Equine

Question 1

Compare natural equine feeding behaviours with how horses are commonly fed in intensive housing, commenting on how these impact on the health and welfare of the stabled horse.

Answer 1

Horses evolved to be trickle feeders grazing up to 16 h/d and maintaining a high gut fill. Due to this, horses also evolved to spend most of their time moving around, eating and chewing, which kept them occupied and producing large quantities of saliva. The diet they evolved to eat is one that is high in fibre, and relatively low in non-structural carbohydrates (NSC). Their blood glucose concentrations would remain relatively low and constant throughout the day. It should not be forgotten that eating is a social pursuit of the horse as it is a herd animal.
We tend to keep horses intensively and/or in isolation, feed them high concentrate, low fibre diets in two big meals per day and confine them to small areas. We also have feeders fed at chest height rather than horses eating at ground level. These large meals are consumed quite quickly with a reduction in chewing which causes teeth to wear abnormally and reduces saliva. Reduction in saliva increases the incidence of gastric ulcers and decreases the lubrication of the ingesta, which can cause choke. The high starch-based meals lead to a large glycaemic response causing the pancreas to have to pump out large amounts of insulin to maintain blood glucose concentrations. This pattern of large, infrequent insulin secretion can result in the insulin becoming less effective leading to insulin resistance and possibly laminitis. The small intestine can become overwhelmed with NSC and is not completely digested, spilling over into the large intestine and caecum leading to hindgut acidosis, endotoxaemia and laminitis. Gas produced from excessive fermentation can result in discomfort manifested as flatulent colic.
A reduction in gut fill due to lower fibre content means there is less water being retained in the gut so impaction colic risk is increased. This lack of gut fill may also enable mesentery to twist back on itself leading to strangulation colic.
Feeding horses at chest height not only means their teeth are not correctly occluded (leading to more dental problems) but has implications for the respiratory tract as it is the up and down movement of the head and neck that facilitates the removal of mucous, debris and microbes from the lungs.
Horses spend only about 15% of their day eating instead of 60–70% leaving them with large periods of time with nothing to do. This leads to the development of stereotypies such as windsucking, crib biting, weaving, and aggression.

Question 2

Why is obesity in horses becoming increasingly important?

Answer 2

It is implicated in equine metabolic syndrome and insulin resistance (IR). Both of these diseases lead to an increased risk of laminitis – a potentially life-threatening disease and a disease that impacts greatly on horse welfare.

Question 3

How does obesity contribute to the disease processes it is implicated in?

Answer 3

While the disease process is not completely understood; a vicious circle is set up with IR promoting adiposity which in turn promotes IR. Adipocytes produce the hormone resistin, which inhibit the actions of insulin. Excessive number or increased activity of omental-like adipocytes contributes to the development of IR.
There is also a role for cortisol as stress may stimulate omental fat deposits which produces 11 β- hydroxysteriod dehydrogenase (11 β-HSD). It converts cortisone to cortisol (which induces elevated insulin due to increased blood glucose) so adipocytes maintain and perpetuate themselves.

Question 4

Explain what an emaciated horse should be fed, how this feeding should be managed and why.

Answer 4

Dietary regimens developed for refeeding emaciated horses must take into account physiologic and physical changes that take place during starvation, such as delay in gastric emptying and slower absorption of nutrients. Successful nutritional rehabilitation is achieved when chronically malnourished horses have regained normal body weight, which usually takes 3 to 10 months.
During starvation, horses are in a catabolic state that depletes body stores of fat, muscle, and electrolytes. Renal adaptation enables the body to maintain serum electrolyte concentrations. Free fatty acids from adipose tissue are the primary source of energy metabolites during fasting or starvation, and high serum concentrations of FFA would, therefore, be expected.

Refeeding Syndrome
Introduction of carbohydrates, specifically glucose, to starved horses results in release of insulin. Insulin prevents release of FFA and causes an intracellular influx of glucose and selected electrolytes, which, in turn, decreases serum concentrations of those substances. Availability or solubility of carbohydrate sources determines the intensity of the glycaemic response.
Insulin stimulates anabolic protein synthesis, which further depletes the body’s marginal mineral and electrolyte stores often leading to severe extracellular hypophosphataemia, hypomagnesaemia, and hypokalaemia. This response can cause depletion of phosphorylated metabolites, especially ATP and 2,3-DPG, and results in RBC dysfunction, including decreased viability, reduced ability to pass through capillary beds, and inability to release oxygen to tissues. Cardiac and respiratory failure may then develop

Feeding management
Lucerne hay is low in starch (< 3%) and high in the insoluble carbohydrate cellulose (25 to 28%) and therefore creates minimal insulin response, In addition, it contains high level and quality protein and major electrolytes, particularly Ca, Mg.
Oaten hay is not recommended as it is too bulky, and low in Ca, Mg and P. It also is predisposes the horse to diarrhoea.
“Complete” feed also contains good quality protein and electrolytes but higher insulin response (and therefore risk Refeeding Syndrome)

Refeeding protocol
§ Days 1-3: 1⁄2 kg high-quality lucerne every 4 h (total of 3 kg/d in six feedings)
§ Days 4-10: slowly increase lucerne and decrease feeding frequency – 2 kg hay every 8 h (total of 6 kg/d in three feedings)
§ Day 10 and following several months: feed as much lucerne as horse will eat. Provide access to a salt block.

Do not feed grain, treats or other supplements until horse has well recovered – complicates return of normal metabolic function. Provide clean, fresh water at all times

Question 5

Describe the effects of both over- and under- nutrition on fertility in the mare.

Answer 5

§ Mares with low BCS during anovulatory period (autumn and winter) experience longer and deeper anoestrus than those in good condition
§ Low energy
o Delayed onset of oestrus cycle
o Irregularcycles
o Morecyclestoconception
o Decreasedconceptionrate
o Lesslikelihoodofmaintainingpregnancy
§ Low protein
o Can delay onset of oestrus
o Lower ovulation rates although mare may exhibit normal cycle length and oestrus behaviour
§ High energy
o Shorter time to first season cycle in spring
o Ovulate earlier during oestrus
o Milky mares have greater tendency to resorb fertilised eggs at first oestrus - Could be reason for association between overfeeding during last 3 months pregnancy and reduced subsequent fertility
§ I2 and Se status have considerable effects on fertility of mare and viability of foal
o Deficiency or excess of either depresses embryonic developmentl

Question 6

What demands are placed on a lactating mare that increase her nutritional requirements?

Answer 6

The mare needs to produce milk to feed her offspring as well as meeting her own requirements. She will also need to be adequately nourished to ensure she is cycling correctly to be rebred. The mare will sacrifice her own bodyweight to maintain the foal on the ground but if inadequately nourished will not fall pregnant for the next year.

Question 7

What are the major nutrients that need to increase in the lactating mare’s diet to ensure she meets these demands?

Answer 7

Water, energy, protein and Ca.

Question 8

Describe how pre- and post-natal nutrition may affect growth and development of the foal.

Answer 8

§ Restriction prior to parturition can induce premature birth
§ Most foetal growth occurs during last 90 d gestation
§ Birth weight critical factor in determining prospects of foals
o Size of mare is major controlling influence
§ Milk yield influenced by
o Mare’s genetic ability for milk production
o Feed intake during late pregnancy
o Availability of water
o Intake of energy and protein during lactation
o Growth rate of foal relative to milk yield of mare
§ When consuming adequate amount of milk and grazing to meet its needs foal will double birth weight in first month
o Double it again by 3 months of age
§ Mare’s milk contains sufficient energy, protein and other major nutrients to meet needs of young foal during first 4 weeks of its life
§ Growth rate dependent on milk yield of mare during first 2 months
§ After peak lactation energy and protein content of mare’s milk and declining milk production
unable to meet foal’s needs for growth
§ Good quality green pasture containing 9-10% CP helps make up shortfall
§ As pastures dry off or grazed down in early to late summer supplementary concentrate feed necessary for both mare and foal
o Supplementary creep feed: 16-18% CP, 13-14 MJ DE/kg DM
§ Should contain at least 20-25% by weight of high quality protein meal (soybean, canola, skim milk powder) for young foals to meet protein, lysine & other EAA requirements for growth
§ Important to monitor foal’s growth rate
o Want to achieve steady rather than maximum or rapid growth
§ Incidence of limb deviations & enlarged growth plates on joints associated with developmental orthopaedic disease (DOD) largely influenced by diet and exercise in young growing horse from 3-9 months of age
§ Supplementary creep feeds should be restricted in quantity to 0.5-0.75 kg/100 kg BW
§ Where evidence of growth abnormalities restrict growth rate by decreasing supplementary feed or by decreasing mare’s feed for 3-4 weeks
o Should not prejudice ultimate mature size if carefully regulated

Question 9

Why is the intensive preparation of young horses for yearling sales at odds with how current research suggests growing horses should be managed?

Answer 9

Young horses should not be fed to achieve maximum growth rate as this increases the incidence of developmental orthopaedic disease. Research shows that the tallest heaviest yearlings bring the better prices at sales. Current research shows that growing horses should only achieve a moderate growth rate at best to decrease the incidence of OCD.

Question 10

How should these horses be managed so they achieve the market ideal but at the same time maintain structural integrity?

Answer 10

If growing horses are going to be fed high energy diets they need to be undergoing high levels of exercise in an effort to limit the incidence of developmental disorders.

Question 11

Describe how feeding a high fat diet to an athletic horse has a glycogen-sparing effect. In the answer include what is considered a high fat diet.

Answer 11

Lipids/fat is three times more energy dense than carbohydrates. Up to 20% lipids in the diet can be tolerated; inclusion of 5-10% results in weight gain. Inclusion at > 5% constitutes a high-fat diet.
§ When feed high fat diet, fat is utilised for aerobic activities in place of glycogen.
§ Feeding high fat diet delays decline in blood glucose concentrations in endurance horses
§ Accelerates recovery of resting pulse and respiration
§ Promotes recovery of resting blood glucose concentration
§ Yields less CO2/mole ATP produced, decreasing plasma PCO2
§ Small increase in plasma pH, with decreased plasma H+ and lactate concentrations and delay in fatigue
§ Stimulation to β-oxidation or fat mobilisation and metabolism, sparing glycogen

Question 12

From a health perspective, why is maximising chewing so important in feeding horses?

Answer 12

Reduction in chewing which causes teeth to wear abnormally and reduces saliva secretion. Less saliva production results in less buffering of the gut thereby increasing the incidence of gastric ulcers as well as decreasing the lubrication of the ingesta, which can cause choke. Decreasing chewing is also linked with increased incidence of stereotypies, such as crib biting, wood chewing and wind sucking.

Question 13

What is the difference between hyperlipaemia and hyperlipidaemia?

Answer 13

Hyperlipidaemia is a normal physiological response in hypophagic and exercising horses. It is characterised by raised or abnormal concentrations of lipids and/or lipoproteins in the blood. It is not due to high fat diet. The condition is corrected when feed intake improves or exercise ceases. It is an acute condition
Hyperlipaemia is the pathophysiological response to prolonged negative energy balance (i.e., chronic condition). It is characterised by gross lipaemia (excess lipids in the blood), marked hypertriglyceridaemia and fat infiltration of body tissues and organ dysfunction. High mortality rate, ranging from 22-80%.

Question 14

How does hyperlipaemia occur?

Answer 14

Food deprivation – accidental, intentional, or relative to increased metabolic demands of pregnancy or lactation

Question 15

What are important predisposing factors for the development of hyperlipaemia?

Answer 15

§ Insulin resistance – influenced by diet/body condition, pregnancy/lactation, breed, inactivity
§ Inadequate dietary intake (especially acute reduction) – leading to negative energy balance
§ Concurrent disease – decreases appetite and increases catabolic hormones
§ Systemic inflammation

Question 16

Outline the important principles for management of an animal with hyperlipaemia

Answer 16

§ Dietary/nutritional management – offer various feedstuffs to reverse negative energy balance i.e., meet resting energy requirement
o If inappetant consider enteric nutrition or if animal is not able to tolerate enteric nutrition, can consider parenteral nutrition (but expensive ad there are some potential complications – thrombophlebitis, hyperglycaemia, etc.)
§ Treat underlying condition
§ Use of insulin? Maybe useful if animal develop hyperglycaemia
§ Address fluid and electrolyte deficits – oral or IV fluids
§ General support care

Question 17

List the common causes and clinical findings in animals with equine metabolic syndrome

Answer 17

Also known as Peripheral Cushing’s Syndrome, Pseudo-Cushingoid Syndrome, Insulin Resistance Syndrome, Syndrome X, Omental Cushing’s syndrome, Insulin refractory state, Prediabetes and central obesity.
§ Obesity, especially in horses aged > 6-8 years
o Ponies are more susceptible
§ Abnormal/excessive fat deposition – often crest, shoulders, gluteal muscles and sheath
§ Females – abnormal ovarian cycling
§ “Easy keepers” – weight loss futile
§ Intra-abdominal (omental) adipose
§ Hyperinsulinaemia (fasting insulin > 300 pmol/L)
§ Insulin resistance (Type II diabetes)
o It is a vicious cycle, whereby IR promotes adiposity which in turn promotes IR through release of the hormone resistin
§ Low grade (chronic) laminitis

Question 18

Outline a suitable management plan for equine metabolic syndrome.

Answer 18

§ Treatment is aimed at the reversal of obesity
§ Dietary restriction and increased exercise
§ Dietary modification: avoid soluble carbohydrates (grains, sweet feeds, lush pastures, pasture at risk of high fructans, e.g., during weather with warm days and cold nights). Feed roughage based diet – hay/chaff/high fibre supplements/pasture with low soluble carbohydrates. Dietary modification will help to reduce body condition and increase insulin sensitivity.
§ Exercise: if no overt laminitis, regular exercise is useful to reduce body condition and increase insulin sensitivity. Farriery for management of laminitis
§ Mediciations? – drugs to try and increase tissue insulin sensitivity, e.g., metformin

Question 19

Discuss the risk (nutrition-related) factors and feed management strategies to minimise the incidence of gastric ulcers and laminitis in performance horses.

Answer 19

Gastric ulcers
§ High-grain, low roughage diets
§ Insufficient chewing – insufficient buffering
§ Large, infrequent meals
o Intermittent feeding shown to cause and increase severity of gastric ulcers
o Horses should be fed hay continuously or every 5-6 h to buffer stomach pH
§ Not all horses show clinical signs, those that do may include:
o Slower growth rate, failure to reach genetic potential, failure to thrive, poor performance
o Intermittentdiarrhoea
o Low-gradecolic
o Poor appetite
o Picky eater or agitated while eating o Graduallossofcondition
o “pot belly” appearance
o Salivation or froth around the lips o Teeth grinding
o Foals – lying on their backs
§ All of these clinical signs relate to the (extreme) discomfort associated with the acid “burning” the stomach lining (in simple words)

Feeding management
§ Practices that mimic natural grazing situation and respect gut function
§ Aimed at removing predisposing factors and decreasing acid production
§ Maximise amount of roughage in the ration
§ When possible, horses should be allowed free-choice access to grass or hay
o More frequent feedings will help buffer acid in stomach
§ Decreased feeding grains that form VFAs may help some horses
§ Energy from grain can be replaced by using feed higher in fat
§ Treatment: acid-suppressive therapy
§ 4 month spell at pasture will usually result in ulcer healing

Laminitis
Laminitis is thought to be a clinical syndrome (rather than a discrete disease) that results from several systemic disease entities or, less frequently, in the supporting limb of a lame horse. Laminitis can be a clinical outcome of endocrine disease, sepsis, or unrelenting unilateral weight bearing (supporting limb laminitis), and despite its prevalence remains without a targeted treatment that can achieve lamellar repair. Endocrinopathic laminitis occurs in association with equine metabolic syndrome. The critical factor in cases of endocrinopathic laminitis appears to be insulin dysregulation (ID), which results from a complex, often multifactorial disruption to the normal interactions between glucose and insulin. The management of ID currently relies on ongoing strategies to mitigate hyperinsulinemia, such as dietary restriction, weight loss, and exercise, the success of which is dependent on owner compliance.

The clinical signs include lameness involving one or multiple hooves, stiffness, weight shifting, a typical ‘saw horse’ stance and reluctance to move, increased digital arterial pulses and sensitivity to hoof tester pressure applied at the toe of the affected digit(s). Many horses also present with gross hoof wall alterations that include divergent rings, increased cap horn or a wider/separated white line, and flat or convex soles.
§ Reversal of obesity
§ Dietary restriction and increased exercise
§ Avoid starch overload
◦ Avoid “aged horse” rations, increase lower quality roughage
§ Role for antioxidants, Vitamin E
§ Pasture-related laminitis - combination of both pasture and horse management
◦ Decrease intake of water soluble carbohydrates (WSC)
◦ Where possible, horse pastures should contain either C4 species, or those C3 species
or varieties that tend to accumulate low concentrations of WSC
◦ Maintain short, leafy grass swards, either by grazing or mowing, and maintain appropriate soil moisture and fertility
◦ Restrict grazing to early morning to avoid intakes of highest concentrations of NSC
§ Prevent susceptible horses from grazing pastures at times of high light intensity and low temperatures
◦ Favour slow growth but high levels of C accumulation
§ Avoid pastures that have ‘gone to seed’ as well as recently harvested stubble where high fructan concentrations may be present in stem
§ Grazing muzzle – physically prevents excessive herbage and NSC intakes
§ Horses on restricted grazing require alternative source of forage

Question 20

Discuss the (nutrition-related) causes of and clinical signs of endotoxaemia in horses.

Answer 20

Endotoxins are lipopolysaccharides (LPS) – the structural components of gram –ve, non-sporing rods of Enterobacteriaceae – Escherichia coli, which normally inhabit the intestines.

Causes
§ Excessive consumption of readily fermentable CHO
§ Inadequate adaptation to diet
§ Ignorance – changing diet too rapidly
§ Accidental access to grain/concentrate

The grain overload increases the numbers of lactobacillus and streptococci, which produce lactic acid. As a consequence caecal pH decreases (from 7 to 4) within 12-24 h. The starch fermenters proliferate faster than cellulose fermenters. The microbes that utilise lactic acid are not adequate and consequently pH plummets, with the number of lactate-utilising microbes declining further. The ciliate protozoa that engulf starch are killed by the low pH, and no longer act as buffers. Normal homeostatic mechanisms are destroyed.

Acid production continues and Enterobacteriaceae die, releasing large amounts of LPS into the gut, compromising the integrity of the colon. The endotoxins overwhelm the mononuclear phagocytic system that normally clears then, resulting in endotoxaemia. Consequently, there is decreased blood perfusion to vital organs, and increased perfusion of GIT.

As a consequence of the changes in perfusion, the extremities are cold. Due to incomplete lung perfusion, hypoxaemia developments. Restricted hepatic blood flow decreases lactic acid removal. Diarrhoea frequently occurs, causing dehydration and further increasing PCV. Stress leads to acute laminitis (ponies are at greater risk).

Question 21

Discuss feed management strategies to minimise the incidence of this condition.

Answer 21

§ Treatment is directed towards preventing laminitis
o Fluidreplacement
o Evacuation of starch overload – mineral oil decreases bacterial fermentation thus slowing down absorption of endotoxin. The oil also assists in evacuation of the GIT.
§ Prevention
o Slowly increase grain/concentrate portion of ration
§ Lactic acid fermenters and protozoa that engulf starch are able to multiply, and thereby act as buffers against decline in pH
o Do not increase the amount of concentrate fed by more than 200 g/d for 550 kg horse  Less for smaller animals
§ Allow 40 d for 0 to 8 kg concentrate o Feed small meals often,
§ Promotes digestion of starch in SI, and prevents ‘spilling’ into LI
§ Feed 0.4% BW/meal
o Processing of grain – gelatinisation enhances digestion in the SI o NSC restricted to 0.25% BW per meal

Question 22

Explain how the clinical signs of exertional rhabdomyolysis in horses are related to inadequate nutritional management.

Answer 22

Although exertion per se is not always involved, such disorders triggered by exercise are often termed equine exertional rhabdomyolysis (ER), literally the dissolution of striated muscle with exercise. Exertional rhabdomyolysis (ER) is becoming one of the most common and economically relevant disorder in horses that perform exercise beyond their conditioning status or those adopting strenuous exercise after a period of inactivity while being fed a high concentrate ration.

There remains uncertainty as to the etiology and pathophysiology of ER. A direct muscle injury or an altering relationship between energy production and energy consumption in muscle has been suggested. There is also evidence that the Ca homeostasis has a pivotal role in maintaining the integrity of the muscle cell. When the muscle is injured by mechanical stress, there is an influx of Na and Ca into the damaged cells which lead to various sequels including persistent contraction of the myofibres, depletion of ATP, and activation of vasoactive molecules besides liberation of phospholipase A2, and increased production of free radicals and Ca overload. Several studies have stated that the disease is associated with multiple complications such as calcification of muscular tissue as well as kidney damage due to excessive myoglobin excretion. Work is currently ongoing looking into the link between excessive glycogen, abnormal polysaccharide and rhabdomyolysis.

Contributory causes/triggers:
§ Exercising after a period of over‐feeding and under‐exercising
§ Provision of too little fibre coupled with too much NSC
§ Electrolyte or mineral imbalances, especially K
§ Deficiency in Se and/or Vitamin E

Clinical signs: muscle spasms or cramps, reluctance to move, stiffness or shortened gait, hard, painful muscles (especially in hindquarters) when palpated, and haematuria.

Question 23

Describe how the horse’s nutritional requirements should be managed to minimise the occurrence of this condition

Answer 23

The actual diet that will be the most beneficial will depend on the horse as an individual, and what they are being used for (as influences energy needs), as well as their history with respect to ERS and the likely underlying cause.

Forage:
§ Less mature hays required for those affected individuals with higher energy requirements, preferably based on grass rather than legume hay.
§ If required (e.g. to potentially help reduce the risk of gastric ulceration), lucerne (chaff or long hay) should be added to the ration gradually as the workload increases but no more than 50% of the hay consumed
o Increasing daily intake of pasture hay or pasture, decrease lucerne hay if previously feeding high levels
§ Feed forages with a reduced NSC content (<12% on a DM basis) to minimise post‐feeding glycaemic and insulinaemic responses
o Whilst soaking hay will not necessarily result in substantial loss of WSC, it may be a helpful supplementary measure.
o In order to help reduce the NSC intake, avoid turning out on ‘lush’ fast growing pastures, especially pastures with a high fructan, high starch or WSC content,
o Prolonged daily periods out in a sparse paddock are often beneficial. Additional energy provision
§ If additional energy required above that of forage, consider using more digestible fibre sources such as soya hulls and unmolassed sugar beet pulp \ and/or supplementary vegetable fats or oil.
§ Grain or NSC – cut out altogether and replace with vegetable oil to meet energy requirements
§ Consider Vit E and Se supplement (anecdotal reports of supplementation preventing further episodes have not been supported to date by scientific studies and there is no good evidence
that oxidative stress plays a primary role in ER).

Electrolytes
§ Ensure the diet provides a sufficient intake of electrolytes in an adequate and balanced manner
§ If wheat bran added to the horse’s diet, it should be fed on a regular basis and any Ca:P imbalance of the diet corrected.

Other factors to take into consideration
§ Do not feed in anticipation of an increase in workload – wait until additional energy is needed before increasing intake.
§ On rest days (which should be avoided if possible), any complementary feed intake should be reduced (for example halved) from the evening before until the evening afterwards.
§ If a more prolonged period of rest is to be given then the type of feed fed should be evaluated and either one of a lower energy density, or forage alone, appropriately supplemented, should be fed.

Question 24

Which of the following is not a hallmark of metabolic syndrome in horses?

a) Obesity.
b) Insulin resistence.
c) Hypoinsulinaemia.
d) Dyslipidaemias.

Answer 24

c) Hypoinsulinaemia

Question 25

Which of the following statements regarding equine metabolic syndrome is incorrect?
a) Is associated with a disruption to insulin signalling pathways leading to insulin resistance.
b) Due to the feeding of a high soluble carbohydrate diet leads to the risk of intestinal
carbohydrate overload and subsequently increased mucosal permeability.
c) Increased mucosal permeability leads to absorption of gasto-intestinal tract derived toxins.
d) None of the above statements are incorrect.

Answer 25

d) None of the above statements are incorrect

Question 26

The incidence of equine metabolic syndrome appears to be more common in ponies, Arabs and Morgans.

a) True.
b) False.

Answer 26

a) True.

Question 27

Increased cholesterol concentration is typically associated with equine hyperlipidaemia.

a) True.
b) False.

Answer 27

b) False

Question 28

Hyperlipaemia is associated with pituitary pars intermedia dysfunction.

a) True.
b) False.

Answer 28

a) True

Question 29

Which of the following statements regarding colic is correct?

a) Is most prevalent in horses older than 10 years of age.
b) Is more common in stallions and geldings than mares.
c) Is the most common cause of death in horses, with an estimated mortality rate of > 25%.
d) More commonly occurs in Arabs than Thoroughbreds.

Answer 29

c) Is the most common cause of death in horses, with an estimated mortality rate of > 25%.

Question 30

Which of the following statements regarding maiden and barren mares is correct?
a) They should be placed on a rising plane of nutrition 6 weeks before joining.
b) Young mares should be provided with a diet containing increased protein, Ca and P.
c) Both types of mares (young and barren) can be maintained on good quality hay or improved
pasture.
d) All of the above.

Answer 30

d) All of the above

Question 31

The large intestine is affected more than the small intestine with strangulation colic.

a) True.
b) False.

Answer 31

b) False

Question 32

The degree of pain is an indication of the seriousness of colic.

a) True.
b) False.

Answer 32

b) False

Question 33

In horses, skeletal muscle damage is characteristic of all myopathies.

a) True.
b) False

Answer 33

a) True

Question 34

Because of the horse’s unique gut architecture and digestive physiology,

a) It is best suited for grazing of roughage in one or two discrete grazing bouts throughout the day
b) Most digestion and nutrient absorption occurs in the intestines
c) Most digestion and nutrient absorption occurs in the stomach.
d) It is nearly impossible to meet nutrient requirements from hay or pasture alone.

Answer 34

b) Most digestion and nutrient absorption occurs in the intestines

Question 35

Compared with grass hays, lucerne hay

a) Has the more balanced Ca:P ratio relative to requirements in horses
b) Is the more concentrated in both energy and protein
c) Is the less palatable
d) Tends to have the greater concentration of neutral detergent fibre (NDF).

Answer 35

b) Is the more concentrated in both energy and protein

Question 36

Manufactured feeds for horses consisting of fortified concentrates
a) are designed to be fed as the sole ration; i.e., alleviated the need to provide forage separately.
b) always need to be supplemented with a protein supplement.
c) are typically formulated to meet nutrient requirements specific to a given stage in the life
cycle, physiological, status, etc.
d) very rarely include liquids such as vegetable oil or molasses because of their high cost.

Answer 36

c) are typically formulated to meet nutrient requirements specific to a given stage in the life
cycle, physiological, status, etc.