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What part of the equine GI tract is the stomach considered?
The foregut
What does the equine stomach do?
It acts as a digestive organ
produces acid continuously
supports bacterial fermentation
secretes digestive enzymes
Why do horses produce stomach acid continuously?
Horses are naturally continuous grazers, so their stomach is adapted to ongoing food intake
Why does roughage help protect the equine stomach?
Roughage buffers stomach acid and helps form a food bolus
What is the protective role of long-stem roughage?
It buffers acid and helps reduce acid splash onto squamous stomach area
What are the two major regions of the equine stomach?
squamous/ non-glandular
glandular
What separates the squamous and glandular stomach?
The margo plicatus
Where is the squamous stomach located functionally?
It connects with the mouth and esophagus
Why is the squamous stomach vulnerable to ulcers?
It is not accustomed to acid exposure
Where is the glandular stomach located functionally?
It connects toward the duodenum/small intestine
What cells secrete acid in the glandular stomach?
Parietal cells
Why is the glandular stomach normally more protected from acid?
It has a thick mucus layer
robust blood flow
buffers
How does stomach acidity change as you move ventrally?
pH decreases; the stomach becomes more acidic
What is a food bolus?
A mass of feed/roughage in the stomach that helps buffer acid and reduce acid splash
What is a gastric ulcer?
A break in the lining of the stomach
What is EGUS?
Equine Gastric Ulcer Syndrome
What are the two main types of EGUS?
Equine Squamous Gastric Disease
Equine Glandular Gastric Disease
What are the two categories of ESGD?
Primary ESGD
Secondary ESGD
What is primary ESGD usually associated with?
Management factors, especially feeding and housing practices that increase acid exposure
What is secondary ESGD usually associated with?
Gastric outflow obstruction or hospitalized/sick horses with gut motility problems
Why is squamous ulceration common in domesticated horses?
Feeding and housing practices often reduce continuous grazing and increase acid exposure
Why do wild horses have less acid splash despite running?
They eat continuously and maintain a food bolus that helps prevent acid splash
Why can glandular ulcers occur even though the glandular lining is normally exposed to acid?
They may result from breakdown of normal defense mechanisms that protect the lining
Is bacterial infection clearly associated with glandular ulcers in horses?
No, do not have clear helicobacter-type association noted
What human risk factors are associated with ulcers but are not the same in horses?
Helicobacter pylori
NSAID use
Why is EGGD less well understood?
The glandular lining is normally acid-exposed, so ulcers likely involve failure of protective mechanisms rather than simple acid exposure
How can exercise contribute to squamous ulcers?
Gaits faster than a walk increase intra-abdominal pressure, pushing acid upward onto the squamous lining.
Why do racehorses have more ulcers?
Intense and long-duration training increases acid exposure and ulcer severity
How is ulcer severity related to endurance riding?
Severity is directly correlated with the distance of the ride
Who gets gastric ulcers?
Risk varies by breed, use, training level, and type of ulceration
What percentage of Thoroughbred racehorses may have ESGD?
About 80–100%
What percentage of show/sport horses may have ESGD?
About 17–58%
What percentage of Australian Thoroughbred racehorses may have EGGD?
About 47–65%
What percentage of sport horses may have EGGD?
About 64%
Are gastric ulcer risk factors simple or multifactorial?
Multifactorial
Why might horses trained in urban areas have higher ulcer risk?
They may have less turnout and more confinement/stress
How does lack of pasture turnout affect risk?
It reduces grazing and food bolus formation, increasing acid exposure
What nutritional factors increase ulcer risk?
Lack of forage
more than 6 hours between forage meals
straw alone as forage
high starch/grain intake
intermittent water access.
Why is alfalfa beneficial for gastric ulcer prevention?
It helps raise gastric pH because it contains calcium and protein that buffer stomach contents
Why does high starch/grain intake increase risk?
Breakdown can produce volatile fatty acids, adding to the acid load in the stomach
Why is intermittent water access a risk factor?
Less water can make stomach contents more concentrated and acidic
Are there pathognomonic clinical signs for EGUS?
No. Clinical signs are nonspecific
What does pathognomonic mean?
A sign that is specific to one disease and strongly indicates that disease
What are common clinical signs of gastric ulcers?
Decreased appetite
poor body condition
weight loss
colic after eating
cinchy/girthy behavior
behavior changes
poor performance
poor coat condition
What behavior changes may be seen with gastric ulcers?
Stereotypic behavior, aggression, or self-mutilation
Is diarrhea a typical sign of gastric ulcers?
No. It is anatomically and physiologically implausible for stomach ulcers.
What is required for definitive diagnosis of EGUS?
Gastroscopy
What length endoscope is usually needed for mature horses?
At least a 3-meter endoscope
What route does the gastroscope take?
Through the esophagus/cardio region into the stomach, with visualization of squamous, glandular, pyloric, and sometimes duodenal areas
What does squamous stomach tissue look like on gastroscopy?
Light pink
What does glandular stomach tissue look like on gastroscopy?
Darker pink
Is there a relationship between the presence of ESGD and EGGD?
No. One does not predict the other, which is why both need to be examined
How is ESGD graded?
From Grade 0, normal, to Grade 4, severe/deep ulceration.
Should EGGD be graded?
No. EGGD grading has minimal validity.
Why should EGGD not be graded?
Visual severity and microscopic appearance correlate poorly, and appearance/contour varies.
What is polypoid ulceration?
A glandular ulcer pattern seen commonly in Warmblood horses
What is omeprazole used for?
It blocks acid production
What are common brand names for omeprazole in horses?
Gastrogard
Ulcergard
What did ranitidine do?
It decreased acid production
unavailable
What does sucralfate do?
Coats the stomach lining and increases blood flow
What is another name for sucralfate?
Carafate
What is misoprostol used for?
It is a synthetic prostaglandin analog used especially for glandular ulcers
How does misoprostol help glandular ulcers?
It increases blood flow to the gut and supports healing
What are prokinetic agents used for?
Secondary ulcers related to gut motility/transit issues
How do prokinetic agents help?
They increase gut transit and move acid/bile along
Why is management change necessary in ulcer treatment?
Medication alone may not prevent new ulcers if risk factors continue
What management changes help prevent recurrence of gastric ulcers?
Pasture grazing
high forage intake
some alfalfa
lower concentrate diets
smaller frequent meals
ad libitum forage
small forage before exercise
constant water access
Why feed a small amount of forage before exercise?
It creates a food bolus to reduce acid splash
Why lower concentrate diets?
They decrease intragastric fermentation and acid load
What is the main caution with supplements for ulcers?
Many lack strong randomized clinical control studies
What may sea buckthorn berry extract help with?
Glandular ulcers but did not improve squamous ulcers in study
What effect can oils such as canola have?
They may lower gastric acid output because of it has an omega 3:6 ratio which is has anti-inflammatory effects
What do antacids do?
They may increase gastric pH but need to be given every 2 hours
When might antibiotics/probiotics help?
Possibly with non-responsive ulcers
What do pectin-lecithin complexes do experimentally?
Increase total mucus concentration in gastric juice
What supplement combination has shown promise as prophylaxis for ESGD and EGGD?
Magnesium hydroxide
pectin-lecithin complex
Saccharomyces cerevisiae
What is strangles?
A contagious respiratory infection of horses caused by Streptococcus equi equi
What organism causes strangles?
Streptococcus equi equi
Why is it called “strangles”?
Swollen lymph nodes can compress the trachea and interfere with breathing
What does severity of strangles depend on?
The horse’s immune status
How do older horses usually respond?
They tend to have less severe disease
When does fever occur after exposure to strangles?
About 3–14 days after exposure
What are common clinical signs of strangles?
Fever
snotty nose
swollen/abscessed submandibular or retropharyngeal lymph nodes
sore throat/pharyngitis
lethargy
Which lymph nodes commonly swell or abscess with strangles?
Submandibular
retropharyngeal
What emergency airway procedure may be needed if swelling prevents breathing?
Tracheostomy
Why might intubation be difficult in severe strangles?
Hard lymph node abscesses and swelling can obstruct the airway
How is strangles spread?
By nasal shedding
When does nasal shedding start?
About 2–3 days after fever begins
How long does shedding usually persist in most horses?
About 2–3 weeks
Can horses shed after appearing recovered?
Yes. Some horses shed longer after recovery
What percentage of horses may become long-term subclinical carriers?
About 10%
Where do long-term carriers often harbor bacteria?
The guttural pouch
What is chronic empyema?
Chronic accumulation of pus, especially in the guttural pouch
What are chondroids?
Hardened pus “stones” that can form with chronic empyema.
What signs may long-term carriers show?
rare but:
Sporadic cough
intermittent nasal discharge
What percentage of horses develop solid immunity after strangles?
About 75%
How long can immunity last after strangles?
Around 5 years or longer
Does Streptococcus equi equi readily persist in the environment?
No. Good sanitation reduces spread
What samples can be used to diagnose strangles?
Nasal swabs
nasal washes
pus from abscesses
What does PCR detect in strangles diagnosis?
bacterial DNA dead or alive