2012- the role of diet in the prevention and management of several equine diseases 1

8/17/2019 2012- The Role of Diet in the Prevention and Management of Several Equine Diseases 1

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Animal Feed Science and Technology 173 (2012) 86–101

Contents lists available at SciVerse ScienceDirect

Animal Feed Science and Technology

journal homepage: www.elsevier.com/locate/anifeedsci

The role of diet in the prevention and management of several equine

diseases

Cristy J. Secombe, Guy D. Lester ∗

Divisionof Health Sciences, School of Veterinary and Biomedical Sciences, Murdoch University, South Street,Murdoch, WesternAustralia, 6150, Australia

a r t i c l e i n f o

Keywords:

Horse

Diet

Equine metabolic syndrome

Laminitis

Exertional myopathy

Selenium

a b s t r a c t

Modern feeding and housing practices of horses are typically directed at achieving a high

level of athletic performance. There are some unfortunate consequences including an

increased incidence of disease. Some of these diseases can be directly linked to dietary prac-

tices, while in others diet contributes as an important co-factor. Breeding practices to select

for specific traits have also inadvertently resulted in the preferential selection of horses

with genetic mutations within several breeds. In several of these genetic disorders specific

dietary management is required for affected horses to achieve an acceptable level of per-

formance. Diseases in which diet has a significant influence are discussed including equine

metabolic syndrome, laminitis, diseases attributed to deficiency of vitamin E and/or sele-

nium, exertional myopathies, nutritional secondary hyperparathyroidism, hyperkalaemic

periodic paralysis, and the developmental orthopaedic disease complex.

© 2011 Elsevier B.V. All rights reserved.

1. Introduction

Diet plays a pivotal role inboth thegenesis andthe management ofseveralcommon diseasesof horses. Animals involvedin

modernhorseactivities commonly receive a diet that differs markedlyfrom that consumed by horses duringrecent evolution

of the species, where the diet was typically fibre-rich and low in starch and was consumed slowly and continuously with

little day-to-day variability in feed type or quality ( Janis, 1976; Durham, 2009). In contrast modern diets commonly include

large high starch meals that are interspersed with variable amounts of roughage. Changes in the type and quality of feed can

vary widely and may predispose horses to a range of problems.

Modern feeding practices are commonly associated with problems of the gastrointestinal tract. For example, sudden

changes in diet have been identified as the most important risk factor in the development of abdominal pain (colic) in horses

(Archer and Proudman, 2006). The risk appears to be increased for upto 14 days after a diet change (Cohen et al., 1999). The

sudden, and typically accidental, consumption of a large amount of starch, often grain, has long been identified as a cause of

colic, abdominal bloat, diarrhoea, toxaemia, and laminitis. Diet has also been recognised as a contributing factor to severalinfectious intestinal diseases of horses, including salmonellosis and clostridiosis (Traub-Dargatz et al., 1990).

Abbreviations: AST, aspartate aminotransferase; Ca, calcium; CK, creatine phosphokinase; DE, digestible energy; DM, dry matter; DOD, developmental

orthopaedic disease complex; EDM, equine degenerative myeloencephalopathy; EMND, equine motor neuron disease; EMS, equine metabolic syndrome;

FFA, free fatty acid; GYS1, glycogen synthetase enzyme; HYPP, hyperkalaemic periodic paralysis; IR, insulin resistance; MJ, megajoule; NSC, non-structural

carbohydrates; Na, sodium; NSH, nutritional secondary hyperparathyroidism; OC, osteochondrosis; P, phosphorus; PSSM, polysaccharide storage myopa-

thy; PTH, parathyroid hormone; QH, Quarter Horse; RER, recurrent exertional myopathy; RYR1, ryanodine receptor; WMD, white muscle disease; WSC,

water-soluble carbohydrate. This paper is part of the special issue entitled Nutrition and Pathology of Non-Ruminants, Guest Edited by V. Ravindran.∗ Corresponding author. Tel.: +61 893607676; fax: +61 893602603.

E-mail address: [email protected] (G.D. Lester).

0377-8401/$ – see front matter © 2011 Elsevier B.V. All rights reserved.doi:10.1016/j.anifeedsci.2011.12.017

http://localhost/var/www/apps/conversion/tmp/scratch_5/dx.doi.org/10.1016/j.anifeedsci.2011.12.017http://localhost/var/www/apps/conversion/tmp/scratch_5/dx.doi.org/10.1016/j.anifeedsci.2011.12.017http://www.sciencedirect.com/science/journal/03778401http://www.elsevier.com/locate/anifeedscimailto:[email protected]://localhost/var/www/apps/conversion/tmp/scratch_5/dx.doi.org/10.1016/j.anifeedsci.2011.12.017http://localhost/var/www/apps/conversion/tmp/scratch_5/dx.doi.org/10.1016/j.anifeedsci.2011.12.017mailto:[email protected]://www.elsevier.com/locate/anifeedscihttp://www.sciencedirect.com/science/journal/03778401http://localhost/var/www/apps/conversion/tmp/scratch_5/dx.doi.org/10.1016/j.anifeedsci.2011.12.017


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C.J. Secombe, G.D. Lester / Animal Feed Science and Technology 173 (2012) 86–101 87

Continuous access to pasture is considered to be protective with the incidence of colic less in this population than in

horses that are predominately stabled (Hudson et al., 2001). Horses at pasture are not immune from colic and can develop

problems with hindgut fermentation when large amounts of fructan-rich pasture are consumed (AlJassim and Andrews,

2009). Overstocking in sandy regions commonly leads to consumption of sand andan associated risk of intestinal obstruction

and colic (Ragle et al., 1989).

The focus of this review is examination of the relationship between diet and several important diseases of horses.

These include the equine metabolic syndrome (EMS), laminitis, diseases attributed to deficiency of vitamin E and/or sele-

nium, exertional myopathies, nutritional secondary hyperparathyroidism, hyperkalaemic periodic paralysis (HYPP), and the

developmental orthopaedic disease (DOD) complex.

2. Equinemetabolic syndrome

A disease with similarities to human metabolic syndrome is recognised in the horse and is termed equine metabolic

syndrome (Frank et al., 2010). Obesity and insulin resistance (IR) are factors shared by both syndromes ( Johnson et al., 2006).

Thepresence of,or history of laminitisis also characteristicof theEMS phenotype (Treiber etal., 2006). Hypertriglyceridaemia

(Frank et al., 2006), hyperleptinaemia (Cartmill et al., 2003), arterial hypertension (Bailey et al., 2008), increased systemic

markers associated with obesity (Vick et al., 2007), and altered reproductive cycling (Vick et al., 2006) are also associated

with EMS.

The domestication of horses led to feeding practices that often differed significantly from the diets consumed in a natural

state. Before domestication the genetic predisposition of “thrifty genes” conferred an evolutionary advantage. The accumu-

lation of fat, development of transient IR and a proinflammatory state was beneficial for survival during times of limited feed

availability. These changes abated when fat stores were depleted, typically at the end of winter ( Johnson et al., 2006). The

subsequent domestication and propensity to overfeed horses has led to year round persistence of adipose tissue with con-

tinual IR and its associated consequences. Adipose tissue is hormonally active and produces adipokines and adipocytokines

(Rasouli and Kern, 2008). More than 100 different adipokines have been identified and it is the inappropriate secretion of

these products over time that results in the pathophysiological consequences of obesity (Hutley and Prins, 2005). Specific

adipokines that have been implicated in EMS include leptin, adiponectin, and resistin. Adipocytokines released by the adi-

pose tissue or from macrophages within fat are pro-inflammatory and lead to a chronic state of low-level inflammation

(Wisse, 2004; Vick et al., 2007; Rasouli and Kern, 2008). Similar to humans it is suspected that specific regions of adipose

tissue in horse may be more hormonally active than other regions. One area is the accumulation of adipose tissue in the

crest of the neck. A neck crest scoring system (the cresty neck score) has been developed to help distinguish horses that

have developed regional rather than generalised obesity (Carter et al., 2009).

Insulin resistance is caused by defective insulin signalling at the cellular level leading to defects in a range of insulin-

dependent metabolic and vascular processes, including insulin-mediated glucose transport (Kashyap and Defronzo, 2007).

There is a compensatory increase in insulin secretion from the pancreas. As described earlier obesity and IR are clearly

linked in EMS (Frank et al., 2006; Treiber et al., 2006; van Weyenberg et al., 2008). The link between IR and obesity may be

due to the adipokine- or adipocytokine-induced down-regulation of insulin signalling pathways and/or the accumulation of

intracellular lipids in insulin-sensitive tissues, such as skeletal muscle, a process termed lipotoxicity (Slawik and Vidal-Puig,

2006). Horses like humans vary in their genetic ability to develop IR; for this reason some obese horses do not exhibit IR

(Frank, 2009).

The common signalment of the equid affected with EMS is the horse or pony between 5 and 15 years of age. The most

common clinical signs at presentation include laminitis and prolonged generalised or regional obesity. It has recently been

shown that supraphysiologic hyperinsulinaemia can induce laminitis in horses (Asplin et al., 2007). It is postulated that

physiologic hyperinsulinaemia is a significant trigger factor in the development of laminitis ( Johnson et al., 2010). The

underlying effect of high insulin levels on the sensitive laminae tissues of the hoof is yet to be fully elucidated, but is

suspected to be mediated by disruption to insulin-mediated vasoregulatory properties (Frank et al., 2010). It is reported that

IR promotes a state of vasoconstriction due to decreased endogenous production of nitrous oxide (Muniyappa et al., 2007).

The diagnosis of EMS requires consideration of the patient signalment, history, physical examination including body

scoring or neck crest measurement, and appropriate laboratory screening tests. Radiographic evaluation of the feet may also

be indicated. The laboratory diagnosis of EMS is typically centred on the single measurement of blood insulin and glucose

concentrations. Testing should be performed between 8 am and 10am in the morning after a minimum of 6 h of grain and

pasture deprivation.A small amount of highlystructured carbohydratecan be fedand is usefulin horses that becomestressed

with feed deprivation (Frank, 2009).

Horses with EMS tend to have a resting blood glucose concentration in the upper end of the normal range rather than

being hyperglycaemic. Type 2 diabetes mellitus should be considered in older horses with persistently elevated resting

glucose when external influences cannot account for the increased glucose. A serum insulin concentration greater than

20U/mL is consistent with IR, although there may be variability between laboratories (Frank et al., 2010). Test specificity

can be affected in a variety of situations; false positives may occur when animals are stressed or experiencing pain, such as

those experiencing laminitis. Testing should only occur when the animal is acclimatised to the environment and is without

lameness or concurrent disease. Sensitivity of the test is affected when the horse is in the early stages of the disease or

if pancreatic insufficiency has occurred due to cell exhaustion resulting in diabetes mellitus type 2 (Frank, 2009; Frank


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88 C.J. Secombe, G.D. Lester / Animal Feed Science and Technology 173 (2012) 86–101

et al., 2010). If a false negative result is suspected dynamic testing using the combined glucose–insulin test is strongly

recommended (Eiler et al., 2005).

The mainstay of management of EMS involves dietary modification and increasing physical activity. Pharmacological

intervention may be used to enhance the response to management changes, but if used alone is unlikely to result in a

successful response. Horses should be fed low quantities of non-structural carbohydrates (NSC) in order to attenuate the

insulinaemic response to meals. Pasture access should be denied or tightly controlled as the digestible energy (DE) from this

source is difficult to quantify and can contribute a significant amount to total daily intake. It has recently been recognised

that dietary fructan, a component of many pasture types, undergoes significant hydrolysis before thelarge intestine, thereby

contributingto theglycaemic response to a meal (Longlandand Byrd,2006). In addition equids exhibiting IR mount an insulin

response to dietary fructan (Bailey et al., 2007). Non-structural carbohydrates can be calculated by adding starch and water-

soluble carbohydrate (WSC) percentages and should be below 100 g/kg of dry mater (DM) intake in affected animals (Frank

et al., 2010). The practice of soaking hay in cold water for 60min to reduceWSC cannot be reliedupon to consistently remove

WSC from roughage (Longland et al., 2009).

Weight loss is essential for successful management of EMS, but horses should not be starved. This may worsen IR or cause

pathologic mobilisation of fat stores. Horses should be fed hay at a recommended rate of 1.5% of body weight daily for the

first 30 days of management, and then further reduced to 1% of body weight daily. Those horses that exhibit IR and regional

adiposity rather than generalised obesity are more challenging to manage and often require the addition of higher energy

but low NSC feedstuffs, such as beet pulp or vegetable oils. It is also recommended to feed regularly spaced small meals

(Frank et al., 2010).

Exercise has been clearly shown to be effective in improving insulin sensitivity in people with IR (Goodyear and Kahn,

1998; Crandall et al., 2008). A similar response to exercise has been documented in horses with IR (Pratt et al., 2006). The

primary limitation to exercise in equids with EMS is the frequent episodes of laminitis. Although the amount of exercise

required to improve insulin sensitivity has been determined in humans, this is not the case in the horse (Bajpeyi et al., 2009).

Thecurrent recommendations in laminitis-free equids are to begin with 2–3 exercise sessions a week of 20–30 min duration,

and slowly increase both the number and intensity of sessions over time (Frank et al., 2010).

Pharmacological management of EMS includes levothyroxine sodium, insulin-sensitising drugs such as metformin, or

supplements such as magnesium and chromium. Levothyroxine has been shown to induce weight loss and improve insulin

sensitivity in horses over the short- and long-term without any reported adverse effects (Frank et al., 2005). There are

conflicting data on metformin improvement in insulin sensitivity in horses (Vick et al., 2006). This may bedue inpartto the

drugs apparent low bioavailability in horses (Hustace et al., 2009).

3. Laminitis

Laminitis is one of the most common diseases of horses. The condition, also known as founder, has a range of inciting

causes, but all result in a common pathologic consequence and consistent clinical signs. The most frequently identified form

of laminitis seen is pasture-induced (Hinckley and Henderson, 1996; USDA-NAHMS, 2000). Although this form has a clear

nutritional basis the exact mechanism that triggers the pathways resulting in laminitis have not been definitely determined.

A digestive and/or metabolic disturbance is postulated (Geor, 2009).

The delivery of a large amount of poorly digested but rapidly fermentable substrate to the caecum and large colon

initiates changes in bacterial flora and mucosal permeability (Krueger et al., 1986; Milinovich et al., 2006). This occurs

classically when large amounts of grain are consumed spontaneously, or when carbohydrate is administered experimentally,

typically in the form of starch. The pathophysiology of pasture-induced laminitis differs from the experimental model of

starch overload. Recently, a model of laminitis has been established using oligofructose, a storage carbohydrate of grasses

in climatic conditions that favour photosynthesis over plant growth (Longland et al., 1999). Such climatic conditions are

associated with an increase in the incidence of pasture-induced laminitis (Hinckley and Henderson, 1996).

Fructans are the primary storage carbohydrate of pasture grasses grown in temperate regions and are located in the

plant stem (Longland and Byrd, 2006). Starch is the storage carbohydrate of the seed of temperate grasses. Starch is also

the primary carbohydrate in the vegetative tissue and seeds of legumes and warm season grasses (Longland, 2007). There

are numerous environmental factors that influence the accumulation of fructans in pasture, including seasonal and diurnal

factors. Fructan concentration is highest in spring in the afternoon of any particular day (Longland and Byrd, 2006). In horses

with 24-h access to pasture it is possible to reach a NSC intake equivalent to or greater than that used to create laminitis in

an experimental model, but this typically would occur over the entire period rather than as a single bolus, thereby sparing

the majority of animals from becoming clinically affected. It is likely that horses with a predisposition to pasture-induced

laminitis will be affected by smaller doses of fructans consumed over relatively short periods of ingestion (Geor, 2009).

It has been observed that a particular phenotype of equid is predisposed to pasture-induced laminitis. There is now a

substantial body of evidence that links obesity, IR, and hyperinsulinaemia as predisposing factors for the development of

pasture-induced laminitis( Johnson et al., 2004; Treiber et al., 2006; Frank, 2009). Grazing of pastures with high NSC(134 g/kg

DM) compared to other times of the year have been shown to exacerbate IR and hyperinsulinaemia in ponies (Treiber et al.,

2008), and recent research has demonstrated that hyperinsulinaemia alone can result in clinical laminitis (Asplin et al.,

2007). Insulin resistance may lower the threshold for induction of laminitis from carbohydrates due to the vasoconstrictive

and pro-inflammatory state it potentiates (Geor, 2009).


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The clinical signs, diagnosis and treatment of laminitis are reviewed elsewhere (Floyd, 2007a, 2007b; van Eps, 2010).

The focus in horses predisposed to founder is to prevent initial occurrence or to limit exacerbation in animals currently or

recently affected. This revolves around the identification and correction of underlying metabolic abnormalities and limiting

dietary NSC intake. The most common metabolic abnormalities associated with pasture-induced laminitis are EMS and

pituitary pars intermedia dysfunction, the latter condition often incorrectly referred to as Equine Cushing’s disease.

Fructans are believed to pose the greatest risk of laminitis, but other NSC may also be important and should be included

in a feed analysis (Longland and Byrd, 2006). Forage analysis of hay and other feedstuffs is easily performed and highly

recommended in order to develop a feeding regimen for these animals. Unfortunately, due to the dynamic nature of carbo-

hydrate storage within pasture, single point analysis may not accurately reflect the range of NSC throughout a 24-h period

(Longland and Byrd, 2006). This limitation usually results in conservative recommendations regarding access to pasture, for

example, animals with active laminitis should have no pasture exposure and horses that are identified as being of high risk

should have highly restricted pasture access. This advice can be tempered through knowledge of geographical, diurnal, and

seasonal variability in NSC content of pasture. Estimates of the amount of pasture that is ingested during pasture access have

been reported (Ince et al., 2005). The current recommendations are that at risk animals should have no access to pasture

during the growing season, but if this is not possible then restriction should be instituted, with animals having access late

at night or early in the morning before fructans reach daily peak concentrations (Longland and Byrd, 2006). Horses should

not be grazed on mature grasses with high stem NSC content and grazing in conditions that favour photosynthesis rather

than growth should be avoided due to preferential fructan accumulation. Recently harvested stubble and pastures that have

gone to seed should also be avoided (Longland and Byrd, 2006). Horses can be managed successfully using grazing muzzles

to limit pasture intake at times of high fructan content, but consideration should be given to changes in social dynamics that

may occur with muzzle use (Harris et al., 2006).

The presence of rapidly fermentable material in the hindgut results in preferential growth of Gram positive bacteria over

Gram negative organisms (Garner et al., 1975, 1978). In a study where horses were fed pelleted diets containing 830 g/kg

ground maize, at rate greater than 20MJ DE per 100kg bodyweight daily, the antibiotic virginiamycin prevented selective

overgrowth of Gram positive bacteria (Rowe et al., 1994). Antibiotic efficacy has been supported by in vitro data with the

maximal benefit reported in starch models and a lesser degree of benefit in response to dietary fructans (Bailey et al., 2002).

Anecdotally prophylactic administration of virginiamycin has not been efficacious in all cases prompting investigation of

other agents (Harris et al., 2006). The results thus far have been disappointing leaving dietary control as the fundamental

preventative strategy (Bailey et al., 2002).

In those animals that have limited or no access to pasture safe dietary alternatives need to be provided. Ideally feed

should be tested for NSC content, with less than 100 g/kg content the ideal. As a general rule mature grass hays will contain

less NSC than immature hays and therefore should be chosen for the at-risk animal. Horses require 2% of body weight of

forage daily to maintain body weight, but forage alone will not provide sufficient mineral, vitamins or protein. Therefore

supplementation should be provided (Geor, 2009).

4. Diseases associatedwith a deficiency in vitamin E/selenium

There are 3 equine conditions where deficiencies of vitamin E and/or selenium have been implicated. Nutritional myo-

degeneration is most commonly expressed clinically as rhabdomyolysis in young, rapidly growing foals and is due primarily

to a deficiency of selenium. A deficiency of vitamin E is postulated to be involved in the pathogenesis of 2 other neurologic

diseases of equids, equine degenerative myeloencephalopathy (EDM) and equine motor neuron disease (EMND). Equine

degenerative myeloencephalopathy is a chronic disease seen in younger horses that causes symmetric ataxia and pare-

sis, more pronounced in the hind limbs and spasticity. Equine motor neuron disease is a neurodegenerative disease of the

somatic lower motor neurons affecting mature horses. Although vitamin E and selenium deficiency is not thought to be

involved in the aetiology of atypical myopathy they may be protective against a potential oxidative stress involved in the

pathophysiology of this disease (Galen et al., 2008).

4.1. Nutritional myodegeneration in foals

Nutritional myodegeneration, or as it is more commonly known white muscle disease (WMD), is a non-inflammatory,

degenerativediseaseof skeletaland cardiac musclecaused by a deficiencyof selenium, andto some degreevitaminE (Higuchi

et al., 1989; Lofstedt, 1997). The disease has been reported in both hemispheres (Dill and Rebhun, 1985; Radostits et al.,

1994) and occurs in areas with selenium deficient soils. Selenium deficient soils are often acidic and volcanic in nature and

produce crops that are also deficient in selenium. A contributing factor is the presence of sulphur, either natively within the

soil or through fertilisation with sulphur-containing fertilisers. Dietary sulphur hinders selenium absorption in animals and

uptake in plants. Rapidly growing plants, in particular legumes, tend to be the most selenium deficient (Maas and Valberg,

2009).

Seleniumhas a variety of functions within thebody includinginhibition of lipid peroxidationand incorporation into some

important amino acids and enzymes (Koller and Exon, 1986). From the perspective of the aetiology of WMD perhaps the

most important enzyme is glutathione peroxidase, which in conjunction with vitamin E, serves to act as an antioxidant and

protect lipid containing organelles and cellular membranes from damage caused by free radicals or highly reactive oxygen


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metabolites (Lofstedt, 1997). Vitamin E scavenges compounds that form reactive metabolites while glutathione peroxidase

destroys formed free radicals and reactive oxygen species. Vitamin E and glutathione peroxidase work synergistically, but

the latter is considered more important, illustrating a critical role for selenium (Lofstedt, 1997). Selenium is also important

in effecting an adequate humoral immune response, a role that has been demonstrated in the horse (Baalsrud and Overnes,

1986; Knight and Tyznik, 1990).

White muscle disease in equids is without breed and gender predilection and clinical signs usually occur within 60 days

of birth, but have been reported at up to 1 year of age and in aborted foetuses (Dill and Rebhun, 1985). The disease may

occur acutely, quickly progressing to cardiovascular collapse and death due to cardiac muscle involvement. A subacute form

of WMD is characterised by signs of profound muscular weakness due to involvement of skeletal muscle (Moore and Kohn,

1991). Dysphagia is a common clinical sign that is often seen in this group of animals and is attributed to involvement of

the pharyngeal and masticatory muscles (Dill and Rebhun, 1985). Although rare in adult horses, the only presenting sign

of nutritional myodegeneration in this age group is dysphagia (Ludvikova et al., 2007). It is important to recognise that

low serum levels of selenium are present in many outwardly healthy foals when reared in selenium deficient areas. Other

compounding factors such as excessive exercise, stress, vitamin E deficiency, or excessive dietary fats may induce clinical

disease (Lofstedt, 1997).

Thediagnosis of WMD is basedon clinical signs of profound muscular weakness, palpablyfirm muscles, or signs of dyspha-

gia. An antemortem diagnosis is confirmed through a variety of biochemical and electrolyte abnormalities and measurement

of whole blood selenium and glutathione peroxidase activity (Dill and Rebhun, 1985; Moore and Kohn, 1991). Biochemical

and electrolyte abnormalities include markedly elevated muscle-derived enzymes creatine phosphokinase (CK) and aspar-

tate aminotransferase (AST), and hyponatraemia, hypochloraemia, hyperkalaemia, and azotaemia. A mixed metabolic and

respiratory acidosis may be present (Dill and Rebhun, 1985). The measurement of whole blood selenium is thought to

accurately reflect the current selenium status of the animal, whereas erythrocyte glutathione peroxidase activity is a good

indicator of selenium status in the months prior to sample collection as selenium is incorporated into the erythrocyte at cell

formation only (Lee et al., 1995). A postmortem diagnosis of WMD typically reveals bilaterally symmetric white streaks in a

variety of muscle groups. Histologically the muscle has hyaline degeneration and fragmentation with lysis of the myofibrils

in acute cases, and calcification and histiocyte infiltration in more long-standing cases (Dill and Rebhun, 1985; Moore and

Kohn, 1991).

Treatment involves minimising physical exertion and stress, supportive therapy, and administration of parenteral sele-

nium and vitamin E (Dill and Rebhun, 1985). Mildly affected animals should improve rapidly after selenium injections

although there is a delay in increase erythrocyte glutathione peroxidase activity. Platelet glutathione peroxidase activity

increases within hours of selenium administration and this may be more reflective of changes that occur within the muscles

after supplementation (Lofstedt, 1997). Despite treatment the prognosis is often guarded, with mortality rates of up to 95%

in the cardiac form and up to 45% in the skeletal form (Combs and Combs, 1986).

Theassessment of herd seleniumstatus, ideally performed in thelast trimester of pregnancy, shouldprovide therationale

for prophylactic supplementation of selenium. This is most efficacious when administered during theprepartum period (Dill

and Rebhun, 1985; Moore and Kohn, 1991). Selenium status of newborn foals is dependent on the mare, and blood levels

are usually lower than the dams if the mare’s selenium status is normal (Lee et al., 1995). The prevention of WMD is through

ensuring themare hasan appropriateselenium intake of 1 mg/dayfor a 500kg horse (National Research Council, 2007). Daily

oral supplementation or annual parenteral seleniumadministration to the mare may be requiredif her existingdietary intake

does not meet requirements (Wichtel et al., 1998), or given to the foal after birth, although this does not prevent in utero

acquired WMD (Lofstedt, 1997).

4.2. Equine degenerativemyeloencephalopathy

EDM is a neurologic disease of horses with an incompletely understood pathophysiology. Vitamin E deficiencies in isola-

tion or in combination with a familial tendency, or exposure to wood preservatives have all been postulated as contributory

factors (Dill et al., 1990). Copper deficiency has been shown to cause degenerative myelopathy in other species but this

appears not to occur in horses (Dill and Hintz, 1989). The case for vitamin E deficiency is supported in part by data collected

from other species where uncomplicated vitamin E deficiency results in axonal degenerative disease in juvenile animals

(Mohammed et al., 2007). The pathological nervous system lesions seen in EDM are similar to those seen in vitamin E defi-

ciency in a variety of other species (Blythe and Craig, 1992a). Vitamin E acts as an antioxidant and prevents abnormal lipid

peroxidation, in the case of deficiency there is excessive membrane lipid peroxidation and an abnormal spinal cord vascular

accumulation of lipopigment (Cummings et al., 1995). This is supported by histological findings of a larger amount vascular

endothelium lipopigment in horses with EDM versus controls (Cummings et al., 1995). The source of the reactive oxygen

metabolites is thought to be endothelial mitochondria, which may explain why lesions are more marked in the spinal grey

matter rather than the spinal roots, as the mitochondria are far more abundant in the cord (Cummings et al., 1995).

Serum vitamin E concentrations arenot always decreasedin affected animals (Dill etal.,1989) and in those farms where a

problem has been identified it has been clearly shown that supplementation with vitamin E (1000–2000 IU/day) has reduced

disease incidence (Mayhew et al., 1987; Dill et al., 1990).

The aetiology of the low alpha-tocopherol levels in affected horses is unknown but several hypotheses have been put

forward, with theinadequatedietaryvitamin E being themost favoured (Miller and Collatos,1997). It has been demonstrated


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that raising foals on dirt lots rather than vitamin E-rich green pastures is a risk factor for the development of the disease

(Dill et al., 1990).

Histopathological lesions of EDM are consistent with a neuronal dystrophy and occur in the brain stem and throughout

the spinal cord (Blythe and Craig, 1992a). The most common clinical presentation is that of a horse less than 1 year of

age presenting with symmetrical ataxia and paresis more pronounced in the pelvic limbs (Dill et al., 1990; Blythe and

Craig, 1992a). There is usually hyporeflexia, manifest as a failure to elicit the cutaneous trunci reflex or reduced or absent

thoracolaryngeal adductor response (aka “slap test”) (Mayhew et al., 1987). Clinical signs are often self-limiting and if a

horse survives, the neurological deficits often remain stable for the duration of the animal’s life (Blythe and Craig, 1992a).

The diagnosis of EDM is often one of exclusion, with cervical vertebral compressive myelopathy, equine herpes myeloen-

cephalopathy, and in somegeographicallocations, equine protozoalmyeloencephalitisbeing the main differential diagnoses.

Serum vitamin E or alpha-tocopherol levels should be measured, but a low value should not lead to a definitive diagnosis

EDM; the only definitive diagnostic test is histopathology (Blythe and Craig, 1992b).

Once clinical signs of EDM develop a full recovery is unlikely, even with vitamin E supplementation, although some

improvement may be achievable. Clinical improvement should begin within 3–4 weeks and may continue for up to a year

following supplementation (6000IU/day) (Blythe and Craig, 1992b). Foals that exhibit risk factors, i.e., familial history, min-

imal access to green pasture, high incidence of the disease on the farm, and exposure to wood preservatives should receive

vitamin E prophylactically (1000–2000 IU/day) (Mayhew et al., 1987).

4.3. Equinemotor neuron disease

EMND was first reported in 1990 and has many similarities to progressive spinal atrophy of man (Cummings et al., 1990).

Thedisease is a neurodegenerativedisorder of somatic lower motor neurons and occurs independently of geographic region,

although thenortheast of theUSA appears over-represented in cases (Hahn and Mayhew, 1993; Sustronck et al., 1993; Gruys

et al., 1994; Kuwamura et al., 1994; De la Rua-Domenech et al., 1997). There have been several EMND epidemiologic studies

performed (Mohammed et al., 1994; De la Rua-Domenech et al., 1995a, 1995b) and risk factors typically include an isolated

mature horse, of either Quarter Horse or Thoroughbred breed, that has been kept in a dry lot with little to no pasture access.

Although pasture access may not be as an important factor as previously thought (McGorum et al., 2006).

The underlying pathophysiology of EMND involves damage and death of somatic ventral motor neuronal cells (Divers

et al., 2001). A neuronal loss of 30% is required before clinical signs are evident (Weber Polack et al., 1998). The loss of the

parental motor neuron cells results in degeneration of the myelinated axons in the ventral roots, peripheral nerves and

muscles with a predominance of type 1 fibres. These muscles, often the postural muscles, are more highly oxidative than

other muscle groups and therefore are more severely affected (Valentine et al., 1994). All brainstem cranial nerve somatic

motor nuclei, except those of cranial nerves 3,4 and 6 are affected, although cranial nerve deficits are rarely appreciated

clinically (Divers et al., 2006b). Lipopigment deposition is seen in both the endothelial cells of the spinal cord capillaries

and retina and occasionally in the liver and the gut; this reflects increased lipid peroxidation, a consequence of widespread

oxidative stress (Cummings et al., 1995; Verhulst et al., 2001).

The aetiology of the disease is again likely to be multifactorial with oxidative stress due to hypovitaminosis E being a

major contributor. This is supported by the experimental induction of the disease by chronic dietary vitamin E deficiency

(Divers et al., 2006a; Mohammed et al., 2007) with the loss of the antioxidant activity of vitamin E (both systemically and

in nervous tissue) and accumulation of oxidative free radicals within tissue. There is more rapid induction of disease when

deficient animals are fed pro-oxidants (Divers et al., 2006a). Deficiency of other antioxidants is not thought to result in

disease (Mohammed et al., 2007). It is likely that additional factors are required to induce disease, as the classic lesions

associated with vitamin E deficiency in other mammals are not present and the disease was not identified until the 1990s,

well after vitamin E deficiency was first recognised in horses (Divers et al., 1994; Mohammed et al., 2007). Interestingly in 3

horses with histologically confirmed EDM, there was concurrent histological evidence of EMND although clinical signs were

absent (Divers et al., 2006b). In addition in the experimental models not all horses fed a vitamin E deficient diet went on to

develop clinical EMND, although ante-mortem diagnostic tests were suggestive of early disease (Mohammed et al., 2007).

It remains unknown if low vitamin E is a consequence of the disease rather than a cause (Wijnberg, 2006). Further work is

required to determine other aetiologic factors.

Antioxidant status depends on a multitude of factors including nutrition, time of year, age and activity (McGorum et al.,

2003). Antioxidant status may be better assessed by repeatedly measuring vitamin E, glutathione peroxidase and selenium

before concluding that a true deficiency exists (Wijnberg, 2006). In addition reference values for each lab should be estab-

lished, as they are notoriously variable (Wijnberg, 2006). This may help explain those sporadic cases in which the disease is

diagnosed post-mortem but vitamin E status is within normal limits (Syrja et al., 2006).

Equine motor neuron disease clinical signs are dependent on the stage of the disease at the time of presentation and are

categorised as subacute or chronic (Divers et al., 1994). Horses suffering from the subacute form often demonstrate muscle

fasciculations, trembling, frequent shifting of weight, abnormal sweating, and spend a large amount of time lying down.

Head carriage is usually low and tail head is usually elevated due to atrophy of the tail head muscles (sacrocaudalis dorsalis).

Appetite is appropriate or increased. Owners often report a loss in muscle mass over the preceding month (Divers et al.,

1994). Around 30% of horses will demonstrate a pigment retinopathy, but vision is usually not affected (Riis et al., 1999).

The chronic form of the disease is usually seen after stabilisation of the subacute stage, but some horses may present in the


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chronic disease state. Clinical signs seen at this stage include fatigue, poor athletic performance, and an unusual gait. Muscle

atrophy resulting in weight loss is usually present and will vary from mild to severe. Muscles most severely affected are

those involved with the stay apparatus (Valentine et al., 1994) and may explain why these horses have extreme difficulty

standing still. Around 40% of horses will deteriorate quickly in around 1 month after diagnosis, 40% will show improvement

within a similar time period with environmental change and/or vitamin E supplementation (2000–10,000U/day), and the

remaining 20% of animals will have permanent muscle atrophy. Each outcome is dictated by the extent of motor neuron

death (Divers et al., 2006b).

Laboratory findings often found in EMND cases are mild increases in CK and AST, and reduced plasma vitamin E concen-

trations


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rhabdomyolysis requires collection of a thorough history, including a detailed description of the clinical complaint, ration

composition, exercise schedule and temperament of the horse (McKenzie and Firshman, 2009).

Horses with PSSM will often have a persistent elevation in serum CK at rest, especially if they are confined (Finno et al.,

2009), but horses with RER typically have a normal serum CK concentration if they have not exercised recently. Creatinine

kinase should be assessed within 4–6 h of 2–20min of trotting exercise, with a greater than a 3–4 fold increase in serum

activity or a total CK concentration greater than 1000IU/L being abnormal (Valberg et al., 1993; De La Corte and Valberg,

2000). In some horses with RER submaximal exercise testing may not result in a reliable increase in CK (McKenzie and

Firshman, 2009). Muscle biopsies may also provide valuable information with both RER and PSSM having consistent but

different findings. The recent discovery of the genetic mutation associated with PSSM allows for genetic testing. Current

recommendations are for Quarter Horses and QH-based breeds to be tested for both the GYS1 mutation and the ryanodine

receptor (RYR1) mutation, which can be done via blood or hair prior to muscle biopsy. The RYR1 mutation is responsible for

a third type of PSSM and is uncommon in QH with an estimated incidence of 0.5%. This is a more severe and possible fatal

PSSM phenotype and is associated with malignant hyperthermia (McCue et al., 2009). A muscle biopsy is recommended in

those horses that have clinical signs of rhabdomyolysis but are negative for the genetic abnormalities to confirm a diagnosis

of non-GYS1 (type 2) PSSM (McKenzie and Firshman, 2009).

Long before a more thorough understanding of chronic exertional rhabdomyolysis and its subtypes were achieved it has

been appreciated that nutritional modification is important in the management of the condition. Regardless of theaetiology,

horses that exhibit rhabdomyolysis are more likely to encounter muscle necrosis on diets high in NSC (McKenzie et al.,

2003b; Ribeiro et al., 2004). In horses with PSSM high NSC may result in enhanced glucose uptake and glycogen storage in

muscle (McKenzie and Firshman, 2009). In horses with RER a high NSC within the diet has been linked with excitability, a

strong triggering factor for the expression of clinical signs (MacLeay et al., 1999).

Horses with PSSM should receive a diet that reduces glucose load and encourages the supply of fat-based substrate to

exercising muscle. The diet should provide 10% or less of the daily energy requirements as starch and a minimum of 13% DE

as fat (McKenzie and Firshman, 2009). Implementation of a regular exercise regimen in horses with PSSM is also beneficial

(Firshman et al., 2003; Ribeiro et al., 2004). It is believed that a low starch, fat-supplemented diet decreases both insulin

concentration and glucose uptake, and by increasing plasma free fatty acids (FFAs) concentrations FFA oxidation is favoured

overglucose metabolism (Ribeiro et al., 2004). Although some authors believe that increasingthe fat supplementation to 20%

DE is beneficial (Valentine et al., 2001) an increase to this level often exceeds caloric requirements, may create unpalatable

rations, andcould reducethe digestibility of other feedstuffs withinthe ration(McKenzie and Firshman, 2009). Improvement

of clinical signs with dietary modification in horses with PSSM without the inclusion of partial confinement (less than 12h

per day) and an exercise regimen appears to be very limited (Firshman et al., 2003).

Horses that have RER appear to only benefit from fat supplementation when the total DE intake is high, exceeding

88 MJ/DE/day (McKenzie and Firshman, 2009). Serum CK levels were significantly lower when horses were fed a high energy

ration where 20% of the DE was supplied as fat, contrasted with a starch-based equivalent energy ration (McKenzie et al.,

2003b). The horses were subjectivity better to handle, had lower resting heat rates and lower packed cell volumes (haemat-

ocrit). As there is close relationshipbetweennervousnessand RERthe addition of fat at theexpenseof starch, but not energy,

may make horses calmer and therefore less predisposed to an episode of rhabdomyolysis (MacLeay et al., 1999; McKenzie

et al., 2003b).

Thecurrentrecommendations forfeeding horses with RERis to limit starchsources to less than 20%of daily DE andinclude

fatat 15–20%of energy requirements(McKenzie et al., 2003a). Clinical improvement with dietary modification in RER horses

has been shown to occur in less than a week and is attributed to neurohormonal changes that reduce anxiety in susceptible

animals (McKenzie et al., 2003b). Exercise modification and other management strategies, including pharmaceuticals, have

an important role as well (McKenzie and Firshman, 2009).

6. Nutritional secondaryhyperparathyroidism

This disease is colloquially been known as “bran disease”, “Millers disease” or “big head”, and has been well recognised

in horses for centuries (Manning, 1882). The disease tends to occur when horses are fed diets that are low in calcium and

high in phosphorus (e.g., rice bran) or have access to pastures that have a high content of oxalates (Walthall and McKenzie,

1976; Bertone, 1992; Toribio, 2009).

Thepathophysiology of the disease is related to the homeostatic need to maintain total serum and ionised serum calcium

within a very narrow range. If a dietary imbalance of high phosphorus, low calcium, or a P:Ca ratio exceeding 3:1 is not

corrected then physiological compensatory mechanisms are activated (Toribio, 2004). Consumption of grasses with a cal-

cium:oxalate ratio less than 0.5, usually occurring in grasses containing more than 0.5% oxalate DM, while typically not high

enough in oxalate to causeoxalate toxicity, willchelate calcium within the gastrointestinal tract and therefore reduce intesti-

nal absorption causing disease (Blaney et al., 1981). Grasses that are commonly oxalate-rich are tropical grasses including

Setaria, Cenchrus, Panicum, Pennisetum clandestinum and Brachiaria species (Walthall and McKenzie, 1976; McKenzie, 1988;

Bertone, 1992).

Extracellular ionised calcium is maintained by a homeostatic system involving three hormones: parathyroid hormone

(PTH); calcitonin; and 1,25-dihydroxyvitamin D3

, and three body systems: renal; gastrointestinal; and musculoskeletal, and

a calcium sensing receptor (Mundy and Guise, 1999; Toribio et al., 2001; Toribio, 2004). The calcium receptors in the chief


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cells of the parathyroid detect changes in the calcium concentration; low calcium and/or elevated phosphorus stimulate

PTH secretion while elevated calcium results in increased calcitonin secretion. PTH increases renal calcium resorption in the

distal nephron, decreases phosphate resorption in the proximal tubules, stimulates renal calcitrol synthesis in the proximal

tubules and stimulates osteoclastic bone resorption. Calcitrol increases intestinal absorption of calcium and increases renal

resorptionof calcium and phosphorus and inhibits PTH secretion (Toribio, 2004). Hyperphosphataemia stimulatesPTH secre-

tion and inhibits renal 1,25 hydroxy vitamin D synthesis, causing parathyroid cell hyperplasia and increased PTH secretion.

Hyperphosphataemia also results in calcium phosphate precipitates and this further contributes to a reduction in serum

calcium (Argenzio et al., 1974). The condition is slowly progressive and as the homeostatic mechanisms are highly effective

in maintaining blood calcium within a normal range horses do not present with the classic clinical signs of hypocalcaemia

(Toribio, 2009).

As the disease causes increased bone resorption clinical signs include ill thrift, a stiff gait, and shifting limb lameness

(Walthall and McKenzie, 1976; Bertone, 1992; Toribio, 2009). The lameness is thought to be due to loss of bony support of

the articular cartilage as a consequence of subchondral bone resorption, microfractures of the subepiphyseal region of long

bones, focal periosteal avulsion fractures, and insertional tendinopathies or desmopathies (Krook, 1968). The classic clinical

sign of NSH is fibrous dystrophyof thefacial bones,colloquially known as “big head”. This is more commonly seen in younger

horses due to a higher rate of bone metabolism (Bertone, 1992; Ronen et al., 1992). Fibrous tissue replaces bone and horses

may develop masticatory difficulties and loose teeth (Walthall and McKenzie, 1976; Bertone, 1992; Toribio, 2009).

Thediagnosis of NSH is basedon dietary history, clinical signs,and theoutcomeof diagnostic tests.Dietaryhistory includes

diets that are high in phosphorus (P:Ca > 3:1) (Toribio, 2009) such as bran or concentrates, or horses that are grazing heavily

on oxalate-rich pastures (David et al., 1997). An inappropriate dietary Ca:P ratio may also cause disease in the absence of

an overtly phosphorus-abundant diet (Little et al., 2000). Osteoporosis is evident radiographically with the lamina durae

dentes demonstrating the earliest change of bone mineral density as they have a high rate of osseous turnover and a thin

discrete radiographic appearance. A decrease of 30% in bone mineral density is required before a subjective decrease can

be appreciated radiographically (Krook, 1968). Facial bones will often be the next radiographically affected and will have

evidence of fibrous proliferation and finally the long bones (Toribio, 2009).

Laboratory testing involves determining calcium and phosphorus serum concentrations and urinary fractional excretion

of key electrolytes, the serum concentration of PTH, and the Ca:P ratio in faeces. Serum concentrations of both calcium

and phosphorus are often normal or there may be a slight increase in phosphorus (David et al., 1997), if this is the case

then urinary fractional excretion is necessary and is considered a sensitive indicator of the disease (Bertone, 1992). Urinary

fractional excretion of phosphorus exceeding 0.5% is consistent with NSH(Bertone, 1992). Measurement of urinary excretion

of calcium is controversial, but if low is also consistent with NSH (Bertone, 1992; Toribio, 2009). Horses with NSH have an

abnormally elevated PTH and measurement has been found to be most accurate using the immunoradiometric assay of

which there are several generations. The third generation assay has now been validated in the horse (Estepa et al., 2003).

The ratio of Ca:P in faeces is often elevated if the horse has been consuming oxalate containing pastures and a ratio of greater

than 2.35:1 is considered significant (Walthall and McKenzie, 1976; Bertone, 1992).

The treatment of NSH involves limiting exercise, providing a ration to correct the Ca:P ratio and reduce the inappropriate

secretion of PTH. The aim is to increase the dietary Ca:P ratio to greater than 4:1 (Toribio, 2009). This can be achieved by

reducing grain intake and increasing hay, in particular lucerne (alfalfa) hay due to high calcium content. Supplementation

with either dicalcium phosphate (Ca:P ratio 22:1.5) and or calcium carbonate (350g/kg calcium) is also useful (McKenzie

et al., 1981; Toribio, 2009). Feeding a ration with a high Ca:P ratio should continue until the radiographic signs have returned

to normal and clinical signs have resolved, this process may take up to 1 year. In some cases the facial swelling may not

regress and lameness may improve but not resolve (Krook, 1968; Bertone, 1992; Toribio, 2009). Prevention of the disease is

easily achieved by ensuring horses have a diet with an adequate Ca:P ratio, especially in young growing animals.

7. Hyperkalaemic periodic paralysis

Hyperkalaemic periodic paralysis is a genetic disease affecting horses descended from the prominent Quarter Horse sire

“Impressive” (Impressive was a cross between a QH and Thoroughbred). Dietary modification is a critical aspect of disease

management (Naylor, 1994b). The disease is characterised as a myopathy and is attributed to a defect in skeletal sodium

(Na) muscle channels (Rudolph et al., 1992; Naylor, 1994b; Meyer et al., 1999). Horses with the genetic mutation were

preferentially selected due to their prominent muscular phenotype (Naylor, 1994a). The disease is well recognised as a

genetic defect and mandatory genetic testing is required before registration with the American Quarter Horse Association

(Groves, 1996).

Hyperkalaemic periodic paralysis is caused by an autosomal dominant point mutation that results in a

phenylalanine–leucine substitution at the voltage-dependent skeletal muscle Na channel alpha subunit (Rudolph et al.,

1992; Naylor, 1997). Sodium channels are usually closed in resting muscle but are triggered to open as the membrane

potential moves toward threshold. The resultant rapid influx of Na leads to membrane depolarisation giving rise to the early

phase of the cell action potential. Once the membrane is fully depolarised the Na channels close and the potassium channels

open, potassium leaves the cell leading to cell repolarisation. In HYPP horses the Na channels remain open following mem-

brane depolarisation resulting in a permanent reduction of membrane potential causing involuntary muscle contraction,

followed by fatigue and weakness (Naylor, 1997). Involuntary contraction occurs when the fibres are sufficiently depolarised


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to reach the threshold for contraction. The simultaneous contraction of groups of fibres appears as visible muscular spasm

or fasciculation and is a feature of mild to moderate attacks. In sustained severe attacks there is muscle fatigue and this

is reflected clinically as weakness (Naylor, 1997). Affected horses maintain a muscle resting membrane potential that is

less negative and therefore closer to reaching the electrical threshold potential (Pickar et al., 1991). Although the mutation

results in a Na channel defect the prominent electrolyte abnormality is hyperkalaemia, which is only present during attacks.

There are some horses that will continue to maintain a normal serum potassium concentration in the face of an HYPP clin-

ical episode (Stewart et al., 1993). Raising extracellular potassium can trigger opening of Na channels and during attacks

there is increased potassium efflux from cells that also contributes to the measurable hyperkalaemia (Naylor, 1997). There

is variation in individual horses susceptibility to attacks, which appears to be due to differential rates of transcription of the

normal and abnormal genes (Zhou et al., 1994).

Clinical signs range from the horse being clinically asymptomatic to daily exhibition of periodic attacks. Heterozygotes

(single loci positive for defect) tend to show signs that occur less frequently and are less severe than homozygotes. In het-

erozygotes the most common and earliest clinical sign is muscle fasciculation that can be misinterpreted as either shivering

or anxiousness (Naylor et al., 1993). Other common clinical signs in heterozygotes include tachypnoea, sweating, and weak-

ness. Less common signs, more likely to be seen in homozygotes, include prolapse of the third eyelid, respiratory stridor,

colic-like signs, recumbency, arrhythmia, or rarely death (Naylor, 1997). During the attack and immediately afterwards

serum potassium is elevated, but in some instances may be normal, more so in homozygotes (Stewart et al., 1993). The

majority of affected heterozygote horses begin to exhibit clinical signs between 2 and 3 years of age and are apparently

normal between episodes (Rudolph et al., 1992; Naylor, 1994b), whereas homozygotes tend to display clinical signs as foals

(Naylor, 1997). Precipitating factors that increase therisk of an attackinclude diets high in potassium, suddenchanges in diet,

transportation, anaesthesia, exposure to cold, co-existent disease, pregnancy, and rest after exercise. Exercise alone does not

cause clinical signs (Reynolds et al., 1998; Spier, 2006). During mild attacks horses usually remain standing with episodes

usually last between 15 and60 min(Spier, 2006). Although horses are clinically normal between episodes electromyographic

examination is abnormal (Naylor, 1994b).

Historically thediagnosis of HYPPhas beenbased on pedigreeanalysis, clinical signs, anddocumentationof hyperkalaemia

during an episode (Naylor, 1997). HYPP was the first veterinary disease to utilise DNA probes for genetic diagnosis (Rudolph

et al., 1992), and since 1998 all Quarter Horses from an Impressive lineage must have genetic testing prior to registration

and from 2007 homozygous HYPP horses could no longer be registered (Spier, 2006). This addendum was likely due to

persistence of the genetic mutation within the breed after mandatory testing was introduced.

Most acute attacks will often pass without requiring any medical intervention. If the event is mild then light exercise may

be sufficient to resolve the episode (Spier, 2006). Corn syrup, grain or glucose may be given to stimulate insulin secretion,

which facilitates intracellular movement of potassium. This along with the administration of adrenalin or the diuretic aceta-

zolamide may reduce the signs associated with mild episodes (Spier, 2006). More severe attacks require more aggressive

treatment and commonly include the intravenous administration of potassium free fluids to dilute and encourage renal

excretion of potassium, the administration of sodium bicarbonate, or intravenous glucose to enhance cellular uptake of

potassium, and intravenous calcium which will reduce membrane threshold (Leitch and Paterson, 1994; Spier, 2006).

Thelonger term control of the disease is focused around the reduction of potassium in thediet, increasing renal excretion

of potassium, and avoiding stressful events or sudden environmental change (Naylor, 1997; Spier, 2006). High potassium

feeds that should be avoided include lucerne/alfalfa (14–24 g/kg potassium DM), electrolyte and kelpsupplements, soyabean

meal, molasses, and some sweet feeds. Feeds that are low in potassium include beet pulp, oats, barley and wheat, and most

pasture grasses (Spier, 2006). Horsesthat sufferrepeatedepisodes shouldbe feda diet with between 6 and11 g/kg potassium

DM and meals should contain less than 33g of total potassium (Reynolds et al., 1998). Some horses will experience recurrent

episodeseven in theface of dietary management and may require medical therapies that increase renal potassium excretion.

Potassium wasting diuretics such as acetazolamide and hydrochlorothiazide are often useful (Naylor, 1997; Spier, 2006).

8. Developmental orthopaedic disease

Developmental orthopaedic disease (DOD) is a non-specific term to describe an assortment of manifestations of bone

disease including osteochondrosis, subchondral bone cysts, physitis, angular limb deformities, flexural deformities and

cervical vertebral compressive myelopathy. Although all of these diseases occur in young growing horses and involve the

musculoskeletal system it remains speculative that they all share a common underlying aetiology ( Jeffcott, 1991). Even

the aetiopathogenesis of the most researched manifestation of DOD, osteochondrosis (OC), remains provisional rather than

definitive at this time ( Jeffcott and Henson, 1998; Ytrehus et al., 2007). It is universally agreed that aetiology of both OC and

DOD are multifactorial and that the contribution of various risk factors is open to debate.

These DOD risk factors include genetic predisposition, nutrition, growth rate/body size, exercise, biomechanical loading,

and endocrinologic factors ( Jeffcott, 1991). Inheritance and the accompanying conformational characteristics are important

contributors to the development of OC in humans, dogs, pigs and horses (Ytrehus et al., 2007). Biomechanical influences

aid in the explanation of the consistent predilection sites of disease, particularly for OC (van Weeren, 2006). Excessive or

inadequate levels of exercise in foals have both been shown to increase the incidence of OC (van Weeren and Barneveld,

1999) and appropriate levels of exercise in the immature horse is important for optimal skeletal development and bone


11/16


growth (Rogers et al., 2008a, 2008b; van Weeren et al., 2008) and may enhance resistance to injury (Barneveld and van

Weeren, 1999).

Nutritional factors that contribute to the aetiopathogenesis of DOD include mineral deficiencies, excesses, or relative

imbalances. Deficiencies of calcium, phosphorus, copper, and zinc have all been postulated to predispose to DOD (Knight

et al., 1985; Lawrence andPagan, 2005). Therole of copperdeficiency in DOD is controversial with some literature supportive

of dietary supplementation with copper to decrease the incidence of DOD (Hurtig et al., 1993; Pearce et al., 1998). However

the roleof copper in maintenance of skeletalintegrity and thereforeDOD remains to be fully elucidated. It has beenspeculated

that copper may be important in the repair and resolution of early cartilage lesions rather than in disease prevention (van

Weeren et al., 2003). Copper supplementation to dams in late gestation or high liver copper levels in foals is not protective

against the development of cartilage lesions (Gee et al., 2007).

Mineral excesses have also been associated with DOD and include excesses in calcium, phosphorus, zinc, iodide, fluoride,

lead, and cadmium (Lawrence and Pagan, 2005). It was proposed that a high rate of calcium supplementation interferes with

trace mineral absorption and could lead to an increase in DOD cases (Krook and Maylin, 1988), but this has been found not

to be the case (Savage et al., 1993a). Excessive dietary phosphorus supplementation will result in the reduction of calcium

absorption and this has been shown to increase the incidence of DOD lesions (Savage et al., 1993b). Excessive zinc intake

has been shown to result in a secondary copper deficiency (Eamens et al., 1984; Cymbaluk and Smart, 1993). Balancing

rations to ensure that appropriate mineral requirements are met has failed as a single strategy to reduce the incidence of

DOD (Lawrence and Pagan, 2005).

Excessive energy intake resulting in rapid growth within a specific time period is postulated to result in an increased

incidence of DOD (van Weeren et al., 1999; Donabedian et al., 2006). It is proposed that excessive energy intake leads to a

strong and sustained postprandial hyperinsulinaemia that is induced by a meal containing a high amount of easily digestible

carbohydrates (van Weeren, 2006). Insulin as well as insulin growth factors 1 and2 directly impactendochondral ossification

and insulin removes thyroid hormones from circulation, which also adversely impacts cartilage differentiation ( Jeffcott and

Henson, 1998). Horses with OC lesions have been shown to have higher insulin and glucose responses to high grain diets

than normal horses (Ralston, 1996; Pagan et al., 2001), but the effect of insulin on thyroid hormones may only occur within

a narrow age range (Glade and Reimers, 1985). Although it is possible to induce OC lesions in horses due to dietary energy

manipulation (Savage et al., 1993a) the lesions produced are not often seen in naturally occurring cases of OC (Glade and

Belling, 1986), giving rise to the belief that although excessive energy intake plays a key role in the development of DOD the

exact mechanism through which this occurs remains to be determined.

Rationevaluation is essential to determineif nutritionis a causativefactor in cases of DOD andthereare multiple common

feeding scenarios thatmay potentiate DOD.Overfeedingof young horses is a common problem thatresults in excessive intake

and growth rates, both of which have been shown to result in DOD (Savage et al., 1993a; Pagan et al., 1996; Lepeule et al.,

2009). Principles have been developed to minimise the incidence of DOD.

Preventative feeding strategies should begin during pregnancy. Many horse owners overfeed their brood mares during

early pregnancy and underfeed them in lactation; these feeding practices have the propensity to lead to overweight brood-

mares (Lawrence and Pagan, 2005). There is anecdotal evidence that over-conditioned brood mares will produce foals that

are at increased risk of DOD, particularly angular limb deformities (Mason, 1981). If a mare is fed appropriately throughout

pregnancy it is unnecessary to supplement a foal until 90 days of age, at which time it can be introduced to grain. A gradual

introduction should be undertaken or there may be the risk of an excessive growth at this time (Lawrence and Pagan, 2005).

The period from weaning to 12 months of age is the most important time in regards to dietary management to prevent DOD.

Weanlings should be having adequate mineral supplementation and be grown at a moderate rate. Often the nutritional

content of pasture is underestimated, again leading to excessive growth rates (Lawrence and Pagan, 2005). Recent research

indicates that feeding concentrates that initiate a low glycaemic response may also be prudent (Pagan et al., 2001). Once

a horse reaches 12 months of age the risk of new DOD lesions is greatly reduced, but it may be an important period for

pre-existing DOD lesions to become clinically apparent.

In young horses that develop DOD nutritional modification can be used to reduce the severity of disease. The rationale of

dietary modification is a slowing of skeletal growthrate through a reduction in energy intake, whilemaintainingappropriate

levels of protein and minerals to promote healthy bone development.

9. Conclusion

Modern equine breeding, feeding and management practices have tended to focus on achieving rapid growth and max-

imising athletic performance. The feeding of concentrate-based diets is an important factor in achieving these outcomes. As

a consequence there are several diseases of horses that may have a direct or indirect causal relationship with diet. It is likely

that dietary modification will be an important tool in the management and prevention of such diseases.

Conflict of interest

None.


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2012- the role of diet in the prevention and management of several equine diseases 1

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