Horses Flashcards
What are the feeding behaviours of horses?
High gut fill
16-17hrs a day grazing
Ingest more food/unit BW than ruminants.
Spend less time chewing.
Peak grazing times early am and late pm, bouts last 30mins to 4hrs.
Grazing is not dependent on feed availability and will consume beyond their needs - evolutionary sense to lay down fat reserves.
Prefer young growth and leaves, graze shorter grasses than ruminants.
Do concentrates or fibres increase the chewing in horses?
Hay has 4 x more chewing than oats (also takes 4 x longer to eat).
What foods enhance saliva production? Why is this important?
Hay has most, then grass, then mixed feed.
Important for bicarbonate (buffer).
Decreased fibre - decreased chewing - decreased saliva - less buffering - more gastric acidity - more ulceration - more stereotypies.
What is neophobic?
Fear of trying new feeds - horses on well balanced diet are reluctant to try different feed stuffs.
What influences food intake?
Taste, smell, visual appraisal, texture, aversions formed when illness immediately follows ingestion.
Voluntary feed intake increases when indigestible fibre present in feed.
What macronutrients does a horse require?
Water
Energy - carbohydrates (glucose, VFA’s)
Lipids - triglycerides, FFA’s
Protein - AA (essential and limiting)
What micronutrients does a horse require?
Macrominerals
Microminerals - trace minerals, trace elements
Vitamins - water and fat soluble
What is the most limiting nutrient after water that a horse requires? Discuss this?
Energy.
Primary source is nonstructural CHO (starch, maltose, sucrose), digested in SI and stored as muscle glycogen.
Structural CHO - cellulose, hemicellulose, pectin. Fermented in caecum to VFA’s.
What factors influence the energy requirements of a horse?
Stage of life Body composition Environment - temp., humidity Intensity and duration of work Weight and ability of rider Condition of working surface/terrain Degree of fatigue
What are the maintenance requirements of a 500kg horse?
DE = 68.5MJ/day
How do you determine DE for a horse?
DE (Mcal/d) = 1.4 + 0.03W
W=weight
to convert to MJ x4.18
What challenges are associated with feeding maiden and barren mares?
Don’t want them to get to fat (above 3,3.5/5 BCS).
Rising plane of nutrition for joining (6wks prior).
What nutritional considerations need to be taken into account when feeding a mare in the last 3rd of gestation?
Last 3 months - rapid growth of foetus (500g/d)
Energy, protein, Ca and P requirements increase.
Lay down fat for lactation.
Intake problems - capacity of GIT.
At what life stage is a horses nutrient needs the highest?
During lactation.
Recovering from parturition and producing milk.
3% BW produced in milk per day in first 3 months.
Body condition suffers before milk production.
How many MJ DE are required to produce 1kg of milk?
3.3MJ DE
What are the requirements of a breeding stallion?
No special requirements.
Maintain good body condition with their increased physical activity.
Extra energy and protein if workload warrants it.
Some evidence that increased omega-3 FA in diet assists sperm quality in stallions with poor transport quality semen.
How much more energy do grains have than hay?
40-60% more
What are some ways to increase energy density?
Feed higher quality hay
Add grain
Substitute grains/concentrate by adding fat (up to 15% by weight)
What are some problems associated with the feeding of excess energy?
Excess body weight
Laminitis
Behavioural problems
Thermal stress
What should obese horses be fed?
Grass hay 1.5%BW
Divide into 2 meals, soak for at least 8hrs to remove WSC.
Balanced vitamin and trace mineral supplement - mix with low energy chaff.
Atleast 1hr/d exercise
Free access to water at all times
Fitted grazing muzzle if turned out.
How much protein should be fed for maintenance?
8%
12% for growing horse in work
Good quality lucerne - 15-20%CP
How much water can you expect a horse to drink?
2-3L/kg DM intake
Lost as urine, faeces, sweat, evaporation from lungs and skin, lactation.
Lactation has requirement 50-70% above maintenance.
What influences water intake?
Water to feed ratio
Increased hay = increased water intake
Temperature - decreased with decreased temp.
Work - increases 20-300%
What causes endotoxaemia?
Excessive consumption of readily fermentable CHO’s.
Inadequate adaptation to diet - rapid change in diet.
Accidental access to grain/concentrate.
What are endotoxins?
Lipipolysaccharides (LPS).
Structural component of gram -ve, non sporing rods of enterobacteriaceae (eg. E.coli)
Inhabit intestines.
Elicit strong immune responses in animals.
Clinical signs mediated by prostaglandins.
Inhibit gastric secretions and increase Na output.
Describe disease progression in the case of endotoxaemia.
Grain overload - increased lactobacillus & streptococci - produce lactic acid - drop caecal pH.
Starch fermenters proliferate faster than cellulose fermenters.
Organisms that utilise lactic acid not adequate - pH drops further.
Ciliate protozoa that normally engulf starch and act as buffers are killed by low pH
Normal homeostatic mechanisms are destroyed - acid production continues.
Enterobacteria die, releasing large amounts of LPS.
Colonic integrity compromised.
Intestinal ischaemia, abetted by lactic acidosis or previous parasitism.
Endotoxins overwhelm mononuclear phagocytic system that normally clears them.
What are the consequences of endotoxaemia?
Decreased blood perfusion to vital organs
Increased perfusion of GIT - cold extremities.
Incomplete lung perfusion - hypoxemia
Anaerobic glycolysis increases lactic acid in muscles.
Restricted hepatic blood flow decreases lactic acid removal
Diarrhoea - further decreases PCV through dehydration.
Major cause of colic and can lead to laminitis.
What is the treatment for endotoxaemia?
Prevent laminitis - stand horses feet in ice bath for up to 48hrs.
Cyclo-oxygenase (COX) inhibitors - NSAIDs
Fluid replacement
Evacuation of starch overload - mineral oil slows absorption of toxin, assists evacuation of GIT.
Virginiamycin - antibiotic, controls lactate producing bacteria
What are some prevention strategies to decrease the chance of endotoxaemia?
Slowly introduce grain/concentrate (200g/d) - allows lactic acid fermenters and protozoa that engulf starch to multiply and act as buffers.
Small meals often - promotes starch digestion in SI, prevents spilling into LI
Processing technique - gelatinisation enhances SI digestion.
NSC restricted to 0.25%BW/meal
What is osteochondrosis dissecans?
Developmental orthopaedic disease
Lesion of growth zone of articular/epiphyseal cartilage
Compromises integrity of articular skeleton and cartilage.
Causes poor performance, lameness, wastage.
Describe the disease process of OCD?
Focal damage during endochondral ossification.
Adjacent to joint surface and articular/epiphyseal cartilage complex.
Development of cartilage core and subsequent subchondral bone damage.
May lead to joint ‘mice’ - small bone fragments.
What are the symptoms of OCD?
Non-painful joint swelling.
More time recumbent
Stiffness, difficulty keeping up with peers.
Development of upright conformation
What causes OCD?
Initiating cause unknown.
Multifactorial - growth, body size, nutrition (overfeeding, mineral imbalance, toxicity), endocrinological factors (Insulin, PTH, TH, GH, Calcitonin, growth factors), genetic predisposition, biomechanics/exercise (high energy, low exercise).
What nutritional factors may contribute to OCD?
Over feeding - rapid growth (0.85kg/d), excess DE (>128%), excess CP.
Ca:P imbalance (excess P or Ca, Ca deficiency)
Excess Zn, Cd
Cu deficiency
High energy causes abnormal cartilage which causes OCD.
How do the endocrinological factors contribute to OCD?
High CHO - hyperinsulinaemia, hyperglycaemia
Temporary hypothyroxaemia - adverse effects on chondrocyte maturation.
Excess Ca - hypercalcitonin, decreased chondrocyte maturation and bone resorption.
What is hyperlipidaemia?
Elevated lipid concentrations in blood (uncontrolled lipolysis) - both FFA’s and triglycerides. Not cholesterol.
Occurs in response to negative energy balance.
What breeds of equine are more likely to be affected by hyperlipidaemia?
Ponies, donkeys, minature ponies/horses.
Individuals suffering from IR, cushings, and systemic inflammation.
What are the clinical signs of hyperlipidaemia?
Dull demeanour, inappetance, colic/diarrhoea, weakness, underlying disease, neurological signs.
How can you diagnose hyperlipidaemia?
Gross appearance of plasma
What is the treatment for hyperlipidaemia?
- Early ID (at risk animals, blood analysis)
- Correct negative energy balance (small amount of CHO, roughage-hay, chaff or grass, anything palatable frequently.) May be inappetent (stomach tube or IV administration of glucose/dextrose).
- Treat any underlying diseases
- Correct fluid and electrolyte deficits.
- Supportive care
How can hyperlipidaemia be prevented?
Avoid negative energy balance and improve insulin sensitivity (diet, exercise, drugs)
Avoid stressful conditions - transport, adverse weather, disease
What is equine metabolic syndrome characterised by?
Obesity Dyslipidaemia Insulin resistance Hyperinsulinaemia Laminitis
Define insulin sensitivity.
Insulin that elicits a half-maximal response.
What is the cause of EMS?
Complex interrelationships - obesity, insulin and glucose dysregulation, laminitis.
Overfeeding and inactivity - imbalance between energy intake and expenditure. High NSC, pasture or cereal grain/sweet feed intake.
Genetic predisposition - dominant inheritance pattern for laminitis in EMS ponies, breeds, enhanced metabolic efficiency.
Diagram - diet linked to obesity and hyperinsulinaemia, hyperinsulinaemia linked to laminitis and insulin resistance. Obesity linked to insulin resistance which is linked to laminitis. Diet indirectly linked to laminitis.
How are obesity and IR linked?
Lipotoxicity - FA uptake by tissues, disruption to insulin signalling pathways.
Production of inflammatory mediators - pro inflammatory cytokines, local cortisol production.
Adipokines - leptin (signals satiety-leptin resistance), adiponectin (insulin sensitising, decreased in EMS).
How does IR cause laminitis?
Altered laminar glucose metabolism -> vascular changes -> oxidative stress -> laminitis
What equids are more predisposed to EMS?
Breeds - ponies, arabs, QH, morgans.
History - easy keepers
Clinical presentation - typical phenotype, overweight, regional adiposity, laminitis.
Does obesity mean the horse has EMS?
No
How can you diagnose EMS?
Screening tests - history, physical examination, blood tests (insulin, glucose).
Dynamic tests - diagnosis and monitoring, assess glucose and insulin responses (combined glucose-insulin test).
Are EMS and Cushings disease the same? How do you differentiate?
No Cushings = Pituitary Pars Intermedia dysfunction.
Endogenous ACTH and dynamic testing of pituitary.
Response to treatment.
What is the treatment for EMS?
Limited options - goal is long term management.
Treatment for laminitis - shoeing, analgesia, housing.
Goals - resolve obesity/regional adiposity, improve insulin sensitivity, resolve hyperinsulinaemia, decrease risk of laminitis.
Done via altering diet (weight reduction - avoid soluble CHO’s - grain/sweet feeds/molasses/treats/pasture), increasing exercise and drugs (Metformin, Levothyroxine).
When should pasture be avoided specifically?
When episode of laminitis
While IR
Once IR improves gradually reintroduce pasture - ongoing restriction requires when high fructans (spring/summer rains/warm days and cool nights/drough/frost stress).
Can limit time on pasture, use grazing muzzle, strip graze or mow.
What should an EMS horse be fed?
High fibre/roughage and low NSC.
Hay - <10% NSC, grass/meadow, mature, can soak to remove water soluble carbs.
Supplement - fibre based feed, add to chaff, 0.5-1kg day
1.5%BW/day of hay general guide - don’t go below 1%
Keep all dietary changes gradual
Monitor BSC
If hay not sufficient to meet energy requirements; sugar beet pulp (no molasses), commercial feeds with low NSC, vegetable oil, stabilised rice bran (20% fat).
What exercise is appropriate for an EMS horse?.
Only if no overt laminitis.
Under saddle or lunging, equal to or over 30 mins trot/canter 4-7 x week.
This will not improve insulin sensitivity on its own, needs dietary management as well.
What are some myopathies that horses experience?
Exertional rhabdomyolysis - sporadic, recurrent
Polysaccharide storage myopathy
Other - ionophore toxicity, nutritional (vit E, Se), toxicity, infectious, traumatic, inflammatory
Recurrent ER, PSSM, and other (nutritional) are the main nutritional ones.
What causes nutritional myopathies?
Involves skeletal muscle damage.
Common in performance horses, various breeds, and various athletic pursuits.
All have similar signs but different pathophysiology.
RER - heritable (thoroughbreds, standardbreds, arabs), defect in intracellular Ca regulation - excessive release from sarcoplasmic reticulum, excessive contraction and damage).
PSSM - QH, paint and draft breeds more likely affected. Glycogen storage disorder. Heritable (glycogen synthase enzyme mutation), QH enhanced insulin sensitivity. Results in myocyte energy deficit.
What are the risk factors for RER?
Female aged 2 years.
Nervous temperament, stress, high CHO diet, rest days prior to exercise.
What factors can influence the incidence of PSSM and RER?
Underlying myopathic cause Diet Age Gender Fitness Exercise intensity Temperament
What are the clinical signs of RER and PSSM?
Poor performance Lameness/stiff gait Painful muscles - lumbar/rump area Sweating Muscle tremors Increased HR and RR Brown urine
How do you diagnose RER and PSSM?
History
Clinical signs - not always present
Laboratory - muscle enzymes (CK, AST), urinalysis, muscle biopsy
Genetic test for PSSM
Response to submaximal exercise - measure CK before and 4-6hrs after.
How do you treat PSSM and RER?
Acute - rest and confinement, analgesia, sedatives, fluid therapy (oral, IV).
How can you prevent PSSM and RER?
Nutritional factors are important - high grain diet (especially after rest) and electrolyte/mineral/vitamin deficiencies. Regulate NSC, try alternate energy sources (oil), align with requirements and exercise load. Specific ration depends upon disease severity, BCS, exercise requirements. Provide good quality forage at more than 1%BW, small amount of concentrate and fats (up to 15-25%)
Training/exercise programs - minimise stall rest, daily turnout, lunge/ride, less than 12hr confinement/day.
Don’t exercise them alone, exercise and feed them before other horses, can use low dose tranq (ace).
What are some of the benefits to feeding fats?
Decreased thermal stress Lower gut fill Lower water requirement Enhanced performance Calmer demeanour Reduced CK
Describe a ration specific for PSSM.
Low starch - less than 10% of DE
Fat Supplementation - at least 13% DE and up to 20%DE (decreases CK, myopathy, amount depends on BCS)
Describe a ration specific for RER.
Low starch - less than 20%DE
Fat Supplementation - 15-25%DE (decreased nervousness, lower CK, myopathy, increased aerobic fat metabolism.
