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