HORSE MEDICINE Flashcards
fWhat are the top 3 differentials for weight loss in a horse
1) Nutrition (low quantity or quality)
2) Dental Disease
3) Parasite
What are your differentials for a horse with weight loss
1) Increased demand - illness, pregnancy/lactation, increased workload, environmental factors
2) Inadequate intake - low quantity, low quality, low uptake (dental disease or GI disease)
3) inappropriate utilization - liver disease, GI disease (malabsorption or maldigestion, parasites)
What should you do if a horse presents to you with weight loss?
-Measure quantity of feed
-Measure quality of feed consumed
-Check teeth
-Perform a fecal
-blood work, abdominal U/S, abdominocentesis, abdominal x-rays, absorption testing
How do you determine the caloric maintenance requirements for a horse
Maintenance: 0.033 x BWT (kg)
light work: x 1.2
moderate work: x 1.4
hardwork: up to x 1.9 DE for maintencane
Charlie is a 12yo QH gelding weighing 500kg (1100Ib) in excellent health and a couch potato. How many calories does Charlie need per day?
Maintenance: 0.033 x 500kg = 16.7 Mcal/day for weight maintenance
This can be divided to 0.8Mcal/Ib (Hay) or 1.3Mcal/Ib
100% forage diet = 20.8Ibs (2% body weight)
90% forage/10% grains = 18.8 Ib forage / 1.3Ib grain
about 4 flakes a day
T/F: grain is an essential part of the horse’s diet
False- grain is not an essential part of the equine diet
*Cornerstone of the diet is hay
Hay should meet as mich of the horse’s protein, energy and fiber needs are possible
T/F: all hay “flakes” are created equally
False
but a flake of small bale hay is about 5Ibs
A flake is about
5 pounds of hay- not all are created equally
The digestible energy and nutritive value (quality) of hay is dependent on the
plant maturity at the time of harvest
Hay analyses look for
Increased in Crude protein
Decreased in acid detergent fiber (ADF: lignin and cellulose (digestibility of nutritionist))
Decreases in neutral detergent (NDF: structural carbohydrates)
Alfalfa that is in early bloom has _________ calories/pound, ________ crude protein, and ______ Ca2+ than alfalfa in full bloom
Early bloom: more calories, more crude protein, more calcium
What hay has the highest Crude protein
a) alfalfa (early bloom)
b) alfalfa (full bloom)
c) orchard grass (early bloom)
d) timothy (early bloom)
alfalfa (early bloom)
What hay has the highest mcal/Ib
a) alfalfa (early bloom)
b) alfalfa (full bloom)
c) orchard grass (early bloom)
d) timothy (early bloom)
alfalfa (early bloom)
What hay has the highest Ca++ %
a) alfalfa (early bloom)
b) alfalfa (full bloom)
c) orchard grass (early bloom)
d) timothy (early bloom)
alfalfa (early bloom)
How often do you need a horse
If possible allow access to feed (hay) 24hrs/day
Preferable feed small meals frequently
Lily is a 4yo TBH mare weighing 450kg (1000Ibs) that is a race horse- hard to keep weight on her. How many calories does Lily need per day?
0.0363 x 450kg x 1.9 = 31Mcal/day for maintenance weight of heavy exercise animals.
Hay= 0.8Mcal/Ib
100% hay diet = 24.8 Ibs hay/day
Grain 1.3Mcal/day
70% hay diet = 17.36 Ib hay/day ; 30% ???
How many calories does hay typically have in it
0.8Mcal/Ib
How many calories does grain typically have in it
1.3Mcal/Ib
How can you add more high fat content into a horse’s diet, which is popular for equine athletes
-Vegetable oils
-Linseeds
-Ricebran
High fat diets in horses, like with vegetable oils, linseeds, and ricebran spares the use of _____________ and increases the use of ___________
this leads to less production of lactic acid and heat during exercise
spares use of glucose/glycogen and increases the use of body fat
*Requires an adaption period of 3 weeks
How long does it take for a horse to adapt to a high fat diet to spare the use of glucose and increase the use of body fat and reduce excitable behavior in horses
about 3 weeks
What effect does carbs (certain grains) have on a horse’s behavior
certain grains can make horses hot
Dietary fats (corn oil) reduce excitable behaviors in horses
Vegetable oils, such as corn oil, may offer natural protection against__________
gastric ulceration
What are the benefits and disadvantages of using a fat supplemented diet in horses
Pros: energy density, no mastication required, less risk of GI disturbance, behavioral benefits, GI protection (ulcers), glycogen sparing effect
Cons: weight gain, reduced palatability, cost, messiness, shelf life (unsaturated FA), insulin sensitivty?
Vegetable oils vary in terms of proportions of
1) Saturated vs unsaturated fatty acids
2) Omega 3 vs omega 6 fatty acids
Canola, corn, flaxseed, olive, soybean, and sunflower are all types of
vegatable oils
differ in their proportions of saturated vs unsaturated fatty acids and omega 3 vs omega 6 fatty acids
Why do we not just feed horses more grain
health problems associated with feeding large grain meals
Digestive disturbances: colic, colitis, diarrhea, gastric ulcers, laminitis (endotoxin)
Metabolic: laminitis (insulin resistance), tying up, obesity, hoint disease, hyperlipemia
How do oats differ from corn
Oats: palatable, best nutrient balanced, starch is foregit digested, “sugar high”
Corn: denser than oats (overfeeding), not nutrient balanced, starch mostly hindgut digested (hindgut acidosis and colic) unless processed
Are oats or corn more likely to cause a sugar high
oats
Are oats or corn more likely to cause hindgut acidosis
Corn- it is mostly hindgut digested (oat is foregut digested) corn needs to be processed
Forage based diets are typically deficient in
trace minerals (copper, zinc) and vitamins
provide vitamin/mineral supplements to the diet
YOu should limit concentrates to about
3Ibs/meal (if they are even needed at all)
To increase the energy content of a horse’s diet ________
supplement with fats, rather than carbohydrates
________ can be fed to a horse whole while ______ needs to be processed
oats ; corn
Asa general rule of thumb, you should aim for approximately _____ percent of a horse’s BW in hay/day
2%
What are good indicators of hay quality
Numerous factors affect the quality of hay and include the type of hay, maturity of the plant at harvest, season of harvest, handling of the crop during harvest and storage condition.
In general, the characteristics of good quality roughage include high leaf-to-stem ratio, fresh smell and appearance, cleanliness, and natural color. Despite the fact that these characteristics are good indicators of quality, hay should be analyzed to determine its actual nutrition content especially if it is being fed to horses suffering from endocrine/metabolic conditions.
The following statement is TRUE or FALSE?
Grain is not an essential part of the equine diet.
True
Despite the fact that many horse owners consider a normal equine diet to consist of hay and grain(s), grains are not an essential part of a horse’s diet. Forage (e.g. pasture, hay) should meet as much of the horse’s proteins, energy, and fiber needs as possible.
When additional energy is needed, it is safer to use fats and fermentable fibers before grains. Modern feeds with added fat and digestible fiber are recommended over high-starch feeds.
T/F The starch contained in whole corn is mostly hindgut digested, thus increasing the horse’s risk of developing hindgut acidosis.
True
Most of the starch (72%) from whole or cracked corn is not digested in the foregut and proceeds to the hindgut where it is rapidly fermented. That process results in the production of lactic acid, which lowers the large intestinal pH (=hindgut acidosis) which can result in bacterial death and endotoxin release. For these reasons, corn should be processed (e.g. ground, pelleted, extruded) for all horses, and pelleted feeds should not contain more than 25% of corn.
Please calculate the energy needs for a 1,200 lbs horse with a normal metabolism that performs a moderate amount of work.
How many flakes of grass hay would you need to feed to provide 100% of this horse’s energy needs?
The energy requirements for a 1,200 lbs horse (=545 kg) with a normal metabolism (0.0333 Mcal/kg) and a moderate workload (X 1.4) are the following:
1.4 X 545 kg X 0.0333 Mcal = ~ 25.4 Mcal/day
Additional information needed:
1 lbs of hay contains approximately = 0.8 Mcal/lbs
1 flake of hay weighs approximately = 5 lbs
The number of flakes of hay this horse needs to be fed to cover 100% of its energy needs is:
25.4 Mcal/day /0.8 Mcal = 31.76 lbs of hay
31.76 lbs / 5 lbs = 6.35 flakes ~ 6 flakes of hay
What are the clinical signs of equine esophageal disease
-Dysphagia
-Frequent swallowing
-Coughing
-Hyper-salivation (ptyalism)
-regurgitation of feed (mouth, nostrils)
-Anxiety, neck stretching
-Swilling, emphysema
T/F you should use barium if perforation is suspected
False- do not use barium if perforation is suspected. barium within the tissue can cause inflammation
What is nasogastric intubation in a horse used for
passage of nasogastric tube can help determine if there is an obstruction present. If esophageal obstruction (choke) is suspected, care should be taken not to damage the mucosa.
can sometimes be passed beyond the obstruction and enter the stomach, giving false impression that either an obstruction did not exist of had been relieved. Esophageal perforation at obstructed site may also allow passage of tube beyond the obstruction. If the perforation is cervically located, the tube may ass subcutaneously to the thoracic inlet
What should you be careful for when doing nasogastric intubation to check for choke
avoid causing more damage to the esophageal mucosa
What is the color of the normal esophageal mucosa
whitish-tan to slightly
The esophagus is normally _______ when coated with the barium solution, allowing visualization of the smooth, longitudinal folds
collpased
What should you give a horse for sedation when performing a good oral examination
-A2 agonists - Xylazine or Detomidine
-Acepromazine
-Buscopan-muscle relaxant
-Methocarbamol (Robaxin)
-Lidocaine (topical)
Why is the use of atropine for oral examination controversial
it will only relax the smooth muscle of the distal 1/3 esophagus, which is not where the chokes usually occur. also risk for colic (GI ileus)?
What is the most common esophageal disorder in horses
esophageal obstruction- usually due to intraluminal impaction
The proximal 2/3 of the horse esophagus has no serosal layer, meaning it
takes longer to heal
What are vital structures adjacent to the esophagus that are at risk with choke
-Vagosympathetic trunk
-Recurrent laryngeal nerve
-Carotid artery
High choke means there is is an esophageal obstruction in the
cervical part of the esophagus- at risk for aspiration pneumonia
Low choke means there is an esophageal obstruction in the
thoracic inlet
Intrathoracic choke is rare but it means that there is an esophageal obstruction in the
lower esophageal sphincter
How do you treat esophageal obstructions in horses
1) Sedation/Muscle relaxation (Xylazine/ Detomidine or Acepromazine and then allow a nasal gastric tube to help pass the obstruction into the stomach. Avoid pressure if not removed do lavage
2) Lavage
3) Drugs : NSAIDs, antibiotics (broad spectrum if aspiration)
4) Support: treat dehydration and electrolytes, treat esophageal inflammation and aspiration pneumonia. Horses with excessive salivation will have hypochloremic metabolic alkalosis - give 0.9% NaCl
T/F you should use lubricating agents, such as mineral oil and softening agents (DSS) during lavage to relieve esophageal obstructions in horses
False- they are contraindicated - cause granulomatous pneumonia because they are non-degradable
What are the predisposing factors of esophageal obstructions in camelids
The bosses that are dominant
greed eaters
pelleted foods
How do you treat esophageal obstructions in camelids
needle trocar if bloated
sedation
antibiotics if aspiration occured
prolonged salivary salivary loss: metabolic derrangements
may need general anesthesia/intubation/gentle lavage
may follow choke
results in weight loss, regurgitation, recurrent choke, recurrent bloat
most are idiopathic but can result from organophosphates and myasthenia gravis
Megaesophagus
What solution should you use when doing lavage to dislodge an esophageal obstruction
warm water, preferably with 0.9% sodium chloride solution
Which of the following clinical signs is NOT found in a horse with esophageal disease?
Dysphagia
Ptyalism
Diarrhea
Stretching of neck
Coughing during swallowing
Diarrhea
The hallmark of esophageal disorders in the horse is dysphagia. Additional clinical signs, particularly for proximal esophageal disorders, include frequent, ineffectual attempts to initiate swallowing, coughing during swallowing, ptyalism (excessive salivation), and nasal regurgitation of feed mixed with saliva. Other clinical signs include anxiety, restlessness, and stretching of the neck.
The following statement in TRUE or FALSE?
An esophageal feed obstruction (choke) should be treated as a medical emergency.
True
Esophageal obstruction should be considered an emergency because prolonged pressure on the esophageal mucosa by the obstructing material can result in extensive tissue damage, with subsequent scar tissue formation and stricture.
Treatment of a horse with an esophageal obstruction (choke) typically consists of administration of heavy sedation, passage of a nasogastric tube, and gentle lavage with warm water.
What is/are the goals for administering sedation?
Relaxation of the esophageal musculature
Allowing safe handling of the horse
Reducing the risk of fluid aspiration when lavaging
All of the above
All of the above
the margo plicatus is a
distinct margin that separates the non-glandular and glandular portion of the stomach.
has stratified squamous epithelium and serves to contain the horse’s food without aiding in the chemical breakdown of the ingesta
non-glandular portion (squamous mucosa)
What are the 4 types of secretory epithelial cells that horses have on their glandular mucosa. What do they secrete?
Mucous cells: secrete an alkaline mucous
Parietal cells: secrete HCl
Chief cells: secrete pepsin
G cells: secrete gastrin
How might equine gastric rupture occur
abnormalities which interfere with the normal aboral movement of fluid through the small intestine may cause the accumulation of fluid in the stomach. Severe gastric dilation can occur and then rupture if not reated
What allows there to be a one-way valve in the equine stomach
the anatomic arrangement of the esophagus and cardia
What kind of horse is gastric ulceration more common in
race horses
What causes gastric ulceration in a horse
an imbalance betweeh the mucosal aggressive factors (HCl, pepsin, bile acids, and organic acids) and the mucosal protective factors (mucus, bicarbonate, and mucosal perfusion)
Mucosa is damaged by excessive exposure to HCl and pepsin. Non-glandular mucosa response to acid irritation by increasing thickness of its keratin layer- only providing minimal protection.
Causes: Anything that impairs mucosal lining, NSAIDs, Stress, Impaired gastric blood flow, reperfusion injury
What is the predominant stimulato to hydrochloric acid secretion
gastric, histamine, and acetylcholine via the vagus nerve.
Gastric- g cells within the gastric glands
histamine- mast cells and enterochromafin-like (ECL)
Ingestion of feed stimulates acid secretion in horses, what is also stimualted by eating to buffer the acid?
bicarbonate-rich salivary secretions
What are the protective factors of equine stomach, secreted by the glandular portion
Mucous cells: alkaline mucous coating mucosa like a gel
also increased PGE2 secretion
What portion of the equine stomach is most sensitive to acid induced injury?
The squamous epithelium (non-glandular) less mucosal protective properties (thick mucus and bicarb later like glandular mucosa has)
What are the 5 causes of gastric ulcerations in horses
1) Strenuous exercise - less blood flow and increased acid contact time
2) Stress/illness- decreased PGE2, blood flow, and mucous with increased HCl
3) NSAIDS- Decreased PGE2, blood flow and mucous with increased HCl
4) Feeding- Lenght of meal, type of feed (saliva production, gastrin release, calcium content)
5) infectious causes- H. pylori
What might be an infectious cause of gastric ulceration?
Helicobacter pylori (sporadically been found in horses with gastric ulceration)
What are the clinical signs associated with gastric ulceration in adult horses
colic, poor body condition, poor hair coat, poor performance, changing appetite, attitude changes, “girthiness”, back pain
What is the difference in clinical signs of gastric ulceration of foals vs adult horses
Foals get diarrhea, excessive salivation (1-4mo),
f*oals can perforate
What are the clinical signs of gastric ulceration in foals
colic, teeth grinding, DIARRHEA, excessive salivation, reduced appetite
What can be unreliable tests for gastric ulceration in adult horses
Fecal occult blood test and constrast radiography
*Testing for fecal occult blood is only of value in young foals isnce the colonic microflora throughly digest hemoglobin
How do you treat gastric ulceration in horses
Management- avoid stress, allow access to feed 24hours/day preferable feed small meals frequently, vegetable oils may offer natural protection against ulceration
Medical to decrease gastric acidity and improve mucosal protection
Antacids- Mallox,
Proton pump inhibitor- omeprazole
Anti-histamines (Cimetidine, Ranitidine, Famotidin)
Mucosal protectants- Sucralafate, bismuth subsalylate, misprostol
PGE2 analog- Misprostol
What are drugs that serve as mucosal protectants for gastric ulceration
Sucralfate (bandage to unprotected surface, immediate pain relief, does promote healing, does not alter gastric pH, does not prevent ulceration)
Bismuth subsalicylate
Misoprostol (Synthetic PGE2 analog
serves as a bandage to unprotected surface, immediate pain relief, does promote healing, does not alter gastric pH, does not prevent ulceration
Sucralfate
Misoprostol is a
synthetic PGE2 analogue used to help gastric ulceration
Misoprostol is a synthetic prostaglandin E analog and has been shown to be effective in the treatment of gastric ulcers in humans and horses. The proposed mechanism of action involves both inhibition of gastric acid secretion and mucosal cytoprotection. Reported adverse effects include colic and diarrhea.
What is omeprazole’s mechanism of action
inhibiting proton pump which is the final pathway in hydrochloric acid secretion used to help with gastric ulceration
What is the prognosis for gastric ulceration
Good: if only squamous mucosa and management changes
Fair: if glandular mucosa
Poor: if perforated
What is the only definitive diagnostic for gastric ulceration
Gastroscopy
While a presumptive diagnosis of gastric ulceration is often based on the presence of age-related clinical signs and response to therapy, gastroscopy is the only definitive diagnosis currently available. Diagnostic procedures aimed at the detection of fecal occult blood or plasma protein (e.g. albumin) are unreliable.
True or false: duodenal ulcers and strictures are more common in adult horses than foals.
False: they are more common in foals.
What is the primary H2 antagonist used in horses with gastric ulcers?
Ranitidine
80% of equine gastric ulcers occur in which part of the stomach?
Squamous
The parietal cells in the glandular mucosa of the stomach produce the gastric hydrochloric acid.
Which of the following does NOT stimulate cellular HCl production?
A) Histamine
B) Prostaglandin
C) Acetylcholine
D) Gastrin
Prostaglandin
Which of the following is considered to be (a) factor(s) in gastric ulcer formation in horses?
Choose all that apply
Decreased PG E2 production
Increased mucosal blood flow
Large grain meals
Feeding alfalfa
Decreased mucosal blood flow
Decreased mucous production
Decreased PG E2 production
Large grain meals
Decreased mucosal blood flow
Decreased mucous production
Factors that have been implicated in gastric ulcer formation in horses include inhibition of prostaglandin E2 synthesis (e.g. by NSAID administration and stress). PG E2 increases blood flow to the stomach mucosa, promotes secretion of bicarbonate-rich mucus (which creates a lumen-to-mucosa gradient in pH from 1.5 to 6.5), and decreases acid secretion. In addition to decreased synthesis of PG E2, other factors that impair gastric blood flow (e.g. intense exercise) may also contribute to ulcer formation. Mucosal capillary perfusion is an integral component of mucosal protection, since disruption of mucosal perfusion readily produces ulcerations. Cellular restitution refers to the regeneration of surface epithelial cells in response to an irritating substance.
Eating behavior has also been shown to have an effect on the risk of gastric ulcer formation. For example, restricting access to roughage and feeding a large amount of concentrate (which reduces the time spent eating and increases postprandial gastrin release) promotes increased gastric acidity. In contrast, high roughage diets tend to stimulate production of bicarbonate-rich saliva, which will help buffer gastric acid. Concentrates stimulate a greater postprandial serum gastrin response than roughage, thus increasing hydrochloric acid production. Moreover, the calcium contained in alfalfa can act as a natural antacid buffer for hydrochloric acid.
What is the best diet for managing horses with gastric ulcers
Alfalfa- high calcium content acting as a natural antacid buffer for HCl
What is the most common gastric neoplasia in the horse
Squamous cell carcinoma (actually originate from squamous epithelium of esophagus)
How do you diagnose gastric neoplasia like squamous cell carcinoma in a horse
pass nasograstric tube for resistance
neoplastic cells may be found in fluid recovered by gastric lavage
Endoscopy- positive diagnosis and biopsy
laparotomy or laparoscopy
What are the equine liver specific enzymes
SDH- hepatocellular
GGT- biliary
What are the equine liver associated enzymes
AST + LDH: Hepatocellular
AP: biliary
Gamma Glutamyl Transferase (GGT)
a biliary specific enzyme
technically not liver specific (Renal tubules-released into urine; Mammary- secreted into colostrum; and pancreas)
What can release GGT
Liver
Renal tubule cells - into urine
Mammary glands - secreted into colostrum
Pancreas
What enzyme is high in colostrum fed ruminant neonates
GGT
T/F ALT is not useful in large animals
True
How do you differentiate between liver disease and liver failure
liver failure: inability to perform its normal function
1) Nutrient metabolism (Carbs, lipids, proteins)
2) Biosynthesis (protein biosynthesis)
3) Detoxification/Excretion (Bilirubin, blood ammonia, BUN, phylloerythrin)
4) Immunity
5) Digestion
Hepatic encephalopathy is a clinical sign of
liver failure
early: agitation, wandering
late: somnolence, coma
due to increased ammonia and decreased BUN excretion through the urea cycle
May be the first clinical sign of pyrrolizidine alkaloid toxicity or biliary obstruction
photosensitization
photosensitization is most severe on
non-pigmented skin where reactive compounds are most directly exposed to the UV spectrum.
What is the photosensitizing compound created during liver failure
phylloerythrin (normally removed from the liver, after chlorophyll is broken, and then removed by the liver and excreted in bile
Primary photosensitization
associated with photodynamic compounds foind in certain plants (Bishops weed, buckwheat, spring parsley, St Johns wort which are absorbed from the digestive react, react with the nonpigmented skin upon IV light.
associated with defective porphyrin metabolism in liver
Can be seen in liver failure because the liver is responsible for the synthesis of numerous factors evolved in coagulation and fibrinolysis
Coagulopathy/ hemorrhagic diathesis
What are the clinical signs of liver failure in horses
1) Hepatic encephalopathy (early: agitation, wandering/ late: somnolence, coma)
2) Photosensitization
3) Coagulopathy
4) Icterus
5) Weight loss
6) Edema and ascites
What are the 3 causes of icterus in the horse
1) Prehepatic - hemolysis
2) Hepatic- hepatocellular dysfuction
3) Posthepatic- cholestasis
*anorexia
in food animals: icterus is more often due to
likely due to hemolytic disease rather than hepatic and biliary disease
icterus is rare in cows
in horses: icterus is most likely caused by
anorexia, followed by hepatic and biliary disease
exception is foals- do not have enough fat stores, likely neonatal isoerythrolysis or Tyzzer’s Disease
How does equine liver disease result in weight loss
decreased feed intake, anorexia, loss of normal hepatocellular metabolic activites
Why do you get ecchymotic hemorhage, epixstaxis, melena, hematuria, and hemotomas in horses with liver disease
failure to synthesize II, V, VII, IX X
What factor has the shortest half life
Factor VII T1/2= 4-5hours
Will see deficiencies in extrinsic pathway first
Why do you see edema and ascites in horses with liver failure
Hypoalbuminemia,
secondary to vascular thrombis (hyperlipidemia in ponies)
half life of albumin is relative long (19-20 days) edema is a rare clinical sign
Why is edema a rare clinical sign in horses with liver failure
half life of albumin is relative long (19-20 days) edema
Blood concentration of bile acids will be _________ with liver disease
increased.
Serum concentration is not impacted by short term fasting (<14 hours). but prolonged fasting (>3days) will increase serum bile acids of three times the baseline.
What are the most commonly used equine liver function tests?
1) Serum bile acid concentrations
2) BUN
3) Dye elimination test - Bromsulphalein
4) Ultrasound and liver biopsy
What is Bromsulphalein (BSP) used for
A test for equine liver function. A substance that when injected is metabolized in the liver. Heparin tubes are collected 3,6,9,12 minutes.
BSP half life is prolonged when greater than 50% of hepatic function is lost
Why is a bile acid elevation not specific to equine liver failure
They are also increased when there is cholestasis and portosytemic shunting
Are CNS signs typically seen in acute or chronic equine liver disease
Acute
Is weight loss typically seen in acute or chronic equine liver disease
Chronic
Is photosensitivity typically seen in acute or chronic equine liver disease
Chronic
T/F: Chronic equine liver disease will often only have mild elevation of liver enzymes
True: Mild
T/F: Acute equine liver disease will often only have mild elevation of liver enzymes
False: often severe elevation in the liver enzymes
Theiler’s Disease typically impacts
adult horses
Tyzzer’s disease typically impacts
foals
Acute hepatitis in adult horses, acute onset with acute hepatic necrosis, liver failure, caused by viral etiology
Theiler’s Disease
What is the etiology of Theiler’s disease
A mystery but has a viral etiology.
Flaviviridae family- Theiler’s disease associated virus
Equine Parvovirus (EqPV-H) associated with antitoxin?
What is the causative agent of Tyzzer’s disease
Clostridium piliforme
What is the prognosis for horses with Theiler’s disease
guarded
What causes acite hepatitis, 7-42 days, often peracute with no signs of disease, killing foals with fever, anorexia, icterus, seizures, and coma
Tyzzer’s disease caused by Clostridium piliforme
What is the prognisis of foals with Tyzzer’s disease
extremely poor
Use supportive care, fluids, NSAIDs, nutrition, tx for hepatic encephalopathy
Does pyrrolizidine alkaloid toxicity cause acute or chronic liver failure in horses
Chronic liver failure- weight loss, photosensitivation, icterus, hepatic encephalopathy
The most common cause of chronic liver failure in horses in certain parts of the US
chronic megalocytic hepatopathy from pyrrolizidine alkaloid toxicity
Pathogenesis of pyrolizidine alkaloids
pyrroles alkylate nucleic acids and proteins (cross links DNA) stopping mitosis and protein synthesis. Hepatocytes then enlarge, forming megalocytes. When megalocytes die- fibrosis (cirrhosis) occurs
Hepatocytes around portal triad (zone 1) are affected first.
bile duct hyperplasia
can cross the placenta and toxic to the fetus
What area of hepatocytes are impacted first from pyrrolizidine alkaloid toxicity
Zone 1 is affected first (hepatocytes surrounding the portal triads)
What results in megalocytes?
pyrroles alkylate nucleic acids and proteins (cross links DNA) stopping mitosis and protein synthesis. Hepatocytes then enlarge, forming megalocytes.
pyrrolizidine alkaloid toxicity is typically diagnosed by presumptive signs, exposure history and lab evidence of hepatic disease. How do you get a definitive diagnosis
Liver biopsy- look for
1) megalocytosis
2) biliary hyperplasia
3) fibrosis
can also be detected in feed by high-performance liquid chromatography
What species is relatively resistant to pyrrolizidine alkaloids?
Sheep
-pre-graze pastures laden with PA containing plants
What is the prognosis for pyrrolizidine alkaloid toxicity
If fibrosis is present-> prognosis is poor
No treatment available
Serum bile acid concentration greater than 50umol/L is suggestive of grave prognosis
How do you manage a field with tons of pyrrolizidine alkaloid containing plants
Sheep
-pre-graze pastures laden with PA containing plants
Is an icteric horse more likely to be experiencing cholastasis or liver disease
Cholestasis
What is the cause of cholelithiasis in horses?
unknown but
Ascending infection, decreased bile flow and salmonella
What is associated with cholelithiasis in horses?
salmonellosis - ascending infection because they lack and exit port sphincter to prevent backflow of intestinal contents into the biliary tract.
Horses do not have an exit port sphincter in their biliary tract. Why is this clinically significant
salmonellosis and other enteric pathogens - ascending infection because they lack and exit port sphincter to prevent backflow of intestinal contents into the biliary tract.
How do you treat cholangitis/cholangiohepatitis in horses
Supportive care, antimicrobials, NSAIDs, liver support
Surgical approach is better (cholelithotripsy or choledochotomy)
What are the 3 clinical signs of cholangitis/cholangiohepatitis in horses?
1) Cholestais- icterus
2) Colic (recurrent)
3) fever (cholangitis)
What is the prognosis of cholangitis/cholangiohepatitis in horses?
poor if hepatic fibrosis is present.
What are your differentials for chronic liver failure in horses
-Pyrrolizidin Alkaloid toxicity
-Cholangitis/Cholangiohepatitis
-+/- Cholelithiasis
what are possible complication with liver biopsy in horses
hemorrhage
pneumothorax
peritonitis
abscess
*keep in mind they might have prolonged coagulation times with liver failure
What would you see on ultrasound if the horse has hepatomegaly
rounded edge and swollen
What are the intermediate hosts for liver flukes (Fasciola hepatica)
Snails
What causes bacillary hemoglobinuria
toxins produced by Clostridium hemolyticum (Clostridium novyi type D)
What is another name for Clostridium hemolyticum, the causative agent of bacilary hemoglobinuria
Clostridium novyi type D
What are the exotoxins that cause bacillary hemoglobinuria
beta toxin: phospholipase C- necrosis and hemolysis
eta toxin: tropomyosinase
theta toxin: lipase
*Cause hepatic necrosis and intravascular hemolysis
What is the pathogenesis of bacillary hemoglobinuria
spores of Cl. hemolyticum are ingested and cross the intestinal mucosa. spores reach the liver by portal circulation and can persist in the liver tissuw for long periods of time within the Kupffer cells. Following a hepatic insult (liver fluke migration, hepatic inflammation or abscesses, liver biopsy)
Creates an anaerobic environment , spores become activated and germinate, Beta, eta, and theta toxins are produced. causing hepatic necrosis and hemolysis, icterus, hemoglobinuria
In most cases, the liver insult seen in Red water disease by Clostrium hemolyticum (novyi type D) is due to
migration of Fasciola hepatica
What are the clinical signs of bacillary hemoglobinuria?
Hemolysis: Red serum/plasma, hemoglobinuria, anemia (pale mm, tachycardia)
icterus (pre-hepatic)
DIC
blood tinged frother (mouth and nose)
Rectal bleeding, blood in feces
ischemic hepatic infarct
What is another differential you need to rule out when an animal has bacillary hemoglobinuria?
Anthrax (Bacillus anthracis)
How do you diagnose bacillary hemoglobinuria
1) Fluorescent antibody test on impression smears taken from liver infarct for Cl. hemolyticum antigens
2) Necropsy- icterus, red urine, petechia, ecchymoses, red-tinged fluids, ischemic infarct
3) Clinically: anemia, increased plasma protein, DIC (fibrin degradation products, decreased platelet counts)
What does Clostridium novyi type D cause
Bacillary hemoglobinuria
What does Clostridium novyi type B cause
Blacks disease
What are the toxins of Clostridium novyi type B? What do they cause
alpha, beta, zeta (local and systemic effects)
Hepatic necrosis, endothelial damage*, resulting in passage of RBCs into tissue, neuronal damage
What are the clinical signs associated with Black’s disease
Animals usually found dead
Clinical signs are nonspecific
no red urine or external (nose/rectal) bleeding
What is seen upon the necropsy of an animal with Black’s disease
hemorrhage of suncutaneous tissues results in black discolaration of carcass - looks like diffuse bruising of all muscles
Diagnose with impression smear taken from the margin of the liver lesion - revealing numerous large gram + rods. Confirm diagnosis with fluorescent antibody testing to identify Cl. novyi type B should be performed
How do you diagnose Black’s disease
Diagnose with impression smear taken from the margin of the liver lesion - revealing numerous large gram + rods. Confirm diagnosis with fluorescent antibody testing to identify Cl. novyi type B should be performed
How do you prevent Blacks disease
vaccination - last 5 to 6 months
control flukes
How do you prevent Bacillary hemoglobinuria
vaccination - last 5 to 6 months
control flukes
Decreased production is a sign of acute or chronic liver failure in cattle
Chronic disease
________ are a common complication of ruminal acidosis
Liver abscesses
What kind of ruminants are at risk for developing liver abscesses
ruminants that are fed excessive amounts of fermentable carbohydrates (grains/concentrations, finely ground silage) generally, starch and sugars
common among feedlot cattle (25-30%)
What causes bovine liver abscesses
during ruminal acidosis (ruminitis), typically when fed excessive amounts of fermentable carbohydrates,, Fusobacterium necrophorum overgrows and invades the eroded wall and is carried by the portal circulation to the liver. Once lodged it produces toxins that destroy keukocytes and aids in pathogenic process
What causes liver abscesses in neonatal calves
ascending infection of the umbilical vein.
Prevent with good hygiene and umbilical disinfection
Symptoms of liver abscesses in cattle
-Subclinical: reduced gain, decreased productivity
Laminitis
Endotoxemia (Rumen acidosis)
Less common: acute hepatitis: fever, arched back, mild colic due to hepatic swelling
Caudal vena cava syndrome- abscess can erode into the caudal vena cava, producing caudal vena cava thrombosis
What is caudal vena cava syndrome
a serious sequela following liver abscesses- erosion into the caudal vena cava
produces caudal vena cava thrombosis
How do you diagnose liver abscesses in cattle
*Farm HX (production, liver abscesses, laminitis
Inflammatory leukogram with hyperfibrinogenmia in acute stage
Increased liver enzymes (SDH, AST, possibly GGT, and AP) in the acute stage
Subacute to chronic- hematology and chem may be normal, although TP may be evident from immunoglobulin production
How do you treat liver abscesses in cattle?
Prognosis for complete recovery is poor
How do you prevent liver abscesses in cattle?
gradual change of the amount of carbohydrates fed (3-4 week period)
feed ration in small amounts frequently
add antibiotics to reduce incidence of liver abscesses in high risk feeder cattle (commonly Tylosin)
Avoid slug feeding with refers to ingestion of large quantities of grain-rich ration.
within the cell wall of all gram negative bacteria
released during replication and death
can cause shock if released into circulation
endotoxins
T/F: endotoxins are within the cell wall of all gram negative bacteria
True
Are endotoxins or exotoxins heat resistance
Endotoxins
What are the components of endotoxins
1) Lipid A (hydrophobic)
2) O-specific polysaccharides (Hydrophilic)
3) Core region (Hydrophilic)
What prevents the absorption of most of the endotoxins from being absorbed?
Mucosa barrier:
epithelial cells
antibodies
enzymes
How does impaired liver function result in endotoxemia?
failure to filter out toxins, bacteria, etc.
How might there be an impairment in the mucosa leading to endotoxemia
ischemia and inflammation allow endotoxins to enter into the circulation
-Inflammation changes the permeability of the mucosa when diseases
this causes massive portal bacterial and toxins overload the liver leading to endotoxemia and sepsis
What happens once endotoxins enter the circulation
it interacts with circulating proteins (LPS binding protein) or it may be removed by macrophages in liver, spleen and pulmonary vasculture.
LPS binding protein interacts with lipid A portion of endotoxin.
Combination of LBP and and endotoxin interact with cell surface receptor, CD14- a patter recognition receptor on phagocytes
Soluble CD14 can also interact with LBP/endotoxin to activate cells without receptor (endothelial cells)
Signals are intracellularly transmitted to signal release of proinflammatory mediators (TNF-a + Tissue factor) and anti-inflammatory mediators (IL-10)
What is released when LPS binding protein and endotoxin is bound to CD14
Proinf: TNF-a and tissue factor
Anti-inflammatory: IL-10
TNF-a is a
proinflammatory mediator/cytokine released after the onset of endotoxemia. Initiates a cascade of responses:
-Hypotension
-Hemoconcentration
-Metabolic acidosis
-DIC
Stimulates synthesis of Interleukins, acute phase proteins, tissue factor
TNF-a concentration has been associated with prognosis for survival
What is a result of TNF-a in endotoxemia
-Hypotension
-Hemoconcentration
-Metabolic acidosis
-DIC
Stimulates: interleukins, acute phase proteins and tissue factor
The majority of the effect seen in endotoxemia are due to
overproduction and release of inflammatory mediators by the immune cells
A glycoprotein synthesized by mononuclear phagocytes and mononuclear in response to endotoxin. Comes into contact with coagulation factor VII in plasma- activating the extrinsic arm of the coagulation cascade. Formation of microthrombi
Makes the vasculature sticky, leaky, and soggy
Tissue factor
What does it mean when endotoxin makes the microvasculature “sticky, leaky, and soggy”
Results in
1) Leukopenia- leukocyte margination
2) Fluid leakage- hypovolemia and hypoproteinemia
3) Pooling of blood in microvasculature- injected blood vessels and hypotension
How does endotoxin cause leukopenia and neutropenia
activated endothelium, margination, from sticking against the vascualar wall
Endotoxemia causes (Hypotension/Hypertension)
Hypotension
What are the clinical diseases associated with endotoxemia
1) Sepsis
2) Colic
3) Colitis
What are the clinical signs of endotoxemia
1) Increased HR and RR
2) Ileus
3) Mild to moderate colic
4) Congested mucous membranes
5) Injected vessels
6) Increased CRT
7) Decreased peripheral pulses
8) DIC- thrombosis, petechiation, ecchymosis
9) Laminitis- may progress after systemic signs improve
10) Hemoconcentration
How do you treat endotoxemia in the horse
1) Prevent uptake of endotoxin into the circulation: Remove source- umbilicus, colic surgery, effusions or bind endotoxin within the GI lumen using a Bio-sponge and activated charcoal
2) Neutralization of endotoxin already present in system: Antiendotoxin antiserum (core and lupud A, enhances opsonization- has some adverse reactions) or polymyxin B- antibiotic that forms complexes beneficial effect seen but has nephrotoxicity
3) Prevention of release of inflammatory mediators
NSAIDS- prevent endotoxin-induced synthesis of prostaglandins and thromboxane- give Flunixin Meglumine- low dose to decrease nephrotoxicity risk
Glucocorticoids- No beneficial effects- increase likelihood of laminitis
4) Prevention of endotoxin-induced cellular activation
Toxic oxygen metabolite scavengers- Allopurinol or DMSO- reduces mucosal injury and prevent receptor interaction and tissue injury
How do you prevent the uptake of endotoxins in the horse
Remove source- umbilicus, colic surgery, effusions or bind endotoxin within the GI lumen using a Bio-sponge and activated charcoal
How do you neutralize endotoxins in the circulation
1) Antiendotoxin antiserum: antibodies directed against the core and lipid A regions to enhance opsonization of intact bacteria, remove endotoxin from the blood- given 1.5ml/kg
2) Polymyxin B- broadspectrum antibiotics that forms a stable complex with lipid A for the treatment of endotoxemia in horses . Can cause respiratory paralysis and nephrotoxicity
broadspectrum antibiotics that forms a stable complex with lipid A for the treatment of endotoxemia in horses . Can cause respiratory paralysis and nephrotoxicity
Polymyxin B
antibodies directed against the core and lipid A regions to enhance opsonization of intact bacteria, remove endotoxin from the blood- given 1.5ml/kg
Antiendotoxin antiserum
Why should you not use glucocorticoids in treating endotoxemia in horses
because it increases the risk of laminitis
Do you want to use low or high dose of Flunixin Meglumine (Banamine) in treating endotoxemia in horses?
Low dose (0.25 mg/kg QID,TID
decreases risk of nephrotoxicity
What NSAID should you use to present inflammatory mediator (prostaglandins and thromboxane) release in horses with endotoxemia?
Flunixin Meglumine (Banamine)
low dose to decrease risk of nephrotoxicity
What is Allopurinol used for
it is a hydroxyl radical scavenger and inhibitor of xanthine oxidase activity, prevents toxic oxygen metabolities from causing damage during endotoxemia
it is a hydroxyl radical scavenger and inhibitor of xanthine oxidase activity, prevents toxic oxygen metabolities from causing damage during endotoxemia
Allopurinol or DMSO
The following statement is TRUE or FALSE?
The presence of photosensitization in horses and livestock species is always indicative of liver disease/failure?
True
False
The statement is false.
Photosensitization can be classified into two basic types; primary and secondary.
Primary photosensitization is associated with photodynamic compounds found in certain plants (e.g. Bishop’s weed, Buckwheat, Spring parsley, St. John’s wort), which once absorbed from the digestive tract, react in the nonpigmented skin with UV light.
Secondary or hepatogenous photosensitization, as the name implies, results when an animal’s liver is sufficiently diseased to be unable to remove plant by-products that can react with UV light. Phylloerythrin, a bacterial breakdown product of chlorophyll, is the photosensitizing compound. Normally, phylloerythrin is removed by the liver and is excreted in bile. Hepatic photosensitization can be further subdivided into that attributable to hepatocellular disease as opposed to that caused by biliary disease and cholestasis.
Which of the following CBC abnormalities is commonly seen in the early stages of endotoxemia?
In the early stages of endotoxemia and sepsis, profound neutropenia with toxic neutrophil morphology with a left shift is often evident. Neutropenia is due to margination and transmigration of cells and occurs within an hour of onset of endotoxemia. Other abnormalities notes on the CBC and biochemistry panel reflect nonspecific secondary changes (e.g. hyperglycemia, polycytemia and metabolic acidosis due to hypovolemia, azotemia due to hypovolemia and hypotension).
Which of the following drugs binds circulating endotoxin, thereby preventing its interacting with receptors and hastening its elimination?
Polymyxin B
Polymyxin B is a broad-spectrum antibiotic that forms a stable complex with lipid A, thus preventing its interaction with cellular receptors and hastening its elimination.
Flunixin meglumine (Banamine) is a NSAID and reduces the synthesis of inflammatory mediators.
Dimethyl sulphoxide (DMSO) is a potent scavenger of hydroxyl radicals.
Allopurinol is a hydroxyl radical scavenger and inhibitor of xanthine oxidase activity
Dexamethasone is a glucocorticosteroid and is a potent inhibitor of inflammatory mediator synthesis. Despite this, no beneficial effects of steroid use was found in large, multicenter studies of humans with gram-negative sepsis. In addition, corticosteroids are also often implied to increase the likelihood of laminitis in endotoxic horses. Thus, corticosteroids are not recommended in the treatment of endotoxemia.
Endotoxemia is unlikely to occur in which of the following disease processes?
Large colon impaction
Strangulating lipoma
Pleuropneumonia
E. coli mastitis
Colitis
In horses, most diseases characterized by endotoxemia/sepsis affect the gastrointestinal tract (e.g. intestinal inflammation or ischemia) or involve bacterial infections of the pleural or peritoneal cavities. In cattle, gram negative mastitis and metritis are common causes for endotoxemia. As large colon impactions typically do not result in an impairment of the intestinal barrier, they are usually not associated with endotoxemia.
Which of the following clinical signs are commonly encountered in endotoxic horses?
Tachycardia
Injected scleral blood vessels
Coughing
Colic
Laminits
Urticaria
Tachycardia, injected scleral blood vessels, colic, and laminitis
Horses given endotoxin experimentally develop tachycardia, a fever, ileus, mild to moderate abdominal pain (e.g. pawing, looking at flank region, stretching out, lying down), congested mucous membranes (+/- a “toxic” line), prolonged the capillary refill time (CRT), as well as signs of dehydration, such as reduced skin turgor, tacky mucous membranes, hemoconcentration (↑ PCV), rapid and weak peripheral pulses, cold extremities, and sweating. Vascular damage and hemorrhagic diathesis may be seen as petechial and ecchymotic hemorrhages. A poor prognostic sign is the development of a hypercoagulative state, with thrombosis of vessels, and subsequent increased bleeding tendency (a consequence of platelet and coagulation factor consumption and uncontrolled activation of fibrinolyis). Signs of laminitis, a complication of endotoxemia, may also develop.
What are the two types of infiltrative intestinal diseases?
1) Inflammatory (IBD) - granulomatous enteritis, lymphocytic-plasmacytic, idiopathic eosinophilic, multisystemic eosinophilic epitheliotrophic disease (MEED)
2) Lymphosarcoma
What do horses with small intestine disease not get?
Diarrhea (diarrhea is apparent in large intestinal disease)
they only get weight loss
What are the clinical signs of equine small intwstinal disease
1) Weight loss and lethargy- thickening of mucosa and blunting of the villi -> malabsorption
2) Edema- loss of tight junctions and ulcerations leading to protein loss and edema
3) Depending on type, severity and location- colic (granulomatous enteritis and eosinophilic enteritis) and skin lesions -eosinophilic enteritis and MEED
How do you get edema with equine small intestinal diseases
loss of tight junctions and ulcerations leading to protein loss and edema
How do you get weight loss with equine small intestinal diseases
Weight loss and lethargy- thickening of mucosa and blunting of the villi -> malabsorption
agregates of macrophages and epitheloid cells, occasionally giant cell macrophages, usually diffuse across the small intestine
granulomatous enteritis
infiltration of the mucosa and submucosa with eosinophils, lymphocytes, and macrophages- segmental/multifocal across small intestine, skin, oral cavity, esophagus, salivary glands, liver, lung, mesenteric lymph nodes, and pancreas
MEED- multisystemic eosinophilic epitheliotrophic disease
How will small intestinal infiltrative disease look like on ultrasonography
thickened small intestine, several loops of moderately distended small intestine
What test can you se to detect malabsorption in horses with granulmatous enterities and lymphocytic-plasmacytic enteritis
Carbohydrate absorption test.
Horse fasted for 18 hours
10% solution of glucose of D-xylose is goven through nasogastric tube
Blood for glucose/D-xylose is collected at 0,30,60,90,120,150,180,210,and 240 minutes
Plasma peak levels should occur between 60 and 120 minutes. Delayed or flattened peaks are consistent with malabsorption diagnosis
when should the peak in the carbohydrate absorption test occur in order to rule out malabsorption
Peak should occur between 60-120 minutes after administering glucose/D-xylose
How is a carbohydrate absorption test performed?
Carbohydrate absorption test.
Horse fasted for 18 hours
10% solution of glucose of D-xylose is goven through nasogastric tube
Blood for glucose/D-xylose is collected at 0,30,60,90,120,150,180,210,and 240 minutes
Plasma peak levels should occur between 60 and 120 minutes. Delayed or flattened peaks are consistent with malabsorption diagnosis
How is infiltrative intestinal disease definitively diagnosed?
Biopsy and histopathology to see the predominant cell type present in the intestinal lesions
-exploratory celiotomy or flank laparotomy is required
How do you treat infiltrative bowel disease
-Corticosteroids (limit timing)
-Metronidazole- anti-inflammatory and antimicrobial (no idea on efficacy
-Anthelmintics (eosinophilic enterocolitis)
Adult horse diarrhea usually involved abnormality in the
large intestine (large colon +/- cecum)
What are your differentials for diarrhea in a horse
1) Salmonellosis *
2) Intestinal clostridiosis (Cl. difficile and Cl. perfringens)*
3) Potomac Horse Fever*
4) Equine coronavirus*
5) antibiotic-associated colitis*
6) NSAID toxicity
7) intestinal parasites
8) nutritional causes
9) sand induced
10) toxin exposure
11) peritonitis *
*=usually acute
Salmonella in a horse typically causes (acute/chronic) diarrhea
usually acute
Intestinal clostridiosis (difficile and perfringens) in a horse typically causes (acute/chronic) diarrhea
usually acute
Potomac horse fever in a horse typically causes (acute/chronic) diarrhea
usually acute
Equine coronavirus in a horse typically causes (acute/chronic) diarrhea
usually acute
Antibiotic-associated colitis in a horse typically causes (acute/chronic) diarrhea
usually acute
What are some common diarrhea causing parasites in horses
Cynthostomiasis
Strongylus vulgaris
Parascaris equorum
Cryptosporidia
What is the diagnostic approach to diarrhea in a horse
-CBC/Chem/VBG, UA
-Abdominal ultrasonography +/- abdominocentesis- assessment of bowel wall thickness (severity and prognosis)- rule out sand and peritonitis
-Fecal examination- PCR analysis (IDEXX diarrhea panel), fecal egg count (cyathostomiasis, ascarids), check for sand (sedimentation)
-Abdominal x-rays (sand and assess amount
-Other test (aerobic culture for salmonella, anaerobic culture for Clostridia spp, CLostridial toxin ELISAs, PHF serology
A gram - facultative anaerobe that causes acute diarrhea in the horse
Salmonella
type species S. bongori and S. enterica
what are the risk factors for salmonellosis in the horse
-Age
-Stress (shipping, surgery, feed changes, illness)
-Disruption of GI flora and motility (colic and ABCs)
-Environment- hot and humid, persistence, multiplication
-Insects (mechanical fectors)
-Birds- vector and resevoir
-Other horses: feco-oral, aergoenous, fomites, water, feeds
-Cattle- Vertical from S.dublin
-Rodents- vector and reservoir
What are the clinical signs of Salmonellosis in horses
1) Asymptomatic: from lower infectious dose, varying prevalence
2) Colitis: fulminant disease- pipe stream diarrea- ileus, colic, and laminitis
3) Abortion- S. abortus equi not seen in US in decades
4) Febrile illness- delayed onset of signs, rapid fecal shedding, mild change in fecal consistency, often self-limiting
5) Sepsis - often fatal, isolation from liver, mesenteric lymph nodes, kidney, foals: joints
How do you diagnose salmonellosis in horses
culture of fecal sample using enrichment techniques (enrichment broth of Selenite or tetrathionate) and selective media (XLD agar: xylose-lysine deso-oxycholate) keep samples chilled and place directly in enriched media
aerorbic culture
potentially PCR
How do you treat Salmonellosis in horses
Early- replace lost fluids
not much that you can do
antibiotics is controversial unless they are neutropenic or patient has signs of septicemia then use a broad spectrum antibiotic
How does intestinal hyperammonemia in horses occur
due to increased blood NH4+ concentration
1) increased absorption due to altered permeability of GI wall
2) Increased production, overgrowth of ammonia producing bacterial
3) Failure of liver to clear ammonia leading to hepatic encephopathy*** most likely
*Prognosis is guarded to poor if severe strcutural gastrointestinal lesions
What is the most likely cause of intestinal hyperammonemia in the horse?
Failure of liver to clear ammonia leading to hepatic encephopathy
What is the pathogenesis of Salmonellosis
1) most commonly oral infection
2) Attachement to mucosal cells- increased if GI stasis is present
3) Inflammation triggered - causes focal and diffuse PMN infiltrates, epithelial necrosis, edema formation
4) Tissue invasion and dissemination- gain entry via mononuclear phagocytes, M cells, and lymphatic system
How does salmonella gain entry
via mononuclear phagocytes, M cells, and lymphatic system
What are the post-mortem findings of a horse with Salmonellosis
Fibrinosuppurative and necrotizing typhlocolitis - inflammation in colon results in fresh blood in feces
Is there increased Salmonella shedding at home or the hospital
at the hospital- stress
host susceptibility plays an important role in the pathogenicity
What is the enrichment broth used to diagnose Salmonellosis
Selenite or tetrathionate
What time of year does equine coronavirus infections typically occur
during the colder months (October to April)
What are the risk factors to equine coronavirus
-Colder months (October to April)
-Midwest
-Draft horse
-Ranch/farm and breeding
an enveloped RNA virus that causes acute diarrhea in horses
Equine Coronavirus
Does Equine Coronavirus cause high morbidity or mortality
high morbidity (field outbreaks 10-83%)
fatalaties are rare
What are the clinical signs of equine coronavirus
-Anorexia (97%)
-Lethargy (88%)
-Fever (83%)
-Diarrhea (23%)
-Colic (19%)
-Neurological signs (3%)
When is equine coronavirus typically shed
incubates for 48-72 hours and then sheds 3-4 days post-infection and can shed up to 25 days
How do you diagnose equine coronavirus in a horse
Detection of the virus in the feces by PCR
How do you treat Equine Coronavirus?
No specific treatment but most adult horses recover within a few days.
Supprotive treatment may include fluids, NSAIDs, electrolytesm and GI protectants
What causes Potomac Horse fever
Neorickettsia risticii (intracellular bacteria)
What does Neorickettsia risticii cause
Potomac horse fever
What is another name for equine monocytic erlichiosis
Potomac horse fever
What time of the year does Potomac horse fever typically occur during
Summer (June through September)
DNA of Neorickettsia risticii has been found in
Aquatic snails
Aquatic larval insects
What cell type does Neorickettsia risticii infect
blood monocytes, it is an intracellular bacteria
has a predilection for intestinal wall, especially the large colon
impaes absorption of Na and Cl from lumen causing a watery diarrhea
How is Neorickettsia risticii transmitted to the horse
Life cycle involving snails (1st intermediate host), cercariae, larva aquatic insect (2nd intermediate horse), adult aquatic insect, and insectivores
How do you diagnose potomac horse fever
serological testing using indirect fluorescent antibody (IFA)
-does not confirm if they are currently infected or if the antibodies were produced during a previous exposure or vaccination
How do you treat Potomac Horse Fever
Tetracycline IV
Vaccination is available
*protection is incomplete as there are different strains- lessens the impact of the disease though
What are the pros and cons of when to use antimicrobial therapy in horses
Pros: Neutropenic patient, risk of sepsis, Clostridial species, Potomac horse fever
Cons: may not alter the course of the disease, may interfere with competing GI flora, toxicity issues
What time of year is Salmonellosis in horses more common
Late Summer months and fall- shedding and occur continuously or intermittently
Which of the following clinical signs is NOT encountered in horses with small intestinal infiltrative disease unless disease?
Colic
Diarrhea
Weight loss
Edema
Lethargy
Diarrhea
The most prominent clinical sign of small intestinal infiltrative disease is weight-loss secondary to malabsorption. Diarrhea is not apparent unless the large intestine is also involved. Additional clinical signs of infiltrative intestinal disease include dependent edema (due to protein loss) and lethargy (due to malabsorption of nutrients). Occasionally, affected horses may be presented with colic.
T/F: Horses with a Salmonella positive fecal culture result always have clinical signs such as diarrhea.
The statement is FALSE. Depending on the population surveilled, approximately 1 to 7% of horses are subclinically infected with salmonella and actively shed the organism without outward signs of clinical disease.
The prevalence of diarrhea caused by which of the following agents is higher in the winter than the summer?
Equine Coronavirus
Potomac Horse Fever
Salmonellosis
Equine coronavirus infections are more commonly seen during the cold weather months (between October through April). In contrast, the incidence of Potomac Horse Fever is highest during the summer months (June through September). The peak incidence of salmonellosis in horses occurs in late summer and fall.
The following statement is TRUE or FALSE?
The use of antibiotics is always indicated in horses with acute colitis.
The statement is FALSE.
The use of antimicrobials in the treatment of diarrhea is controversial. In cases of colitis caused by N. risticii, the efficacy of tetracycline intravenously has been documented clinically and experimentally. In contrast, the effect of antimicrobials in diarrhea caused by other microorganisms (e.g. Salmonella spp.) is not well documented and is associated with potential risks (e.g. interference with competing GI flora). In severely neutropenic patients the use of broad-spectrum antibiotics is justified to provide systemic protection from bacteremia.
Do equine endocrine disorders have an increasing incidence?
-Aging horse population (more common with age)
-Improved diagnostics
-Awareness and education about endocrine disorders
What are the two most common equine endocrine disorders
Equine Cushings Disease ( PPID)
Equine Metabolic Syndrome (EMS)
*also pheochromocytoma, thyroid disease in foals, diabetes insipidus
In horses: Cushing’s disease is always caused by
abnormal function of the pituitary gland
*not necessarily high levels of cortisol in the blood like seen in dog and human (pars distalis)
What part of the pituitary has increased secretion in Equine Cushing’s
Pars intermedia
The pars intermedia of the anterior pituitary is composed of a homogenous population of
Melanotrophs - contain propiomelanocortin (POMC)produces a-MSH, b-END, and corticotropin-like intermediate lobe peptide (CLIP)
The pars distalis of the anterior pituitary is composed of these 5 cell types
1) Somatotrophs- Growth hormone
2) Lactotrophs- Prolactin
3) Corticotrophs- POMC- ACTH, a-LIP, b-END
4) Thyrotrophs- TSH
5) Gonadotrophs- FSH and LH
Within the anterior lobe of the pituitary, How are signals from the hypothalmus arrived to the pars distalis vs the pars intermedia
-Pars distalis- hormones released from hypothalmus, reach pituitary by portal system
-Pars intermedia- poorly vascularized- secretion is controleld by neurotransmitters that are released from axons (hypothalmus)
How does POMC in the melanotrophs (pars intermedia) and the corticotrophs (pars distalis) differ
POMC (pars distalis) : ACTH (high), LPH, MSH, b-END)
ACTH acts on the adrenal gland to make cortisol
POMC (pars intermedia): MSH, b-end, ClP, ACTH (small) - POMC peptides serve various functions
What inhibits the secretion from the melanotrophs of the pars intermedia
Dopamine
What modulates secretion from the melanotrophs of the pars intermedia?
-Serotonin
-Epinephrine, Norepinephrin
-y-aminobutyric acid (GABA)
T/F Melanotrophs respond to negative feedback
False: they do not
In the horse- increased secretion of pars intermedia (always) - POMC; a-MSH, bEND, etc (ACTH only a small amount)
Why is Equine Cushing’s called PPID
because the pars intermedia is dysfunctioning to always secrete POMC: a-MSH, bEND, etc
No negative feedback
How does PPID occur?
abnormal function of the pars intermedia because of a loss of hypothalamic control
Dopamine inhibits hormone secretion of the pars intermedia and dopamine’s inhibition decreases over time as nerve cells die off
Without inhibition of secretion, pituitary cells enlarge and may even undergo neoplastic change
What is the signalment of horses with PPID
older horses (typically >15 years old)
Average 19-21 years old
All breeds affected
Increased in ponies? - pituitary adenomas
Youngest: 6 years
What are the clinical signs of PPID?
1) Hypertrichosis/hirsutism (long shaggy hair coat, usually associated with abnormal shedding patter - late shedding or no shedding in spring)
2) Hyperhidrosis- excessive sweating
3) PU/PD (maybe)
4) Muscle loss
others in association with above and hoof abscess
1) Chronic/recurrent laminitis
2) lethargy
3) Chronic infections* (respiratory and sinus, GI parasites- ascarids) and delayed wound healing
4) Bulging of supraobrital fat
5) Blindness (rare)
T/F: laminitis is common in horses with PPiD
True but not every horse with laminitis has PPID
T/F you get clinical signs of hypertrichosis and hyperhirsutism in early PPID
False, not all signs have to be present. These typically arent common in early disease
ACTH and cortisol may not be elevated in _______
early disease
ACTH and cortisol levels are typically higher in what time of year?
fall time- CSU doesnt offer fall reference ranges
Why might there be a false positive in testing for PPiD
1) ACTH and cortisol levels are typically higher in the fall
2) Stress (pain and trailering) can falsely elevated ACTH and cortisol
What is the best test to run if you suspect early PPID in a horse
THR stimulation test (Thyroid Releasing Hormone Stim test)
When given TRH, Cushings horses will release the expected triiodothyronine (T3) and thyroxin (T4) but will also increase plasma ATCH concentration for 15 minutes. Useful for borderline cases (horses with clinical signs but normal resting endogenous ACTH levels) Collect 10-30 min following administration TRH IV. 30 minute sample is more reliable. Cutt offs are 100pg/mL at 10min post TRH and 35pg/mL at 30min post TRH
Positive: Initiate treatment
Negative: re-assess in 3-6 months
Thyroid Releasing Hormone Stim Test
When given TRH, Cushings horses will release the expected triiodothyronine (T3) and thyroxin (T4) but will also increase plasma ATCH concentration for 15 minutes. Useful for borderline cases (horses with clinical signs but normal resting endogenous ACTH levels) Collect 10-30 min following administration TRH IV. 30 minute sample is more reliable. Cutt offs are 100pg/mL at 10min post TRH and 35pg/mL at 30min post TRH
Positive: Initiate treatment
Negative: re-assess in 3-6 months
What is the best test to run if you have a horse with history and clinical signs consistent with PPID and you suspect moderate to advanced PPID
Baseline ACTH
Measuring the endogenous plasma ACTH
Positive: Initiate treatment
Negative: Do a TRH stim test (Positive initiate treatment, if not re-assess in 3-6 months)
Of all the diagnosis methods of PPID, which are not affected by stress/pain
-Domperidone response test and a-MSH
-CT and MRI
What are the methods used to diagnose PPID in a horse?
1) Dexamethasone suppression test (DST)
2) Resting plasma (endogenous) ACTH level
3) Resting plasma cortisol level
4) Thyroid-releasing hormone (TRH) response test
5)Domperidone response test and a-MSH **
6) Urinary cortisol:cretinine ration
7) CT and MRI **
*****= stress/pain do not impact these
Used to be the golden standard for diagnosing PPID but has since fallen out.
Administration of dexamethasone in late afternoone should depress cortisol production to less than 10ng/ml in the morning
Horses with Cushings typically show a small degree of suppression which will not persist for the 17 to 19 hours in which the overnight protocol is performed
Dexamethasone Suppression Test
May be a promising new test for diagnosis of PPID. Horses with PPID react to domperidone admin with exagerrated icnrease in endogenous ACTH concentration 2-4 hours after administration.
Domperidone Response test- not impacted by stress and pain
How do you treat PPID in horses?
1) Dopamine agonists: Pergolide and Bromocriptine
2) Antiserotonergic actions: Cyproheptadine
What is probably the most effective drug at treating PPID
Pergolide - a long-acting oral dopaminergic agonist
What are the two dopaminergic agonists used for treating PPID
1) Pergolide (better)
2) Bromocriptine
Bromocriptine
a dopaminergic agonist used to treat PPID
expensive and Pergolide works better
Pergolide is used to treat
PPID in horses
Cyprohepatadine
an antiserotonergic agent that has been used with limited success in treating parsintermedia dysfunction in horses.
Wide safety margin
T/F: Mitotane/Op-DDD (Lysodren) can be used to treat PPID in horses
False- not effective- causes selective necrosis of zona fasiculata and reticularis)
commonly used to treat pituitary Cushings in dogs though
Trilostane
a competitive inhibitor of 3-b-hydroxysteroid dehydrogenase to attempt to block endogenous cortisol production by the adrenal gland
not potent enough to block cortisol synthesis in patients with hypercortisolism
Pergolide seems to be better
Is the prognosis for PPID good?
good if endocrinological control has been achieved and laminitis is well managed
How should you monitor response to PPID therapy
-Clinical signs
-Endogenous ACTH
-Dexamethasone suppression test
Adjust therapy as needed
What are the clinical signs of equine metabolic syndrome (EMS)
-Obesity (crest of neck, gluteal region, sheath, omental fat)
-“easy keepers”
-Laminitis
-Difficult to breed
-PU/PD (rare)
What are the breed predilection for equine metabolic syndrome?
Peruvian Pasos, Ponies, Saddlebreds, Morgan Horses, Warmbloods, and “hardy” breeds
What age of horses does EMS typically affect?
Adult to middle aged horses (6 to 20 years of age)
Dogs with hypothyroidism have similar clinical signs as horses with __________
Equine Metabolic Syndrome (Normal thyroid gland)
-Hypoactive
-Weight gain
-Obesity
-Dry hair coat
-Reproductive dysfunction
-Increased cholesterol
if low resting T3 and T4 are detected: consequences of EMS rather than the problem
Hypothyroidism in foals
-Goiter
-Prognathism
-Ruptured common digital extensor tendons
-Forelimb contracture
-Retarded ossification
-Crushing of cuboidal bones
-Goiter
-Prognathism
-Ruptured common digital extensor tendons
-Forelimb contracture
-Retarded ossification
-Crushing of cuboidal bones
hypothyroidism in foals
What is the hallmark of equine metabolic syndrome
insulin resistance (glucose intolerance)
similar to type 2 diabetes mellitus
Horses with EmS have glucose intolerance, what does that mean
following glucose administration, resolution of hyperglycemia is delayed
Normal response to glucose vs those with insulin resistance
Normal: Horse eats grain, blood glucose increases, insulin is secreted (b-cells), insulin binds to cellular receptor, cells take up glucose and utilize it, blood glucose normalized)
Insulin resistance: Horse eats grain, insulin is secreted, cells do not respond to insulin, blood glucose does not normalize appropriately, b-cells continue to secrete insulin (hyperinsulinemia)
What would the blood sample show of a horse with insulin resistance
Elevated insulin and low G:I ratio
What is the role of adipocytes in insulin resistance
adipocytes are active participants in energy regulation
metabolically active products are released and interfere with insulin action
-Leptin, adiponectin, resistin, TNF-a, and IL-6
How do you diagnose EMS
Fasting hyperinsulinemia
Dynamic glucose (+/- insulin tolerance test) - oral glucose tolerance test and CGIT
Oral sugar test: use when baseline insulin is WNL. at least 8 hours of fasting overnight. Administer 0.15mL/kg Karo Light Corn Syrup PO and administer insulin and glucose: baseline and 60 and 90 minutes- spin and separate serum and chilled/freeze for shipping
Abnormal predictive proxies (G:I rato)
When should you do an Oral sugar test
when you suspect EMS and baseline insulin is within normal limits
at least 8 hours of fasting overnight. Administer 0.15mL/kg Karo Light Corn Syrup PO and administer insulin and glucose: baseline and 60 and 90 minutes- spin and separate serum and chilled/freeze for shipping
when you suspect EMS and baseline insulin is within normal limits
at least 8 hours of fasting overnight. Administer 0.15mL/kg Karo Light Corn Syrup PO and administer insulin and glucose: baseline and 60 and 90 minutes- spin and separate serum and chilled/freeze for shipping
Oral sugar test
How do you differentiate between PPID and EMS
EMS- testing of hypothalamic/pituitary/adrenal axis should be WNL in horses
caution-laminitic horse*
How do you improve insulin sensitivity in horses with EMS
weight reduction
-reduce caloric intake and provide adequate exercise
this might be problematic in horses with active laminitis
When you are trying to reduce the weight of a horse. What precautions should you take
Do not feed less than 1% of their body weight
Hyperlipidemia, hepatic lipidosis worsening IR, stereotypical behaviors
Feed 1.5% of the desired body weight
Avoid feed with a high glycemic index (GI) such as grain and molasses (ex: sweet feed is high, alfalfa is low)
Choose the right hay and restrict grazing (sugars in pasture grass)
What are the medical therapy and supplements for EMS?
-Levothyroxine- start at high dose and gradually reduce dose over 3-6 months
-Sodium-glucose co-transporter 2 inhibitors (ertuglflozin) - inhibit the reuptake of glucose in the kidney, decreases insulin required for euglycemia
complication: hypertriglyceridemia *expensive
-Metformin- only effective in small number of horses, may lose efficacy over time
-Magnesium?
-Chromium?
-Resveratrol?
Levothyroxine
used as therapy for EMS.
start at high dose and gradually reduce dose over 3-6 months and take them off
inhibit the reuptake of glucose in the kidney, decreases insulin required for euglycemia
complication: hypertriglyceridemia *expensive
Sodium-glucose co-transporter 2 inhibitors (ertuglflozin)
Combined glucose-insulin test (CGIT)
used to diagnose EMS in horses
Administer 150mg/kg dextrose and 0.1 U/kg regular insulin is given. Blood samples are collected at 1,5,15,25,35,45,60,75,90,105,120,135, 150 minutes after.
Insulin resistance is diagnosed when blood glucose concentration is higher than baseline at 45 min or insulin concentration is greater than 100uU/mL at 45 min
Metformin
Antidiabetic- suppresses hepatic glucose production by activating AMP-activated protein kinase, which inhibits gluconeogenesis and lipogenesis while increasing fatty acid oxidation and lipolysis. Only small number of studies have been done in horses
some shown it decreases insulin concentration but failed to improve
Does EMS have a good prognosis?
Good prognosis if laminitis is controlled, husbandry is good, and nutrition is appropriate
Which of the following clinical signs can be observed in both horses suffering from Pituitary Pars Intermedia Dysfunction (PPID) AND in horses with Equine Metabolic Syndrome (EMS)?
Choose all that apply.
Laminitis
Pu/Pd
Hypertrichosis
Cresty neck
Hyperhidrosis
Laminitis
Pu/Pd
The clinical signs associated with PPID include:
Hypertrichosis/hirsutism
Hyperhidrosis (excessive sweating)
Pu/Pd
Muscle loss
Chronic/recurrent laminitis
Lethargy
Chronic infections and delayed wound healing
Bulging of the supraorbital fat
Blindness (rare)
The clinical signs associated with EMS include:
Obesity with regional adiposity in specific locations including the crest of the neck (“cresty neck”), over the gluteal region/close to the tail head and in the prepuce (“swollen sheath”) or mammary gland region.
“Easy keepers”
Difficult to breed successfully due to abnormal ovarian cycling activity
Laminitis
Pu/Pd (rare, with overt diabetes mellitus)
Which of the following can assist you in differentiating horses suffering from PPID from horses with EMS?
Choose all that apply.
Age at onset of disease
Abnormal glucose tolerance test
Radiographic evidence of laminitis
Abnormal dexamethasone suppression test
Age at onset of disease
Abnormal dexamethasone suppression test
As laminitis and insulin resistance can be clinical signs of PPID as well as EMS, it is important to differentiate these two conditions from each other. EMS may be differentiated from PPID by:
1. Age of onset. The EMS phenotype is generally first recognized in younger horses, whereas PPID is more common in older horses (note: these conditions may coexist in some cases).
2. Clinical signs. Clinical signs suggestive of PPID but not EMS include delayed or failed shedding of the winter haircoat, hirsutism/hypertichosis, excessive sweating, and skeletal muscle atrophy.
3. Positive diagnostic test for PPID. For example, detection of an increased plasma adrenocorticotropin hormone concentration in the absence of cofounding factors such as pain and stress.
The following statement is TRUE or FALSE?
The most effective treatment of PPID involves the administration of a dopamine agonist.
True. Hormone secretion of the pars intermedia is controlled by neurotransmitters released from axons that extend directly from the hypothalamus to the pars intermedia. Secretory control is primarily through inhibition by dopamine (with additional modulation by serotonin, b-adrenergic and g-aminobutyric acid (GABA)-ergic inputs). Therefore, the most effective way to reduce pars intermedia secretion is by administering a dopamine agonist. Probably the most effective drug currently available is pergolide, a long-acting oral type 2 dopaminergic agonist.
You diagnose a severely obese horse (BCS 9/9, 670 kg = 1,471 lbs) with Equine Metabolic Syndrome (EMS) As part of your management plan you recommend to put the horse on a diet to induce weight loss. Your estimation of the horse’s ideal body weight is 520 kg (1,144 lbs).
How many kilograms of a low NSC grass hay should the horse be fed/day to achieve the desired weight loss without the risk of adverse health or behavioral consequences?
Weight loss should be induced in obese horses by restricting the total number of calories consumed and by increasing the horse’s level of physical activity. An obese horse should be placed on a diet consisting of hay fed in an amount equivalent to 1.5% of the ideal body weight (1.5 lbs of hay per 100 lbs bwt). If the horse fails to lose weight after a horse has been fed at an amount equivalent to 1.5% of ideal body weight for 30 days, this amount can be lowered to 1%. However, amounts fed should not fall below 1%, as severe calorie restriction may lead to hyperlipemia, worsening of IR, and stereotypical behaviors.
For the horse in this example:
Desired weight = 520 kg
1.5% of body weight = 7.8 kg
Horses are hypsodont and anelodont, what does that mean
Hysodont- very long crown and short root
Naelodont- no new tooth length can be added
occlusal surface
has sharp enamel points. what occludes with other teeth
What does coronal mean
towards the crown of the tooth
Crown located occlusal to the attaced gingiva and visible within the oral cavity
What ate the portions of the horse teeth
1) Occlusal- occlusal surface
2) Coronal: toward the crown- clinical and reserve crown
3) Apical: toward the root tip
4) Radicular root
Toward the cheek, premolars and molars
buccal
towards the lips,
canine and incisors
labial
toward the tongue
lingual
toward the palate
palatal
the space between adjacent teeth
interproximal space
surface adjacent to tooth in front
mesial surface
surface adjacent to tooth behind
distal surface
What is the eruption rate of horse’s teeth
3mm per year on average
What is the dental formula of the horse
3-1-3(4)-3
3-1-3-3
Why is it important that the pulp horn is located on the labial aspect of the clinical crown
if the incisor is fractured and the labial peripheral enamel has been broken off the tooth it is very common to have pulp exposure
Where are the pulp horns on the horse incisor
on the labial aspect
What is the bright white structure that surrounds the tooth
peripheral enamel
What lays over the pulp horn on the incisor
dentin
what surrounds the infundibular cementum
infundibular enamel
T/F: horse’s teeth continually erupt
False
What kind of horses have canines
ALL MALE HORSES
Rudimentary in 7-28% of females
How many root canals and pulp horns do equine incisors have
1root canal
1 pulp horn
How many root canals and pulp horns do equine canines have
1 root canal and 1 pulp horn
What is another name for the first premolar tooth
Wolf teeth
25% females
15% males
erupts at 6 months of age and +/- shed by 2.5 years
less common on mandibular
What tooth is the Wolf tooth
1st premolar
25% females
15% males
erupts at 6 months of age and +/- shed by 2.5 years
less common on mandibular
1st premolar
25% females
15% males
erupts at 6 months of age and +/- shed by 2.5 years
less common on mandibular
Wolf tooth
The majority of horses with exfoliate the Wolf tooth when________
the permanent maxillary secondary premolar tooth erupts around age 2-3 years
as long as not in abnormal place and causing periodontal disease do not need to remove
How many mandibular cheek teeth are there in the horse
6 (3 premolars and 3 molars)
two roots each
What are the characteristics of mandibular cheek teeth
3 premolars
3 molars
-Two rooths
-5-6 pulp horns (extra PM2 and M3)
-No infundibulum
Where is the extra pulp horn on mandibular premolar 2 and 3 located (6 pulp horns total)
on the mesial aspect of premolar 2 and the distal aspect of molar three
**This is where the large hooks form
When dealing with pulp horns, ensure that there isnt over reduction of else the pulp horn will be exposed
In horses, peripheral enamel encircles the
pulp horns
What mandibular cheek teeth have 5 pulp horns?
Premolar 3 and 4
Molar 1 and 2
What mandibular cheek teeth have 6 pulp horns
Premolar 2 (mesial)
Molar 3 (distal)
What do the mandibular premolars and molars do not have
an infundibulum
Why do horses have peripheral cementum
due to their teeth continually erupting throughout their life
as the periodontal ligament must always be able to connect to alveolar bone and cementum
the largest pulp horn of mandibular cheek teeth are always located
BUCALLY
-PH 1 and 2 are always located bucally
What are the largest pulp horn of mandibular teeth
-PH 1 and 2
always located bucally
How many maxillary cheek teeth are there in the horse
3 premolar and 3 molar teeth
-all of which have 3 roots
How many roots do the maxillary cheek teeth have
all have 3 roots (2 lateral and 1 palatal)
What maxillary cheek teeth have 5 pulp horns
Premolar 3 and 4
Molar 1 and 2
What maxillary cheek teeth have extra pulp horns (6-7)
Premolar 2 and Molar 3
(1-2 extra)
*Located on the mesial aspect of premolar 2 and the distal aspect of molar 3 - where do the hooks form
Where do the hooks form in the maxillary mandibular teeth
pulp horns located on the mesial aspect of premolar 2 and the distal aspect of molar 3 - where do the hooks form
What teeth are located in the caudal maxillary sinus
2nd and 3rd molar teeth
What sinus are the 2nd and 3rd molar teeth located in
the caudal maxillary sinus
What sinus is the 1st molar located in
the rostral maxillary sinuses
What teeth are located in the rostral maxillary sinus
-1st molar
-Distal aspect of 4th premolar tooth can be located in the rostral maxillary sinus, especialy when a horse is young and teeth are young. As horse ages, the tooth may erupt away from the sinus and no longer maintains the relationship
What sinus is the distal aspect of the 4th premolar located within
Distal aspect of 4th premolar tooth can be located in the rostral maxillary sinus, especiialy when a horse is young and teeth are young. As horse ages, the tooth may erupt away from the sinus and no longer maintains the relationship
T/F: maxillary teeth do not have infundibulum
false- they have 2 infundibulum (5-7 cm depth) length of reserve of crown
Dental disease of ______________ can result in secondary sinusitis
Premolar 4 and all molars
-PM4 and M1- Rostral maxillary sinus
-M2 and M3- Caudal maxillary sinus
What color do pulp horns appear
brown
When do the wolf teeth erupt
around 6 months of age
will be gone by 2.5 years
What is the last equine tooth to completely erupt
canine tooth (about 4-5 years)
When do deciduous incisors erupt
I1-3 (6 days, 6 weeks, 6 months)
When do permanent incisors erupt
I1-3 (2.5 y, 3.5y, 4.5y)
When do the incisors erupt
Deciduous 6d, 6week, 6 month
Permanent: 2.5y, 3.5y,4.5y
When do the deciduous premolars erupt
2 weeks
When do cheek teeth erupt
M1: 1 year
M2: 2 year
PM2: 2.5y
PM3: 3 y
M3: 3.5y
PM4: 4 y
How do you discern what a deciduous tooth is
in a young horse, they will look very worn down “caps”? idk
Horses with PPID can cause ______ dental disease
periodontal disease - can get really nasty oral-nasal fistulas
What are historical indicators for dental pathology
-Weight loss
-Abnormal mastication
-Excessive salivation
-Quidding
-Headshaking
-Response to bit
-Choke or colic
*Most common to have no signs
used for when horses drop feed from their mouths while they are chewing, or leave balls of partially chewed hay or other food behind in their feed buckets
sign of dental pathology
quidding
What can you see stall side observation for dental pathology
-Body condition score
-observe mastication
-symmetry of face (temporal muscles can atrophy)
-fiber in feces about 1 inch of length- mastication is adequate
What is the significance of the point of the facial crest
it marks the line between the maxillary premolars and molars
What equipment is used to perform an equine dental exam
-Adequate sedation
-Flush mouth thoroughly
-Full mouth speculums
-Head support
-Quality light source
*look for impacted feed- tells you where problem is
What is the normal gingival sulcus depth in horse
0-1mm
What do you palpate for an extraoral facial exam in a horse
-Point of facial crest
-Region of sinuses
-Periorbital region
-Retropulse the eye- push lightly on the eye
-Zygomatic arch
-Temporomandibular joint
-Muscles of mastication
-Ears (temporal teratoma- ear tooth)
-Parotid salivary gland
-Mandibular lymph nodes
-Intermandibular region
-Mandible (lingual and buccal)
-Rostral mandibular
-Incisive one region
-Nares
-Rostral maxilla
What do you examine in an equine intraoral exam
-Mucocutaneous junction
-All regional soft tissue structures
-labial and alveolar mucosa
-Gingival attachment
-Dentral structures
-Interproximal spaces
abnormal placement of individual teeth in any plane
resulting in pain (soft tissue laceration), abnormal attrition, and reduced masticatory function
Malocclusion
What is a result of malocclusions in horses
pain (soft tissue laceration), abnormal attrition, and reduced masticatory function
The average horse spends ______ hours eating forage
16 hours (12.5kg forage)
When taken off pasture- decreases to 11.5 hours (8kg forage and 4 kg concentrates)
3kg forage and 7 kg concentration- 6.1 hours eating
leads to malocclusion
What is a class 1 malocclusion (MAL 1)
arcades appropriately aligned but individual tooth malpositioned in any plane
-Tooth overgrowth:
Sharp enamel points
Steps
Wave
Hooks (in conjunction with MAL2/3
-Rotation or tipped
Sharp enamel points
a type of MAL 1 where anisognathic jaws lead to portions of the teeth that arent in contact with one another when at rest
Lead to ulceration or laceration- buccal or lingual mucosa
Maxilla-Buccal
Mandibular- Lingual
horses have anisognathic jaws meaning
the mandible is skinnier than the maxilla
Sharp enamel points happen on the _________ aspect of the maxilla and the ________ aspect of the mandible
Buccal aspect of maxilla
Lingual aspect of the mandible
Sharp enamel points can lead to
ulceration and laceration of the buccal and lingual mucosa
Step/Wave mouth
A type of MAL 1 where there is overgrowth in the middle of the arcade
Step-one tooth
Wave- multiple teeth
Nidus: missing teeth, expiring teeth, fractured teeth
occluding tooth problem
Hook
when a portion of the mesial 2 PM or distal 3M tooth overlong
causes: Mal 2 or 3, bit seats, offset cheek teeth arcades, missing teeth and collapse of arcade
Where do hooks typically form in
PM 2 (mesial)
M3 (distal)
*do not get them in the middle of the arcade
When missing tooth on the mandible, what would result
overgrowth of the maxillary tooth that touch it
What causes the formation of hooks
1) Mal 2 or 3 malocclusions
2) Bit seats: practice to increase performance, rounding mesial aspect of tooth. if only doing it on max/mand then it will overgrwo
3) offset cheek teeth: nx jaw lengths but one of the arcades si shifted
4) Missing teeth and collapse of arcade
What is the oldest tooth and typically wears out first, could potentially lead to wave
The first molar tooth on the maxilla
What type of malocclusion is mandibular brachygnathism “Parrot mouth”
Class 2 Malocclusion (MAL 2)
Hooks 106/206 and 311/411
mandibular brachygnathism “Parrot mouth” leads to
Hooks on the maxilla 106/206 and 311/411
*Class two malocclusion
Maxillary malocclusion “undershot/underbite/monkey-mouth/ sow mouth” is a Class ______ Malocclusion
Class 3
Hooks form on mandible 306/406 and 111/211
Maxillary brachygnathism leads to
Hooks on mandible 306/406 and 111/211
Mandibular brachygnathism (Class 2 MAL) results in ________ on _________ while mandibular brachygnathism (Class 3 MAL) results in _________ on _______
Mandibular Class 2: Hooks on 106/206 and 311/411
Maxillary Class 3: Hooks on 306/406 and 111/211
Forms hooks on 306/406 and 111/211
Maxillary brachygnathism (Class 3) Underbite
(Maxillary M3 have hooks when maxilla is short)
Forms hooks on 106/206 and 311/411
Mandibular brachygnathism “Parrot mouth” (Class 2)
(Mandibular M3 have hooks when mandible is short)
Class 4 Malocclusion
one quadrant asymmetrical growth “Wry mouth or wind swept)
Maxilla shifts to one side in comparison to mandible
causes: post-trauma and congenital conformation
Mild maxillary is very common- require continual maintenance
Severe= respiratory distress because nose is curved
What are the causes of Class 4 Malocclusion
post-trauma and congenital conformation
*Maxilla shifts to one side in comparison to mandible
What is Wry mouth or wind swept
Class 4 Malocclusion one quadrant asymmetrical growth - slant or diagonal *eat and masticate normally typically
Maxilla shifts to one side in comparison to mandible
causes: post-trauma and congenital conformation
Mild maxillary is very common- require continual maintenance
Severe= respiratory distress because nose is curved
reduction of overgrown dental material
Most common-reduction in enamel points- rounded to level of cementum and dentin
manages malocclisions
Odontoplasty “Float”
What are the precautions of odontoplasty
remove no more than 3-4 mm every 3 months if more than just enamel is involved
just take of sharp enamel points
do not flatten completely- can expose pulp
just need to be comfortable for eating
How do you manage older horses with expired teeth
shift from hay/pasture to older/senior maintenance feed because they do not have much dental structure
