagus.
• Esophageal lavage in the horse
• Accumulations of feedstuffs, which occur
most commonly in the horse, can be removed
by careful lavage or flushing of the obstructed
esophagus.
• Surgical removal of foreign bodies
– Surgical removal by esophagostomy may be
necessary if other measures fail.
– Gastrotomy may be necessary to relieve
obstructions of the caudal portion of the
esophagus adjacent to the cardia.
 EQUINE COLIC (ADULT HORSES)
• Gastrointestinal disease causing signs of
abdominal pain in horses is commonly
referred to as colic.
• Colic is a frequent and important cause of
death
• Considered the most important disease of
horses encountered by practicing
veterinarians
ETIOLOGY of equine colic
• Several classification systems of equine colic
have been described including a disease-
based system classifying the cause of colic as:
– Obstructive
– Obstructive and strangulating
– Nonstrangulating infarctive
– Inflammatory (peritonitis, enteritis)
• Colic cases can also be classified on the basis
of the duration of the disease:
– acute (24-36 h),
– chronic (> 24-36 h) and
– recurrent (multiple episodes separated by periods
of > 2 days of normality).
• Horses with acute transient colic relieved by
analgesics are often referred to as having
spasmodic colic.
– Spasmodic or gas colic was the cause of 35% of
horses with colic examined in the field by
veterinarians. Large -colon impaction (20%) and
undiagnosed (13%) were the other largest
diagnostic categories.
 EPIDEMIOLOGY
• Occurs Worldwide
• The case fatality rate is 6-13%.
• Death due to colic accounts for 28% of all
horse deaths.
• Age, sex, breed, management, watering,
housing, exercise, and weather/climate may
affect the occurrence and type of colic.
• Colic may be associated with tapeworms,
cyathostomes and/or large strongyles
PATHOGENESIS
• The features common to severe colic are
– pain
– gastrointestinal dysfunction
– intestinal ischemia
– endotoxemia
– compromised cardiovascular function (shock) and
metabolic abnormalities
• Pain
• Pain is the hallmark of gastrointestinal disease
in horses
• attributable to distension of the
gastrointestinal tract and stimulation of
stretch receptors in the bowel wall and
mesentery, stretching of mesentery by
displaced or entrapped bowel, and
inflammation and irritation of the bowel,
peritoneum or mesentery.
• Gastrointestinal pain has an inhibitory effect
on normal gastrointestinal function,
– the pain inhibits normal gut motility and function,
allowing accumulation of ingesta and fluid,
resulting in distension and further pain.
• Horses can respond very violently to
abdominal pain and may injure themselves
when rolling or thrashing.
Gastrointestinal dysfunction
• Colic is almost invariably associated with
impaired gastrointestinal function,
– usually alterations to motility or absorptive
function.
– Gastrointestinal motility
• may be increased, as is presumed to be the case in
spasmodic colic,
• altered in its character or coordination, as in some cases
of impaction colic, or
• absent, such as in ileus secondary to inflammation or
ischemia of the bowel or to the presence of
endotoxemia.
• Increased or uncoordinated gastrointestinal
motility probably causes pain through
excessive contraction of individual segments
of bowel or distension of bowel because of
the loss of normal propulsive activity.
• Ileus is associated with fluid distension of the
small intestine and stomach and fluid and gas
distension of the large colon, both of which
cause severe pain and can lead to gastric or
colonic rupture.
• The absorptive function of the intestine may
be decreased by inflammation or ischemia,
which results in
– distension of the small intestine or large colon,
– pain and
– potentially rupture of the stomach or colon.
• Impairment of the barrier function of the
gastrointestinal mucosa by inflammation or
ischemia can result in leakage of endotoxin
and endotoxemia.
Ischemia of the intestinal wall
• most forms of lethal colic involve some degree
of ischemia of the intestine,
• with subsequent loss of barrier function,
evident in its most extreme form as rupture of
the viscus, endotoxemia, bacteremia,
cardiovascular collapse and death.
• Ischemia may be the result of, impaired blood
flow to or from the intestine
– because of torsion, volvulus of the intestine,
hernias, strangulation
• Ischemia may also result from severe
gastrointestinal distension,
• Mild ischemia probably impairs normal
intestinal motility and function.
Endotoxemia
• When the affected viscus ruptures secondary
to distension, or
• When ischemia and/or infarction damages a
segment of bowel wall (barrier function),
– Endotoxemia is due to the absorption of
endotoxins from the peritoneum or the gut lumen
into the systemic circulation.
Shock (compromised CV function)
• The usual cause of death in severe colic is
cardiovascular collapse secondary to
endotoxemia and hypovolemia.
• Hypovolemia
– is due to the loss of fluid and electrolytes into the
lumen of the gastrointestinal tract or loss of
protein from the vascular space
– Hypovolemia impairs venous return to heart and
therefore cardiac output, arterial blood pressure
and oxygen delivery to tissues
• Measures of circulatory status are good
predictors of the outcome of colic.
• Cardiorespiratory function is impaired if there
is severe distension of gut, because of
restricted respiration by pressure on the
diaphragm and reduced venous return to the
heart because of pressure on the caudal vena
cava.
Overview of the pathogenesis of common
colics
• Simple obstructive
– there is obstruction to the passage of ingesta but
no ischemia or strangulation of bowel.
– In the terminal stages there is often ischemia
caused by distension of the intestine.
Obstructive and strangulating
• Diseases that cause both obstruction and
strangulation as an initial event,
– such as torsion of the small intestine or volvulus of the
large colon,
– result in severe and unrelenting pain that is little relieved
with analgesics.
– Obstruction causes distension and strangulation causes
ischemia, loss of barrier function and endotoxemia.
– These diseases have a short course, usually less than 24 hours
and sometimes as short as 6 hours, and profound clinical signs.
– Endotoxemia and cardiovascular collapse are characteristic of
these diseases.
Infarctive
• Infarctive diseases, such as thromboembolic
colic, are characterized by ischemia of the
intestinal wall with subsequent alterations in
motility and absorptive and barrier functions.
– Ileus causes distension of the intestines and
stomach and altered barrier function causes
endotoxemia.
– The course of the disease is usually less than 48
hours and is terminated by cardiovascular collapse
and death.
Inflammatory
• Inflammation of the intestine or peritoneum
alters gastrointestinal motility and absorptive
function leading to accumulation of fluid and
ingesta, distension and abdominal pain.
 Clinical findings
• Visual examination
• Behavior
– Pain is manifested by pawing, stamping or kicking
at the belly or by restlessness, pacing in small
circles, repeatedly getting up and lying down,
– looking or nipping at the flank, rolling, and lying
on the back.
– Often the penis is protruded without urinating or
with frequent urination of small volumes.
– Continuous playing with water without actually
drinking (sham drinking) is common.
• Horses in the terminal phase of the disease
may have a marked diminution of pain
associated with relief of pressure after
rupture of distended bowel and depression
caused by toxemia and shock.
• a horse that goes down and rolls almost
certainly has alimentary tract colic.
Posture
• the horse stands stretched out with the
forefeet more cranial and the hindfeet more
caudal than normal - the so- called 'saw-horse'
stance.
• Some horses lie down on their backs with
their legs in the air suggesting a need to
relieve tension on the mesentery.
Abdomen size
• Distension of the abdomen is an uncommon
but important diagnostic sign.
• Symmetrical, severe distension is usually
caused by distension of the colon, sometimes
including the cecum.
• asymmetrical enlargement in the right
sublumbar fossa- If only the cecum is distended
• Maximum distension of stomach or small
intestines does not cause appreciable
distension of the abdomen.
Vomiting
• Projectile vomiting or regurgitation of
intestinal contents through the nose is very
unusual in the horse and is a serious sign
suggesting severe gastric distension and
impending rupture.
Defecation and feces
• in the very early stages of acute intestinal
obstruction there may be normal feces in the
rectum, and the animal may defecate several
times before the more usual sign of an empty
rectum with a sticky mucosa is observed.
Physical examination
• Heart and respiratory rates
• The heart rate is a useful indicator of the
severity of the disease and its progression
– heart rates less than 40/min indicate mild disease
– heart rates above 120/min usually indicate
terminal stages of severe disease
• The respiratory rate is variable and may be as
high as 80/min during periods of severe pain.
Mucous membranes and extremities
• Mucous membranes of normal horses are
pink, moist and regain their normal color
within 2 seconds
• Dehydrated horses have dry mucous
membranes, although the capillary refill time
and color are normal.
• Horses with impaired cardiovascular function
have pale, dry mucous membranes with
delayed capillary refill (> 2 s).
• Endotoxemic horses will often have bright red
mucous membranes with normal or delayed
capillary refill.
• As the disease becomes more severe the mucous
membranes develop a bluish tint and capillary
refill is longer than 3 seconds.
• Terminal stages of disease are associated with
cold, purple, dry mucous membranes with a
capillary refill time of more than 3 seconds;
• necrosis of the mucosa of the gingival margins of
the gums, the so called 'toxic line', is often seen.
• Cool extremities may be indicative of
compromised cardiovascular function but
should be interpreted with caution and only in
the context of the rest of the clinical
examination.
• Sweating is common in horses with severe
abdominal pain and, when present in a horse
with cool extremities and signs of
cardiovascular collapse, is indicative of a poor
prognosis.
Auscultation; percussion
• Auscultation
• diagnostic and prognostic information
• All four quadrants (dorsal and ventral, left and
right sides) of the abdomen should be
examined for at least 1 minute at each site.
• Attention should be paid to the intensity,
frequency and characteristics of the
spontaneous gut sounds (borborygmi).
• Continuous, loud borborygmi distributed in
all or most quadrants are indicative of
intestinal hypermotility and consistent with
spasmodic colic, impending diarrhea or the
very early stages of a small-intestinal
obstructive strangulating lesion.
• The absence of sounds, or the presence of
occasional high-pitched, brief sounds,
sometimes with a splashing character, is
consistent with ileus.
Rectal examination
• Probably the most important part of the
clinical examination in colic and should not be
neglected.
• Abnormal findings- detected by rectal palpation
– One should be able to recognize gas and fluid
distension of the cecum and colon, fluid
distension of the small intestine, impaction of the
large and small colon, and displacement of the
large colon. Impaction is evident as columns of
firm ingesta in the large or small colon.
• Nasogastric intubation
– Passage of a nasogastric tube is an essential part
of the examination of a horse with colic because
of the diagnostic information it provides and
because relief of gastric distension may be life-
saving.
CLINICAL PATHOLOGY
• Increases in both hematocrit and total protein
concentration
• Plasma total protein concentrations may
decline
• Leukopenia and a left shift are consistent with
the endotoxemia
• abnormalities in coagulation
• Most horses with severe colic have metabolic
acidosis
• Abdominocentesis
• Analysis of peritoneal fluid is an important
component of the complete examination of a
horse with colic.
– there is an increase in the total protein
concentration,
– a change in the color to red or blood-tinged, and
– an increase in the leukocyte count in peritoneal
fluid,
DIFFERENTIAL DIAGNOSIS
• The following diseases may be mistaken for
colic:
– Laminitis, Pleuritis, Enterocolitis, Obstructive
urolithiasis, Uroperitoneum, Foaling and dystocia,
Uterine torsion, Peritonitis, Cholelithiasis,
Ovulation and ovarian pain, Esophageal
obstruction, Anterior enteritis, Gastric ulceration,
Testicular torsion, Rabies,
TREATMENT
• Medical treatment
• varies and depends on the nature of the lesion
and the severity of the disease.
• principles common to the treatment of most
colic are:
– Provision of analgesia
– Correction of fluid, electrolyte and acid-base
abnormalities
– Gastrointestinal lubrication or administration of fecal
softeners
– Treatment of underlying disease
Analgesia
• relieves the horse's discomfort,
• minimizes the physiological consequences of
pain, including the pain-induced reduction in
gastrointestinal motility,
• permits a thorough clinical examination and
• reduces the likelihood of the horse injuring
itself.
• Analgesics can be divided into NSAIDs,
sedating analgesics and spasmolytics.
Nonsteroidal anti-inflammatory drugs
• Flunixin meglumine and ketoprofen should
only be used to control pain when the
diagnosis is clear or when surgical
intervention is not an option.
• phenylbutazone -has relatively weak
analgesic effects in colic patients
• Dipyrone -a weak analgesic that is useful in
treatment of mild cases of colic.
• Alpha-2 agonists
– xylazine, detomidine, romifidine provide potent
analgesia, especially when combined with the
opiate butorphanol.
• Opiates
– butorphanol, meperidine (pethidine), morphine
and pentazocine, are potent analgesics useful in
the management of abdominal pain in the horse.
• Antibiotics
– when there is evidence of toxemia because of
presumed bacteremia.
– a broad spectrum- including Gram-negative and
positive and anaerobic bacteria
• Fluid and electrolyte therapy
– Horses with evidence of dehydration,
compromised cardiovascular function
or electrolyte imbalances should be
administered fluids intravenously,
– preferably a balanced, isotonic,
polyionic fluid such as lactated Ringer's
solution.
Intestinal lubricants and fecal softeners
– The intestinal lubricant of choice is mineral
oil.
– Mineral oil is useful in cases of mild
impaction colic and is often administered
when the cause of the colic is not known,
– Other fecal softeners include magnesium
sulfate and sodium sulfate.
• Trocarization
– Occasionally in severe cases of flatulent (gas) colic
or in cases of colon torsion in which the
abdominal distension is impairing respiration,
– usually performed through the right paralumbar
fossa immediately caudal to the last rib.
– The exact place for trocarization can be located by
simultaneous flicking the body wall with a finger
and listening with a stethoscope. The area of
loudest ping will indicate the point of insertion of
the trocar.
• A suitable trocar is a 12.5-15 cm 14-16-gauge
needle.
• The trocar should be kept in position as long
as gas is escaping.
• It is advisable to administer systemic
antibiotics to horses that have been
trocarized.
Surgery
• The only definitive treatment for many causes
of equine colic is surgical correction or
removal of the lesion.
• Gastrointestinal surgery should not be
attempted by those untrained or
inexperienced in the necessary techniques or
without the facilities to provide postoperative
care.
 ENTERITIS
• Inflammation of the intestinal mucosa
• In many cases, gastritis also occurs together
with enteritis.
ETIOLOGY AND EPIDEMIOLOGY
• Enteropathogens include bacteria, viruses,
fungi, protozoa and helminths.
• Many chemicals and toxins can also cause
enteritis.
PATHOGENESIS
• Normal intestinal absorption
– Under normal conditions, a large quantity of fluid
enters the small intestine from the saliva,
stomach, pancreas, liver and intestinal mucosa.
– This fluid and its electrolytes and other nutrients
must be absorbed, mainly by the small intestines,
– The brush border membrane of the villous
epithelial cells is of paramount importance for the
absorption of water, electrolytes and nutrients.
• Mechanisms of diarrhea
– Any dysfunction of the intestines will result in
failure of adequate absorption and diarrhea.
– Depending on the causative agent, intestinal
malabsorption may be the result of at least four
different mechanisms:
• Osmotic diarrhea
• Exudative diarrhea
• Secretory diarrhea
• Abnormal intestinal motility
Osmotic diarrhea
• when substances within the lumen of the
intestine increase the osmotic pressure over a
greater than normal length of intestine,
• resulting in an osmotic movement of an
excessive amount of fluid into the lumen of
the intestine. The fluid is not reabsorbed and
accumulates in the lumen.
• Examples include saline purgatives, overfeeding,
indigestible feeds and disaccharidase
deficiencies.
• A deficiency of a disaccharidase→ incomplete
digestion →large quantities of undigested
material, which acts as a hypertonic solution.
• Malabsorption is associated with several
epitheliotropic viruses that affect the villous
absorptive cells
– E.g. TGE (transmissible gastroenteritis) virus in
newborn piglets, and rotavirus and coronavirus
infections in newborn calves and other species..
Exudative diarrhea
• Acute or chronic inflammation or necrosis of
the intestinal mucosa results in a net increase in
fluid production, inflammatory products,
including loss of serum proteins, and a
reduction in absorption of fluids and
electrolytes.
• E.g. many of the diseases associated with
bacteria, viruses, fungi, protozoa, chemical
agents and tumors.
– The classic example is enteric salmonellosis, in which there is
severe inflammation with the production of fibrinous,
hemorrhagic enteritis.
Secretory diarrhea
• A secretory-absorptive imbalance results in a
large net increase in fluid secretion with little
if any structural change in the mucosal cells.
• The enterotoxin elaborated by
enterotoxigenic E. coli results in intestinal
hypersecretion.
• The villi and crypts remain intact
– secretion is increased beyond the absorptive
capacity of the intestines, resulting in diarrhea.
• The increased secretion is due to an increase
in cyclic adenosine monophosphate, which in
turn may be stimulated by prostaglandins.
– E.g. enterotoxic colibacillosis
• The mucosa remains relatively intact and
retains normal absorptive capacity. Fluid
replacement solutions containing water,
glucose and amino acids can be given orally
and are absorbed efficiently.
Abnormal intestinal motility
• Hyperexcitability, convulsions and the stress
of unexpected sudden confinement may
result in diarrhea,
• which may be due to increased peristalsis
→reduced intestinal absorption due to rapid
passage of intestinal fluids in an otherwise
normal intestine.
• This can occur in animals that are being
assembled for transportation and during
transportation.
Dehydration, electrolyte and acid-base imbalance
• The fluid that is lost consists primarily of water,
the electrolytes sodium, chloride, potassium and
bicarbonate, and varying quantities of protein.
• Protein is lost (protein –losing enteropathy) in
both acute and chronic inflammation, leading to
hypoproteinemia in some cases.
• The loss of bicarbonate results in metabolic
acidosis, which is of major importance in acute
diarrhea.
Chronic enteritis
• the intestinal wall thickens and mucus secretion
is stimulated
• the absorption of intestinal fluids is decreased
(but not of the same magnitude as in acute enteritis)
• decreased digestion and absorption →negative
nutrient balance → body wasting.
• In some cases depending on the cause, there is
continuous loss of protein→clinical
hypoproteinemia. E.g. Intestinal helminthiasis,
Johne's disease of ruminants, and chronic
diarrheas of the horse are examples.
CLINICAL FINDINGS
• The major clinical finding in enteritis or
malabsorption is diarrhea.
– Dehydration, abdominal pain, septicemia and
toxemia with fever occur commonly
– In acute enteritis, the feces are soft or fluid in
consistency and may have an unpleasant odor,
may contain blood (dysentery), fibrinous casts and
mucus
Systemic effects
• Septicemia, toxemia and fever are common in
the infectious enteritides.
• Dehydration (4-6 % of body weight -just barely
detectable, 10-12% of body weight, clinically
very evident.
• In acute enteritis, there may be severe
abdominal pain, which is most severe in the
horse.
Intestinal sounds in enteritis
• Auscultation of the abdomen usually reveals
sounds of increased peristalsis and fluid-
rushing sounds in the early stages of acute
enteritis.
• Later there may be paralytic ileus and an
absence of peristaltic sounds with only fluid
and gas tinkling sounds.
Chronic enteritis
• the feces are usually soft and homogeneous in
consistency,
• contain considerable mucus and
• usually do not have a grossly abnormal odor
• Progressive weight loss and emaciation or
'runting' are common
• usually no systemic abnormalities
CLINICAL PATHOLOGY
• Fecal examination
• Examination of intestinal tissue sample
• Hematology and serum biochemistry
DIFFERENTIAL DIAGNOSIS
• the diarrheas caused by lesions of the small
intestine are profuse and the feces are liquid and
sometimes as clear as water.
• The diarrheas associated with lesions of the large
intestine are characterized by small volumes of
soft feces, often containing excess quantities of
mucus.
• The presence of toxemia and fever, marked
changes in the total and differential leukocyte
count suggest bacterial enteritis, possibly with
septicemia.
Differential diagnosis (cont’d)
• The presence of frank blood and/or fibrinous
casts in the feces usually indicates a severe
inflammatory lesion of the intestines.
• A chronic diarrhea with a history of chronic
weight loss in a mature cow suggests Johne's
disease.
TREATMENT
The principles of treatment of enteritis are:
• Removal of the causative agent:
– anthelmintics
– antiprotozoan agents
– antimicrobial agents
• Alteration of the diet
• Fluids and electrolytes
• Intestinal protectants and adsorbents
• Antidiarrheal drugs
 SIMPLE INDIGESTION
• Common in dairy cattle and stall-fed beef
cattle
• because of the variability in quality and the
large amounts of feed consumed
ETIOLOGY
• dietary abnormalities of minor degree
including
– indigestible roughage, particularly when the
protein intake is low, moldy, overheated and
frosted feeds, and
– moderate excesses of grain and concentrate
intake
– Prolonged or heavy oral dosing with
antimicrobials
PATHOGENESIS
• Changes in the pH of its contents markedly
affect the motility of the rumen
– overeating on grain →an increase in acidity
– High protein diets (excessively large quantities of
legumes or urea) → sharp increase in alkalinity →
depress motility
– The simple accumulation of indigestible food may
physically impede ruminal activity.
– Putrefaction of protein may also play a part in the
production of atony.
CLINICAL FINDINGS
• A reduction in appetite is the first clinical
finding,
• in milking cows slight drop in milk production.
• The anorexia may be partial or complete
• There is mild depression and dullness
• Rumination ceases and the ruminal
movements are depressed in frequency and
amplitude and sometimes are almost absent.
Clinical findings (cont’d)
• The rumen may be larger than normal if the
cause is sudden access to an unlimited supply
of palatable feed.
• There may be moderate tympany, especially
with frozen or damaged feeds or in allergy,
• the usual finding is a firm, doughy rumen
without obvious distension
Clinical findings (cont’d)
• 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;
• There is no systemic reaction
• Mild abdominal discomfort may be present
for several hours.
• Most cases recover spontaneously or with
simple treatments in about 48 hours.
CLINICAL PATHOLOGY
• Examination of the urine for ketone bodies -
to differentiate from acetonemia
• Tests to assess the activity of the ruminal
microflora.
• Examination of the rumen juice for pH using
indicator paper
DIFFERENTIAL DIAGNOSIS
• diseases of the forestomachs and abomasum in
which ruminal atony is a common clinical
finding, and
• diseases of other body systems that cause
secondary ruminal atony
– Acetonemia, Traumatic reticuloperitonitis,
Carbohydrate engorgement, Left-side displacement
of the abomasum (LOA), Right-side dilatation of
abomasum, Abomasal volvulus, Vagal indigestion,
Phytobezoars, Secondary ruminal atony
TREATMENT
Spontaneous recovery
• Most cases recover spontaneously
• Small quantities of fresh, good-quality,
palatable hay should be provided several times
daily to encourage eating and to stimulate
reticulorumen motility
Rumenatorics
• Administered to stimulate reticulorumen
motility and to stimulate appetite.
– However, their use is questionable.
Treatment (cont’d)
• Magnesium hydroxide - a potent alkalinizing
agent- should be used only in cattle with
rumen acidosis
Parasympathomimetics
• used to stimulate reticulorumen activity but
have the disadvantage of inducing undesirable
side effects and being very transitory in effect
– Carbamylcholine chloride, physostigmine and
neostigmine are most commonly used.
Treatment (cont’d)
– Epsom salts (0.5-1.0 kg per adult cow) and other
magnesium salts are reasonably effective
• Alkalinizing and acidifying agents
– If an excessive quantity of grain is the cause of the
simple indigestion, the use of alkalinizers, such as
magnesium hydroxide is recommended when the
rumen contents are excessively acid.
– Acetic acid or vinegar is used when the rumen
contents are alkaline as a result of the ingestion of
high-protein concentrates.
Treatment (cont’d)
• Reconstitution of ruminal microflora
• In cases of indigestion that have run a course
of more than a few days, and in animals that
have been anorexic for prolonged periods,
there will be significant loss of ruminal
microflora, especially if there have been
marked changes in pH.
– From abattoir or
– Live animals
ACUTE CARBOHYDRATE ENGORGEMENT
OF RUMINANTS
(RUMINAL LACTIC ACIDOSIS, RUMEN
OVERLOAD)
• ETIOLOGY
• The sudden ingestion of toxic doses of
carbohydrate-rich feed, such as grain
EPIDEMIOLOGY
• Occurrence
• Cattle, sheep and goats are susceptible
• but the disease occurs most commonly in
feedlot cattle and dairy cattle fed on high-
level grain diets.
Previous diet and change of ration
• the type and level of ration consumed by a
ruminant affects the numbers and species of
bacteria and protozoa in the rumen,
• a change from one ration to another requires a
period of microbial adaptation.
• 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.
• This results in the rapid onset of abnormal
fermentation.
Accidental consumption of excess carbohydrates
• accidental consumption of toxic amounts of
grain
• also following the irregular feeding of large
quantities of other less common animal feeds
and byproducts, such as bread, baker's dough
and wet brewers' grain
• The accidental feeding of a high-level grain
ration to cattle that are on a highlevel
roughage ration is a common cause of the
disease
• Morbidity and case fatality rates
• Depending on
– the grain,
– the total amount eaten and
– the previous experience of the animals,
• the morbidity will vary from 10-50%.
• The case fatality rate may be up to 90% in
untreated cases, while in treated cases it still
may be up to 30-40 %.
Types and toxic amounts of feeds
• Wheat, barley and corn grains are the most
toxic when ingested in large quantities.
• Oats and grain sorghum are least toxic.
• 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.
PATHOGENESIS
Changes in rumen microflora
• The ingestion of excessive quantities of highly
fermentable feeds by a ruminant is followed
within 2-6 hours by a marked change in the
microbial population in the rumen.
• There is an increase in the number of
Streptococcus bovis, which utilize the
carbohydrate to produce large quantities of
lactic acid.
• In the presence of a sufficient amount of
carbohydrate (a toxic or a lethal amount) the
organism will continue to produce lactic acid,
→rumen pH drops to 5 or less →destruction
of the cellulolytic bacteria and protozoa
Volatile fatty acids and lactic acid in the rumen
• The concentration of volatile fatty acids
increases initially, contributing to the fall in
ruminal pH.
• 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, which
markedly increases ruminal osmolality, and
water is drawn in from the systemic circulation,
causing hemoconcentration and dehydration.
• Some of the lactic acid is buffered by ruminal
buffers
• but large amounts are absorbed by the rumen
and some moves into and is absorbed further
down the intestinal tract.
• 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.
Systemic lactic acidosis
• In severe cases of lactic acidosis 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.
• Renal blood flow and glomerular filtration rate
are also decreased, resulting in anuria.
Eventually there is shock and death.
Chemical and mycotic rumenitis
• The high concentration of lactic acid in the
rumen causes chemical rumenitis, which is the
precursor for mycotic rumenitis in those that
survive; this occurs about 4-6 days later.
• The low pH of the rumen favors the growth of
Mucor, Rhizopus and Absidia spp. which
invade the ruminal vessels, causing
thrombosis and infarction. Severe bacterial
rumenitis also occurs.
• Widespread necrosis and gangrene may affect
the entire ventral half of the ruminal walls and
lead to the development of an acute
peritonitis. The damage to the viscus causes
complete atony and this, together with the
toxemia resulting from the gangrene, is
usually sufficient to cause death
Hepatic abscesses
• 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.
CLINICAL FINDINGS
• Speed of onset and severity
• a few hours after engorgement, the only
abnormalities that may be detectable are a
distended rumen and abdomen,
• In the mild form, affected cattle are anorexic
and still fairly bright and alert, and the feces
may be softer than normal.
– Rumen movements are reduced
– Affected cattle do not ruminate for a few days but
usually begin to eat on the third or fourth day
without any specific treatment.
Clinical findings (cont’d)
• Individual animals
• Depression, dehydration, inactivity, weakness,
abdominal distension, diarrhea and anorexia
are typical.
• The temperature is usually below normal,
36.5-38.5oC.
• The heart rate is usually increased and
continues to increase with the severity of the
acidosis and circulatory failure.
Clinical findings (cont’d)
• In general, the prognosis is better in those
with heart rates below 100/min than those
with rates up to 120-140/min.
• The respirations are usually shallow and
increased up to 60-90/min.
• A mucopurulent discharge is common because
animals fail to lick their nares.
• Diarrhea -usually profuse, light-colored with
sweet-sour odor.
Clinical findings (cont’d)
• The feces commonly contain an excessive
quantity of kernels of grain
• The dehydration is severe and progressive. (In
mild cases-about 4-6% BW, and with severe
involvement up to 10-12% BW)
• Anuria
• The rumen contents may feel firm and doughy
in cattle that were previously on a roughage
diet and have consumed a large amount of
grain.
Clinical findings (cont’d)
• the rumen is rather resilient In cattle that
have become ill on smaller amounts of grain
• The primary contractions of the reticulorumen
are usually totally absent,
• low-pitched tinkling and gurgling sounds
associated with the excessive quantity of fluid
in the rumen are commonly audible on
auscultation of the rumen.
• The ruminal fluid is a milky green to olive
brown color and has a pungent acid smell.
• Collection of a sample of ruminal fluid in a
glass beaker will reveal an absence of foam.
The pH of the rumen fluid is usually below 5.
• Severely affected animals have a staggery,
drunken gait and their eyesight is impaired.
• They bump into objects and their palpebral
reflex is sluggish or absent.
• Acute laminitis may be present
• Affected animals are lame in all four feet,
• Recumbency –usually after about 48 hours
• Affected animals lie quietly, often with their
heads turned into the flank.
• Evidence of improvement during this time
includes a fall in heart rate, rise in
temperature, return of ruminal movement
and passage of large amounts of soft feces.
CLINICAL PATHOLOGY
Ruminal fluid pH
• The pH of the ruminal fluid can be measured in
the field using wide-range pH (2-12) Indicator
paper.
• must be examined immediately because the pH
will increase upon exposure to air
• A pH of 5-6 suggests a moderate degree of
abnormality
• a pH of less than 5 suggests severe grain
overload and the need for energetic treatment.
Clinical pathology (cont’d)
Ruminal microflora
• Microscopic examination of ruminal fluid will
reveal the absence of ruminal protozoa,
– a reliable indicator of an abnormal state of the
rumen, usually acidosis.
– The predominantly Gram-negative bacterial flora
of the rumen is replaced by a Gram-positive one.
The hematocrit/PCV rises to 50-60% in the
terminal stages and is accompanied by a fall in
blood pressure.
Clinical pathology (cont’d)
Serum biochemistry
• Blood lactate and inorganic phosphate levels
rise and blood pH and bicarbonate fall
markedly.
Urine pH
• The urine pH falls to about 5 and becomes
progressively more concentrated; terminally
there is anuria.
NECROPSY FINDINGS
• the contents of the rumen and reticulum are thin
and porridge-like and have a typical odor
suggestive of fermentation.
• The cornified epithelium may be mushy and easily
wiped off, leaving a dark, hemorrhagic surface
beneath.
• Abomasitis and enteritis
• The abomasum may contain large quantities of grain.
• There is a pronounced thickening and darkening of
the blood and the visceral veins stand out
prominently.
Necropsy findings (cont’d)
• the wall of the reticulum and rumen may be
gangrenous (In cases that have persisted for
3-4 days)
• In affected areas the wall is 3 or 4 times ticker,
• show a soft black mucosal surface raised
above surrounding normal areas and have a
dark red appearance visible through the
serous surface.
• The thickened area is very friable and on
cutting has a gelatinous appearance.
DIFFERENTIAL DIAGNOSIS
• Simple indigestion: the ruminal pH and
protozoan numbers and activity are normal
• Parturient paresis
• Toxemias
• Subacute ruminal acidosis
TREATMENT
The principles of treatment are:
• Correct the ruminal and systemic acidosis and
prevent further production of lactic acid
• Restore fluid and electrolyte losses and
maintain circulating blood volumes
• Restore forestomach and intestinal motility to
normal.
Treatment (cont’d)
When cattle are found engorging themselves,
the following procedures are recommended:
• Prevent further access to feed
• Do not provide any water for 12-24 hours
• Offer a supply of good-quality palatable hay
equal to one-half of the daily allowance per
head
• Exercise all animals every hour for 12-24 hours
to encourage movement of the ingesta through
the digestive tract.
Treatment (cont’d)
• those cattle that have continued to eat hay,
after 18-24 hours, may be allowed free access
to water.
• Those with clinical evidence of grain overload
must be identified and treated accordingly.
Treatment (cont’d)
Rumenotomy
• In severe cases, in which there is recumbency,
severe depression, hypothermia, prominent
ruminal distension with fluid, a heart rate of 110-
130/min and a rumen pH of 5 or below; a
rumenotomy is the best course of action.
• The rumen is emptied, washed out with a siphon
and examined for evidence of and the extent of
chemical rumenitis, and a cud transfer (10-20 L of
rumen juice) is placed in the rumen along with a
few handfuls of hay.
Treatment (cont’d)
• Intravenous sodium bicarbonate and fluid
therapy
• The systemic acidosis and the dehydration are
treated with intravenous solutions of 5%
sodium bicarbonate followed by isotonic
sodium bicarbonate (1.3%).
Treatment (cont’d)
• Rumen lavage
• an alternative to a rumenotomy
– In less severe cases,
• affected cattle are still standing but are depressed
• heart rate - 90-100/min,
• moderate ruminal distension and the rumen pH between 5 and
6
• warm water is pumped in until there is an obvious
distension of the left paralumbar fossa; the rumen is
then allowed to empty by gravity flow. The rumen
can be almost completely emptied by 10-15
irrigations.
Treatment (cont’d)
Intraruminal alkalinizing agents
• In moderately affected cases, the use of 500 g
of magnesium hydroxide per 450 kg BW, or
magnesium oxide in 10 L of warm water
pumped into the rumen and followed by
kneading of the rumen to promote mixing will
usually suffice.
CONTROL AND PREVENTION
• Cattle can be started, grown and finished on
high-level grain rations successfully, providing
they are allowed a gradual period of
adaptation during the critical period of
introduction. The important principle of
prevention is that the ruminant can adapt to
an all-concentrate ration.
 RUMINAL TYMPANY (BLOAT)
• 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 to
form pockets of free gas above the level of the
contents and finally are eliminated by eructation.
ETIOLOGY
Primary ruminal tympany (frothy bloat)
• caused by the production of a stable foam
that traps the normal gases of fermentation in
the rumen.
• coalescence of the small gas bubbles is
inhibited and eructation cannot occur.
• Pasture and feedlot bloat
– Leguminous or pasture bloat is due to the foaming
qualities of the soluble leaf proteins in bloating
legumes
– Feedlot bloat is caused by feeding finely ground
grain, which promotes frothiness of rumen
contents
Secondary ruminal tympany (free-gas bloat)
• Physical obstruction to eructation
• occurs in esophageal obstruction or in
obstruction of the cardia.
• Tetanus in cattle is usually accompanied by
secondary freegas bloat due to spasm of the
esophagus and inability to eructate normally
EPIDEMIOLOGY
Occurrence
• Pasture bloat
• occurs in both dairy and beef cattle that graze
pastures consisting of bloating forages
• The incidence is highest when the pasture is
lushest and leaves of the plants contain a high
concentration of soluble proteins.
Feedlot bloat
• occurs in feedlot cattle when cattle are fed
large quantities of grain and small quantities
of roughage.
• In some cases the use of pelleted, finely
ground feed has been associated with
outbreaks of feedlot bloat.
PATHOGENESIS
• A grassfed cow can produce 100 L during the first
hour of feeding. A cow maintained on a legume
diet may produce 200 L per hour.
• In frothy bloat, the gas bubbles remain dispersed
throughout the rumen contents, producing an
abnormal increase in the volume of the
ruminoreticular contents and, consequently,
inhibiting eructation.
• The characteristic frothiness of ruminal contents
is caused by inadequate coalescence of gas
bubbles.
Pathogenesis (cont’d)
• In free-gas bloat the gas bubbles coalesce and
separate from the rumen fluid but the animals
cannot eructate the pockets of free gas
because of abnormalities of the reticulorumen
or esophagus.
• freegas bloat is characterized by the
accumulation of free gas due to esophageal
obstruction or ruminal atony.
Pathogenesis (cont’d)
• Frothiness of the ruminal contents interferes
with function of the cardia and inhibits the
eructation reflex.
• Rumen movements are initially stimulated.
Terminally there is a loss of muscle tone and
ruminal motility.
• The most distinctive aspect of bloated cattle is
abdominal distension, particularly the left
abdomen, due to distension of the rumen.
Pathogenesis (cont’d)
• The volumes of gas in a bloated cow are large,
50-70 L,
• increase in intraruminal pressure
• As the intraruminal pressure increases,
occlusion of the vena cava occurs, causing
congestion of the caudal part of the body.
• In addition, the pressure exerted by the
distended rumen on the diaphragm is very high,
• which results in reduced lung capacity and death
from hypoxia.
CLINICAL FINDINGS
Primary pasture or feedlot bloat
• sudden death (or found dead)
• distension of the rumen which occurs quickly,
• the animal stops grazing
• There is discomfort and the animal may stand
and lie down frequently, kick at its abdomen
and even roll.
• Frequent defecation and urination are
common.
Clinical findings (cont’d)
• Marked dyspnea accompanied by mouth
breathing, protrusion of the tongue, salivation
and extension of the head.
• The respiratory rate is increased up to 60/min.
• The course is short (death does not usually
occur in less than 3-4 hours)
• Collapse and death almost without struggle
• only small amounts of gas are released during
trocarization or passage of a stomach tube
Clinical findings (cont’d)
Secondary bloat
• the excess gas is present as a free gas cap on top of
the ruminal contents.
• There is usually an increase in the frequency and
strength of ruminal movements in the early stages
followed by atony.
• Passage of a stomach tube or trocarization results in
the release of large quantities of gas and
subsidence of the ruminal distension.
• If an esophageal obstruction is present it will be
detected when the stomach tube is passed.
Clinical finding (cont’d)
• In both severe primary and secondary bloat
there is
– dyspnea and
– a marked elevation of the heart rate up to 100-
120/min in the acute stages.
CLINICAL PATHOLOGY
• Laboratory tests are not necessary for the
diagnosis of ruminal tympany
NECROPSY FINDINGS
• protrusion and congestion of the tongue
• marked congestion and hemorrhages of lymph
nodes of the head and neck, epicardium and
upper respiratory tract,
• friable kidneys and mucosal hyperemia in the
small intestine
• The lungs are compressed
• congestion and hemorrhage of the cervical
portion of the esophagus but the thoracic
portion of the esophagus is pale and blanched.
Necropsy findings (cont’d)
• In general, congestion is marked in the front
quarters and less marked or absent in the
hindquarters.
• The rumen is distended but the contents are much
less frothy than before death.
• A marked erythema is evident beneath the ruminal
mucosa, especially in the ventral sacs.
• The liver is pale because of expulsion of blood
from the organ.
• Occasionally, the rumen or diaphragm have
ruptured
TREATMENT
• depends on
– whether the bloat is frothy or due to free gas, and
– whether or not the bloat is life threatening.
Treatment (cont’d)
Emergency rumenotomy
• Using a sharp knife, a quick incision 10-20cm
in length is made over the midpoint of the left
paralumbar fossa into the rumen. Followed by
irrigation and cleaning of the incision site
followed by standard surgical closure
Treatment (cont’d)
Trocar and cannula
• for the emergency release of rumen contents
and gas
• the standard sized trocar and cannula does
not have a large enough diameter to allow the
very viscous stable foam in peracute frothy
bloat to escape quickly enough to save an
animal's life
Treatment (cont’d)
Promote salivation
• For less severe cases, owners may be advised
to tie a stick in the mouth to promote the
production of excessive saliva, which is
alkaline and may assist in denaturation of the
stable foam.
Treatment (cont’d)
Stomach tube
• The passage of a stomach tube of the largest bore
possible
• In free gas bloat there is a sudden release of gas
• in frothy bloat it may be impossible to reduce the
pressure with the stomach tube
• Walking animals for a few minutes usually help
them to eructate.
• Walking may result in loss of stability of foam and
thereby help to coalescence
Treatment (cont’d)
Antifoaming agents
• Any nontoxic oil, especially a mineral oil
• Their effect is to reduce surface tension and
foam.
• A dose of 250 mL is suggested for cattle but
doses of up to 500 mL are commonly used.
• detergent such as dioctyl sodium
sulfosuccinate.
• synthetic surfactants, poloxalene
Treatment (cont’d)
Rumenotomy
• If other methods fail to correct the condition
rumenotomy should be conducted.
Control and Prevention
• To prevent pasture bloat it is important to
feed hay before turning cattle on pasture.
• continual administration of an antifoaming
agent during the risk period
• To prevent feedlot bloat, rations should
contain ≥10-15% cut or chopped roughage
mixed into the complete feed.
• Grains should be rolled or cracked, not finely
ground.
 ACUTE INTESTINAL OBSTRUCTIONS IN
LARGE ANIMALS
• seen in all large animal species
• but are most common in horses
• Cattle are the most commonly affected
ruminants; diagnosis in sheep and goats is rare.
• obstructions are mechanical or functional
• They can interrupt the flow of ingesta, and
vascular integrity may or may not be
compromised (strangulating or simple
obstruction).
Etiology and Pathogenesis:
• Functional obstructions are associated with
altered intestinal motility, often due to dietary
or management factors, parasite infection,
enteritis, or peritonitis.
• Mechanical obstructions (physical blockage of
ingesta) occur due to abnormalities in the
bowel lumen, in the wall, or outside the tract.
Etiology and pathogenesis (cont’d)
• In the horse, impactions and other luminal
obstructions can result from
– coarse feeds, reduced water intake, enteroliths, or
ingested foreign material
• Other causes of intestinal obstruction in
horses are volvulus (twist on the mesenteric
axis) and torsion (twist along the long axis of
the bowel)
Etiology and pathogenesis (cont’d)
• Obstruction occurs either due to incarceration
of the intestine (usually small) by herniation
or because of fibrous bands (e.g. adhesions)
Etiology and pathogenesis (cont’d)
• In cattle, specific causes include
intussusception and volvulus
Clinical Findings and Diagnosis:
• Intestinal obstruction in horses generally
manifests as abdominal pain.
• In cattle, signs of abdominal pain include
treading, stretching, and kicking at the
abdomen, and less commonly rolling and
bellowing.
• signs in cattle are generally more subtle than
in horses
Clinical Findings and Diagnosis (cont’t)
• cattle with intestinal obstruction are anorectic
and pass few or no feces, and
• The feces that are passed may be covered
with mucus, or mixed or coated with blood.
• Thick, raspberry-colored blood mixed with
scant feces is characteristic of small-intestinal
bleeding, particularly that associated with
intussusception.
Clinical findings and diagnosis (cont’d)
• Blood from the colon or rectum is generally
brighter red.
• Melena is typical of abomasal bleeding.
Treatment:
• of functional obstructions in cattle is generally
symptomatic and supportive
• If present, dehydration and electrolyte
imbalances should be corrected by
appropriate fluid therapy (PO or IV).
• Mechanical obstructions almost always
require surgery.
TRAUMATIC RETICULOPERITONITIS (TRP)
ETIOLOGY
• Traumatic reticuloperitonitis is caused by the
penetration of the reticulum by metallic
foreign objects (pieces of wire, nails) that have
been ingested
EPIDEMIOLOGY
Occurrence
• Adult dairy cattle are most commonly affected
• much more common in cattle fed on prepared
feeds
• The incidence is low in sheep and goats
PATHOGENESIS
Ingestion of foreign body
• Lack of oral discrimination by cattle leads to
the ingestion of foreign bodies that would be
rejected by other species.
• may lodge in the upper esophagus and cause
obstruction or in the esophageal groove and
cause vomiting, but in most instances they
pass to the reticulum.
Pathogenesis (cont’d)
Penetration of reticulum
• If the reticular wall is injured without
penetration to the serous surface no
detectable illness occurs, and the foreign body
may remain fixed in the site for long periods
and gradually be corroded away.
Pathogenesis (cont’d)
Acute local peritonitis
• The initial reaction to perforation is one of acute
local peritonitis and clinical signs commence about
24 hours after penetration.
• The peritonitis causes ruminal atony and
abdominal pain.
• If the foreign body moves back into the reticulum
spontaneous recovery may occur.
• the ventral aspect of the reticulum becomes
adherent to the abdominal floor and diaphragm→
decreased reticular motility.
Pathogenesis (cont’d)
• Reticular abscesses are common complications
• Persistent local peritonitis →reduced
reticulorumen motility, inappetence to
anorexia, a capricious appetite (may eat hay
not concentrate), chronic ruminal tympany,
persistent mild fever, abdominal pain on deep
palpation,
• passage of poorly comminuted feces
characterized by an increased proportion of
large particles
Pathogenesis (cont’d)
Generalized peritonitis and extension of
disease
• In cows that calve at the time of perforation
and in cattle that are forced to exercise
spread of the inflammation causing
generalized or diffuse peritonitis may occur.
• Immobility is a prominent clinical finding
• Generalized peritonitis results in toxemia,
alimentary tract stasis, dehydration and shock
CLINICAL FINDINGS
Acute local peritonitis
• sudden onset
• complete anorexia and a marked drop in milk
yield.
• Subacute abdominal pain
• The animal is reluctant to move and does so
slowly.
• Walking, particularly downhill, is often
accompanied by grunting.
Clinical findings (cont’d)
• Most animals prefer to remain standing for long
periods and lie down with great care.
• In others there is recumbency and reluctance to
stand
• Arching of the back occurs in about 50% of cases.
• Defecation and urination cause pain and the acts
are performed infrequently and usually with
grunting.
• This results in constipation, scant feces and in
some cases retention of urine.
Clinical findings (cont’d)
• Rarely, acute abdominal pain with kicking at the
belly and stretching occurs.
• A moderate systemic reaction (To 39.5-40°C, HR
about 50/min and RR about 30/min).
• The respirations are usually shallow
• Rumination is absent
• Reticulorumen movements are markedly
depressed and usually absent.
• Moderate distension of the left paralumbar
fossa.
Clinical findings (cont’d)
• Pain can be elicited by deep palpation of the
abdominal wall just caudal to the xiphisternum.
– Palpation is done using short, sharp pushes with
the closed fist or knee
– while listening with a stethoscope over the trachea
for evidence of a grunt.
• Pinching the withers to cause depression of the
back and eliciting a grunt
• sharp elevation of a solid rail held horizontally
under the abdomen in large cows
Clinical findings (cont’d)
Chronic local peritonitis
• the appetite and milk yield do not return to
normal after prolonged therapy with
antimicrobials.
• The body condition is usually poor,
• the feces are reduced in quantity and there is
an increase in undigested particles.
• In some cases, the temperature may be within
the normal range
Clinical findings (cont’d)
• A persistent slightly elevated temperature →
chronic inflammatory lesion.
• The grunt test may be positive or negative
• The gait may be slow and careful
• occasionally, grunting may occur during
rumination, defecation and urination.
• Rumination activities are infrequent, the rumen
is usually smaller than normal, chronic
moderate bloat is common and there is ruminal
atony or some moderate reticulorumen activity.
CLINICAL PATHOLOGY
Hemogram
• The total and differential leukocyte counts
• In acute local peritonitis
– a neutrophilia and a left shift are common.
– Lasting for up to 3 days,
• In chronic cases the levels do not return
completely to normal for several days or
longer periods and there is usually a moderate
leukocytosis, neutrophilia and a monocytosis.
Clinical pathology (cont’d)
• In acute diffuse peritonitis a leukopenia with a
greater absolute number of immature
neutrophils than mature neutrophils
(degenerative left shift) occurs
Clinical pathology (cont’d)
• Plasma protein and fibrinogen
– High mean plasma protein concentration
– In severe diffuse peritonitis the fibrinogen levels
may be increased
• Abdominocentesis and peritoneal fluid
– A nucleated cell count above 6000 cells/μL and
total protein above 3 g/dL
• Other methods of diagnostic importance
include metal detectors, laparoscopy,
radiography and ultrasonography.
NECROPSY FINDINGS
• fibrinous adhesions between the cranioventral
aspects of the reticulum and the ventral
abdominal wall and the diaphragm.
• Adhesions and multiple abscesses may extend
to either side of the reticulum involving the
spleen, omasum, liver, abomasum and ventral
aspects of the rumen.
• Large quantities of turbid, foul-smelling
peritoneal fluid may be present, containing
fibrinous clots.
Necropsy findings (cont’d)
• The foreign body can usually be found
perforating the cranioventral aspect of the
reticulum.
• In acute diffuse peritonitis a fibrinous or
suppurative inflammation may affect almost
the entire peritoneal cavity with extensive
fibrinous adhesions. Large quantities of turbid,
foul-smelling fluid containing clots of fibrin are
usually present.
DIFFERENTIAL DIAGNOSIS
• must be differentiated from those diseases in
which sudden anorexia, sudden drop in milk
production, ruminal atony, abdominal pain and
abnormal feces are common.
• Simple indigestion, Acute carbohydrate
engorgement, Acute intestinal obstruction,
Abomasal volvulus (following rightside dilatation),
Pericarditis, Acute pleuritis, Perforated abomasal
ulcer, Postpartum septic metritis, Acute local
peritonitis, Pyelonephritis, Acute hepatitis or
severe hepatic Abscess, Acetonemia
TREATMENT
• Two methods of treatment are in general use:
– conservative treatment with or without the use of a
magnet, and
– rumenotomy.
• Conservative medical therapy
• comprises immobilization of the animal,
administration of antimicrobials and the oral
administration of a magnet to immobilize the
foreign body. The cow is tied or confined in a box
stall for several days.
• Immobilization facilitates the formation of adhesions.
Antimicrobials
• broad-spectrum antimicrobial.
• a high rate of recovery is recorded with
antimicrobials combined with immobilization
Rumenotomy
• Surgical removal of the foreign body through a
rumenotomy incision
• It has the advantage of being both a
diagnostic procedure and a satisfactory
treatment.
Treatment (cont’d)
• A rumenotomy is the best treatment
• unnecessary in many cases because of the
tendency of the foreign body to return to the
reticulum.
• treat the animal conservatively for 3 days and
if marked improvement has not occurred by
that time consider a rumenotomy
PREVENTION
• All processed feed should be passed over
magnets to remove metallic material before
being fed to cattle.
• Use synthetic string instead of wire
• Reticular magnets
• Small cylindrical or bar magnets, 7.5 mm long
by 1.0-2.5 cm diameter with rounded ends,
are used to prevent the disease but are also
used in acute cases to minimize penetration of
the foreign body.
 DIETARY ABOMASAL IMPACTION IN
CATTLE
• occurs in cattle when the animals are fed
poor-quality roughage.
• The disease is most common in pregnant
cattle due to increased feed intake in an
attempt to meet the increased needs of a
higher metabolic rate.
ETIOLOGY AND EPIDEMIOLOGY
• The consumption of excessive quantities of
poor-quality roughage which are low in both
digestible protein and energy
• Impaction of the abomasum with sand can
also occur in cattle if they are fed hay on
sandy soils or root crops that are sandy or
dirty.
PATHOGENESIS
• Chopped roughage and finely ground feeds
pass through the forestomachs of ruminants
more quickly than long roughage
• perhaps in this situation the combination of
low digestibility and excessive intake leads to
excessive accumulation in the forestomachs
and abomasum.
Pathogenesis (cont’d)
• Once impaction of the abomasum occurs, a
state of subacute obstruction of the upper
alimentary tract develops.
• The hydrogen and chloride ions are
continually secreted into the abomasum and
an alkalosis with hypochloremia results.
• Varying degrees of dehydration occur
because fluids are not moving into the
duodenum for absorption.
Pathogenesis (cont’d)
• dehydration, alkalosis, electrolyte imbalance
and progressive starvation occur
• Potassium ions are also sequestered in the
abomasum, resulting in a hypokalemia.
CLINICAL FINDINGS
• Usual presenting complaints given by the owner
include:
– Complete anorexia, scant feces and moderate distension
of the abdomen
• The onset is usually slow and progressive
• considerable weight loss and too weak to rise
• The body temperature is usually normal
• May be subnormal during cold weather, which
suggests that the specific dynamic action of the
rumen is not sufficient to meet the energy needs of
basal metabolism.
Clinical findings (cont’d)
• The heart rate varies from normal to 90-100/min
– May increase to 120/min in advanced cases where
alkalosis, hypochloremia and dehydration are
marked.
• The respiratory rate is commonly increased
• Expiratory grunt due to the abdominal
distension may be audible
• A mucoid nasal discharge usually collects on the
external nares and muzzle, because of the failure
of the animal to lick its nostrils
Clinical findings (cont’d)
• The rumen is usually static and full of dry
contents, or it may contain an excessive
quantity of fluid in those cattle that have been
fed finely ground feed.
• The pH of the ruminal fluid is usually within
the normal range (6.5-7.0).
• The rumen protozoan activity ranges from
normal to a marked reduction in numbers and
activity
Clinical findings (cont’d)
• Severely affected cattle will die in 3-6 days
after the onset of signs.
• Rupture of the abomasum has occurred in
some cases and death from acute diffuse
peritonitis and shock occurs precipitously in a
few hours.
CLINICAL PATHOLOGY
• A metabolic alkalosis, hypochloremia,
hypokalemia, hemoconcentration and
• a total and differential leukocyte count within
the normal range
NECROPSY FINDINGS
• At necropsy the abomasum is commonly
grossly enlarged to up to twice normal size
and impacted with dry rumen-like contents.
• The omasum may be similarly enlarged and
impacted with the same contents as in the
abomasum
• The rumen is usually grossly enlarged and
filled with dry ruminal contents or ruminal
fluid.
Necropsy findings (cont’d)
• The intestinal tract beyond the pylorus is
characteristically empty and has a dry
appearance.
• Abomasal tears, ulcers, and necrosis of the
walls of the rumen, omasum or abomasum
may occur.
DIFFERENTIAL DIAGNOSIS
• abomasal impaction as a complication of
vagus indigestion,
• omasal impaction,
• diffuse peritonitis and
• acute intestinal obstruction due to intestinal
accidents or enteroliths and lipomas
TREATMENT
• Salvage or treatment?
• Those that have a severely impacted abomasum
and are weak with a marked tachycardia (100-
120/min) are poor treatment risks and should be
slaughtered.
• Rational treatment would appear to consist of
– correcting the metabolic alkalosis, hypochloremia,
hypokalemia and dehydration and
– attempting to move the impacted material with
lubricants and cathartics, or
– surgically emptying the abomasum
CONTROL
• Prevention is possible by providing the
necessary nutrient requirements
• Adequate amounts of fresh drinking water
should be supplied at all times.
• Consumption of excessive roughage is
reduced by supplementation with appropriate
sources of energy and protein.