<%BANNER%>

Epidemiologic Study of Anhidrosis in Florida Horses

Permanent Link: http://ufdc.ufl.edu/UFE0022784/00001

Material Information

Title: Epidemiologic Study of Anhidrosis in Florida Horses
Physical Description: 1 online resource (54 p.)
Language: english
Creator: Johnson, Eric
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2009

Subjects

Subjects / Keywords: anhidrosis, equine, florida
Veterinary Medicine -- Dissertations, Academic -- UF
Genre: Veterinary Medical Sciences thesis, M.S.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: Anhidrosis is a serious condition that affects horses in hot, humid climates. Ability to effectively eliminate heat accumulation by sweating can be severely compromised. Horses suffering from the syndrome require medical management and reduced workload (or removal from physical activity). To date, the only dependable treatment for anhidrosis is removal from the hot humid client to a cooler, drier one. Little is known about the prevalence and risk factors of anhidrosis. Our objective was to estimate the prevalence of, and to identify risk factors associated with, anhidrosis in horses. We included 500 farms and 4620 horses in the determining the prevalence of the syndrome. We enrolled 2444 horses to determine risk factor information. The study design contains cross-sectional and a case-control components. A questionnaire was structured and mailed to horse owners to obtain information related to diagnosis of anhidrosis in horses and exposure factors associated with the disease. The frequency of investigated farm- and horse-level risk (exposure) factors was compared between affected and non-affected farms and between affected and non-affected horses. The prevalence of anhidrosis was 11% at the farm level and 2% at the animal level. The odds of anhidrosis were 2 and 4 times higher in farms located in Central and South Florida, respectively, compared to farms in North Florida (P less than 0.05) . The odds of anhidrosis were 3 and 5 times higher in racing and show operations, respectively, compared to ranch operations (P less than 0.05). At the horse level, breed (Thoroughbred and warmblood), foaling place (West, Mid-West United States), use (non-racing performance, retired) and family history of anhidrosis were identified as risk factors for anhidrosis. Our study provides new information on the prevalence of anhidrosis and risk factors for anhidrosis in horses. Breed (Thoroughbreds, warmbloods), use (non-racing performance, retired), foaling place (West and mid-West regions in the United States), as well as family history of anhidrosis were identified as risk factors for anhidrosis. Horses with a family history of anhidrosis should be evaluated for anhidrosis by a veterinarian before they are exposed to exercise in hot and humid conditions.
General Note: In the series University of Florida Digital Collections.
General Note: Includes vita.
Bibliography: Includes bibliographical references.
Source of Description: Description based on online resource; title from PDF title page.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The University of Florida Libraries, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Statement of Responsibility: by Eric Johnson.
Thesis: Thesis (M.S.)--University of Florida, 2009.
Local: Adviser: Hernandez, Jorge A.

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2009
System ID: UFE0022784:00001

Permanent Link: http://ufdc.ufl.edu/UFE0022784/00001

Material Information

Title: Epidemiologic Study of Anhidrosis in Florida Horses
Physical Description: 1 online resource (54 p.)
Language: english
Creator: Johnson, Eric
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2009

Subjects

Subjects / Keywords: anhidrosis, equine, florida
Veterinary Medicine -- Dissertations, Academic -- UF
Genre: Veterinary Medical Sciences thesis, M.S.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: Anhidrosis is a serious condition that affects horses in hot, humid climates. Ability to effectively eliminate heat accumulation by sweating can be severely compromised. Horses suffering from the syndrome require medical management and reduced workload (or removal from physical activity). To date, the only dependable treatment for anhidrosis is removal from the hot humid client to a cooler, drier one. Little is known about the prevalence and risk factors of anhidrosis. Our objective was to estimate the prevalence of, and to identify risk factors associated with, anhidrosis in horses. We included 500 farms and 4620 horses in the determining the prevalence of the syndrome. We enrolled 2444 horses to determine risk factor information. The study design contains cross-sectional and a case-control components. A questionnaire was structured and mailed to horse owners to obtain information related to diagnosis of anhidrosis in horses and exposure factors associated with the disease. The frequency of investigated farm- and horse-level risk (exposure) factors was compared between affected and non-affected farms and between affected and non-affected horses. The prevalence of anhidrosis was 11% at the farm level and 2% at the animal level. The odds of anhidrosis were 2 and 4 times higher in farms located in Central and South Florida, respectively, compared to farms in North Florida (P less than 0.05) . The odds of anhidrosis were 3 and 5 times higher in racing and show operations, respectively, compared to ranch operations (P less than 0.05). At the horse level, breed (Thoroughbred and warmblood), foaling place (West, Mid-West United States), use (non-racing performance, retired) and family history of anhidrosis were identified as risk factors for anhidrosis. Our study provides new information on the prevalence of anhidrosis and risk factors for anhidrosis in horses. Breed (Thoroughbreds, warmbloods), use (non-racing performance, retired), foaling place (West and mid-West regions in the United States), as well as family history of anhidrosis were identified as risk factors for anhidrosis. Horses with a family history of anhidrosis should be evaluated for anhidrosis by a veterinarian before they are exposed to exercise in hot and humid conditions.
General Note: In the series University of Florida Digital Collections.
General Note: Includes vita.
Bibliography: Includes bibliographical references.
Source of Description: Description based on online resource; title from PDF title page.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The University of Florida Libraries, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Statement of Responsibility: by Eric Johnson.
Thesis: Thesis (M.S.)--University of Florida, 2009.
Local: Adviser: Hernandez, Jorge A.

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2009
System ID: UFE0022784:00001


This item has the following downloads:


Full Text

PAGE 1

1 EPIDEMIOLOGIC STUDY OF ANHIDROSIS IN FLORIDA HORSES By ERIC JOHNSON A THESIS PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE UN IVERSITY OF FLORIDA 2009

PAGE 2

2 2009 Eric Johnson

PAGE 3

3 To my parents: th ank you for all of your support ; and to my brother: you are missed

PAGE 4

4 ACKNOWLEDGMENTS First and foremost, I thank my supervisory committee : Drs. Robert MacKay, Jorge Hernandez, Thomas Vickroy, and Dana Zimmel. This thesis would not have been possible without their endless effort and guidance. Secondly, I thank Sally McConnell. She is a shining example of what it means to go beyond the call of duty. Sally took it upon herself to help me through great personal adversity. I would also like to thank Jorge Garcia -Pratts and Christy Meyer of the USDA NASS who endure d countless phone calls I also owe many thanks to my friends and family for their su pport and encouragement. Finally, I would like to thank everyone at the University of Florida College of Veterinary Medicine for their thoughts and prayers after a great personal tragedy.

PAGE 5

5 TABLE OF CONTENTS page ACKNOWLED GMENTS .................................................................................................................... 4 LIST OF TABLES ................................................................................................................................ 7 LIST OF FIGURES .............................................................................................................................. 8 LIST OF ABBREVIATION S .............................................................................................................. 9 ABSTRACT ........................................................................................................................................ 10 CHAPTER 1 INTRODUCTION ....................................................................................................................... 12 2 EQUINE SWEATING AND ANHIDROSIS ........................................................................... 14 The Sweat Gland ......................................................................................................................... 14 Structure ............................................................................................................................... 15 Receptor Type ...................................................................................................................... 16 Control of Sweating .................................................................................................................... 16 Mechanisms of Sweat Production .............................................................................................. 17 Thermore gulatory Function ........................................................................................................ 18 Training and Acclimation .................................................................................................... 19 Hypo and Hyperhydration ................................................................................................. 20 Fluid Loss ............................................................................................................................. 20 Sweat Composition .............................................................................................................. 20 Anhidrosis .................................................................................................................................... 21 Cl inical Syndrome ............................................................................................................... 21 Possible Pathologies ............................................................................................................ 21 Unlikely Causal Factors ...................................................................................................... 22 Aggravating Factors ............................................................................................................ 23 Why Only Some Horses Are Affected ............................................................................... 23 Practical Tests ...................................................................................................................... 23 Treatment ............................................................................................................................. 24 Study Objectives .................................................................................................................. 24 3 MATERIALS AND METHODS ............................................................................................... 25 Study Population ......................................................................................................................... 25 Classification of Study Animals ................................................................................................. 25 Development of Questionnaire ................................................................................................... 25 Study Design ............................................................................................................................... 26 Statistical Analysis ...................................................................................................................... 27

PAGE 6

6 4 RESULTS .................................................................................................................................... 29 Response Rate ............................................................................................................................. 29 Prevalence of Anhidrosis ............................................................................................................ 29 Epidemiologic Analysis (Farm L evel) ...................................................................................... 29 Epidemiologic Analysis (AnimalL evel) ................................................................................... 30 Case Control Study ..................................................................................................................... 30 5 DISCUSSION AND CONCLUSIONS ..................................................................................... 44 REFERENCES ................................................................................................................................... 50 BIOGRAPHICAL SKETCH ............................................................................................................. 54

PAGE 7

7 LIST OF TABLES Table page 4 1 Frequency distribution, odds ratios, 95% confidence interval and P values of investigated operation -level risk factors associated with anhidrosis. ................................. 33 4 2 Final logistic regression model for investigated operationlevel risk factors associated with anhidrosis ..................................................................................................... 35 4 3 Frequency distribution, odds ratios, 95% confidence inter val and P values of investigated animal level risk factors associated with anhidrosis. ...................................... 36 4 4 Final logistic regression model for investigated animal level risk factors associated with anhidro sis. ...................................................................................................................... 38 4 5 Case -control study. Univariable analysis of investigated animal level risk factors associated with anhidrosis. .................................................................................................... 39 4 6 Case -contro l study: Final conditional logistic regression model for investigated animal level risk factors associated with anhidrosis. ........................................................... 41 4 7 Frequency, clinical signs, and severity of syndr ome in 79 horses classified as anhidrotic. ............................................................................................................................... 42 4 8 Anhidrotic horses: Treatment type and average monthly duration. .................................... 43

PAGE 8

8 LIST OF FIGURES Figure page 4 1 Map of Florida showing the northern, central and southern regions in the state. .............. 31 4 2 Month of the year when horses were first diagnosed as affected by anhidrosis during the study period: January to December 2005. ...................................................................... 32

PAGE 9

9 LIST OF ABBREVIATION S AQP 5 Aquaporin 5 cAMP Cyclic adenosine monophosphate HCl Hydrogen chloride USDA NASS United Sta tes Department of Agriculture National Agricultural Sta tistics Service

PAGE 10

10 Abstract of Thesis Presented to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Master of Science EPIDEMIOLOGIC STUDY OF ANHIDROSI S IN FLORIDA HORSES By Eric Johnson May 2009 Chair: Jorge Hernandez Major: Veterinary Medical Sciences Anhidrosis is a serious condition that affects hors es in hot, humid climates. A bility to effectively eliminate heat accumulation by sweating can be s everely compromised. Horses suffering from the syndrome require medical management and reduced workload (or removal from physical activity). To date, the only dependable treatment for anhidrosis is removal from the hot humid client to a cooler, drier one. Little is known about the prevalence and risk factors of anhidrosis. Our objective was to estimate the prevalence of and to identify risk factors associated with anhidrosis in horses. We included 500 farms and 4620 horses in the determining the prevalenc e of the syndrome. We enrolled 2444 horses to determine risk factor information. The study design contains cross -sectional and a casecontrol components A questionnaire was structured and mailed to horse owners to obtain information related to diagnosis of anhidrosis in horses and exposure factors associated with the disease. The frequency of investigated farm and horse -level risk (exposure) factors was compared between affected and non affected farms and between affected and nonaffected horses. The prev alence of anhidrosis was 11% at the farm level and 2% at the animal level. The odds of anhidrosis were 2 and 4 times higher in farms located in Central and South Florida,

PAGE 11

11 respectively, compared to farms in North Florida ( P less than 0.05) The odds of an hidrosis were 3 and 5 times higher in racing and show operations, respectively, compared to ranch operations (P less than 0.05). At the horse level, breed (Thoroughbred and warmblood), foaling place (West, Mid West United States), use (non racing performan ce, retired) and family history of anhidrosis were identified as risk factors for anhidrosis. Our study provides new information on the prevalence of anhidrosis and risk factors for anhidrosis in horses. Breed (Thoroughbreds, warmbloods), use (nonracing p erformance, retired), foaling place (West and mid -West regions in the United States), as well as family history of anhidrosis were identified as risk factors for anhidrosis. Horses with a family history of anhidrosis should be evaluated for anhidrosis by a veterinarian before they are exposed to exercise in hot and humid conditions .

PAGE 12

12 CHAPTER 1 INTRODUCTION Sweating is the primary means of heat dissipation in the horse .13 In hot, humid climates, the ability to dissipate heat through evaporation of sweat becomes even more important due to the lack of dissipation through conduction, convection, and radiation.1,4 The reduction or complete lack of sweat o utput to an appropriate stimuli is defined as anhidrosis .1 This syndrome is especially important in tropical climates .5,6 Horses affected by a nhidrosis are athletically less effective than their free-sweating counterparts .7,8 Anhidrosis first gained attention i n horses exported from England to Malaysia in the early 1900s .9 Clinical signs include partial or complete loss of sweating ability, hyperthermia, tachypnea, reduced appetite, decreased water intake, alopecia, dull hair coat and depression .6,8,10,11 Onset of anhidrosis can be sudden, usually after a period of profuse sweating, or gradual with a sweat response slowly decrea sing over time .12 Horses suff ering from the syndrome1,13 require medical management and reduced workload ( or removal from physical activity). To date, the only dependable treatment for anhidrosis is removal from the hot humid client to a cooler, drier one .8,11 Anhidrotic horses forced to perform can suffer severe consequences, including multiple organ failure due to hyperthermia and in some cases, death .14 The etiology of anhidrosis has yet to be determined .11 The epidemiologic aspects of anhidrosis in horses are not well understood. In 1982, in a survey1 of 24 horses affected with anhidrosis in Florida, the frequency of anhidrosis was higher in native horses (16/24) than in imported horses (8/24). In that study1, healthy horses were not included. Thus, it was not possible to assess the orig in of horses (i.e., native versus imported) as a risk factor for anhidrosis. In another study9 conducted in Florida 5 years later, the prevalence of anhidrosis was 6% (52/834). In that study9, the frequency of the syndrome was higher in training horses, co mpared to yearlings, lactating mares, barren or maiden mares, and stallions. The

PAGE 13

13 syndrome was reported more frequently in the summer months, and it was associated with recent transport of horses from geographic regions with a more temperate climate. This s econd study9 was limited to 4 Thoroughbred farms with a history of anhidrosis. Farms without a history of anhidrosis were not included. Thus, it was not possible to examine potential risk factors associated with anhidrosis at the farm and horse level.

PAGE 14

14 CHAPTER 2 EQUINE SWEATING AND ANHIDROSIS The Sweat Gland The equine sweat gland ha s been classified as apocrine .15,16 However, this definition needs revision There are currently two methods of classifying sweat glands ; by method of secretion and the level of association with hair follicles Apocri ne glands secrete their product by sloughing the apical portion of the secretory c ell into the lumen of the gland according to the first method of sweat gland classification Apocrine sweat glands can also secrete their product through a merocrine process; the binding of secretory vesicles to the cell wall and release of the product by exocytosis Eccrine sweat glands release secretory products through specific channels in the apical portion of the cellular membrane, are controlled by the sympathetic nervou s system and are stimulated by the release of acetylcholine15. The second method of classifying sweat glands is through the level of association with a hair follicle. Apocrine sweat glands are closely associated with hair follicles. One sweat gland empties into, or in close proximity to, a ha ir follicle .17 Eccrine sweat glands are not associated with hair follicles; the sweat gland lumen empties directly onto the skin surface .17 Therefore, eccrine sweat glands can be much more abundant than apocrine sweat glands which are limited by the number of hair follicles present. In this classification system, equine sweat glands are considered apocrine. The ducts of the sweat glands mostly empty into associated hair follicles. Occasionally, the lumen will open onto the j unction of the hair follicle and the external skin surface, or even more rarely directly onto the external skin surface Horses were classically considered to possess apocrine sweat glands in both classification schemes .5,18 It is now thought that, while still associated with hair follicles, equine sweat glands

PAGE 15

15 produce the secretory product through both methods of secretion.5,17,18 Electrolytes enter the sweat gland lumen via gap junctions between the epithelial cells, or by passive transport through channels in the cellu lar membrane .19 The water portion of equine sweat enters the lumen through aquaporin 5 channels in the cellular membrane .20 The proteinaceous portion of equine sweat is most likely secreted into the lumen via exocytosis (a merocrine form of secretion). This can be explained by the gradual decrease in protein concentration in equine sweat corresponding to the d ecrease in epithelial secretory vesicles .4,21 Structure The equine apocrine sweat gland consists of a highly coiled secretory portion (fundus) and a straighter duct portion that generally parallels the associated hair follicle .17,22 The duct is lined by 1 to 2 layers of cuboidal epithelium. Surrounding the epithelium is the myoepithelium, which rests on the basal membrane. The duct primarily empties into the follicular canal. H owever, it has also been shown to occasionally open into a depression adjacent to the follicular canal and rarely onto the epithelial surface. The fundus is composed of two layers of cuboidal to columnar epithelium, which is also enveloped by myoepithelium and a basal membrane .17 A well developed capillary bed, with associated nerve fibers, can be found external to the myoepithelium .23,24 There appears to be a brush border present on the apical portions of the innermost secretory epithelial cells in the fundus .17 Rather than expelling luminal contents into the hair follicle through myoepithelial contraction, it appears that sweat is propelled by well developed microvilli .17 While disputed in the literature it is now thought that the nerve fibers affect th e vasculature around the sweat gland and not the secretory cells .25 The horse, in contrast to other species, has an ex tensive vascular system supplying the sweat glands. This vasculature is capable of delivering large quantities of epinephrine to the sweat glands.

PAGE 16

16 Receptor Type Scientific literature16,19,2628 demonstrates that the predominant receptor type of the equine 2adrenergic receptor. This receptor type has a strong affinity for epinephrine, and a much lower affinity f or norepinephrine .16 This affinity for epinephrine has been demonstrated in the clinical setting. Systemic and local administration of epinephrine causes extensive sweat production in the free -sweating horse .16,26 Local and systemic administration of norepinephrine (the primary post -synaptic sympathetic neurotransmitter) produces piloerection .15,16 There are also inconsistent minimal sweat responses at large doses of norepinephrine .16 Control of Sweating The literature seems to favor a dual control of equine sweating; both humoral and 2adrenergic receptors are activated by epinephrine circulating in the bloods tream.16,18 Despite the clos e proximity of nerve fibers to the sweat gland secretory epithelium ,23 i t has been demonstrated that the nervous system does not directly control the equine sweat gland epithelium as it does in man. Evans reported a study15 performed by Dupuy in 1816 where a horse had one vagosympathetic nerve surgically transected. It was thought that sympathetic denervation of the head and neck would render these areas unable to produce a sweat response. However, the denervated areas produced copious amounts of sweat. Therefore, the sweat gland epithelium cannot be under direct sympathetic control as it is in man. This finding was repeated and found to be a valid result of sympathetic denervation. It was then postulated that the sympathetic nervous system normally acts as a vasoconstrictor to the blood vessels supplying the sweat glands. By removin g the sympathetic control, it is thought that these vessels underwent vasodilation, which would increase the amount of epinephrine reaching the 2adrenergic receptors on the sweat gland epithelium. Therefore, it appears that increasing

PAGE 17

17 circulating epinephrine or increasing cutaneous vasodilation can both produce an increased sweat response. Nitric oxide can also play a r ole in equine sweating .29,30 Nitric oxide is a known local acting vasodilator. A sweat response is most likely induced by nitric oxide by increasing the amount of epinephrine stimulating the sweat gland epithelia by vas odilation. It has also been demonstrated that decreased blood supply to the skin can decrease or eliminate the sweat response .16 In an experiment performed by Evans ,16 horses were administered adrenaline systemically. This produced a sweat response over the entire body. A cuff was placed on one hind limb and inflated. This effectively cut off the circulation to the limb distal to the cuff. The horse continued to sweat freely over the entire bod y surface, but all sweating on the limb distal to the cuff was eliminated. The area began sweating again (at a rate similar to the rest of the body) when the cuff was removed. This experiment demonstrated that equine sweat glands will not produce sweat wit hout an adequate blood supply. Therefore, it appears that the equine sweat gland is controlled primarily by epinephrine circulating in the bloodstream, and secondarily by autonomic nervous system control of the sweat gland vasculature. Mechanisms of Sweat Production Equine sweat is composed of many different elements, and different mechanisms31 33 control the secretion of these elements into the sweat gland lumen. The basic secr etory mechanism starts 2adrenergic receptors by circulating epinephrine. A G -protein complex is activated by the stimulated receptors, which then activates adenylate cyclase. This results in an increase in the cytoplasmic concentra tion of cAMP The increased cytoplasmic concentration of cAMP has several effects .34 Luminal cAMP -dependent chloride ion channels are opened, allowing the passive transfer of chloride ions into the lumen of the swe at gland. Basolateral cAMP -dependent potassium ion channels are opened, which allows the passive transfer of potassium ions to the extracellular environment. The simultaneous opening of the cAMP -

PAGE 18

18 dependent potassium ion channels allows the cell to return to the resting electrochemical state. Intracellular concentrations of ionized calcium may play a role as a secondary messenger as well. Wilson demonstrated that intracellular concentrations of ionized calcium increase upon adrenergic receptors .19 The increased calcium may activate calcium dependent chloride channels. Water enters the lumen via apical aquaporin 5 channels and through the tight -junctions between the epithelial cells. The mechanism that drives the e xocytosis of the protein rich secretory vesicles has not been elucidated. Secretory products may also be delivered into the sweat gland lumen by cell death. Dead sweat gland epithelial cells have been shown in the lumen of sweat glands after a sweat respon se. It is unknown if the death of these cells is a method by which sweat is produced, or a sloughing of damaged or dead cells during the normal sweating process. Sweat is released onto the skin surface by pressure produced from the fundus of the gland and no t by myoepithelial contraction. Thermoregulatory Function Sweating is the primary mechanism by which horses dissipate heat accumulation during exercise.7,8,35 When the ambient temperature is below the normal skin temperature, horses dissipate body heat by conduction, convection, radiation, and evaporation (of sweat and fluid in the respiratory tract). A small percentage of heat is lost through the elimination of urine and feces. When the ambient temperature rises above skin temperature; conduction, convection, and radiation are no longer effective at dissipating heat .12 Evaporation is the o nly process of heat dissipation that is still functional when the ambient temperature exceeds body temperature .36 However, in hot, humid conditions, evaporation becomes much less effective, and horses have a difficult time in dissipating body heat. In cool, dry conditions, eva poration of sweat accounts for 5 0% of the dissipated body he at in the exercising horse .37 Evaporation of fluid from the respiratory tract accounts for an additional 30% of the dissipated body heat .37 Without a

PAGE 19

19 functioning sweat mechanism, exercising horses accumulate body heat rapidly. The internal body temperature rises quickly, thus affecting many body systems The resulting hyperthermia can even result in the death of the horse .14 The thermoregulation of horses has often been compared to humans due to the copious amounts of sweat produced under stimuli. Horses produce much more sweat per uni t area than any other domestic species. Unlike humans, the thermally challenged horse is limited by the skin surface area. Horses have much less skin surface area (5 times) when compared to total body mass than do humans .37 Consequently, the copious sweat produced by the thermally challenged horse mostly falls ineffectually to the ground. This design results in the rapid accumulation of body heat during moderate to heavy exercise, even under idea l conditions. The thermal load of the horse at exercise without a properly functioning sweat mechanism would increase at a rapid rate. Training and Acclimation It has been demonstrated that many species gradually introduced to an exercise program in hot, humid conditions exhibit increased tolerance to high thermal loads .36 In fact, many competitors in the 1996 Olympic Games were given advanced not ice that detrimental health effects of the hot, humid climate might be avoided if the owners transported the equine athletes into the region several weeks prior to the games. It was also suggested that animals acclimated to the ambient conditions would hav e a better chance of avoiding exercise intolerance and diminished athletic performance while competing. As a result, many competitors arrived to the Atlanta area several weeks before the opening ceremony of the Olympic Games. It had been demonstrated that horses provided with a 3 week acclimation period accumulated body heat slower and trained for a longer duration than they had at the beginning of the study.38 Unfortunately, this benefit only applied to hot dry conditio ns.

PAGE 20

20 Hypo and Hyperhydration The literature shows that increased level s of hydration did not affect sweating rates or core body temperature of horses during exercise .39,40 Exercise induced dehydration can increase body heat storage though However, hyperhydration, while failing to aid in t hermoregulation, may assist in maintaining high sweat rates during long periods of exercise .40 Fluid Loss For every liter of sweat evaporated, a 400kg horse would have a lower body temperature of 1.8C .12 Horses can lose large amounts of fluid as a result of strenuous long-term exercise. In a study by Kingston e t al., included horses lost about 34 liters of fluid over 3 15 kilometer workouts at 40% maximum oxygen intake .39 Dehydration can follow such a regimen, especially given the fact that horses do not completely replenish fluid losses after strenuous exercise Horses lose up to 4% of their body weight after 6 hours of heat exposure due to sweating .4 They can lose 5% 10% of their body weight during exercise in a high ambient temperatures .2 Sweat Composition Horse sweat is comprised of many components. These include: water, electrolytes, protein, bicarbonate, minerals, trace elements, and urea. Water is the primary component of equine sweat, accounting for the large volumes of sweat produced. Horse sweat is hypertonic when compared to plasma levels of sodium, potass ium, and chloride. The levels of each vary with the type of sweat response (thermal, exercise) and the intensity/duration of exposure to the stimulus. The proteinaceous portion of equine sweat consists primarily of glycoproteins and a small portion of immu noglobulins. It has been postulated the glycoproteins may act as surfactants, thus improving the effectiveness of the expelled sweat product .41 The bicarbonate portion of equine sweat is thought to serve as a buffer, possibly as an adjustment for exercise -induced respiratory alkalosis. Bicarbonate helps k eep the pH of sweat around 8.0.

PAGE 21

21 Anhidrosis Clinical Syndrome The diagnosis of anhidrosis is usual ly based on the characteristic clinical signs which are easily recognized. These include obvious signs of heat stress such as exercise intolerance, hyperthermia (rectal temperature up to 108oF) and tachypnea (rates generally in the 60 120 breaths per min ute range, but can be higher) and less specific signs including alopecia, flaky skin or dull, dry haircoat, anorexia; decreased water co nsumption and depression .1,11,13,42 Development of anhidrosis appears to occur along two different pathways. Horses gradually lose the ability to sw eat appropriately, and others sweat profusely shortly before losing the ability to sweat.11,12 Reduced sweating is first seen along the cervical and costal regions, and then progresses to other areas of the body, such as at the base of the mane and in the pectoral region. In some cases, horses lose the ability to sweat over their entire body.12 Possible Pathologies adrenergic receptors undergo desensitization and down regulation when exposed to consistently high levels of epinephrine .43 Su demonstrated that adrenergic receptor affinity for a specific agonist was greatly diminished after stimulation of these receptors by a catecholamine. The decreased affi nity was a result of an uncoupled state of the receptor to adenylate cyclase. The initial reaction was reversible after removal of the catecholamine (half -life of approximately 7 minutes). However, after longterm exposure to isoproterenol, little functi on of the adrenergic receptors returns. This reaction was not performed on equine sweat gland epithelium, but was repeated in several different cell types with similar adrenergic receptor and adenylate cyclase coupling. Therefore, it is reasonable to assert that a possible mechanism resulting loss of 2adrenergic receptors after long term stimulation by increased levels of circulating epinephrine Anhidrotic

PAGE 22

22 horses have demonstrate d higher resting plasma catecholamine (specifically norepinephrine and epinephrine) levels than free -sweating horses .44 This theory is supported by the observation that some horses, usually mildly to modera tely anhidrotic, return to normal sweating patterns during the cooler winter months. This would indicate the gradual return to the coupled state upon removal of the catecholamine agonist. Also, it has been described that intradermal injection of epinephr ine produces a local anhidrotic condition that is resistant to sweat inducing stimuli for 2448 hours after injection .15,16 These areas did not sweat when exposed to intradermal or systemic epinephrine, nor did they sweat when the horse was exercised. The water channel aquaporin 5 (AQP 5) may play a role in the pathogenesis of this syndrome .20 In a recen t study, an immunohistochemistry analysis revealed a strong AQP 5 like activity reaction at the apical membrane of the glandular secretory cells in freely sweating horses .20 In horses with long -term anhidrosis, however, very little AQP 5 like activity was detected, hence implicating water channel impairment as a possible factor in the development of this syndrome On the other hand, aquaporin channels terminate the secondary messenger cascade. The impairment could be at any step in the cascade, including failure of a drenaline to 2 adrenoceptor. It has been established that up to 10% of sweat glands from severely anhidrotic horses have undergone atrophy and ductal blockage .1 It is presumed that this is a result of anhidrosis, and not a cause. Unlikely Causal Factors Several other cau ses of anhidrosis have been proposed and summarily dismissed due to lack of evidence or production of contradictory evidence. The idea that anhidrotic horses may have a deficiency in production of epinephrine was dismissed when it was demonstrated that anh idrotic horses possess a higher concentration of circulating catecholamines than do free-sweating

PAGE 23

23 horses .12,15,44 Likewise, it was postulated that the sweat glands of these horses were inadequately perfused. Scientific literature does not support this hypothesis. Theoretically, a deficiency in plasma T3 (triiodothyronine) levels could induce an anhidrotic state. In fact, one of the signs of hypothyroidism in horses is a failure to sweat adequately. This theory was discounted as well when anhidrotic horses were shown to possess adequate concentrations of T3. Aggravating Factors Diets ri c h in fat a nd protein, which cause increased heat production, can further increase the difficulty of the anhidrotic horse in regulating body temperature12. Exercise can also aggravate the condition of anhidrosis. The conversion of chemical energy to mechanical energy in skeletal muscle is an ine fficient process. Up to 80% of the converted energy is released as heat .7 This heat can accumulate rapidly in the exercising horse. It is estimated that the body temperature of a galloping horse would increase to 108F after two miles in the absence of a sweat response Why Only Some Horses Affected adrenergic receptors could explain why the syndrome affects a small proportion of the equine population. Such polymorphisms have been found to be differentially sensitive to downregulation in response to adrenergic agonists in various human tissues .45 As a result, these genes displayed varying levels of cAMP. Practical Tests The most commonly used test to diagnose anhidrosis is the semi -quantitative intradermal 2adrenergic agonist) on the lateral side of t he neck. The quantity of sweat produced by each injection is subjectively measured by the clinician. Horses that do not suffer from anhidrosis sweat freely from each injection area. Mild to moderately anhidrotic horses exhibit decreased or no sweat respons e from the areas injected by the lower concentrations of terbutaline, but sweat

PAGE 24

24 freely from the areas of high concentration of the drug. Severely anhidrotic horses do not sweat from any concentration of injected terbutaline. A quantitative intradermal swea t test has been developed, but is impractical in the clinical setting. It involves collection and measurement of sweat produced at each injection site. Treatment The only effective treatment of the condition is removal of the horse from the hot, humid cli mate. This can be done by placing the horse in an air -conditioned stall, or by transportation to a cooler climate. There have been many anecdotal claims of the effective treatment of various products in alleviating the signs of anhidrosis. However, none of these products have been scientifically proven to reduce the effects of anhidrosis. A full understanding of the mechanism of the syndrome may be necessary before an effective treatment can be found. Study Objectives T he objectives of the study reported he re were to estimate the prevalence of anhidrosis in horses in F lorida and to identify farm level and horse level risk factors associated with the syndrome.

PAGE 25

25 CHAPTER 3 MATERIALS AND METHOD S Study Population Considered for inclusion in our study were 12, 750 horse farms and approximately 400,000 horse s residing in Florida. Census data from the 2002 USDA NAS S46,47 were used for identification of the study farms Farms with at least one horse -but no more than fifty h orses residing on the premises were included in the study. Due to a probable poor response rate from large training facilities, farms with greater than 50 horses were excluded from the study. Up to ten free -sweating and five anhidrotic horses were included from each farm that was included in the study via random selection. Gender, age, breed, use, and origin were not factored in the inclusion and exclusion of animals in this study. Classification of Study Animals In this study, horses were classified as anh idrotic by the study respondent Horses affected with anhidrosis were those that sweated poorly or not at all under conditions in which a normal horse would sweat freely and that had at least one of the following signs: rapid shallow breathing (usually mor e than thirty breaths/ minute) in hot conditions; a rectal temperature above 102 F when resting; loss of ha ir over the face or chest; dull coat, and/or dry flaky skin. Alternatively, horses were classified as anhidrotic if the diagnosis had been made by a veterinarian. Horse farms with a history of anhidrosis were those with one or more horses classified as affected with anhidrosis during the study period. Development of Questionnaire A structured questionnaire was developed for collection of epidemiologic data. Information requested pertained to farm level and horse -level risk factors. Farm level information included: geographic location of the premises (North, Central, South Florida) ( Figure 4 -1 ), type of

PAGE 26

26 operation (ranch, boarding, racing, pleasure, instr uction, show, other), grass on the premises (yes, no), type of feed c oncentrate, type of roughage, source of water, type of electrolytes supplemented, size of the operation (acres), number of horses on the premises, horses diagnosed with anhidrosis (yes, no); if yes, number of horses affected with anhidrosis. For each horse on the premises, the following information was requested: horse affected with anhidrosis (yes, no), age, gender, breed, color, use (racing, breeding, non racing athletic, halter/pleasu re, retired, other), origin (Florida born: yes, no), diet (free -salt minerals: yes, no) and family history of anhidrosis (father or mother with history of anhidrosis: yes, no, dont know). In addition, for horses affected with anhidrosis, the following inf ormation was requested: month of onset, clinical signs, severity (mild, moderate, severe), duration of illness and treatment (type, length and efficacy). Finally, among farms with horses affected with anhidrosis, the questionnaire was structured to gather information on every anhidrotic horse (maximum of 5 horses) and up to 10 nonanhidrotic (control) horses per farm. A randomized list to use for selection of control horses was sent to each farm along with the survey. The questionnaire was organized and de livered in collaboration with the USDA -NASS. The questionnaire was mailed during November and December of 2006. All questions pertained to events of anhidrosis and conditions in the horse farm during 2005. Study Design To accomplish the first objective, t he epidemiologic questionnaire was mailed to horse farm managers in Florida. A sample size of 585 horse farms was initially calculated using the following assumptions: prevalence of anhidrosis at the farm level = 3%; confidence = 99.5%; and accepted error = 2%. On the basis of a projected 33% response rate, a sample size of 1820 farms was selected. However, because of funding limitations, the final enrollment included 1207 farms, which were randomly selected from a total of 12,750 horse farms. Prevalence of

PAGE 27

27 anhidrosis in horses was estimated by dividing the number of affected horses by the total number of horses at risk. A total of 4620 horses were considered for inclusion. Prevalence of anhidrosis at the farm level was estimated by dividing the number of fa rms with one or more affected horses by the number total number of farms at risk. The approach to the second objective was to compare the frequency of investigated risk factors between farms with and without a history of anhidrosis, as well as between hor ses classified as affected and unaffected with the syndrome. First, a cross -sectional approach was used to identify risk factors associated with anhidrosis at the farm and horse levels. A total of 2444 horses were enrolled. Second, a case -control study approach was used to identify risk factors associated with anhidrosis at the horse level only. In this second approach, horses from farms with one or more horses affected with anhidrosis were included. Case and control horses were matched by farm, and the fre quency of investigated risk factors was compared between horses classified as affected (cases) or unaffected (controls) with anhidrosis. The rationale was to control for possible confounding effects that farm conditions might have had on anhidrosis. A tota l of 79 cases and 329 controls were enrolled in this approach. Statistical Analysis Differences in response rates were compared between regions by using a chi -square test. Prevalence of anhidrosis was calculated by dividing the number of farms with one or more affected horses by the total number of study farms. At the horse level, the prevalence was calculated by dividing the number of affected horses by the total number of study horses. In addition, ninety -five percent confidence intervals (95% CI) were ca lculated for each prevalence estimate. Prevalence of anhidrosis was compared between regions by using a chi -square test. In the cross -sectional study, logistic regression was used to model the odds of being a farm or a horse affected with anhidrosis. Initi al screening of potential risk factors for anhidrosis was

PAGE 28

28 performed by use of univariable logistic regression. Initially, variables associated ( P the outcome of interest (anhidrosis) were entered into the model, and a forward stepwise approach was used to identify which variables were associated with anhidrosis using two -sided P values to enter and to remove of 0.05 and 0.10, respectively. Two-way interaction terms were included in the final model and tested for significance ( P y, in the case -control study, the associations between investigated horse -level risk factors and anhidrosis were studied by using conditional logistic regression analysis. Values of P

PAGE 29

29 CHAPTER 4 RESULTS Response Rate A t otal of 500 horse farms participated in the study; a response rate of 41%. Response rates in North (45%), Central (39%) and South Florida (41%) were not significantly different ( P = 0.60). Prevalence of Anhidrosis At the farm level, the prevalence of anhi drosis was 57/500 or 11.4% (95% CI = 8.7 to 14.1%). The prevalence of the syndrome was different between regions: 5.2% in North, 13.4% in Central and 26.5% in South Florida ( P < 0.01). At the horse level, the prevalence of anhidrosis was 82/4,620 or 1.8% (95% CI = 1.4 to 2.2%). The prevalence of the syndrome was also different between regions: 0.8% in North, in 1.7% Central and 4.3% in South Florida ( P <0.01). In our study, among 57 farms with one or more horses affected with anhidrosis, 82 of 411 ( 20%) hor ses were diagnosed with clinical signs of anhidrosis. The median age when horses were first affected with anhidrosis was 10 years (1st, 3rd quartiles = 5, 18). Most horses were first diagnosed as affected with anhidrosis during the summer months of May thr ough September. Epidemiologic Analysis (Farm -level) In the univariable analysis, the following variables were associated with anhidrosis ( P number of horses on the farm, region, type of operation, type of property, type of feeding concentrate and type of roughage fed (Table 4 1). In the multivariable analysis, number of horses on the farm, region and type of operation were identified as risk factors associated with anhidrosis (Table 4 2). A positive dose response effect was observed between number of horses

PAGE 30

30 on the farm and the odds of the syndrome. The odds of anhidrosis were 2 times higher in farms located in Central Florida (OR = 2.13; 95% CI = 0.99 to 4.59) and 4 times higher in farms located in South Florida (OR = 4.40; 95% CI = 1.58 to 12.23), compared to farms in North Florida. In addition, the odds of anhidrosis were 5 times higher in show operations and 15 times higher in instruction operations, compared to ranch operations ( P < 0.05); the odds of anhidrosis were 3 times higher in racing oper ations, compared to ranch operations (OR = 3.69; 95% CI = 0.94 to 14.53; P = 0.06). Epidemiologic Analysis (Animallevel) In the univariable analysis, the following variables were associated with anhidrosis: gender, breed, geographic origin, use, and famil y history of anhidrosis ( P (Table 4 3). In the multivariable analysis, Thoroughbred horses, Warm Blood horses, horses that originated from Western or Midwestern states, retired horses, and horses with a family history of anhidrosis were identified at high risk of anhidrosis (Table 4 4). Horses reported as positive for anhidrosis displayed a classical depiction of the onset of the disease, with the vast majority first showing signs of anhidrosis during the hot, humid summer months. Case -Control Study Among horses from farms affected with anhidrosis, the following variables were associated with anhidrosis in the univariable analysis: breed, use and family history of anhidrosis ( P (Table 4 5). In the multivariable analysis, the odds of anhidrosis were 4 times higher in Thoroughbreds and 13 times higher in Warm Blood horses, compared to Quarter Horses ( P 0.01) (Table 4 6). In addition, the odds of anhidrosis were 6 times higher in horses with a family history of anhidrosis, compared to horses without a family history ( P < 0.01). The most common clinical sign of horses with anhidrosis noted by the surveyed owners was tachypnea (70/79 horses) (Table 4 7). OneAC was reported as the most effective treatment (Table 4 8).

PAGE 31

31 Figure 4 1. Map of Florida showing the northern, central and southern regions in the state Original map courtesy of Florida County Maps: www.floridacountiesma p.com

PAGE 32

32 0 10 20 30 Number of horses J F M A M J J A S O N D Figure 4 2. Month of the year when horses were first diagnosed as affected by anhidrosis during the study period: January to December 2005

PAGE 33

33 Table 4 1. Frequency -distribution, odds ratios, 95% confidence inter val and P values of investigated operation -level risk factors associated with anhidrosis Variable Anhidrosis Yes n = 56 (100%) Anhidrosis No n = 444 (100%) Crude OR 95% CI P Horses 1 2 3 4 5 10 11 + Acres 1 10 11 25 26 100 101+ Region in F l North Central South Operation Ranch Boarding Racing Pleasure Instruction Show Other Property type Improved Unimproved Stables Other Grass No Yes 1 (2) 8 (14) 14 (25) 33 (59) 18 (32) 15 (27) 16 (29) 7 (12) 11 (20) 32 (57) 13 (23) 4 (7) 8 (14) 7 (13) 13 (23) 3 (5) 12 (22) 9 (16) 36 (64) 10 (18) 7 (13) 3 (5) 2 (4) 54 (96) 141 (31) 100 (23) 119 (27) 83 (19) 122 (27) 97 (22) 115 (26) 108 (25) 202 (46) 206 (46) 36 (8) 94 (21) 24 (6) 26 (6) 221 (50) 1 (<1) 30 (7) 45 (10) 358 (81) 38 (9) 9 (2) 36 (8) 16 (4) 428 (96) 1.00 11.28 16.58 56.05 1.00 1.05 0.94 0.44 1.00 2.85 6.63 1.00 7.83 6.33 1.38 70.50 9.40 4.70 1.00 2.62 7.74 0.83 1.00 1.01 Reference 1.42 89.86 2.19 125.49 7.68 409.15 Reference 0.50 2.19 0.46 1.94 0.18 1.09 Reference 1.40 5.79 2.76 15.91 Reference 2.18 28.22 1.72 23.29 0.44 4.35 5.93 837.76 2.82 31.34 1.37 16.09 Reference 1.20 5.69 2.72 22.01 0.24 2.83 Reference 0.23 4.48 NA 0.02 < 0.01 < 0.01 NA 0.90 0.87 0.07 NA < 0.01 < 0.01 NA < 0.01 < 0.01 0.79 < 0.01 < 0.01 0.01 NA 0.02 < 0.01 1.00 NA 0.99

PAGE 34

34 Table 4 1 continued. Variable Anhidrosis Yes n = 56 (100%) Anhidrosis No n = 444 (100%) Crude OR 95% CI P Concentrate None Sweet Complete Oats Other Sweet + Comp Sweet + Oats Sweet + Other Comp + Oats Comp + Other Oats + Other Other + Other Roughage None T&A Alfalfa Timothy Coastal Orchard Other T&A + Alfalfa T&A + Other Alf. + Timothy Water P/L/ R Well/P Well/A City, Other Electrolytes None Salt Block Loose Sm artPack Other Block + Loose B+L+ SmartPack Loose + Other 5 (9) 14 (25) 15 (26) 1 (2) 4 (7) 7 (13) 4 (7) 2 (4) 1 (2) 3 (5) 0 (0) 0 (0) 15 (27) 12 (21) 11 (20) 3 (5) 9 (16) 3 (5) 2 (4) 0 (0) 1 (2) 0 (0) 3 (5) 47 (84) 2 (4) 4 (7) 45 (80) 4 (7) 2 (4) 0 (0) 3 (5) 1 (2) 1 (2) 0 (0) 79 (18) 175 (39) 66 (15) 9 (2) 38 (9) 30 (7) 13 (3) 17 (4) 6 (1) 8 (2) 1 (<1) 2 (<1) 209 (47) 37 (8) 32 (7) 7 (2) 127 (29) 4 (1) 26 (6) 1 (<1) 0 (0) 1 (<1) 65 (15) 347 (78) 12 (3) 19 (4) 378 (85) 19 (4) 30 (7) 1 (<1) 14 (3) 1 (<1) 0 (0) 1 (<1) 1.00 1.26 3.59 1.76 1.66 3.69 4.86 1.86 2.63 5.93 ND ND 1.00 4.52 4.79 5.97 0.99 10.45 1.07 ND ND ND 1.00 2.94 3.61 4.56 1.00 1.77 0.56 ND 1.80 8.40 ND ND Reference 0.44 3.63 1.24 10.41 0.18 16.75 0.42 6.55 1.09 12.52 1.15 20.52 0.33 10.40 0.26 26.33 1.19 29.52 ND ND Reference 1.96 10.43 2.02 11.35 1.40 25.48 0.42 2.32 2.14 51.06 0.23 4.96 ND ND ND Reference 0.89 9.72 0.54 23.97 0.94 22.19 Reference 0.58 5.43 0.13 2.42 ND 0.50 6 .51 0.52 136.72 ND ND NA 0.80 0.02 0.50 0.48 0.04 0.04 0.61 0.39 0.05 ND ND NA < 0.01 < 0.01 0.03 1.00 0.01 1.00 ND ND ND NA 0.09 0.20 0.07 NA 0.30 0.76 ND 0.42 0.21 ND ND

PAGE 35

35 Table 4 2. Final logistic regression model for investigated operationle vel risk factors associated with anhidrosis Variable Anhidrosis Yes n = 56 (100%) Anhidrosis No n = 444 (100%) Adjusted OR 95% CI P Number of horses 1 2 3 4 5 10 11+ Region in Fl North Central South Operation Ranch Racing Show Instruction Pleasure Board ing Other 1 (2) 8 (14) 14 (25) 33 (59) 11 (20) 32 (57) 13 (23) 4 (7) 8 (14) 7 (13) 13 (23) 3 (5) 12 (22) 9 (16) 141 (31) 100 (23) 119 (27) 83 (19) 202 (46) 206 (46) 36 (8) 94 (21) 24 (6) 26 (6) 221 (50) 1 (<1) 30 (7) 45 (10) 1.00 10.80 14.07 30. 22 1.00 2.13 4.40 1.00 3.69 5.26 15.40 1.80 2.71 2.90 Reference 1.34 87.06 1.83 107.90 3.95 231.10 Reference 0.99 4.59 1.58 12.23 Reference 0.94 14.53 1.49 18.59 1.20 197.37 0.55 5.91 0.69 10.60 0.79 10.59 NA 0.02 0.01 < 0.0 1 NA 0.05 < 0.01 NA 0.06 < 0.01 0.03 0.33 0.15 0.10 Hosmer Lemeshow Statistic = 7.96; P value = 0.43; DF = 8

PAGE 36

36 Table 4 3. Frequency -distribution, odds ratios, 95% confidence interval and P values of investigated animal level risk factors associated wit h anhidrosis Variable Anhidrosis Yes n = 79 (100%) Anhidrosis No n = 2365 (100%) Crude OR 95% CI P Age 1 2 3 5 6 10 11+ Gender Stallion Female Gelding Color Palomino Bay Chestnut Black Grey Paint Other Breed QH Arab TB Warmbloods Other Origin South North East MidWest West Unknown Foreign 2 (3) 5 (6) 17 (22) 20 (25) 35 (44) 4 (5) 34 (43) 41 (52) 3 (4) 32 (41) 20 (25) 8 (10) 7 (9) 5 (6) 4 (5) 13 (16) 0 (0) 32 (41) 12 (15) 22 (28) 57 (72) 3 (4) 7 (9) 0 (0) 4 (5) 8 (10) 173 (7) 164 (7) 393 (17) 682 (29) 952 (40) 261 (11) 1220 (52) 884 (37) 145 (6) 626 (26) 440 (19) 146 (6) 253 (11) 214 (9) 541 (23) 908 (38) 190 (8) 356 (15) 62 (3) 849 (36) 1950 (82) 32 (1) 67 (3) 38 (2) 176 (8) 102 (4) 1.00 1.82 3.02 1.00 2.47 2.20 2.65 1.34 1. 13 0.36 1.00 ND 6.28 13.52 1.81 1.00 3.21 3.57 ND 0.78 2.68 Reference 0.65 5.07 1.09 8.37 Reference 0.75 8.18 0.64 7.50 0.69 10.19 0.34 5.25 0.27 4.80 0.08 1.62 Reference ND 3.26 12.10 5.92 30.88 0.91 3.62 Reference 0.95 10.78 1.57 8.13 ND 0.28 2.17 1.25 5.78 NA 0.25 0.03 NA 0.18 0.32 0.22 1.00 1.00 0.17 NA ND < 0.01 < 0.01 0.12 NA 0.05 < 0.01 ND 0.63 0.01

PAGE 37

37 Table 4 3 continued. Variable Anhidrosis Yes n = 79 (100%) Anhidrosis No n = 2365 (100% ) Crude OR 95% CI P Use Halter Racing Breeding Non -racing Retired Other Relatives No Yes Unknown 15 (19) 10 (13) 10 (13) 13 (16) 19 (24) 12 (15) 11 (14) 6 (8) 62 (78) 1132 (48) 172 (7) 371 (16) 195 (8) 221 (9) 273 (12) 1303 (55) 24 (1) 1038 (44) 1 .00 4.39 2.03 5.03 6.49 3.32 1.00 29.61 7.08 Reference 1.94 9.93 0.91 4.57 2.36 10.74 3.25 12.97 1.54 7.17 Reference 10.12 86.66 3.71 13.51 NA < 0.01 0.10 < 0.01 < 0.01 < 0.01 NA < 0.01 < 0.01

PAGE 38

38 Table 4 4. Final logistic regression m odel for investigated animal level risk factors associated with anhidrosis Variable Anhidrosis Yes n = 79 (100%) Anhidrosis No n = 2365 (100%) Adjusted OR 95% CI P Breed Quarter Horse Arab Thoroughbred Warmbloods Other Origin South North East Mid West & West Unknown Foreign Use Halter Racing Breeding Non -racing Retired Other Relatives No Yes Unknown 13 (16) 0 (0) 32 (41) 12 (15) 22 (28) 57 (72) 3 (4) 7 (9) 4 (5) 8 (10) 15 (19) 10 (13) 10 (13) 13 (16) 19 (24) 12 (15) 11 (14) 6 (8) 62 (78) 908 (38) 190 (8) 356 (15) 62 (3) 849 (36) 1950 (82) 32 (1) 105 (5) 176 (8) 102 (4) 1132 (48) 172 (7) 371 (16) 195 (8) 221 (9) 273 (12) 1303 (55) 24 (1) 1038 (44) 1.00 ND 4.87 7.26 1.66 1.00 2.08 2.57 0.64 1.24 1.00 1.46 1.45 2.57 4.73 2.21 1.00 21.67 6.18 Reference ND 2.37 10.04 2.89 18.21 0.81 3.38 Reference 0.56 7.70 1.07 6.15 0.22 1.85 0.52 2.95 Reference 0.57 3.76 0.61 3.49 1.13 5.87 2.28 9.83 0.96 5.10 Reference 6.96 67.51 3.18 12.00 NA ND < 0.01 < 0.01 0.16 NA 0.27 0.03 0.40 0.62 NA 0.43 0.40 0.02 < 0.01 0.06 NA < 0.01 < 0.01 Hosmer Lemeshow Statistic = 2.87; P = 0.89; DF = 7

PAGE 39

39 Table 4 5. Case -control study. Univariable analysis of investigated animal -level risk factors associated with anhidrosis Variab le Anhidrosis Yes n = 79 (100%) Anhidrosis No n = 327 (100%) Crude OR 95% CI P Age 1 2 3 5 6 10 11+ Gender Stallion Female Gelding Color Palomino Bay Chestnut Black Grey Paint Other Breed Quarter Horse Arab Thoroughbred Warm Blood Other Origin South N orth East Midwest & West Unknown Foreign 2 (3) 5 (6) 17 (22) 20 (25) 35 (44) 4 (5) 34 (43) 41 (52) 3 (4) 32 (41) 20 (25) 8 (10) 7 (9) 5 (6) 4 (5) 13 (16) 0 (0) 32 (41) 12 (15) 22 (28) 57 (72) 3 (4) 7 (9) 4 (5) 8 (10) 29 (9) 29 (9) 53 (16) 63 (19) 152 (47) 35 (11) 145 (44) 147 (45) 12 (4) 114 (35) 76 (23) 22 (7) 46 (14) 19 (6) 38 (11) 69 (21) 24 (7) 98 (30) 23 (7) 113 (35) 244 (75) 11 (3) 22 (7) 10 (3) 40 (12) 1.00 1.93 1.60 1.00 0.93 0.66 0.85 0.37 1.05 0.36 1.00 ND 5.25 15.51 2.17 1.00 0.69 1.10 1.85 0.56 Reference 0.59 6.28 0.47 5.44 Reference 0.20 4.23 0.13 3.17 0.15 4.80 0.06 2.07 0.17 6.49 0.05 2.43 Reference ND 1.61 17.12 3.34 72.05 0.75 6.27 Reference 0.12 3.69 0.30 3.97 0.37 9 .25 0.18 1.71 NA 0.27 0.44 NA 0.93 0.60 0.85 0.25 0.95 0.29 NA ND < 0.01 < 0.01 0.15 NA 0.66 0.87 0.44 0.31

PAGE 40

40 Table 4 5 continued. Variable Anhidrosis Yes n = 79 (100%) Anhidrosis No n = 326 (100%) Crude OR 95% CI P Use Halter Racing Bre eding Non -racing Retired Other Relatives No Yes Unknown 15 (19) 10 (13) 10 (13) 13 (16) 19 (24) 12 (15) 11 (14) 6 (8) 62 (78) 57 (17) 37 (11) 59 (18) 70 (21) 34 (10) 70 (21) 138 (42) 17 (5) 172 (53) 1.00 1.00 0.97 0.07 2.48 0.53 1.00 7.54 11.53 Reference ND 0.31 3.04 0.01 0.49 0.84 7.34 0.15 1.86 Reference 1.92 29.64 4.49 29.62 NA ND 0.96 < 0.01 0.09 0.32 NA < 0.01 < 0.01

PAGE 41

41 Table 4 6 Case -control study : Final conditional logistic regression model for investigated animal level risk factors associated with anhidrosis Variable Anhidrosis Yes n = 79 (100%) Anhidrosis No n = 327 (100%) Adjusted OR 95% CI P Breed Quarter Horse Arab Thoroughbred Warm Blood Other Relatives No Yes Unknown 13 (16) 0 (0) 32 (41) 12 (15) 22 (28) 11 (14) 6 (8) 62 (78) 69 (21) 24 (7) 98 (30) 23 (7) 113 (35) 138 (42) 17 (5) 172 (53) 1.00 ND 4.37 13.88 2.14 1.00 6.87 9.86 Reference ND 1.23 15.45 2.48 77.47 0.68 6.69 Reference 1.82 25.92 3.82 25.45 NA ND 0.02 < 0.01 0.18 NA < 0.01 < 0. 01

PAGE 42

42 Table 4 7. Frequency, c linical signs and severity of syndrome in 79 horses classified as anhidrotic. Variable Number of horses Clinical Sign Tachypnea Profuse sweating, then none Dull coat and/or (skin) scaling Fatigue Alopecia Hyperthermia Decrea sed appetite Decreased water intake Severity Mild Moderate Severe 70 33 31 23 22 9 9 6 22 22 34

PAGE 43

43 Table 4 8. Anhidrotic horses : Treatment type and average monthly duration. Treatment Duration of treatment ( months ) OneAC 6 (3, 12) Ventipulmin 6 (6, 6) Electrolytes 12 (12, 12) A/C or Fan 6 (4, 6) Other 5 (0, 9.5) Data reported as median (1st and 3rd Quartiles)

PAGE 44

44 CHAPTER 5 DISCUSSION AND CONCLUSIONS Results showed that the prevalence of anhidrosis was 11% at the farm level and 2% at the horse lev el. To our knowledge, there are no other reports on the prevalence of the disease at the farm level in the US states bordering the Gulf of Mexico, where the disease is commonly diagnosed. In a previous study9 conducted on 4 farms with a history of anhidros is in Florida, 52 of 834 (or 6%) horses were diagnosed with clinical signs of anhidrosis. In that study,9 the main objective was not to estimate the prevalence of anhidrosis, but rather to compare clinical findings and results from a clinico pathologic ana lysis between affected and nonaffected horses in a selected number of farms. Furthermore, in that study, Thoroughbred was the only breed represented in the study po pulation. In our study, among 57 farms with one or more horses affected with anhidrosis, 82 of 411 (20%) horses were diagnosed with clinical signs of anhidrosis. It is difficult to compare these 2 prevalence estimates, as the study objectives, sampling and diagnostic methods were all different. In this study, most horses were first diagnosed as affected with anhidrosis during the summer months of May through September. This finding was expected, and it is in line with previous studies .6 In one study ,48 a group of 8 horses with a history of anhidrosis was exposed to riding school training during the summer, autumn and winter seasons in Hong Kong. Skin sam ples were processed and examined by electron microscopy. Blockage or collapse of the sweat gland ducts was observed in 13/28 (46%) ducts in the summer versus 7/22 (32%) in the autumn and 8/31 (26%) in the winter. Finally, it has been suggested that the atr ophy of sweat glands and the blockage of sweat gland ducts are a result of anhidrosis and not an etiologic factor of this syndrome.

PAGE 45

45 At the farm level, geographic region and type of operation were identified as risk factors for anhidrosis. The odds of anhidrosis were 2 and 4 times higher in equine farms located in Central and South Florida, respectively, compared to farms in North Florida. One explanation for this observed association is exposure to increasingly hot and humid conditions in Central and South Florida, compared to the northern region in that state. Anhidrosis results from prolonged stimulation of the sweat glands by epinephrine secreted as a response to conditions of hot humid climate.7 Previous studies have hypothesized that the sweat glands ac commodate to the raised epinephrine content of the blood thus becoming insensitive to it. The clinical signs can be reversed by rest in a cooler and less humid climate.7 Anhidrotic horses can display an increased prop ortion of atrophied and occluded sweat glands .48 Finally, in this study, the odds of anhidrosis were 3, 5 and 15 times higher in racing, show and instruction farms, compared to ranch farms. These associations c an be explained in part by high exercise intensity in these 3 subpopulations of horses. Exercise in hot weather with high humidity can raise the basal metabolism of affected horses, exacerbate water loss, or influence heat loss and affect body heat control .49 In this study, the odds of being diagnosed with anhidrosis were higher in Thoroughbreds and W armblood horses, compared to Quarter Horses. Thoroughbreds, in particular, have consistently been the focus of seve ral studies on anhidrosis. The disease was first reported in British Thoroughbreds taken to tropical colonies in the early 1900s .14 Anhidrosis was obser ved in Puerto Rico in imported Thoroughbreds in the 1950s and 10 years later in 2-year old native horses .13 In 1981, the disease was reported in a 10-year -old Thoroughbred gelding that had been purchased in Wisconsin and moved to K ansas in July .10 During September 1979 and March 1980, the disease was reported in 12 Thoroughbreds, 6 Quarter Horse and 4 Arabian horses in Florida. Although sudden heat stress and change during acclimation was suspected to play a role

PAGE 46

46 in the development of anhidrosis for some horses, native horses were also affected.11 The disease was also reported in 4 equine farms in Florida, wher e 52 of 834 Thoroughbreds were diagnosed with anhi drosis during June -August 1981. Warmblood horses were also identified at high risk of anhidrosis. Warmblood horses typically have larger body sizes than other breeds of horses. This larger body size results in a decreased skin surface area to body mass ratio, which can effectively limit the thermoregulatory capacity of the sweat mechanism .37 The decreased thermoregulatory efficiency of the sweat m echanism can lead to increased body heat storage, placing horses at high risk of anhidrosis .37 Finally, none of the 190 Arab horses included in this study were classified as anhidrotic. One poss ible explanation for this observation could be the differences in breeding regimes between Arab horses and other breeds. The Arab horse was first domesticated in what was known as the Fertile Crescent, a crescent -shape area of land extending from present -d ay Iraq to Egypt .50 The breed has been evolving in this area for several centuries .50 The Arab horse has adapted to survive in much higher temperatures than have other breeds, especially Thoroughbred and W armblood horses .50,51 Two of the 3 founding sires of the Thoroughbred breed were Arabs, but the breed has undergone extensive selective breeding over the past 300 years since this origin.51 Furthermore, the breed was developed in England a climate that is generally cooler in temperature than the Fertile Crescent These differences in evolution may have affected the sweat gla nd epithelia of these breeds and all owed for polymorphisms among adrenergic receptors .45 Our study results support the hypothesis that horses originating from more temperate climates are at high risk of anhidrosis when transported to hot humid climates for racing or exercise. In this study, the odds of anhidrosis were 2.5 times higher in horses that originated

PAGE 47

47 from the West or mid West regions of the United States, compared to horses that originated from the South. In a previous study1 of 24 horses affected with anhidrosis in Florida, 15 of 24 horses were native horses a nd the remaining 9 horses were imported horses. Because that study1 did not include healthy horses, it was not possible to estimate and compare the prevalence of anhidrosis between these 2 subpopulations of horses. Thus, while this and other studies1,2 sho w that native horses are susceptible to develop anhidrosis, our study results provide epidemiologic evidence that horses from temperate climates are at higher risk of the disease when imported into Florida, compared to native horses. In this study, the odds of anhidrosis were 4.7 times higher in retired horses and 2.5 times higher in nonracing athletic performance horses, compared to halter horses. Among 240 horses classified as retired, most were Quarter Horses (30%) and Thoroughbreds (20%). It is very l ikely that horses diagnosed with anhidrosis were retired after the diagnosis, more so if they remained in a hot humid environment. Anhidrosis is a severe condition that can affect performance possibly ending a horses career. In addition, it is a serious w elfare problem because of the considerable distress experienced by affected horses .41 Non -racing athletic performance horses were also identified a t high risk of anhidrosis. This category is consists largely of show horses, who often contend with large amounts of heat stress. The typical show horse is a W arm blood with a body condition score between 6 and 7 out of 9. T hese horses are typically exercised during the daylight hours when the ambient temperature and humidity can reach levels of 95 F and 85% during the summer months in Flo rida The effects of heavily muscled, overweight body types exercising in the summertime heat provide a more than adequate reason for these horses to show an increased risk of anhidrosis.

PAGE 48

48 Our study results support the hypothesis that there is a hereditary predisposition associated with anhidrosis in horses. A hereditary predisposition to anhidrosis was first suggested in a review3 published in 1976. However, to our knowledge, this is the first study that has generated data which supports this hypothesis. In our study, results of the epidemiologic analysis revealed a strong association between family history of anhidrosis and risk of disease. In two separate analyses (Tables 4 and 6), the odds of anhidrosis were 20 and 6 times higher in horses with a family history of anhidrosis, compared to horse without a history. We examined the foaling place data of the 30 horses with a family history of anhidrosis, and almost all horses (n = 29) were foaled in the South; an indication in the epidemiologic analysis that th e association between anhidrosis and family history was not influenced by the high risk origin (temperate climate) of the West and mid West Unites States. Horses with a family history of anhidrosis should be evaluated for anhidrosis by a veterinarian befor e they are exposed to exercise in hot and humid conditions. Future studies comparing the level of AQP 5 expression and lack of sweat production from sweat glands between horses with and without a family history may further advance our limited, current know ledge on the genetic susceptibility as a causative factor for anhidrosis in horses. OneAC was reported as the most effective treatment OneAC contains L -tyrosine, choline bitartrate, niacin, pyridoxine HCl, d -calcium pantothenate. L -tyrosine, an amino acid, is an important building block for many proteins, especially dopamine and epinephrine (both play large roles in the sweating mechanism of the horse). Niacin (vitamin B3) can influence cellular metabolism as well as improve the removal of toxins .52 Pyridoxine HCL (vitamin B6) is also involved in cellular metabolism and assists the production of dopamine. d -calcium pantothenate (vitamin B5) helps with vitality and boosts the immune system. Choline works well with seve ral

PAGE 49

49 B-vitamins to help boost cellular metabolism. Choline is also involved in the synthesis of other essential proteins. The exact mechanism by which OneAC improves the clinical signs of anhidrosis is not well understood. However, there is much anecdotal evidence supporting the claim that OneAC can help reduce or el iminate the signs of anhidrosis. It is this anecdotal evidence that has helped establish OneAC as one of the most common treatment modalities for anhidrosis.

PAGE 50

50 REFERENCES 1 Cu rrie AK, Seager SWJ. Anhidrosis. American Association of Equine Practioners 22nd Annual Meeting 1976:249251. 2 Cymbaluk NF, Christison GI. Environmental effects on thermoregulation and nutrition of horses. Vet Clin North Am Equine Pract 1990;6:355372. 3 Thom sett LR. Noninfectious skin diseases of horses. Vet Clin North Am Large Anim Pract 1984;6:5978. 4 Kerr MG, Snow DH. Composition of sweat of the horse during prolonged epinephrine (adrenaline) infusion, heat exposure, and exercise. Am J Vet Res 1983;44:15711577. 5 Warner A, Mayhew IG. Equine anhidrosis: a review of pathophysiologic mechanisms. Vet Res Commun 1983;6:249264. 6 Mayhew IG, Ferguson HO, 2nd. Clinical, clinicopathologic, and epidemiologic features of anhidrosis in central Florida Thoroughbred horses. J Vet Intern Med 1987;1:136141. 7 Hodgson DR, Davis RE, McConaghy FF. Thermoregulation in the horse in response to exercise. Br Vet J 1994;150:219235. 8 Geor RJ, McCutcheon LJ. Thermoregulation and Clinical Disorders Associated with Exercise and Heat Stress Comp Cont Educ Pract 1996;18:436444. 9 Wright T, Tull T. A preliminary report of an investigation of a condition known as dry coat in horses. Vet J 1925;81:235240. 10. Peter JE, Boge P, Morris PG, et al. Anhidrosis in a thoroughbred. Vet Med Small Anim Clin 1981;76:730732. 11. Warner AE, Mayhew IG. Equine anhidrosis: a survey of affected horses in Florida. J Am Vet Med Assoc 1982;180:627629. 12. Evans SCL, Smith D, Ross K, et al. Physiological Factors in the Condition of "Dry Coat" in Horses. The Veterinary Record 1957;69:19. 13. Correa JE, Calderin GG. Anhidrosis, Dry Coat Syndrome in the Thoroughbred. JAVMA 1966;149:15561560. 14. Barnes J. "Dry Sweating" in Horses. Veterinary Record 1938;50:977978. 15. Evans SCL. Sweating in relation to sympathetic innervation. British Medical Bullentin 1957;13:197201. 16. Evans SCL, Smith D. Sweating responses in the horse. Proc R Soc Lond B Biol Sci 1956;144:6183.

PAGE 51

51 17. Sorensen VW, Prasad G. On the fine structure of horse sweat glands. Z Anat Entwicklungsgesch 1973;139:173183. 18. Evans SCL. Physio logical mechanisms that underlie sweating in the horse. British Veterinary Journal 1966;122:117123. 19. Wilson SM, Pediani JD, Ko WH, et al. Investigation of stimulus -secretion coupling in equine sweat gland epithelia using cell culture techniques. J Exp Biol 1993;183:279299. 20. Bovell DL, Lindsay SL, Corbett AD, et al. Immunolocalization of aquaporin 5 expression in sweat gland cells from normal and anhidrotic horses. Vet Dermatol 2006;17:1723. 21. Montgomery I, Jenkinson DM, Elder HY. The effects of thermal stimulation on the ultrastructure of the fundus and duct of the equine sweat gland. J Anat 1982;135:1328. 22. Scott DW. Large Animal Dermatology. W.B. Saunders, Philidelphia, PA 1988:1718. 23. Takagi S, Tagawa, M. Nerve fibers supplying the horse sweat gland. Jpn J P hysiol 1961;11:158161. 24. Takagi S, Tagawa M. A cytological and cytochemical study of the sweat gland of the horse. Jpn J Physiol 1959;9:153159. 25. Jenkinson DM. Comparative physiology of sweating. British Journal of Dermatology 1973;88:397406. 26. Anderson MG, Aitken, M. M. Biochemical and physiological effects of catecholamine administration in the horse. Research in Veterinary Science 1977;22:357360. 27. Snow DH. Identification of the receptor involved in adrenaline mediated sweating in the horse. Res Vet Sci 1977;23:246247. 28. Bijman J, Quinton, PM. Predominantly beta adrenergic control of equine sweating. American Journal of Physiology 1984;246:R349R353. 29. Mills PC, Marlin DJ, Demoncheaux E, et al. Nitric oxide and exercise in the horse. J Physiol 1996;495 (Pt 3):863874. 30. Mills PC, Marlin DJ, Scott CM, et al. Nitric oxide and thermoregulation during exercise in the horse. J Appl Physiol 1997;82:10351039. 31. McCutcheon LJ, Geor RJ, Hare MJ, et al. Sweating rate and sweat composition during exercise and recovery in ambient heat and humidity. Equine Vet J Suppl 1995:153157. 32. Dahlborn K, Jansson A, Nyman S, et al. Sweat production and localisation of carbonic anhydrase in the eqine sweat gland during exercise at two ambient temperatures. Equine Vet J Suppl 1999;30:398403.

PAGE 52

52 33. Rose RJ, Arnold KS, Church S, et al. Plasma and sweat electrolyte concentrations in the horse during long distance exercise. Equine Vet J 1980;12:1922. 34. Levitzki A. From epinephrine to cyclic AMP. Science 1988;241:800806. 35. McConaghy FF, Hodgs on DR, Hales JR, et al. The horse as a model for thermoregulatory responses to exercise. Int J Sports Med 1998;19 Suppl 2:S100102. 36. Geor RJ, McCutcheon LJ. Thermoregulatory adaptations associated with training and heat acclimation. Vet Clin North Am Equine Pract 1998;14:97120. 37. Lindinger MI. Exercise in the heat: thermoregulatory limitations to performance in humans and horses. Can J Appl Physiol 1999;24:152163. 38. Geor RJ, McCutcheon LJ, Ecker GL, et al. Heat storage in horses during submaximal exercise befo re and after humid heat acclimation. J Appl Physiol 2000;89:22832293. 39. Kingston JK, Geor, R. J., McCutcheon, L. J. Rate and composition of sweat fluid losses are unaltered by hypohydration during prolonged exercise in horses. J Appl Physiol 1997;83:11331143. 40. Geor RJ, McCutcheon LJ. Hydration effects on physiological strain of horses during exercise -heat stress. J Appl Physiol 1998;84:20422051. 41. Jenkinson DM, Elder HY, Bovell DL. Equine sweating and anhidrosis Part 1: equine sweating. Vet Dermatol 2006;17:361 392. 42. Barnes P. Beta adrenergic receptors and their regulation. American Journal of Respiratory and Critical Care Medicine 1995;152:838860. 43. Su YF, Harden TK, Perkins JP. Catecholamine -specific desensitization of adenylate cyclase. Evidence for a multist ep process. J Biol Chem 1980;255:74107419. 44. Beadle R, Norwood, GL, Brencick, VA. Summertime plasma catecholamine concentrations in healthy and anhidrotic horses in Louisianna. American Journal of Veterinary Research 1982;43:14461448. 45. McNamara DM, MacGowan GA, London B. Clinical importance of beta adrenoceptor polymorphisms in cardiovascular disease. Am J Pharmacogenomics 2002;2:7378. 46. Team FSAR. Livestock and Horses: Introducing Florida's Livestock and Horse Industries. 47. Service USDoA NAS. 2002 Census of Ag riculture. 48. Jenkinson DM, Loney C, Elder HY, et al. Effects of season and lower ambient temperature on the structure of the sweat glands in anhidrotic horses. Equine Vet J 1989;21:5965.

PAGE 53

53 49. Jenkinson DM, Elder HY, Bovell DL. Equine sweating and anhidrosis Part 2: anhidrosis. Vet Dermatol 2007;18:211. 50. Arabian Horse Association 19962009. Arabian Horse History & Heritage : Origin of the Arabian Horse Aurora, CO. http://www.arabi anhorses.org/education/education_history_origin.asp. 51. The Ultimate Horse SiteSM 20002005. Thoroughbred Breed Information. Corvallis, OR. http://www.ultimatehorsesite.com/breedsofhorses/thoroughbredhorsebreed.html 52. Higdon J, Drake VJ. Linus Pauling Instit ute 20002009. Niacin. Oregon State University, Corvallis, OR. http://lpi.oregonstate.edu/infocenter/vitamins/niacin/

PAGE 54

BIOGRAPHICAL SKETCH The author was born in Batavia, New York in 1980. He graduated with honors from Holley Senior High School (Holley, New York ) in 1998. He then completed his Bachelor of Science degree in 2002 from Colorado State University in Fort Collins, C olorado. He majored in equine sciences with a science con centration. The author began his employment at Palm Beach Equine Clinic (Wellington, FL) in 2003 and continued until 2005. He began work on his M aster of S cience degree in 2007 at the University of Florida College of Veterinary Medicine and graduate d in Ma y 2009. The author entered the doctor of veterinary medicine program at the University of Florida College of Veterinary Medicine in 2007 and is scheduled to graduate in May 20 09.