Equine Laminitis Study

RUNNING HEAD: Laminitis Study 1

Actuarial Science, the Equine Insurance Industry and the Etiology of Laminitis

Theresa Yardas

Faculty Advisor: Victor Roeske

Ivy Tech Community College


The Equine Insurance Industry, Actuarial Science and an Overview of Laminitis

Rationale for Research

The equine insurance industry has become a blossoming business due to advances in veterinary

care. Owners and farm managers purchase this insurance in an effort to safeguard against

financial ruin. Actuaries that work for these companies are responsible for modeling risk to

calculate competitive rates while maintaining profit. One of the most common, and often

preventable, health risks that threaten any equine investment is Laminitis. Many of the world’s

most valuable animals have succumbed to this disease. The great American thoroughbred

racehorses Secretariat in 1989, and Barbaro in 2007, died as a result due to complications due to

this debilitating disease. Out of these terrible tragedies has arisen some hope. Due to the

notoriety of their circumstances, indirectly, the loss of these champions has generated

tremendous funding of research for this disease. The purpose of this thesis is to present a general

summary of the condition, the current etiologies for its origins specifically concentrating on

pasture associated laminitis, present the widely accepted risk factors that predispose animals to

this disease, review the scientific literature on these risk factors, most notably the role of fructan

concentrations in forages and feedstuffs; offer data for consideration, finally to propose practical

solutions and recommendations, in order to minimize risk.

What is Laminitis? Why is it important?

To anyone in the industry, or private owner hearing the diagnosis of laminitis generates

thoughts of loss. Any horse is susceptible to this disease, and usually most animals experience it

at least once in their lifetime. The Michigan Equine Monitoring System found that “lameness

was the most common health problem reported and had the second longest duration and highest

number of performance days lost of all disease problems reported” “The cost of

lameness(including laminitis) in 1998 was estimated at $678 million with 110 days of lost use


per lameness event” (USDA, 2000). “Summary data from a survey involving 1,178 horse

operations totaling 28,026 horses, estimated that 13 percent of the operations had one or more

horses with laminitis over a twelve month period” (academies, 2007). It is easy to deduce that

in order to minimize risk to life and property some successful preventative measures and

management practices need to be implemented.

The components of a horse’s foot that enable its superior locomotion abilities are a hard

hoof that encases a single toe bone at the end of each limb. This tough exterior protects the

delicate structures encased with in it, and allows the horse relative protection against a variety of

weather and terrain. While these animals are biomechanically well suited for speed and agility,

they are relatively vulnerable to crippling lameness should the mechanism, the lamenae, that

attach these structures to the hoof fails (Pollitt). Laminitis or “founder” as it is often called,

refers to damage to the hoof that causes horses to become lame and resistant to lifting their

limbs. In the case of laminitis of the forefeet, the afflicted horse rests its weight on its hind limbs

in a rocked backwards “laminitis stance.” Sometimes the horse will shift weight from one foot

to the other or refuse to move when asked to walk in a certain direction. Horses are more likely

to develop laminitis in their front feet because they carry about “60 percent” of their total body

weight there (Pollitt). The clinical definition of laminitis is that it is a systemic disease in which

“the junction between the dermal and epidermal laminae serves to attach the distal phalanx to the

hoof wall. Failure of the attachment between the dermo-epidermal junction is the signature

lesion of laminitis” (Politt, et al., 2003). The progression of the disease manifests itself in “four

distinct phases: developmental, acute, subacute, and chronic” (Hood, 1999a). The

developmental phase can be described as the period of time between initiation and the first

physical signs of lameness. This phase lasts typically an average of 40 hours. The second phase


of laminitis is the acute phase. In this phase the disease proceeds in one of these two directions:

it will either continue for up to 72 hours without any “physical or radiographic collapse” or

terminate with the “rotation or sinking of the distal phalanx” (Herthel, 1999). If there is no

collapse the disease enters the subacute phase. This phase is can last an average of 10 weeks and

is considered to be a period where the horse is in recovery. Chronic laminitis or founder is the

fourth phase and this phase is applicable only to those animals that have experienced a digital

collapse. If there is any evidence either radiographical or physical, of collapse, the horse will be

considered to be in the chronic phase of the condition (Herthel, 1999). Failure to recover from an

episode of laminitis will often result in the most humane choice of euthanasia. The key point in

this discussion is that other seemingly unrelated crisis often precedes the initiation of laminitis.

These can include but are not limited colitis, duodenitis/proximal jejunitis, septic metritis,

diarrhea such as associated with Potomac Horse Fever, retained placenta, septicemia,

endotoxemia, pleuropneumonia, and rhabdomyolysis or “tying- up”. By the time the foot pain

appears, the connective tissue in the lamellar structures is already on its way to being

compromised (Pollitt). The best practice is anticipation of the possible developments and

proactive management.

Modern Theories on the Pathogenesis of Laminitis

While the definitive cause for laminitis may be multifaceted and unclear, there are several

modern theories that are widely studied. The first is the vascular hemodynamic theory which

proposes that some unknown mechanism “alters blood supply to the laminae and results in the

failure of the dermal epidermal junction” (Moore, 2004). The second is the traumatic or

mechanical overload theory proposes that after experiencing some trauma or mechanical

overload the associated inflammation that results somehow compromises the blood flow to the


foot separating the dermo-epidermal junction (Hood, The pathophysiology of developmental and

acute laminitis, 1999b). The final theory, and the one most suited to proactive and ongoing

management practices is the toxic, metabolic, or enzymatic theory. This theory proposes that

“an unknown trigger delivered in the bloodstream activates the metallic matrix

metalloproteinases (MMP’s), which lead to the breakdown of the basement membrane and the

separation of the dermo-epidermal junction (Moore, 2004) (French, 2004). This research group

discovered an apparent link between the intake of feedstuffs that are high in rapidly fermentable

carbohydrates and the digital ischemic events that are thought to herald an attack of laminitis

(French, 2004). There are several events that precipitate this last type of laminitis that may in

part be truly preventable with education, training and management. One is grain overload that

occurs when a horse inadvertently has access to a large amount of grain. Grain founder results

“when a horse consumes too much grain either by accidental ingestion or intentional increase by

the keeper” (Burba). The side effects of grain overload as pertaining to laminitis most likely

follow the endotoxemia and lactic acidosis associated with it. These side effects are as follows:

“the digital arteries become dilated due to the endotoxins and lactic acid, this both increases the

blood flow to the feet and constricts the capillaries which supply blood to the lamenae, these

capillaries then begin to swell due to lack of blood and oxygen, and the swollen lamenae

compress against the hoof wall and begin to die” (Burba). The foot will be noticeably hot and

have a “pounding pulse” as the horse begins to assume the classic laminitis stance (Burba).

Grass founder or pasture associated laminitis occurs when horses are given unrestricted access to

grazing in lush pastures (King, 2002). In a recent survey on lameness and laminitis performed

by the USDA, grazing in lush pastures was most commonly perceived as the cause for laminitis

(45.6 percent) (USDA, 2000), by comparison, grain overload was perceived to be the cause in


7.4 percent of the cases. The sugar that is of growing concern to equine professionals, owners,

and managers is called fructan. “It was thought that high levels of fructans accumulated in

grasses under certain conditions (Longland A. C., 1999) and that these were not digested in the

small intestine, but were instead fermented in the large intestine to produce acid, which decreases

pH and can launch a cascade of events leading to laminitis (Huntington, 2008). Fructan,

specifically inulin (Watts, 2009) , is composed of oligo-and polyfructosyl surcrose . “Typically

forages or hay are higher in fructan than grain based feed. A feed can be low in sugar and/or

starch but if it has a high amount of fructan, problems occur in the hindgut” (Striegel, 2008).

Even though the link between overconsumption of carbohydrates, specifically fructan, and

laminitis has not been irrefutably proven, there is enough evidence and research to suggest that it

is probable that they play a substantial role in stimulating this condition in at risk animals. It is

therefore been suggested that both systems of pasture and horse management practices be put

into place to limit exposure to this substance. Fructan can be accumulated in pasture grasses

(Longland A. B., 2006). “Most are cool-season grasses that are commonly found in horse

pastures in the upper Midwest and may be high in sugar” (Duncanson, 2010). In order to

provide management and education on the content of fructan in selected forages a crude

estimation was undertaken using the forage analysis results found in the Dairy One main library

online.

Dairy One

Dairy One is the recognized industry leader in forage analysis. They maintain an updated

database library online, both nationally and internationally for feeds and forages. They use “near

infrared reflectance spectroscopy (NIR) for rapidly and reproducibly measuring the chemical

composition of forage and feed samples” (Dairy One Forage Laboratory Services, 2012). They


measure the amounts of carbohydrate composition as “(ESC) ethanol soluble carbohydrates,

which are simple simple sugars; water –soluble carbohydrates (WSC), which combines simple

sugars and fructans; and nonstructural carbohydrates (NSC) as starch plus water soluble

carbohydrates. Thus it is possible to crudely estimate the fructan content of a forage as WSC-

ESC” (Huntington, 2008). This is the analysis that I have decided to undertake in order to

provide some primitive information that will be useful in the planning process.

(1) % fructan = % water-soluble carbohydrates – %ethanol soluble carbohydrates

Identifying At Risk Populations

Assessment of obesity using body condition scores on a (1-9) scale and a cresty neck

score on a (1-5) scale provides an accurate method for predicting the occurrence of pre-laminitic

metabolic syndrome. “In order to reduce subjectivity in BCS and CNS assessments

morphometric measurements could be substituted. A girth-to- height ration >1.28 can replace

BCS and crest height >10cm. could replace CNS” (Huntington, 2008).

Basic Plant Mechanics and Sample Selection

Through the process of photosynthesis, plants produce simple sugars. Excess sugars

(produced in the vacuoles) are stored as reserves (in the stem). “The vegetative

(nonreproductive) tissues of temperate (cool season, C3 plants) pasture grasses accumulate

fructan …because there is no self-limiting mechanism for the production of fructan in C3

species, high concentrations of it can accumulate” (Longland A. B., 2006). Warm season grasses

and legumes (C4 plants) accumulate starch as their energy reserves and do not accumulate

fructan, and the starch production that takes place in the choloroplasts (when saturated) is a self-

limiting process (Longland A. B., 2006). The sample selection for the purpose of this analysis


will be limited only to cool season C3 grasses. Other environmental factors also come into play

regarding levels of fructan in forages. The levels of fructan fluctuate with the season and time of

day. After a day of full sun (greater production), after a period of stress (greater storage), after

“an evening of temperatures less than 40 ° F, or after quick and rapid drying of cut grass and

hay” (Striegel, 2008).

How Much Fructan is Too Much?

The consumption of fresh pasture as a percent of total body weight has been reported to

range from 1.5 % to 5.2 % per day (Hayward, 1983) (McMenniman, 2000). According to

calculations presented in a paper on “Pasture Nonstructural Carbohydrates and Equine

Laminitis” by Byrd and Longland, a 500 kg horse would consume 7.5 kg per day of dry matter

on a 1.5% body weight consumption scale. On the high end, a 5.2% body weight consumption

scale, a 500kg horse would consume 26 kg per day of dry matter. Grazing pastures with high

fructan concentrations were categorized as pastures containing 384 g of water-soluble

carbohydrates per kg dry matter. Grazing pastures with low fructan concentrations were

categorized as pastures containing 100g of water-soluble carbohydrates per kg of dry matter.

According to these figures, fructan estimated mean intakes per day ranges from 0.56 kg per day

to 1.95 kg per day of low fructan concentration pastures. The fructan estimated mean intakes per

day of high fructan concentration pastures ranged from 2.1 kg per day to 7.3 kg per day. For

higher levels of intake, above the 2.5 % - 5.2 % body weight per day consumption range, the

fructan levels ingested range between 3.5 and 7.3 kg of fructan per day. “These amounts are

similar to and almost double the amount of fructan known to activate laminitis when delivered as

a single dose” (Politt, et al., 2003). For the purpose of this paper, data analysis regarding

estimated mean daily intake of fructan in high concentration and low concentration pastures, for


2.5 % and 5.2% body weight consumption model, will be performed using the breed specific

typical body weights, both low and high range; from the tables available on the Equi-

Analytical.com website.

Data Analysis



Conclusions

Even at low water soluble carbohydrate concentration pastures, horses would be estimated to

ingest by dry matter intake as based on body weight, 2.13-4.31 kg of Fructan per day. Current


research suggests that these amounts are almost double what are needed to induce laminitis in the

laboratory, as described by the literature from the 49th Annual Convention of the American

Association of Equine Practioners (Huntington, 2008). While a direct link between the amount

of Fructan in food supplies and laminitis has not been proven, most horse owners and breeders

should err on the side of caution when planning the nutritional needs of their animals, because of

the exhaustive amounts of recommendations by professionals concerning this topic. In fact the

key to prevention is planning the nutritional needs of their animals based on research and

science, rather than accepted practices or gut instincts. It also should be noted, that while some

breeds tend to appear to have lower risks of pasture associated laminitis, all breeds are

susceptible to overload from grazing unrestricted in lush pastures. As noted in this research

whether body size is in the low or high range, the daily intake of Fructan is still within the danger

zone. After analyzing the Equine Laminitis Risk Calculator results of the test subject, it is

evident that unrestricted grazing on lush pasture is a concern for equine obesity as a

predisposition for a laminitis event. Other concerns were body condition scores, activity level,

and prior history of a laminitis event, as well as commercial feed variations and amounts.

Proactive Nutritional Management for Laminitis Prone Equine

Grazing recommendations (from the Colorado State Extension Office): Limit grazing on high

Fructan grasses; less than one hour per day for high risk animals, use grazing muzzles as needed,

don’t overgraze pastures, fertilized fields contain less Fructan, grazing is safer early in the

morning (Striegel, 2008). Soak hay for 30 minutes before feeding to release the sugars. As a

preventative, the supplement called Founderguard can be added to the animals feeding regime to

act as a buffer (Huntington, 2008).

Therapy


Cryogenic boots have been successful at halting the progression of laminitis.

Referencesacademies, N. r. (2007). Nutrient requirements of horses. Washington, D.C.: National

Academies Press.

Burba, D. P. (n.d.). Grain overload in horses. Retrieved from Equine health tips: equine health studies, school of veterinary medicine, Louisiana State University: http://evrp.lsu.edu/healthtips/GrainOverload.htm

Cerfogli, J. (2009). Biomechanical considerations in equine laminitis. Retrieved from Iowa State Digital Repository: http://lib.dr.iastate.edu/etd/10847/

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Duncanson, A. G. (2010, November 23). Low sugar hay and pasture. Retrieved from University of Minnesota extension: http://www.extension.umn.edu/forages/pdfs/Low_sugar_hay_and_pastures.pdf

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References

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Longland, A. B. (2006). Pastural nonstructural carboydrates and equine laminitis. The Waltham International Nutritional Sciences Syposia (pp. 2012-2099). Blacksburg: Journal of Nutrition.

Longland, A. C. (1999). Seasonal and diurnal changes in fructan concentration in Lolium perenne: implication for the grazing management of equine predisposed to laminitis. Conference proceedings of 16th annual nutritional physiology society symposium (pp. 258-259). Raleigh: Nutritional Physiology Society.

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Moore, R. E. (2004). Evidence for vascular and enzymatic events in the pathophysiologyof acute laminitis: which pathway is responsible for the initiation of this process in horses? Equine Veterinary Journal, 204-209.

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Striegel, N. (2008, October). Sugar content in feed and forage affects horses' health. Retrieved from Colorado Sates University extension fact sheets: http://www.ext.colostate.edu/pubs/livestk/01818.html

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Watts, K. A. (2009). Carbohydrates in forage: what is safe grass? Versailles: Kentucky Equine Research.

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Equine Laminitis Study