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Nutrient Requirements of Horses: Sixth Revised Edition (2007)

Chapter: 12 Unique Aspects of Equine Nutrition

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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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Suggested Citation:"12 Unique Aspects of Equine Nutrition." National Research Council. 2007. Nutrient Requirements of Horses: Sixth Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/11653.
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12 Unique Aspects of Equine Nutrition NURSING AND ORPHAN FOALS liquid milk replacer consumed less than 1 kg grain mix per 100 kg BW daily up to 1 month of age, then increased intake During the first week of life, healthy foals will nurse up to 1.5–2 kg grain mix per 100 kg BW daily at 7 weeks of age to seven times per hour, with each nursing bout lasting 1 to (Cymbaluk et al., 1993). Foal body weight averaged about 2 minutes (Carson and Wood-Gush, 1983). Subsequently, 60 kg at birth, and average daily gains ranged from a low of there is a decrease in the frequency and duration of nursing 0.18 kg/d during the first 2 weeks of age to 1.43 kg/d be- bouts; at 4 weeks of age, foals nurse about three times per tween 16 and 24 weeks of age. In another trial, creep feed hour (Carson and Wood-Gush, 1983). During the first 24 intakes of extensively managed nursing foals averaged hours of life, foals consume approximately 15 percent of 0.56–0.84 kg/d (Coleman et al., 1999). Initially, foals were body weight (BW) as milk, increasing to 22–23 percent on approximately 2 months of age with a mean BW of 140 kg. day 2, and approximately 25 percent of BW (15 liters for a At 4 months of age (the end of the study), mean BW was ap- 50 kg-foal) by 7 days postpartum (Ousey et al., 1996). One proximately 200 kg. study of Thoroughbred foals indicated that the digestibility Management of the orphan foal is dependent upon the age of mare’s milk is 98 percent (Ousey et al., 1997). Although at which the foal loses its dam. Young foals should be fed a the dam’s milk will normally supply all the nutritional needs milk-based diet to ensure satisfactory growth and develop- of foals for the first 6–8 weeks of life, foals will begin to ment, whereas older foals may develop adequately with a consume small portions of solid feed within days of birth. diet of high-quality forage and creep feed. For foals orphaned Foals will increasingly seek solid feed sources to supply on the 1st day of life, an important consideration is provision their nutrient needs by consumption of the dam’s feed, or if of high-quality colostrum that contains immunoglobulins available, feed supplied by creep feeding. Creep feeding has vital to competency of the foal’s naïve immune system. Fol- advantages of supplying a nutrient-dense source of feed to lowing ingestion by the foal, immunoglobulins in colostrum foals that is protected from ingestion by mares. are absorbed by specialized cells throughout the epithelium Average daily gain of foals fed creep feed before wean- of the small intestine. The absorption process is most effi- ing can be higher when compared to foals not receiving cient following the first few feedings postpartum, with a creep rations (Coleman et al., 1999). Additionally, foals that rapid decline in uptake efficiency over the first 12 hours of become accustomed to consuming dry feed prior to weaning life. By 24 hours, the small intestine is no longer permeable have reduced weaning stress (McCall et al., 1985; Hoffman to colostral immunoglobulins (Jeffcott, 1972). Colostrum et al., 1995). Creep rations are typically formulated to con- should be fed before any milk replacers to ensure maximal tain 16–20 percent high-quality crude protein (CP), 0.8–1 absorption of immunoglobulins (Stoneham, 2005). The im- percent calcium, and 0.6–0.8 percent phosphorus, although munoglobulin content of colostrum declines rapidly after the there has been limited research to assess the optimal nutri- onset of nursing in postpartum mares. Milk samples col- ent composition of creep feeds for foals. lected 4–8 hours after birth have 15 percent of the im- The decision to provide creep feed will depend on de- munoglobulin concentration of samples collected in the first sired growth rates and post-weaning nutritional programs. 3 hours postpartum (Naylor, 1979). Therefore, the colostrum Voluntary intake of creep feed is expected to vary between fed to orphan foals should have been harvested from mares foals and to be influenced by factors such as herd behavior, soon after parturition. placement of creep feeders, and presence of other foals con- Fostering to a nurse mare is the preferred option for man- suming feeds. One trial reported that orphan foals receiving agement of orphan foals less than 6 to 8 weeks of age. Foals 235

236 NUTRIENT REQUIREMENTS OF HORSES that cannot be fostered should be fed a mare’s milk substi- lates to physiological function and uses the decline in phys- tute. Fortified cow’s milk, goat milk, and commercially iological function as a threshold for old age. Demographic available milk replacer products specifically designed for age reflects survivorship of an age-group subpopulation rel- foals have been used (Naylor and Bell, 1985; Pugh and ative to the whole. No exact chronological threshold for old Williams, 1992). Milk substitutes should be designed to age in horses has been identified. Several investigators have mimic the nutrient concentrations in mare’s milk (Naylor used 20 years of age to define the threshold of old age (Ral- and Bell, 1985). Research findings on composition of ston et al., 1988, 1989; Malinowski et al., 1997; Brosnahan mare’s milk are provided in Table 16-8. On a dry matter and Paradis, 2003). The 1998 National Animal Health Mon- (DM) basis, foal milk replacers should contain approxi- itoring Systems study (USDA, 1998) estimated that 7.5 per- mately 15 percent fat and 22 percent CP, with a fiber content cent of the horse population (total horse population esti- of less than 0.5 percent (Naylor and Bell, 1985). Milk re- mated at approximately 7 million) was 20 years of age or placers should be fed as a 10–15 percent solution. Milk from older. farm animal species (i.e., goat, pig, sheep, and cow) is dis- Although 20 years of age may serve as an estimate of the similar to mare’s milk. Therefore, commercially available threshold for old age, the degree of variation of this estimate milk replacers are the preferred milk substitute for foals. is not known. Therefore, the combination of chronological However, cow’s milk is suitable if some of the fat is re- age and physical signs of aging may be the most effective moved and sugar added. One recommendation is to feed 2- means of establishing the “old-age” threshold for individual percent-fat skimmed milk to which dextrose has been added horses. Physical signs of aging may include chronically low at the rate of 20 g/L (40 ml of 50 percent dextrose per liter body condition score, loss of muscle mass over the top line of milk) (Naylor and Bell, 1985). yielding a sway-backed appearance, hollowing out of the It is advisable to gradually increase the volume of milk grooves above the eyes, graying of the coat, and dental dis- fed over a 7- to 10-d period. One recommendation is to start ease (Ralston et al., 1988, 1989; Ralston and Breuer, 1996; at 5–10 percent BW at day 1, increasing to 20–25 percent Paradis, 2002). BW by day 10 (Naylor and Bell, 1985). Initially, many small meals should be provided to somewhat mimic natural feed- Energy Requirements of Aged Horses ing patterns (e.g., every hour). As the foal begins to eat solid feed, the frequency of feedings can be gradually reduced. Energy requirements are a function of energy expendi- Alternatively, the foal can be given free choice access to ture and the efficiency with which gross energy (GE) pres- milk in a pail or by use of an automated feeding device de- ent in feeds is converted to net energy (NE). Both of these signed for calves. Fresh water should be available at all factors have the potential to be affected by age. times (Cymbaluk et al., 1993). Orphan foals can be weaned Maintenance energy requirements typically constitute the from milk at 10–12 weeks of age (Naylor and Bell, 1985). largest proportion of total energy expenditure. Maintenance energy requirements in aged humans and dogs have been re- ported to be 15–20 percent lower when compared to OLD AGE younger populations (Harper, 1998a; Bosy-Westphal et al., Several challenges exist in defining nutrient requirements 2003). The decline in maintenance energy expenditure is of old horses. The first challenge is to establish criteria that thought to be a function of declining fat-free mass associ- define the threshold for old age in horses. Secondly, nutrient ated with aging (Bosy-Westphal et al., 2003). Decreased requirements are a function of metabolic requirements and physical activity is thought to be a primary factor in the age- the efficiency of nutrient digestion, absorption, and metabo- related decline in fat-free mass (Harper, 1998a; Roubenoff, lism. Therefore, knowledge of age-related changes in diges- 1999). Whether an age-related decline in maintenance en- tion, absorption, and metabolism is necessary to define the ergy requirement occurs in horses is unknown. Although ap- nutrient requirements of old horses. Finally, the effect of parent loss of muscle mass has been observed in old horses aging-associated disease on nutrient requirements must be (Ralston et al., 1989), age-related change in fat-free mass determined and should be viewed separately from the effects and subsequent changes in maintenance energy requirement of aging itself. Old age is not synonymous with the term have not been quantified in horses. Nor is the effect of age “geriatric,” which refers to diseases of the aged. on physical activity in horses well characterized. Therefore, the extent to which aging alters the maintenance energy re- quirements of horses is not known. Some disease conditions Defining Old Age may increase energy requirements. Mean resting energy ex- Paradis (2002) described three types of age that may be penditure was increased by approximately 41 percent in useful in establishing old age threshold for horses: chrono- horses with recurrent airway obstruction as compared to logic, physiologic, and demographic. Chronologic age is the controls (Mazan et al., 2004). actual number of years of life from birth. Physiologic age re- Fecal energy typically accounts for the largest proportion of gross energy lost from feedstuffs. Therefore, factors that

UNIQUE ASPECTS OF EQUINE NUTRITION 237 influence DM digestibility have a large impact on digestible Micronutrient Requirements energy yield. Mean crude fiber apparent digestibility tended Requirements for micronutrients in old horses remain (P = 0.10) to be lower (~ 5 percent) in a group (n = 7) of old relatively uninvestigated. Only two reports related to the ef- horses (26 ± 5 years of age) when compared to a small group fect of aging on micronutrient nutrition were identified as of (n = 5) of younger horses (2.3 ± 0.5 years of age) (Ralston this writing. Ralston et al. (1989) found decreased phospho- et al., 1989). Because the magnitude of this change in crude rus apparent digestibility (–4 ± 19 vs. 11 ± 6 percent) in old fiber apparent digestibility was similar to that of the young (26 ± 5 years of age) vs. younger (2.3 ± 0.5 years of age) horses used in the study following resection of left and right horses. Additionally, initial reports suggested vitamin C sta- colons, the authors suggested that aged horses have a re- tus may be different between young and old horses (Ralston duced absorptive and/or digestive function in the large in- et al., 1988), but more recent evidence does not support this testine (Ralston et al., 1989). This is in contrast to findings idea (Deaton et al., 2004). in humans and dogs that suggest gastrointestinal function, at least with regard to macronutrients, is well preserved with aging (Harper, 1998b; Russell, 2000). It is also likely in Feed Form some instances that age-related changes to teeth may impair Dental abnormalities, which are common in older horses a horse’s ability to masticate feed, subsequently decreasing (Paradis, 2002; Graham, 2002), can limit the ability to pre- digestibility in the remainder of the digestive tract. hend and chew feed, decrease the digestibility of nutrients, Another area of potential interest in old horses is the ef- and lead to substantial loss of body weight. Alterations in fect of caloric restriction on aging and age-related disease. the physical form of the ration can be beneficial for old Caloric restriction has been demonstrated to extend the life- horses with dental disease. A common approach is to feed span in a variety of species (Heilbronn and Ravussin, 2003). older horses processed, complete feeds. In one study, the Larson et al. (2003) reported that lifetime dietary restriction feeding of a complete feed containing extruded ingredients improved glucose tolerance and had a favorable effect on was more effective at maintaining the body weight of old disease and survival in dogs. horses with low body condition (condition score less than 3) Equine Cushing’s disease is a chronic progressive disease when compared to a more traditional ration consisting of a of the intermediate pituitary gland of older horses. This dis- grain mix and timothy-alfalfa hay (Ralston and Breuer, ease is discussed in detail elsewhere (McCue, 2002). Hyper- 1996). Other options include the feeding of ensiled forage glycemia and hyperinsulinemia are common findings in (haylage) or chopped hay (e.g., early cut alfalfa) or forage horses with equine Cushing’s disease (Garcia and Beech, cubes that have been soaked in water. Oil can be added to in- 1986). Therefore, providing calories from sources that do crease the energy density of the ration. not contribute substantial quantities of glucose to the blood stream (e.g., fiber) appears prudent. Conclusion The true effect of aging and age-related disease on nutri- Protein and Amino Acid Requirements ent requirements remains to be determined in horses. There The effect of aging and age-related disease on protein re- appears to be a large degree of variation in the way old quirements of horses is unknown. Ralston et al. (1989) re- horses respond to similar diets (Ralston and Breuer, 1996), ported lower crude protein apparent digestibility (67 ± 3 vs. suggesting chronological age alone is not sufficient to cate- 73 ± 3 percent) in aged horses (26 ± 5 years of age) when gorize horses relative to age-related changes in nutrient compared to younger horses (2.3 ± 0.5 years of age). requirements. Whether this finding reflects the old horse population in general and significantly impacts protein requirements of FEEDING MANAGEMENT OF HORSES IN COLD OR old horses remains to be determined. Supplemental lysine HOT WEATHER and threonine (0.25 percent on a DM basis or approximately 20.0 g/d and 0.2 percent of DM or 15 g/d, respectively) have Chapter 1 includes a discussion of the effects of climate been suggested to maintain muscle mass in old (22.4 ± 0.87 on heat production in horses and also describes factors that years) as well as younger horses (9.1 ± 0.29 years) under- affect upper critical temperature (UCT) and lower critical going light exercise (Graham-Thiers and Kronfeld, 2005). temperature (LCT) for horses. The UCT is the upper range Healthy humans appear to have a decreased protein require- of the thermoneutral zone and is the temperature above ment with aging. Millward et al. (1997) reported a 33 per- which evaporative heat loss must be increased to control cent reduction in protein metabolic demand and no signifi- body temperature. The LCT is the lowest temperature in the cant impairment in efficiency of protein utilization in thermoneutral zone and is the temperature below which healthy, mobile, elderly persons, suggesting a decline in pro- metabolic heat production must be increased to maintain tein requirements with aging. body temperature. For horses kept in environments outside of the thermoneutral zone, adjustments in nutrient require-

238 NUTRIENT REQUIREMENTS OF HORSES ments will occur and changes in feeding management may TABLE 12-1 Guidelines for Feeding Horses during Cold be necessary. Weathera 1. The lower critical temperature (LCT) for young horses can range from –11 to 0°C and for adult horses can be as low as –15°C in northern Feeding in Cold Weather continental climates. In more temperate climates, LCT was reported to Two studies with growing horses reared in cold, outdoor be 5°C. Specific horses may have higher or lower LCT. If cold weather persists at temperatures below LCT, then an increased provision of di- weather gave differing results concerning voluntary feed in- etary energy may become necessary. take (Cymbaluk and Christison, 1989a; Cymbaluk, 1990). 2. Growing horses may require an additional 1.3 percent digestible en- As temperatures fell below LCT, yearling horses in the first ergy (DE) for each degree below LCT plus the DE required for weight study were found to eat less, not more, feed and, therefore, gain (Cymbaluk, 1990). Adult horses should be given an additional 2.5 consumed less digestive energy (DE). Although decreases in percent DE for maintenance per degree below LCT (McBride et al., 1985). DE intakes were only 5.7 percent and 8.8 percent less at tem- 3. Hays should be provided free-choice to allow horses to eat to their en- peratures below –10° and below –20°C compared to above ergy demands. Use of digestible hays facilitates higher total intake –10°, weight gains were lower than expected (Cymbaluk and (Dulphy et al., 1997). Concentrate may need to be added to ensure ad- Christison, 1989a). In the second study, growing horses ate equate energy intake especially for growing, thin, worked, or aged 0.2 percent more feed per Celsius degree decrease in ambi- horses. If a concentrate is to be fed, the horse must be fully adapted to this feed. ent temperature below LCT (Cymbaluk, 1990). Based on 4. Additional mineral and vitamin supplementation does not appear to be this study, DE intakes for growing horses must be increased necessary during cold weather beyond the requirements needed for the by 1.3 percent per Celsius degree below LCT. By compari- specific production level of the horse. son, maintenance DE for adult horses must be increased 5. Water should be provided ad libitum and can be heated up to 20°C to 2.5 percent per Celsius degree below their LCT of –15°C maximize intake (Kristula and McDonnell, 1994). (McBride et al., 1985). The disparity between feeding rec- 6. Well-bedded and wind-protected shelter should be provided to mini- mize energy loss. ommendations for adults and growing horses is that the LCT aSOURCE: Modified from Cymbaluk and Christison (1990). for adults was based on maintenance only, and those for young horses was based on energy intakes for maintenance and gain. Young, thin, or aged mature horses are less cold- tolerant than mature horses. When cold weather occurs, diet 1995, 1999; McCutcheon and Geor, 1996). The primary changes for susceptible horses must be made much sooner electrolytes lost in sweat are sodium, potassium, and chlo- than for mature horses in good body condition. ride. The amount and type of electrolyte supplementation The overall conclusion from the preceding data is that depends on the extent of heat stress and the amount and du- cold weather creates an increased demand mainly for en- ration of physical stress that is imposed. At a minimum, ergy. Modified guidelines to those previously published for free-choice access to salt should be available to horses dur- feeding horses in cold weather are given in Table 12-1 ing hot weather (McCutcheon and Geor, 1996). General (Cymbaluk and Christison, 1990). Feeding good-quality hay guidelines for feeding horses during hot weather are given in free-choice may be the simplest way to supply additional Table 12-2. DE for most idle, adult horses during cold weather. The in- In hot weather conditions, the feeding program for idle fluence of diet composition and nutrient content on energy horses should be designed to minimize heat load. Although metabolism during cold weather is described in Chapter 1. high-fat diets may prove potentially useful in reducing heat In addition to diet, the effects of cold weather on non- load in hot weather (Kronfeld, 1996; Kronfeld et al., 1998), acclimated horses can be ameliorated through physical mod- few studies have critically examined the metabolic effects of ifications including housing or application of a rug or blan- high-fat diets on thermoregulation of idle horses in hot ket. Shelters, rugs or blankets, and shelters plus rugs or weather conditions. Under normal thermal conditions, blankets reduced heat loss during cold exposure by 9, 18, and horses fed high-fat diets reportedly had lower respiratory 26 percent, respectively (MacCormack and Bruce, 1991). exchange ratios than those fed high-carbohydrate diets (Pagan et al., 2002). Lower blood pH, higher blood glucose, a calculated reduction in urine volume, reduced feed and Feeding in Hot Weather water intake, and weight gain have also been reported Water intake is markedly increased (30–75 percent) by (Zeyner et al., 2002). Mathiason-Kochan et al. (2001) ob- both acute and chronic heat loads (Geor et al., 1996; Marlin served that horses fed a fat-supplemented diet (a concentrate et al., 2001). The high intake of water compensates for water with 10 percent fat of DM, fed in a 65:35 ratio with hay) had lost through rapid respiration and increased sweating rate higher sweat losses after a high-intensity standard exercise when conditions are hot and dry but not hot and humid (Mc- test (SET) but lower packed cell volumes than horses fed a Cutcheon et al., 1995). The increased sweating rate in hot high-hay diet (60 percent hay) or the basal diet with no conditions, especially when superimposed with exercise, re- added fat. The authors suggested this might reflect an in- sults in substantial electrolyte losses (McCutcheon et al., crease in extracellular fluid, but in the absence of plasma

UNIQUE ASPECTS OF EQUINE NUTRITION 239 TABLE 12-2 Guidelines for Feeding Horses during Hot codes for the sodium channel, a membrane protein involved Weather in the regulation of cellular sodium and potassium content. 1. The upper critical temperature (UCT) for horses is about 38°C for This ion channel facilitates movement of potassium into the foals and 25°C for adults, depending on duration of exposure to hot cell and outward movement of sodium. ambient temperatures. Climatic conditions of an area will determine the absolute value of the UCT of the horses living in those regions. 2. At ambient temperatures that exceed UCT, water should be supplied in Etiology and Genetic Basis a manner that allows voluntary intake by the horse. There appears to be no preference for iced water by horses exposed to warm ambient In normal muscle cells, an electrical gradient is estab- temperatures (McDonnell and Kristula, 1996). lished across the cell membrane as sodium is pumped out- 3. Although the benefit of feeding grain-based and fat-supplemented diets side of the cell and potassium into the cell. That electrical to horses in hot weather is unclear, these types of diets may be theoret- gradient is typically on the order of 85 millivolts (mV) and ically useful for horses. is maintained in part by the ability of the sodium channel to 4. Salt should be available to horses during hot weather (McCutcheon and Geor, 1996). restrict entry of sodium into the cell. As long as that gradi- 5. A shade, preferably that allows unimpeded air movement, may reduce ent is maintained, the cell is at rest and no muscle contrac- heating effects of direct sunlight. Coat clipping may help dissipate heat tion occurs. During excitation, a nerve impulse is received in horses with a long hair coat (Morgan et al., 2002). by the muscle cell that results in a conformational change of the sodium ion channel and the generation of an “action po- tential.” During this event, sodium rushes into the cell, protein data, the effect on body fluid distribution is difficult potassium rushes out, and the electrical gradient approaches to interpret. 0 mV. This action potential, in a coupled reaction, causes the Conflicting data have been reported on the impact that fat release of calcium from storage sites within the sarcoplas- may have on utilization of other nutrients (see Chapter 3; mic reticulum of the muscle cell, with movement of calcium Beynen and Hallebeek, 2002). Although soybean oil added ions to the area of the muscle fibrils actin and myosin. Cal- to provide dietary fat at 5–10.8 percent resulted in reduced cium binds to sites on myosin, and the muscle contracts and dry matter, fiber, and protein digestibility by horses (Worth remains contracted until the calcium is resequestered in the et al., 1987; Jansen et al., 2001), no effect of fat was found storage sites by the action of a calcium pump. on nutrient digestion coefficients derived by various meth- In the muscle cells of horses with the HYPP trait, regula- ods (Meyers et al., 1987; Bush et al., 2001). Others have tion of the movement of sodium and potassium ions via the found an increase in fiber utilization (Hughes et al., 1995; sodium channel is disturbed such that there is a constant Julen et al., 1995). Fat supplementation of diet did improve “back leakage” of sodium ions into the cell. As a conse- utilization of either natural or β-carotene or α-tocopherol by quence, there is repetitive depolarization of some muscle horses (Keinzle et al., 2003). More importantly, the stability cells. Under certain conditions, these repetitive contractions and effects of long-term storage of high-fat horse diets under become more severe and are clinically recognized as muscle high heat conditions have not been fully explored. fasiculations. During clinical episodes of HYPP, fasicula- tions are often first evident over the rib cage and flank areas, but may spread to other muscle groups. There can be pro- NUTRITIONAL MANAGEMENT OF SPECIFIC lapse (eversion) of the third eyelid and the horse may show DISEASE CONDITIONS signs similar to colic. In severe episodes, the contractions become tetanic; the horse may sit like a dog and later Hyperkalemic Periodic Paralysis become recumbent. Death due to respiratory failure is pos- Hyperkalemic periodic paralysis (HYPP) is a co-dominant sible. In horses that experience severe episodes, serum single autosomal gene disorder that appears to have originated potassium concentrations may increase from 3 to 4 mEq/L as a point mutation in the Quarter horse stallion Impressive to as much as 12 mEq/L or higher (Meyer et al., 1999). (Spier et al., 1994). The genetic nature of this condition has Recognition of such a marked increase in serum potassium been well documented and a highly reliable test based on concentration is useful in differentiating HYPP from other polymerase chain reaction (PCR) technology has been devel- muscle diseases. oped to identify horses with this condition (Meyer et al., 1999). The test was developed originally for a condition in Nutritional Management humans that is essentially the same genetic abnormality (Lehmann-Horn et al., 2002). To be affected, the horse must Treatment and management of HYPP aims to limit in- have inherited the defective gene from an affected parent de- creases in serum potassium concentration by one or a com- scended from Impressive. Affected horses are either het- bination of three methods: (1) limiting the dietary intake of erozygous (H/N) or homozygous (H/H) for HYPP. Horses potassium, (2) promoting entry of potassium into cells, or that are homozygous are more severely affected than those (3) eliminating excess extracellular potassium from the that are heterozygous (Carr et al., 1996). The gene in question body via the urine.

240 NUTRIENT REQUIREMENTS OF HORSES The most important management practice for HYPP- Exertional Rhabdomyolysis Syndromes positive horses is a restriction in potassium intake. Recent Exertional rhabdomyolysis (ER) in horses is a syndrome work has demonstrated that the risk of clinical episodes is of muscle pain and cramping associated with exercise. It can heightened when dietary potassium exceeds 1 percent of the be categorized into sporadic exertional rhabdomyolysis, in total diet (Reynolds, 1997; Reynolds et al., 1998a,b). When which horses have sporadic or infrequent episodes of mus- dietary potassium content is maintained below this 1 cle necrosis and pain associated with exercise, or chronic ex- percent threshold, HYPP episodes can often be controlled ertional rhabdomyolysis, in which affected horses have re- without other preventative measures. peated episodes (Valberg et al., 1999a). Two forms of The largest single source of potassium in a horse’s diet is chronic exertional rhabdomyolysis have been described: (1) forage (hay). Grains contain potassium, but are generally recurrent exertional rhabdomyolysis (RER), which com- less than 0.5 percent potassium. Forages may, on the other monly afflicts Thoroughbreds but also may affect other hand, contain in excess of 3 percent potassium. Forages vary breeds such as Standardbreds and Arabians; and (2) poly- widely in their potassium content by type, region of the saccharide storage myopathy (PSSM), which predominantly country, and even different areas within a single field. Fer- affects Quarter horses but also has been described in other tility level of the field, rainfall or irrigation, and stage of ma- breeds including Paints, European Warmbloods, Ap- turity all have an effect on the potassium content of forages. paloosas, Morgan horses, and draft breeds (Valberg et al. Higher fertility levels, increased moisture, and cutting hay at 1999a). In Thoroughbreds, RER has been identified as a her- an early stage of maturity all tend to increase the potassium itable defect in intracellular calcium regulation that leads to concentration of the forage (Minson, 1990). Given this wide muscle necrosis during exercise (MacLeay et al., 1999). variation in potassium content, even within forage types, Polysaccharide storage myopathy involves increased storage laboratory analysis is required for accurate estimation of of glycogen and abnormal polysaccharide in skeletal mus- potassium content. However, in general, grass forages tend cle. In both RER and PSSM, there is some evidence that a to have less potassium than legume forages. reduction in dietary starch and sugar and/or an increase in In view of the potassium concentrations in feeds, the use dietary fat are beneficial in the management of affected of grass hays or pastures such as Bermudagrass, prairie hay, horses (see McKenzie et al., 2003). or timothy instead of legume hays or pastures such as alfalfa seems prudent. If alfalfa must be included in the diet, then other preventative measures may be necessary. Also, the use Polysaccharide Storage Myopathy of cereal grains as a major portion of the diet will reduce the overall potassium content of the ration. In addition, grain in- Polysaccharide storage myopathy is characterized by take will stimulate insulin release that may facilitate the up- high concentrations of glycogen and glucose-6-phosphate in take of potassium by muscle cells. However, the inclusion of muscle and the accumulation of amylase-resistant, periodic commercially prepared concentrates that contain large acid Schiff (PAS)-positive inclusions in up to 30 percent of amounts of molasses, soybean meal, or dehydrated alfalfa type II muscle fibers (Valberg et al., 1992). Clinical signs in- should be monitored, as these feed ingredients may be rela- clude ER, exercise intolerance, muscle stiffness, back pain, tively high in potassium (> 2 percent). shifting lameness, gait changes, muscle atrophy, a camped- In cases where control of potassium intake is insufficient out stance, and colic-like signs. Detection of amylase- to manage episodic events, additional interventions may be resistant polysaccharide in muscle of horses with a history required. The uptake of potassium by the cells is enhanced of recurrent ER is considered diagnostic for PSSM. How- by a number of factors, including mild exercise, insulin re- ever, the accumulation of polysaccharide may be a gradual lease, and administration of other cations into the extracel- process. In a small group of Quarter horse foals with clini- lular fluid. Insulin concentrations can be increased by oral or cal and laboratory evidence of chronic, intermittent ER, intravenous (IV) glucose administration, or the feeding of polysaccharide accumulation in skeletal muscle was not ap- cereal grains high in starch. Cations such as sodium and parent until 2 years of age (De La Corte et al., 2002). calcium-administered IV promote the intracellular move- A glycogen storage disorder also has been described in ment of potassium in order to maintain electrical neutrality Warmblood horses (Hunt et al., 2005), draft horses and re- of the extracellular fluid (ECF). As a further preventive lated breeds, and Welsh ponies (Valentine et al., 1997, 2000, measure, a diuretic such as acetazolimide may be adminis- 2001a,b). In draft horses, this disorder has been termed tered under the supervision of a veterinarian. This drug in- equine polysaccharide storage myopathy (EPSM) (Valentine creases the excretion of potassium in urine. et al., 2001a). Clinical signs of polysaccharide myopathy in draft horses and related breeds include muscle soreness of the hindquar- ters and back, stiffness, muscle atrophy, and occasionally overt ER. In Belgian draft horses, PSSM may occur concur-

UNIQUE ASPECTS OF EQUINE NUTRITION 241 rently with “shivers,” a disorder characterized by muscle exercise and/or turnout, in addition to diet change, showed tremors and hindlimb hyperflexion that may progress to significant clinical improvement (Hunt et al., 2005). Quarter muscle atrophy, weakness, and recumbency (Firshman et horses with PSSM also were more likely to show improve- al., 2005). The results of one epidemiologic study indicated ment in the severity and frequency of ER when changes in that PSSM and shivers are common but unrelated disorders both diet and physical activity were instituted vs. a change of Belgian draft horses (Firshman et al., 2005). in diet only (Firshman et al., 2003). Nutritional Factors Pathogenesis There is evidence that diet modifies the clinical expres- The mechanisms underlying enhanced glycogen storage sion of PSSM (and EPSM). In clinical reports, the frequency in Quarter horses with PSSM have been partially elucidated. and severity of ER episodes were higher when PSSM- Unlike skeletal muscle glycogenoses in humans and other affected horses received little exercise and were fed energy species (DiMauro and Lamperti, 2001), excessive glycogen concentrates containing moderate amounts of starch and storage is not due to reduced capacity for glycogen utiliza- sugar such as straight grains or sweet feed mixes (Valentine tion. During controlled exercise protocols, net glycogen et al., 2001b; McKenzie et al., 2003). Conversely, controlled breakdown and accumulation of lactate in skeletal muscle laboratory experiments in Quarter horses with PSSM (middle gluteal m.) were similar in affected Quarter horses (Ribeiro et al., 2004) and uncontrolled clinical trials in and controls (Valberg et al., 1999a,b). Similarly, the activi- Quarter horses (Firshman et al., 2003), Warmblood horses ties of key glycolytic enzymes, measured in homogenates of (Hunt et al., 2005), and draft horses (Valentine et al., 2001a) muscle biopsies, did not differ between affected and control with evidence of muscle polysaccharide accumulation have horses (Valberg et al., 1998). Instead, excessive muscle shown that the feeding of a ration with restricted starch and glycogen storage may be related to enhanced insulin sensi- sugar content (on a total ration basis, < 8 percent DE from tivity and uptake of glucose into skeletal muscle. Glucose starch and sugar) and added fat (> 10 percent of total DE clearance following bolus intravenous administration of glu- from fat) resulted in clinical improvement of affected cose (0.5 g/kg BW) was 1.5 times faster in affected Quarter horses. horses when compared to healthy control horses, while glu- In one study, Quarter horse mares (n = 4) were fed cose concentrations after oral glucose administration were isocaloric diets ranging in DE from 21.2 percent (diet A), significantly lower (De La Corte et al., 1999a). Affected 14.8 percent (B), 8.4 percent (C), to 3.9 percent (D) for horses had lower resting insulin concentrations and lower starch, and 7.2 percent DE (diet A), 9.9 percent (B), to 12.7 insulin concentrations than controls after intravenous or oral percent DE (diet C and D) for fat (Ribeiro et al., 2004). The administration of glucose. Furthermore, intravenous insulin diets were fed for 6-week periods in a 4 × 4 Latin square de- resulted in a more profound hypoglycemia when compared sign. During the last 4 weeks of each period, the horses un- to controls (De La Corte et al., 1999a). Blood glucose and derwent 15–30 minutes of treadmill exercise (trotting). insulin concentrations were also lower in affected horses Blood samples for measurement of serum creatine kinase than in healthy controls after consumption of a meal of (CK) activity were taken 4 hours after each exercise session. sweet feed (De La Corte et al., 1999b), findings consistent The log of serum CK activity was significantly (P < 0.05) with enhanced glucose clearance and insulin sensitivity. The higher when horses were fed diets A, B, and C when com- strongest evidence of enhanced insulin sensitivity in PSSM pared to diet D. Postprandial glucose and insulin responses was provided by a more recent study that demonstrated a were lower in diet D when compared with diet A, while 2-fold higher rate of glucose clearance in affected vs. con- serum free fatty acid (FFA) concentrations (measured 4 trol horses during a euglycemic-hyperinsulinemic clamp hours after exercise) were consistently higher in diet A when (Annandale et al., 2004). compared to the other diets. However, muscle glycogen and glucose-6-phosphate concentrations and the percentage of Nutritional Management muscle fibers with abnormal polysaccharide accumulation did not differ among the diets (Ribeiro et al., 2004). Dietary recommendations (Firshman et al., 2003; Whereas there are reports that draft horses with PSSM McKenzie et al., 2003) for management of horses with can show clinical improvement with diet change alone PSSM include: (1) feeding a minimum of 1.5 percent of BW (Valentine et al., 2001b), studies in Quarter horses (Firsh- as forage per day, ideally a grass or oat hay as these forages man et al., 2003) and Warmbloods (Hunt et al., 2005) have have lower nonfiber carbohydrate content when compared demonstrated that both a change in diet and institution of to legumes; (2) removal of all concentrates containing grain daily exercise (including turnout) are necessary for a favor- and molasses from the ration; and (3) use of alternative en- able response. In a study of 65 Warmblood or Warmblood- ergy sources such as vegetable oil, rice bran, and/or non- cross horses with PSSM, only horses that received regular molassed beet pulp when DE requirements are higher than

242 NUTRIENT REQUIREMENTS OF HORSES that provided by forage alone. Clinical improvement of degree of ALD. It was predicted that 40 percent of these horses with PSSM may be dependent upon the addition of foals would need corrective hoof trimming, 8 percent would fat to the ration. It has been reported that signs of muscle need surgical correction, 3–5 percent would develop con- dysfunction can persist when affected horses are fed an all- tracted tendons, 6 percent would become wobblers, 5 per- forage ration with low starch and sugar content (< 10 per- cent would develop OC, and 10 percent would be unsold as cent DE) content, whereas clinical signs of muscle dysfunc- yearlings because of the bone abnormalities. Leibsle et al. tion abate when even a small amount of vegetable-source fat (2005) found that only 3 percent of newborn (average age 2 is added to the ration (McKenzie et al., 2003). There are days) Thoroughbred foals had “straight” carpal conforma- conflicting views on the amount of dietary fat required for tions compared to 55 percent with correct fetlocks. At 1 to clinical improvement of horses with PSSM. Valentine et al. 1.5 years of age, only 7 percent of the same foals were con- (2001b) reported that horses with ESSM showed greatest sidered straight at the carpus (knee), while 79 percent were improvement when fed a ration that provided, on a total diet straight at the fetlock. Since a considerable number of young basis, at least 20–25 percent of DE from fat. Other re- horses are born with less than perfectly aligned joints, sub- searchers have reported clinical improvement when affected sequent mismanagement of the dietary program and hus- horses were fed rations with only 10–15 percent of DE pro- bandry of the foal could potentially exacerbate any develop- vided by fat (Firshman et al., 2003; Ribeiro et al., 2004). As ing osteochondral problems. some horses with PSSM are overweight, the feeding of a Bone growth disorders in young horses have multifactor- high-oil diet is problematic without instigation of an exer- ial causes. Pool (1993) divided the causes of OC into those cise program. On balance, it appears that a reduction in di- that are idiopathic or acquired. Idiopathic causes are consti- etary starch and simple sugar is the most important dietary tutional and hereditary; acquired causes are associated with recommendation for horses with PSSM. When forage alone biomechanically induced trauma or nutritional, toxic, iatro- does not meet daily DE needs, a source of fat such as veg- genic, and other determinable causes. Thus, the collective etable oil (as much as 600 ml/d for a 500-kg horse), rice risks for bone growth disorders in a foal originate with breed bran (0.5–2 kg/d), or other sources of fat should be added to risk, the conformation of the foal inherited from its dam and the diet. For horses in heavy training, other feedstuffs such sire, its prenatal and postnatal diet, and the husbandry meth- as nonmolassed beet pulp may be needed to meet DE re- ods and housing practices used during the critical growth pe- quirements and ensure palatability of the diet. riod from birth to at least 2 years of age. Future studies to As mentioned, the implementation of a daily exercise elucidate the etiology and pathogenesis of DOD will con- regimen is also important for successful management of tinue to provide conflicting and nonedifying conclusions Quarter horses and Warmbloods with PSSM. A combination until all of these factors are controlled and all criteria used of a low-starch, high-fat diet and regular exercise may result to confirm the clinical and pathological diagnoses of DOD in clinical improvement via a decrease in muscle glycogen are standardized. The extent to which these criteria were storage (Firshman et al., 2003) and/or an increase in lipid controlled and standardized should be considered in the in- metabolism in muscle (Ribeiro et al., 2004). terpretations of conclusions in the studies described below. Developmental Orthopedic Disease Pathogenesis Developmental orthopedic disease (DOD) is a complex Developmental orthopedic diseases originate from abnor- of musculoskeletal abnormalities that can afflict growing malities of endochondral ossification in one or both of the horses. These conditions include angular limb deformities growing areas of bone, articular-epiphyseal cartilage com- (ALD, or “crooked-legged foals”), physitis, subchondral plex and the growth plates (physis) (Pool 1993; McIlwraith, bone cysts, osteochondrosis (OC), flexural limb deformities 2004). Osteochondrosis is the pathologic description of (“contracted tendons”), and cervical vertebral malformation bone diseases of young horses in which there is failure of or (“wobbler syndrome”) (Pool, 1993; McIlwraith, 2004). abnormal cartilage maturation. The abnormalities of joint Congenital contracted tendons are not considered part of the cartilage and subchondral bone in osteochondrosis dissecans DOD complex (Kidd and Barr, 2002) and will not be dis- (OCD) have progressed to cracks and fissures in the carti- cussed here, nor will cervical vertebral malformation. lage. If osteochondrotic cartilage loosens, bone chips or The incidence of DOD disorders (physitis and OC) sub- joint mice may occur within the joint or synovial space mitted to a North American veterinary hospital and in young (McIlwraith, 2004). Although OC and OCD are often used Irish Thoroughbreds was 68–81 percent (Gabel, 1986; interchangeably, the pathology associated with OCD is more O’Donohue et al., 1992). Of these foals, 11.3 percent re- advanced than that seen in OC. Clinical symptoms and quired treatment (O’Donohue et al., 1992). Conformational pathologies are different depending on the affected site and leg abnormalities in the neonate are high (Aldred, 1998; affected bone. A detailed review of the cellular pathogenesis Leibsle et al., 2005). Aldred (1998) reported that 80 percent of equine osteochondrosis can be found in Jeffcott and Hen- of Thoroughbred foals born in Australia annually have some son (1998) and some of the site specific modulators of the

UNIQUE ASPECTS OF EQUINE NUTRITION 243 physeal growth zones including dietary nutrients were re- (Mase, 1987; Firth and Hodge, 1997; Whitton, 1998) lead- viewed by Orth (1999). ing to carpal physitis or other forms of DOD. Osteochondrosis has been described as a dynamic bone The impact of genotype on osteochondrosis has been re- disorder that can develop or regress in specific joints de- ported in several studies. Based on a survey of 753 Swedish pending on the joint’s “window of susceptibility” (Pool, Standardbred trotters aged 6–21 months, 14.3 percent had 1987; Dik et al., 1999; Barneveld and van Weeren, 1999). In tibiotarsal OC while 11.8 percent had fetlock joint involve- 1987, Pool suggested that the pathologic insult to a suscep- ment (Grondahl and Dolvik, 1993). The incidence of fet- tible bone likely was of short duration and occurred ran- lock, hock, and stifle OC ranged from 17, 6, and 3 percent domly during the period of joint vulnerability. This hypoth- and 24, 6, and 11 percent, respectively, in nonlame and clin- esis appears to be supported by subsequent studies. Mild to ically lame Swedish Warmblood horses (Beneus, 2005). Ra- moderate radiographic abnormalities were observed in the diographic evidence of OC was found in 16.6 percent of 350 intermediate ridge of the distal tibia in 67.4 percent of 1- Maremmano Warmblood horses with a heritability index of month-old Dutch Warmblood foals (Dik, 1999; Dik et al., 0.14, which increased with inbreeding (Pieramati et al., 1999; van Weeren et al., 2003), but tended to regress over 2003). These authors predicted that through genetic selec- time so that at 11 months of age, only 18.4 percent of hocks tion, OC in their studied population could be reduced from were still abnormal. Stifle abnormalities occurred between 16 percent to 2 percent within five generations. 3–4 months of age but reverted to normal by 8 months of In North America, the breeds with the highest incidence age. Similarly, Sondergaard (2003) observed an age-related of DOD were Quarter horses, Thoroughbreds, Arabians, and decrease in radiographic OCD from weaning through 2 Paints (Wagner, 1986), while Standardbred followed by years. Although most lesions were temporary, the “age of no Thoroughbred horses were at highest risk of OC (Mo- return” when regression was less likely to occur in the hock hammed, 1990). Ponies and draft horses have been sug- was after 5 months of age and for the stifle was after 8–12 gested to have a low incidence of osteochondrotic bone dis- months of age (Dik, 1999; Dik et al., 1999). The important orders (Stromberg, 1979). In a veterinary hospital, only 5 nutritional conclusion from these observations is that dietary percent of the admitted draft horse population had OCD mismanagement preceding and during these critical ages and/or subchondral bone cysts (Riley et al., 1998). The may tip the balance from regression to progression of sub- heavy breeds most often presented in the latter study were clinically abnormal cartilage and bone to clinical lesions. Clydesdale and Percheron horses. Hence, a balanced and appropriately managed diet is neces- Foals at risk for osteochondrosis were described as those sary prior to and at the time of weaning. that are the most rapidly growing foals in the group (Turner and Fretz, 1977; Stromberg, 1979; Thompson et al., 1988a,b), which is consistent to observations in other species (Olsson, Genetics and Growth Rate 1978; Stromberg and Rejno, 1978; Stromberg, 1979). Some The genetic growth potential of the foal, including its ambiguity between the association of weight gain with DOD conformational traits and growth, are governed by the geno- has been raised (McIlwraith, 2004), and this uncertainty is type of the dam and sire (Saastamoinen, 1990; Preisinger et supported by the conflicting data presented in studies exam- al., 1991; Árnason and Bjarnason, 1994; Koenen et al., ining these relationships. Foals affected with hock OC 1995; Molina et al., 1999; Zechner et al., 2001; Leibsle et tended to have heavier birth weights, had higher average al., 2005). Skeletal dimensions and conformation were mod- daily gain (ADG), and were heavier at 1.5 years of age, but erately to highly heritable traits in Andalusian and Lipiz- those with palmar/plantar osteochondral fragments tended zaner horses (Molina et al., 1999; Zechner et al., 2001) and to weigh less than nonaffected foals (Sandgren, 1993). Foals Trakehner foals (Preisinger et al., 1991). Associations be- with stifle OC were significantly taller at the withers and tween parent and progeny were found for carpal but not fet- had 7–20 percent higher weight gains only at 3 and 5 months lock conformation (Leibsle et al., 2005). These authors also of age; there was no relationship between rates of weight reported a significant relationship between heavier birth gain and OC in the hock joint (van Weeren et al., 1999). The weights and an offset carpal conformation (P < 0.01) and average incidence of DOD in Thoroughbred foals evaluated fetlock inward deviation at 46 days (P < 0.005), effects that between 4 through 18 months of age was 16.1 percent persisted beyond 1 year of age (Leibsle et al., 2005). Foals (range 12.9–28.8 percent) and the highest incidence was with hock OC and palmar/plantar osteochondral fragments recorded at 4 months of age (Jelan et al., 1996). Body tended to have outwardly rotated limb axes and periodically weights were not statistically different between affected and had a more upright pastern (Sandberg, 1993). The high inci- nonaffected foals, although the authors noted that affected dence of conformational imperfections in foals (Leibsle et foals were generally heavier. Based on farm data, OCD- al., 2005), coupled with the relative immaturity of the radio- affected and normal Thoroughbred or Hanoverian foals did carpal physis at birth (Mase, 1987), and/or a high body mass not differ in body weight (Pagan, 2003; Vervuert et al., could exacerbate abnormal biomechanical pressure, asym- 2003). The total incidence of hock and fetlock osteochon- metrical growth, or direct trauma occurring at the physis drotic lesions in the latter study was 31.5 percent. Foals in

244 NUTRIENT REQUIREMENTS OF HORSES controlled studies fed excess energy or starch did not differ Thoroughbreds monitored from birth through 2 years oc- in final body weights or average daily gain, although curred post-weaning in early winter and gradually resolved dyschondroplasia was prevalent in one study (Savage et al., over the next year (O’Donohue et al., 1992). Seasonal fluc- 1993a) but not the other (Ott et al., 2005). tuations in DOD were also evident in yearlings fed high That genotype affects the rate of weight gain is evident starch (SS) or high fat-fiber (FF) diets (Hoffman et al., from the wide range of weight gains of various breeds of 1999). The most severe clinical physitis in suckling foals oc- horses (see Chapter 1), but certain lines of horses within curred over 2 months in late summer and autumn, and were breeds are also recognized to have different body dimen- not influenced by the foal’s growth rate or sex (Finkler- sions (Zechner et al., 2001). A highly positive correlation Schade et al., 1999; Gee et al., 2005b). However, in other (0.97) was found between body weight and growth rate at 12 studies the seasonal clinical observations were coincident months in Finnhorses indicating that selection for rapid with changes in serum bone markers, including osteocalcin, growth rates is possible in horses (Saastamoinen, 1990). The carboxypropeptide of type I collagen and type III collagen heritability for body weight from birth to 2 years of age was propeptide, and with average daily gain (Price et al., 1997, 0.22–0.88 (SE = 0.46 to 0.87); the overall heritability from 2001). The production of sex hormones may also stimulate birth to 48 months was 0.86 ± 0.32 (Saastamoinen, 1990). growth spurts. Weight gains increased abruptly in 14-month- The variance in growth rates exceeded variance in absolute old Thoroughbred fillies concurrent with a pubertal spike in body measurements. Variation in absolute body weight progesterone secretion (Nogueira et al., 1997). ranged from 7.3–14.9 percent and from 2.4–4.6 percent for Thus, sustained modest growth rates may be preferred for withers height. Variance in ADG in the age categories from young horses to minimize some DOD-like conditions, espe- birth–6 months, 6–12, 12–24, 24–36, 36–48, and 0–48 cially prior to the earliest window of susceptibility for spe- months was 10.9, 26.8, 24.1, 64, 45.3, and 7.9 percent, re- cific joints. Supplying creep feed to suckling foals at 2–3 spectively. The calculated variances in biweekly ADG for months of age has been suggested as a method to maintain weanlings fed a high-forage diet (70 percent alfalfa) in lim- growth during the suckling period and to minimize the im- ited amounts or free-choice, or a high-concentrate diet (34.7 mediate post-weaning weight loss seen in foals (Coleman et percent alfalfa) fed free-choice were 7.8, 14.2, and 17 per- al., 1999; Peterson et al., 2003). Although creep feeding did cent, respectively, indicating a more fluctuating weight gain not entirely prevent weight loss post-weaning, creep-fed with ad libitum feeding (Cymbaluk, 1989). Thus, rate and foals were perceived to be less stressed than noncreep-fed amplitude of weight gain are not only affected by diet but by foals just after weaning (Coleman et al., 1999). method of feeding, which is further confounded by heri- tability of gain. Dietary Nutrients and Bone Growth Disorders Fluctuating growth rate may be a precursor to DOD (Barneveld and van Weeren, 1999), yet fluctuating biweekly The potential effect of dietary nutrient intake on bone weight gains are evident even in normal Thoroughbred foals growth in foals has been reviewed by Jeffcott and Savage between birth and 1 year of age (Thompson, 1995). Al- (1996) and Harris et al. (2005). Documented evidence has though erratic weight gains were more prevalent in free- confirmed that horses kept under pratical management situ- choice than in limit-fed foals (Cymbaluk, 1989), it was un- ations are often fed diets that may not be adequately de- clear whether this alone would contribute a sufficient signed to meet the predicted nutrient requirements (Knight biomechanical insult during the critical window of suscepti- et al., 1985; Hacklander et al., 1996; Finkler-Schade et al., bility to alter endochondral ossification. Other management 1999; Gibbs and Cohen, 2001; Paragon et al., 2003). The conditions that have been reported to result in nonuniform most common nutrient imbalances identified included ex- growth rates are dietary stress (Hintz et al., 1976), environ- cess energy intake, and excesses or deficiencies in protein, mental stress (Rooney, 1984; Cymbaluk and Christison, macromineral, and trace mineral content, as well as calcium/ 1989a; Cymbaluk, 1990), season (Jelan et al., 1996; Hoff- phosphorus imbalances. Feeding programs on Thorough- man et al., 1999), hormonal maturation (Noguiera et al., bred and Quarter horse breeding farms were well managed 1997), and unidentified factors (Jelan et al., 1996). Con- on about half of the farms, but the remaining farms were felt tracted tendons and/or physitis in young horses followed a likely to be using unbalanced diets (Gibbs and Cohen, suspected compensatory gain following a switch from nutri- 2001). Although the role of diet in foal growth cannot be tionally marginal to abundant diets (Hintz et al., 1976), fol- disputed, the complexity of the relationships among nutri- lowing environmental stress either as extreme cold (Cym- ents and their interactions in abnormal bone growth are not baluk and Christison, 1989a) or prolonged inclement yet fully elucidated. It is, however, important to recognize weather (Rooney, 1984). that when formulating practical diets, nutrient concentra- Seasonal growth spurts were associated with an increased tions can deviate from NRC recommendations without caus- occurrence of bone abnormalities in young horses (O’Dono- ing abnormal growth in young horses (Ott and Kivipelto, hue et al., 1992; Hoffman et al., 1999). The peak incidence 2002). However, all variances in dietary nutrient concentra- (4.1 percent) of clinical musculoskeletal conditions in young tions in horse diets should be evaluated to ensure that the

UNIQUE ASPECTS OF EQUINE NUTRITION 245 nutrient concentration falls into an accepted normal range fed a fat-fiber (FF) concentrate. However, Ropp et al. (2003) for the class of horse for which the diet is intended. compared the insulin-glucose responses of weanling Quar- ter horses fed a more typical concentrate containing 33.9 percent nonfiber carbohydrates vs. a concentrate containing Energy, Protein, and Fat Intake 10 percent fat and 24 percent nonfiber carbohydrate for 75 Excessive energy intake has received considerable inter- days and found no treatment by time interactions on day 0 est in the etiology of equine DOD in part based on the hy- or 60 for glucose and no interaction effect for insulin on day pothesis that excessive amounts of nonfiber carbohydrates 0 or 30. There was no change in growth hormone secretion may contribute to hormonal abnormalities in foals, specifi- or plasma insulin-like growth factor I (IGF-I) concentra- cally through modified insulin responses (Kronfeld et al., tions, and only a minor glucose sparing effect. Ott et al. 1990). High-energy diets were felt to cause OCD irrespec- (2005) fed weanling horses either a medium- (2.9 starch/kg tive of feed composition (Stromberg, 1979). The data of BW) or high- (6.5 starch/kg BW) starch diet without induc- Savage et al. (1993a), who fed weanling foals diet contain- ing changes in bone mineral content or creating new osteo- ing 29 percent more energy than recommended by NRC chondrotic bone lesions. During the study, the incidence of (1989), supported this hypothesis. Histological dyschon- preexisting radiographic OCD bone lesions decreased about droplastic changes in the stifle, hock, and fetlock joints were 29 percent irrespective of whether the foals were fed hay observed in all foals fed high-energy diets (29 percent above plus a concentrate containing either 17 or 37.5 percent control) created by adding 0.25 kg of corn oil to a basal diet starch. These data confirm that foals fed some types of of 13 percent oaten chaff and 77 percent rice-based pellets grain-based concentrates can have altered insulin responses. (Savage et al., 1993a). The source of the additional dietary Unlike growing horses, ponies were significantly more hy- energy in the high-energy diet in this study was derived from perglycemic and hyperinsulinemic when fed a high-fat (11.1 corn oil, but all diets were based on rice concentrate, a feed percent) diet than when fed a high-sugar diet (Schmidt et al., that is high in starch, and the foals were partially confined. 2001). The role of insulin resistance in developmental bone The foals in this study had similar net gains in skeletal and disorders is unclear and conflicts with the observation that weight growth to control foals (Savage et al., 1993c); con- ponies are more insulin resistant than horses (Rijnen and van sequently, the dyschondroplastic bone lesions may have der Kolk, 2003), yet have an apparently low incidence of been induced through a hormonal alteration, although this DOD or osteochondrosis (Stromberg, 1979). was not verified. The suspicion that insulin resistance may contribute to Dietary composition, in addition to absolute nutrient con- developmental bone disorders (Kronfeld et al., 1990) has tent, of foal diets has also been scrutinized as a possible in- stimulated interest in finding alternative energy sources to fluence on the incidence of DOD. The assumption that rapid nonstructural carbohydrates. Fat, in limited amounts (< 11 growth obtained through use of grain-based, high nonfiber percent), was added to highly fibrous constituents (oat straw, carbohydrates has contributed to a higher incidence of DOD soybean hulls–FF) (Hoffman et al., 1999; Staniar, 2002) or has led to examination of dietary effects on the insulin- to concentrate-based supplements (Ropp et al., 2003) to glucose axis and the role of insulin sensitivity in foals. The lower the nonfiber carbohydrate while maintaining energy plasma insulin-glucose response to feeding a diet of 50:50 content of the diet. Carpal physitis scores and joint effusion textured grain:alfalfa-grass hay was compared in OCD- did not differ between FF and SS foals, but hind fetlock affected to normal young horses (Ralston, 1996). Although physitis was higher (P < 0.5) for the SS group at 8 and 12 glucose:insulin ratios did not differ, plasma insulin concen- months (Hoffman et al., 1999). Foals in the FF group had tration was 29–79 percent higher in OCD-affected horses higher (P < 0.05) scores for angular limb deformities at than controls. Pagan (2003) correlated the post-meal feeding 1 month, 8 months, and 10 months of age. (2 h) plasma insulin concentrations of 218 10-month-old The conflicting data obtained on the effects of energy in- foals to surgical OCD lesions present at the time of blood take on the incidence of DOD have in part arisen through sampling or which developed over the next 6–10 months and different methods of feeding. Regulated feeding of concen- observed that the 27 OCD-affected foals had higher plasma trate mixes has not resulted in increased bone abnormalities glucose and insulin concentrations but no difference in the (Ott and Asquith, 1989; Reynolds et al., 1992; Ott et al., glucose:insulin ratio compared to normal cohorts. Yearling 2005). Quarter horse weanlings fed a diet of 25 percent Thoroughbreds fed a 72 percent hydrolysable carbohydrate Bermudagrass hay plus 75 percent concentrate (given twice diet had a significantly higher glycemic (P < 0.043) and in- daily) from 6 to 12 months of age gained weight at 0.65 sulinemic (P < 0.031) response than foals fed a high fat-fiber kg/d, and all subchondral and cystic lesions, except for the concentrate (Staniar, 2002). That high nonfiber carbohy- cystic carpal lesions, identified radiographically at 6 months drate concentrates modify the insulin responsiveness was had regressed by 1 year of age (Reynolds et al., 1992). Un- shown by Treiber et al. (2005), who observed a 37 percent regulated feeding of any diet, whether high in fiber or not, reduction in insulin sensitivity in weanlings fed a 49 percent has led to transient physitis and flexural limb deformities nonfiber carbohydrate (SS) concentrate compared to foals (Cymbaluk and Christison, 1989b). In addition to the effect

246 NUTRIENT REQUIREMENTS OF HORSES on the somatotrophic axis, the use of FF concentrates (Hoff- epidemiological study, which found a higher incidence of man et al., 1999) requires further study to verify its useful- clinically diagnosed disorders in foals fed low-copper diets ness in preventing developmental bone disease. (Knight et al., 1985). Although copper was implicated in the High-protein diets do not appear to influence the occur- clinical conditions, foals on farms with a higher incidence rence of DOD. Although feeding excessive protein, specifi- of OC and physitis also fed diets low in calcium and high cally soybean meal, has previously been proposed as a cause in phosphorus. Subsequently, controlled studies on DOD of flexural limb deformities in growing horses (Fackelman, (Knight et al., 1990; Hurtig et al., 1993; Pearce et al., 1980), others have suggested minimal to no effect of high 1998a,b,c; Grace et al., 2002; van Weeren et al., 2003; Gee dietary protein intake on DOD occurrence (Stromberg, et al., 2005a,b, 2006) have examined the role of copper in 1979; Boren et al., 1987; Savage et al., 1993a). Addition of foal bone development with contradictory outcomes. Knight 0.2 percent lysine or 0.2 percent lysine and 0.1 percent thre- et al. (1990) evaluated bone development in 21 foals whose onine to diets of yearling horses had no effect on bone min- dams were either fed 13 (control) or 32 mg Cu/kg BW (sup- eral content or skeletal growth rates (Graham et al., 1994). plemented) during the last 3–6 months of gestation and dur- ing lactation. Foals received a creep ration containing 15 mg Cu/kg concentrate (control) or 55 mg Cu/kg concentrate Mineral Intake (supplemented). Postmortem findings of 90-day-old foals The effect of excesses and deficiencies of minerals on revealed predominantly physeal abnormalities that were not foal growth has been reviewed in Chapter 5. Macrominerals, different between groups. Equal numbers of physeal lesions especially calcium (CA), phosphorus (P), and magnesium, occurred in the forelimbs of 180-day-old foals although con- form the mineral complex in bone. Bone mineral density, trol foals had more physeal and articular-epiphyseal lesions ash, and calcium content in subchondral and trabecular bone in the hindlimbs. Notably, at both 90 and 180 days of age, increased in horses up to 4 years old (van der Harst et al., one individual in the control group accounted for 59 percent 2005), suggesting that an inadequate or an imbalanced or 35 percent of the bone lesions, respectively. Hurtig et al. macromineral intake could affect bone development and (1993) fed 18 foals, including 2 with preexisting DOD, diets strength up to this age. Dietary mineral content may affect containing either 8 or 25 mg Cu/kg feed. A higher incidence the severity of OCD as shown by Firth et al. (1999), who ob- of cartilaginous flaps and/or thinning was observed for foals served comparatively lower bone mineral density in the third fed the diet containing 8 mg Cu/kg feed. No significant dif- carpal bone and the distal radial bone of young horses with ference was observed between treatment groups in the tibial severe signs of OCD. Imbalances in dietary calcium and or radial growth plates, calcified cartilage area, metaphyseal phosphorus also increased the risk of DOD. Weanling bone formation, or epiphyseal bone formation rates or in the Warmblood foals fed diets with either a normal Ca:P ratio biochemical properties of the bone or growth plate cartilage. (2.5:1) or a low Ca:P ratio (1:2.5) had normal weight gains, Pearce et al. (1998a,b,c) compared feeding supplemental but all foals developed physitis, synovial distension, and, ex- copper to pregnant mares (0.5 mg/kg BW or 28 mg Cu/kg cept for one foal, all others developed OCD in two or more diet) to a control group grazing pasture containing 4.4–8.6 joints (Staun et al., 1989). Savage et al. (1993b) observed mg Cu/kg. Foals born to these mares were randomly allo- that weaned foals fed a high-calcium diet (1.95 percent) had cated to either a copper-supplemented or a copper-control a similar number (33 percent) of histological dyschon- group. Copper-supplemented foals received 0.2 mg Cu/kg droplastic lesions as foals (17 percent) fed a control diet with BW from 21 to 49 days of age and 0.5 mg Cu/kg BW to 150 a Ca:P ratio of 1.3:1. A companion study in which weaned days of age. Only those foals whose dams were given sup- foals were fed a diet containing adequate calcium and excess plemental copper in the latter part of pregnancy had a lower phosphorus (1.7 percent) whose calcium:phosphorus ratio incidence of OC (Pearce et al., 1998c). The incidence of was imbalanced resulted in an 83 percent incidence of histo- bone and cartilage lesions was low in all foals irrespective of logical dyschondroplasia of the shoulder, hock, and/or inter- copper intake by dam or foal. Providing the foals with sup- vertebral joints (Savage et al., 1993c). Joint lesions were plemental copper (0.5 mg/kg BW) from 1.5–5 months of attributed to a nutritional secondary hyperparathyroidism in- age did not further eliminate bone or cartilage lesions duced by a Ca:P imbalance. These data support the need for (Pearce et al., 1998c). Subsequently, Grace et al. (2002) sup- an adequate macromineral intake and an acceptable Ca:P plemented yearling horses on pasture (7.9 mg Cu/kg DM) ratio during postnatal growth, but they also indicate that even with 130 mg copper daily so that copper-supplemented when macrominerals are supplied in adequate amounts, yearlings consumed a total of 186 mg Cu/d compared to 56 some foals may develop bone abnormalities. mg/d for controls. Neither weight gain nor incidence of Dietary micromineral content, particularly copper physitis differed between copper-supplemented and control through lysyl oxidase, has been shown necessary for forma- yearlings. Gee et al. (2006) administered injectable copper tion and repair of collagen, the main component of bone ma- (calcium copper edentate) to pregnant mares starting at trix. Copper (Cu) was first linked to OC and physitis in an about 7 months through parturition and observed no differ-

UNIQUE ASPECTS OF EQUINE NUTRITION 247 ence in osteochondral abnormalities between foals born to Vitamins the treated and untreated mares. All osteochondral lesions The effect of deficient and excessive intake of vitamins were considered minor and there were no differences in foal has been described in Chapter 6. The fat-soluble vitamins A or dam hepatic copper concentrations. The authors con- and D have been implicated in developmental abnormalities cluded that injectable copper was an unsuitable method of of the growth plate. Feeding vitamin A in amounts 1,000- copper supplementation and did not confer the protective ef- fold greater than control (12 µg/kg BW) produced histolog- fect against the development of osteochondrotic bone le- ical osteochondrotic lesions in growth plates of growing sions observed in foals born to dams given oral copper three ponies (Donoghue, 1980). Deficiencies of vitamin D can times weekly (Pearce et al., 1998c). lead to poorly mineralized bone but excesses also have been Hepatic copper decay in neonatal foals followed a pattern shown to result in weakened, porous bone. Unexpectedly, of rapid decline in concentration from birth to weaning (Gee serum vitamin 1,25 (OH)2 D and parathyroid hormone con- et al., 2000; van Weeren et al., 2003). Two distinctive pat- centrations were higher in osteochondrotic foals than those terns of hepatic copper decay were observed; a normal and without or with few lesions and, perhaps, indicate that higher an accumulator pattern (Gee et al., 2000). Neonatal hepatic hormone levels are needed to maintain plasma calcium copper concentration (374 mg/kg DM liver) in normal foals concentration in this condition (Sloet van Oldruitenborgh- declined to adult values (21 mg/kg DM liver) by 160 days of Oosterbaan et al., 1999). age. Accumulator foals had a much slower rate of hepatic copper decay. At weaning, liver copper concentrations were still high (162 mg/kg DM liver). Although hepatic liver cop- Exercise and Training per concentrations and OCD status in foals were not corre- lated (van Weeren et al., 2003), a higher hepatic copper sta- Weight bearing and exercise have been shown to posi- tus at birth appeared to promote the regression of OCD tively affect bone turnover and remodeling (Lanyon, 1992) lesions present in the stifle at 11 months of age but not at 5 and may also act as a stimulus for collagen development in months of age. Van Weeren et al. (2003) proposed that cop- subchondral bone of horses (Brama et al., 2002). In most of per deficiency may not initiate OC lesions but rather may the Thoroughbred and Quarter horse breeding farms sur- stimulate the repair mechanism in abnormal cartilage. The veyed in Texas, young horses were kept in semiconfinement collective conclusions of copper studies in foals support the and received free exercise (Gibbs and Cohen, 2001). Volun- following: (1) copper supplementation of the pregnant dam, tary exercise (foals kept on pasture) tended to protect the ar- not the weanling foal, may have reduced incidence of DOD ticular cartilage from development of OC lesions compared in foals; (2) experimental copper deficiency in foals pro- to complete confinement in 5-month-old Dutch Warmblood duced inconsistent cartilage pathology, which may differ to foals (Barneveld and van Weeren, 1999). Benefits in bone that of clinical OC; and (3) copper deficiency may not initi- mineral content of the third metacarpal bone were also re- ate OC, but supplemental copper may be beneficial for OC- ported for weanling Arabians and Quarter horses given vol- affected foals by promoting repair of developing osteochon- untary (pasture) or enforced exercise (82 m/d, 5 d/wk) (Bell dral lesions. et al., 2001; Hiney et al., 2004). Exercise produced site- Dietary trace mineral supplementation of diets for foals specific increases in calcium and collagen cross-links in the did not dramatically change the incidence of bone abnormal- subchondral bone of 5-month-old foals (Brama et al., 2001, ities in foals fed diets marginally adequate in trace minerals. 2002) and increased bone mineral density by 5–8 percent in The addition of a trace mineral and/or calcium mixture to a 2-year-old Thoroughbred fillies compared to idle controls, concentrate mix fed with a Bermudagrass hay containing 7 suggesting a beneficial mechanical effect of exercise (Jack- mg Cu/kg and 57 mg Zinc (Zn)/kg to yearling horses had no son et al., 2003). In contrast, bone mineral density did not effect on feed intake (P < 0.1) but increased bone mineral differ whether foals were kept in box stalls, boxed and exer- content of the third metacarpal bone only when the basal diet cised, or on pasture for 5 months then turned out for volun- was supplemented to provide 11 mg Cu/kg and 69 mg Zn/kg tary exercise on pasture for an added 6 months (Firth et al., (Ott and Asquith, 1989). A subsequent study in which a basal 1999). Sondergaard (2003) observed that group-housed diet, marginal in calcium (0.36 percent) and phosphorus growing horses were more active than foals housed alone, (0.29 percent), but which contained 11 mg Cu/kg and 40 mg but the increased voluntary activity did not influence the in- Zn/kg, was compared to the same diet supplemented to sup- cidence of radiographic OCD. ply the following mineral concentrations: calcium (0.53 per- Intensive exercise may also cause negative effects. En- cent), phosphorus (0.38 percent), copper (14 mg/kg), and forced exercise of 2-month-old foals for 12 months reduced zinc (45 mg/kg). None of the yearlings showed any clinical the number of thyroid C cells required for calcitonin secre- abnormalities in either study, and there was no effect on bone tion involved in calcium homeostasis and also produced a mineral content of yearlings fed the diets for 112 days. trend to lowered bone mineral density of the hind cannon bone (Ueki et al., 2003). Box-stalled foals required to do

248 NUTRIENT REQUIREMENTS OF HORSES gallop sprints up to 5 months of age, then turned out to pas- • Voluntary exercise may be beneficial in reducing DOD ture until 11 months of age, had a reduced glycosaminogly- compared to confinement. Enforced exercise may benefit can content and hypermetabolic chondrocytes in articular bone mineral content but may negatively affect chondrocytic cartilage compared to unexercised and pastured foals, sug- metabolism. gesting that the enforced exercise regimen reduced the vital- ity of the chondrocyte (Barneveld et al., 1999; van den Practical nutritional management to prevent bone growth Hoogen et al., 1999). A positive effect, however, of enforced disorders was discussed by Lewis (1995). Although, the re- exercise was an enhancement in bone mineral density com- search data cited by this author are only current to 1995, pared to foals given voluntary exercise (pasture) and sus- many of the feeding management suggestions are still valid. tained confinement. Laminitis Summary of Studies on Developmental Orthopedic Laminitis is a systemic disease that manifests in the foot Diseases in Foals and results in significant pain and lameness. The junction The following conclusions can be inferred about foal de- between dermal and epidermal laminae serves to attach the velopmental bone disorders based on current information: distal phalanx to the hoof wall. Failure of the attachment be- tween the dermo-epidermal junction is the signature lesion • The causes of DOD are numerous and likely interrelated. of laminitis (Pollitt et al., 2003). The progression of lamini- • The incidence of DOD can be as low as 1 foal in 20 to tis can be categorized into four phases: developmental, as high as 1 foal in 3. acute, subacute, and chronic. Hood (1999a) defines the four • Osteochondral abnormalities were observed early in phases as follows. The developmental phase is the period life (1 month of age) but most lesions regress. Joints appear between the initial causative insult and the first appearance to have different windows of susceptibility after which re- of lameness and lasts an average of 40 hours (range 24–60). gression of lesions may be less likely to occur. The “age of The acute phase follows the developmental phase and takes no return” was felt to occur about 5 months of age for the one of two courses: continuation for 72 hours without phys- hock and 8–12 months for the stifle. ical or radiographic collapse or termination abruptly upon • Genotype affects growth rate and likely impact the in- occurrence of digital collapse (i.e., rotation or sinking of the cidence of DOD. Weight was highly heritable but rate of gain distal phalanx). The subacute phase follows the acute phase may or may not be directly related to the incidence of DOD. in the absence of physical or radiographic collapse, lasts • The normal variability seen in foal weight gain up to 1 from 8–12 weeks, and is considered a period of recovery year of age was increased when diets were fed ad libitum, ir- from the damage done during developmental and acute respective of composition (either high concentrate or high phases. The terms chronic laminitis and founder are fre- forage). An irregular growth rate may be a factor in the oc- quently used synonymously and are reserved for the horse currence of DOD and can be created through dietary and en- having mechanical collapse of the foot. Thus, any horse with vironmental stresses, seasonal and hormonal changes, and radiographic or physical evidence of digital collapse is cate- unidentified factors. gorically considered to have chronic laminitis, regardless of • Creep feeding may help smooth the growth pattern of the duration of the disease. Specific clinical features associ- foals in the transition from suckling through weaning. ated with acute and chronic laminitis have been discussed in • Practical diets fed to foals and broodmares may or may detail (Herthel and Hood, 1999; Swanson, 1999). not be balanced in the critical nutrients—energy, protein, Laminitis is considered a major disease of the horse due macrominerals, and trace minerals—required for bone to the associated pain, lameness, and potential debilitation. growth. There are limited data on the prevalence of laminitis in • Diet composition can affect hormonal responses. equids. Summary data from a survey involving 1,178 horse Specifically, concentrates high in nonfiber carbohydrates operations, totaling 28,026 horses, estimated that 13 percent have resulted in higher insulin-glucose responses to feeding of the operations had one or more horses with laminitis over and lower insulin sensitivity when compared to high-fat a 12-month period, and the overall incidence of laminitis (> 10 percent) and fiber concentrates. However, the source was 2.1 ± 0.3 percent (USDA, 2000). A slightly higher inci- of energy in the concentrate does not appear to affect the in- dence (7.1 percent) was reported in a survey involving cidence of clinical osteochondral abnormalities. 113,000 horses in the United Kingdom (Hinckley and Hen- • Feeding excess protein does not appear to affect DOD. derson, 1996). The incidence of laminitis in geriatric horses • Imbalances in calcium and phosphorus (Ca:P ratio < 1) (> 20 years of age) was 6.4 percent, according to a survey can produce dyschondroplasia. involving 467 geriatric horses (Brosnahan and Paradis, • Copper deficiency may not initiate osteochondral ab- 2003). normalities. Supplementation of the pregnant dam, not the Several factors have been implicated in the etiology of weanling foal, may reduce incidence of DOD in foals by acute laminitis. These include excessive ingestion of rapidly promoting repair of developing osteochondral lesions. fermentable carbohydrate (e.g., starch, sugars, and/or fruc-

UNIQUE ASPECTS OF EQUINE NUTRITION 249 tans) (Garner et al., 1978; Rowe et al., 1994; Pollitt et al., clinical signs of laminitis in 23 of 31 horses following ad- 2003), endotoxemia (Garner et al., 1978; Moore et al., 1989; ministration of a cornstarch-wood flour gruel (mean 40 Rowe et al., 1994; Pollitt et al., 2003), black walnut shavings hours; range 24–48 hours), via stomach tube, that delivered (Minnick et al., 1987), excessive concussion (Hood, 1999a), approximately 15 g starch/kg BW. Rowe et al. (1994) re- obesity and insulin resistance (Jeffcott et al., 1986; Treiber ported lameness, characteristic of laminitis, in 4 of 4 horses et al., 2005, 2006), glucocorticoid administration (Johnson after 4 days of consuming 2 meals/d, 12 hours apart, each et al., 2004a), and endocrine disturbances (Johnson et al., containing approximately 3.75 to 6.8 g starch/kg BW (cal- 2004b). Although several factors have been associated with culation assumes corn contains 75 percent starch). There- the onset of laminitis, the exact mechanism(s) by which fore, the recommendation by Potter et al. (1992) of no more these factors trigger laminitis is unknown. than 2 to 4 g starch/kg BW/meal (assuming 2 to 3 meals/d) may be prudent in the prevention of acute laminitis. How- ever, it should be noted that not all starch is created equal in Pathogenesis terms of prececal digestion as stated in Chapter 8. The pathogenesis of acute laminitis is uncertain (Bailey The ingestion of pasture grasses rich in water-soluble et al., 2004; Moore et al., 2004). Three primary theories carbohydrates (glucose, fructose, sucrose, and fructan) may exist: (1) vascular hemodynamic theory; (2) toxic, meta- precipitate laminitis (Bailey et al., 2004). It has been pro- bolic, or enzymatic theory; and (3) traumatic or mechanical posed that ingestion of fructans can result in disturbances to overload theory. These theories have been discussed in de- hindgut function in a similar way to undigested starch tail (Hood, 1999b; Moore et al., 2004; Bailey et al., 2004). (Longland and Cairns, 2000), with triggering of laminitis. Briefly, the vascular theory states that a yet to be identified However, a direct relationship between the onset of lamini- factor(s) initiates a change in digital vascular function, tis and ingestion of specific pasture carbohydrates has not resulting in impaired blood supply to the laminae and sub- been demonstrated. Furthermore, there is limited informa- sequent damage resulting in the failure of the dermal- tion on the quantities of pasture fructan or other storage car- epidermal junction (Moore et al., 2004). One research group bohydrate required to cause significant changes in hindgut (Bailey et al., 2004) proposed that vasoactive monoamines function that may increase risk of laminitis. Longland et al. formed and released from the hindgut might be the link be- (1999) reported fructan concentrations in specific varieties tween ingestion of feedstuffs rich in rapidly fermentable car- of perennial ryegrass (Lolium perenne) ranging from 100– bohydrates and the digital ischemic events thought to pre- 420 g fructan/kg DM, depending on environmental condi- cede the onset of laminitis. The toxic, metabolic, or tions. In general, pasture content of storage carbohydrates enzymatic theory states that an unknown trigger factor de- (including fructans) is highest in spring, lowest in mid- livered in the bloodstream activates metallic matrix metallo- summer, and intermediate in autumn. However, there also proteinases (MMPs), which leads to the breakdown of the can be marked daily fluctuations that coincide with patterns basement membrane and separation of the dermo-epidermal of energy storage (photosynthetic activity) and utilization. junction (Moore et al., 2004; French and Pollitt, 2004). The Thus, pasture water-soluble carbohydrate tends to rise dur- traumatic or mechanical overload theory states that trauma ing the morning, reaching maxima in the afternoon, and de- or mechanical overload and/or associated inflammation and clining overnight. Horses grazing in the afternoon, when altered blood flow through the foot leads to separation of the compared to nighttime or morning, may ingest between 2 dermo-epidermal junction (Hood, 1999b). and 4 times as much water-soluble carbohydrate. Assuming a dry matter intake of 2.5 percent of body weight for a 500- kg horse, the fructan intake from the perennial ryegrass pas- Nutritional Management and the Prevention of Acute ture studied by Longland et al. (1999) could range from Laminitis 2.5–10.5 g fructan/kg BW. The upper end of this range falls Strict nutritional guidelines for the prevention of acute within a range of oral fructan dosage (7.5–12.5 g/kg BW) laminitis have not been determined. It is well documented reported to induce laminitis in horses (French and Pollitt, that disturbance of normal fermentation pattern in the 2004). Smaller dosages of fructan also may alter the hindgut hindgut resulting from the fermentation of rapidly fer- environment and increase risk of laminitis. In ponies, the mentable carbohydrates (e.g., starch, fructans) can precipi- consumption of inulin (a fructan extracted with chicory tate laminitis (Garner et al., 1977, 1978; Pollitt et al., 2003). root) at 1 g or 3 g/kg BW resulted in a significant decrease However naso-gastric bolus was the means of delivering the in fecal pH (Crawford et al., 2005). Vervuert et al. (2005) re- rapidly fermentable carbohydrate used in these experiments, ported fructan concentrations in cool-season grass-legume which makes extrapolation to oral ingestion of a meal or pasture ranging from 18 ± 8 to 57 ± 17 g/kg DM. Using sim- meals difficult. Potter et al. (1992) suggested that the starch ilar assumptions on DM intake as above, the fructan intake intake per meal (assuming 2 to 3 meals/d) should not exceed from the cool-season grass-legume mix pasture studied by 2 to 4 g starch/kg BW in order to minimize postileal starch Vervuert et al. (2005) is considerably lower (0.45–1.4 g digestion and the subsequent potential for disturbance of fructan/kg BW) than the range reported capable of inducing normal fermentation patterns. Garner et al. (1977) induced laminitis by French and Pollitt (2004). Hoffman et al. (2001)

250 NUTRIENT REQUIREMENTS OF HORSES reported that the rapidly fermentable carbohydrate content termed osteodystrophia fibrosa. Subsequent bone thicken- of grass-legume pasture (a large proportion of which was as- ing results in physical distortion of the head, accounting for sumed to be fructan) ranged from 22.9–145 g/kg DM which the disease’s descriptive name “big head.” Changes to max- could result in an intake of approximately 0.57–3.6 g rapidly illary and mandibular bones are bilateral, but not necessar- fermentable carbohydrate/kg BW. Although the role of pas- ily symmetrical. Affected horses may first present with ture carbohydrates in the pathogenesis of laminitis has not clinical signs associated with upper airway breathing diffi- been unequivocally demonstrated, the disease occurs most culty or noise (Clarke et al., 1996). As the disease pro- commonly in equids kept at pasture (USDA, 2000). There- gresses, horses may have difficulty chewing as a result of fore, for horses and ponies with a history of pasture- decreased bone integrity of dental alveoli and associated associated laminitis, there is rationale for restricted access to dental pain. Reduced feed intake results in weight loss and pasture, particularly during the growing seasons. poor body condition. Nutritional secondary hyperparathyroidism was preva- lent among working horses in the early 1900s. Working Nutritional Management and Chronic Laminitis horses fed large amounts of bran byproduct, especially those Specific, objective information regarding nutritional man- used to mill wheat, were most often afflicted, hence the agement of horses with chronic laminitis is not available. names “bran disease” and “miller’s disease” were used to However, a logical approach to feeding horses with chronic describe the condition. Presently, NSH is not considered a laminitis is to prevent excess body weight in order to mini- common condition, but inappropriate dietary management mize mechanical stress on the foot and supply nutrients nec- relative to calcium and phosphorus intake can lead to lesion essary for hoof growth and repair (Hood, 1999c). Rations development in individual or groups of horses. having low-caloric density (e.g., low-quality forage only) are often recommended in an effort to prevent excess body Nutritional Factors weight. If unsupplemented, low-calorie rations may have the potential to be deficient in protein, amino acids, and various Nutritional situations in which available dietary calcium micronutrients (Hood, 1999c). Hoof wall growth has been is insufficient to meet daily requirements can result in de- demonstrated to be influenced by overall plane of nutrition velopment of NSH. Inadequate dietary calcium can result (Butler and Hintz, 1977), as well as biotin supplementation from a primary or secondary deficiency. Diets consisting of (Buffa et al., 1992; Reilly et al., 1998). Therefore, based on mature grass forage with large amounts of cereal grain- limited information, providing a ration that does not exceed based supplements are often low to deficient in dietary cal- digestible energy requirements but contains at least adequate cium with adequate to slightly excessive phosphorus. Grass protein and micronutrients should be a feasible approach to forages vary in calcium content, but generally have a Ca:P promote hoof wall growth and repair. ratio less than 2:1 compared to legume forages that have Ca:P ratios greater than 4:1. Cereal grains of all varieties contain very low calcium (< 0.1 percent DM) and high Nutritional Secondary Hyperparathyroidism phosphorus (0.3–0.4 percent DM), resulting in a Ca:P ratio Nutritional secondary hyperparathyroidism (NSH) is a of 1:6 or more. Mature warm-season grasses may have a metabolic bone disease associated with the feeding of ra- Ca:P ratio of 1:1 or slightly less, and their feeding with large tions with an excess of phosphorus or a deficiency of avail- amounts of cereal grain supplements has been implicated in able calcium (Joyce et al., 1971; Capen, 1983; Bertone, reported cases of NSH (Joyce et al., 1971; Ronen et al., 1992). Although associated skeletal lesions are generalized, 1992; David et al., 1997; Wisniewski et al., 1999). bony changes do not occur uniformly or consistently within Excessive dietary phosphorus can induce a secondary skeletal regions. Horses from weaning up to 7 years of age calcium deficiency. Diets supplemented with large amounts are most often affected. Early signs of the disease include a of wheat or rice bran have been reported to induce NSH shifting lameness of one or more legs, tenderness of joints, (Joyce et al., 1971; Clarke et al., 1996). Fiber bran byprod- reluctance to move, and a stiff, stilted gait. These signs are ucts of wheat and rice contain between 1.3 and 2.3 percent associated with bone demineralization and resultant devel- DM phosphorus and low calcium (< 0.2 percent DM). Diets opment of subepiphyseal microfractures, loss of trabecular containing large amounts of wheat or rice bran contain ei- bone integrity with disruption of articular cartilage, and tear- ther adequate or slightly deficient calcium with excessive ing or detachment of tendons and ligaments. In advanced phosphorus, resulting in a dietary Ca:P ratio less than 1:1. cases, spontaneous fractures may occur, most often of the Supplementing a diet with a high phosphorus mineral with- sesamoids, phalanges, or both. out calcium could also result in a dietary calcium and phos- Bones of the head are most often visibly affected. Min- phorus imbalance (Lewis, 1995). Feed byproducts of cereal eral content of facial bones and mandible is replaced with grain processing also contain high concentrations of phos- increased amounts of osteoid and fibrous tissue, a process phorus and have low calcium to phosphorus ratios. For ex-

UNIQUE ASPECTS OF EQUINE NUTRITION 251 ample, corn distillers’ byproducts and corn gluten feed con- TABLE 12-3 Grasses That May Contain Excessive tain high concentrations of phosphorus (> 1 percent DM) Amounts of Oxalates with low calcium (< 0.15 percent DM). Dietary supplements Common Name Scientific Name containing large amounts of these byproducts can result in Buffel grass Cenchrus cilaris excessive phosphorus intake and a low dietary Ca:P ratio. Blue or green panic grasses Panicum spp. Availability of dietary calcium is reduced in the presence Dallis grass Paspalum spp. of dietary oxalates resulting in a secondary calcium defi- Foxtail millet Setaria italica ciency (Swartzman et al., 1978; Blaney et al., 1981; McKen- Kikuyu grass Pennisetum clandistinum zie et al., 1981a), and NSH has been reported in horses that Napier, mission grass Pennisetum spp. Purple pigeon grass Setaria incrassate consumed oxalate-containing plants as their primary forage Pangola grass Digitaria recumbens source over a prolonged period of months (Walthall and Setaria grass Setaria sphacelata McKenzie, 1976; Blaney et al., 1981; McKenzie, 1988). A number of tropical warm-season grasses (Table 12-3) can contain potentially harmful amounts of oxalate (Walthall and McKenzie, 1976; McKenzie, 1988; Lewis, 1995; David centration is tightly controlled by the counterregulatory hor- et al., 1997). Alfalfa hay (n = 11; mean ± standard deviation mones PTH and calcitonin (CT). A primary or secondary [SD], 0.56 ± 0.15 percent DM) and pelleted alfalfa meal calcium deficiency results in decreased plasma-ionized cal- (n = 22; mean ± SD, 0.36 ± 0.1 percent DM) were found to cium and increased PTH secretion. PTH in conjunction with contain variable oxalate concentration, but comparable in biologically active vitamin D promotes increased calcium magnitude to grasses shown to induce NSH (Hintz et al., uptake from the gut, bone, and kidneys. In dietary situations 1984). Cymbaluk et al. (1986) reported total oxalate con- of limited calcium availability, bone resorption becomes the centration in legume hays (n = 68; mean ± SD, 0.83 ± 0.27 primary source of calcium. PTH promotes increased resorp- percent DM) and showed legume hay oxalate concentration tion of bone by activation of osteoclasts. The result is loss of to be greater compared to mixed legume-grass, various skeletal calcium and phosphorus (bone demineralization). In grass, or cereal grain hays. Diets containing more than 0.5 the kidney, PTH promotes phosphorus excretion and calcium percent DM total oxalate and with a Ca:oxalate ratio of 0.5:1 reabsorption. or less pose greater risk for induction of calcium deficiency Blood phosphorus concentration is directly related to di- and NSH (Blaney et al., 1981; McKenzie et al., 1981a). As etary phosphorus intake (Capen, 1983). Therefore, con- a result of higher calcium content associated with legume sumption of a diet with excessive phosphorus will result in forages, Ca:oxalate ratios range from 1.7 to over 7:1 (Hintz a state of hyperphosphatemia. Hyperphosphatemia will re- et al., 1984; Cymbaluk et al., 1986), which are well above duce blood calcium concentration, by law of mass action, ratios associated with greater risk. Conversely, native and and suppress PTH’s ability to stimulate renal activation of other grass species were found to have lower available cal- vitamin D, further decreasing digestive absorption effi- cium, due to their lower calcium content, and posed a ciency (Capen, 1983; Bertone, 1992). Insoluble dietary ox- greater risk for dietary calcium deficiency (Cymbaluk et al., alates bind dietary calcium forming indigestible calcium ox- 1986). Calcium digestibility was not found to be adversely alates, which are excreted in the feces (Swartzman et al., affected by oxalate content of alfalfa (Hintz et al., 1984; 1978; Blaney et al., 1981). Lowered availability of dietary Cymbaluk et al., 1986). Oxalate-induced calcium deficiency calcium induces hypocalcemia and subsequent stimulation can occur in any horse, but lactating mares and weanlings of PTH secretion. Prolonged exposure to the imbalanced are most susceptible as a result of their higher calcium re- diet results in hypertrophy and hyperplasia of parathyroid quirements and greater feed intake (Lewis, 1995). glands in support of increased secretory activity (Fujimoto et al., 1967; Capen, 1983). Although NSH is induced by a dietary imbalance of cal- Pathogenesis cium and phosphorus, blood concentrations of these miner- Clinical signs of NSH are the result of sustained secretion als are not useful for diagnosis. Increased PTH concentra- of parathyroid hormone (PTH) and mobilization of bone cal- tion with normal to slightly low blood calcium and normal cium in an effort to maintain normal blood ionized calcium to slightly high blood phosphate concentrations are typical concentration in the face of dietary imbalances that induce a in horses with NSH (Roussel et al., 1987; Benders et al., state of hypocalcemia (Joyce et al., 1971; Capen, 1983; 2001; Estepa et al., 2003). This is in contrast to primary hy- Bertone, 1992; Hunt and Blackwelder, 2002). Ionized cal- perparathyroidism where elevated PTH concentrations are cium plays critical roles in muscle contraction, neuromuscu- associated with hypercalcemia (Frank et al., 1998; Peauroi lar activity, blood coagulation, and membrane permeability, et al., 1998). Increased urinary fractional clearance of phos- as well as many other intracellular regulatory processes phate (4 percent or greater, normal 0–0.5 percent) results (Capen, 1983). Consequently, plasma-ionized calcium con- from PTH effects on increased renal clearance of phospho-

252 NUTRIENT REQUIREMENTS OF HORSES rus and is suggestive of NSH (Ronen et al., 1992; David et agus. It has been suggested that inflammation of the duode- al., 1997; Ramirez and Seahorn, 1997). Serum alkaline num results in functional impairment of gastric emptying, phosphatase activity will be elevated as a result of increased with irritation and ulceration of the gastric and esophageal bone osteoclastic activity, but this is not specific for NSH. mucosa probably due to prolonged exposure to acidic lumi- Ration evaluation in conjunction with presenting clinical nal contents. This condition may occur in mini-outbreak signs is the best method for diagnosis of NSH. form on an individual farm and may be preceded by episodes of diarrhea, leading to speculation that a viral or bacterial infection precipitates disease. Gastric mucosal in- Nutritional Management and Prevention flammation and ulceration in foals post-weaning has been Horses affected by NSH can be effectively treated by di- associated with cribbing (Nicol et al., 2002). Cribbing be- etary alterations to increase available dietary calcium intake havior in these foals was decreased after administration of to meet daily requirements, along with a reduction in dietary antacids and ulcer healing, suggesting a cause-and-effect re- phosphorus to an appropriate ratio with calcium. High Ca:P lationship between gastric ulceration and cribbing (see ratios in the range 3:1 to 6:1 have been advocated in the Chapter 11). early treatment of the disease (David et al., 1997; Ramirez Erosion or ulceration of the squamous mucosa is the pre- and Seahorn, 1997). Reversal of clinical signs associated dominant form of EGUS in mature horses (Andrews and with bony changes occurs over a period of months. Progno- Nadeau, 1999; Lester, 2004). The squamous mucosa adja- sis for recovery is good in older horses, although some fa- cent to the margo plicatus is most frequently affected, par- cial distortion may be permanent, and guarded in young ticularly on the lesser curvature. The pathogenesis of these growing horses depending upon severity of bony lesions and lesions is likely multifactorial (see below), but it has been remodeling of long bones (Hunt and Blackwelder, 2002). suggested that diet and feeding practice may alter risk for Prevention of this disease can be accomplished by feed- development of squamous ulcer disease. Ulceration of the ing a diet appropriately balanced to provide sufficient gastric glandular mucosa, alone or in combination with amounts of available calcium and phosphorus and maintain nonglandular squamous lesions, also occurs in mature a dietary Ca:P ratio of between 1 to 2.5:1 (David et al., 1997; horses but is much less common than the squamous form of Ramirez and Seahorn, 1997). Diets containing large EGUS. Clinical signs of EGUS, such as poor appetite and amounts of cereal grains or bran products must have the abdominal pain after feed ingestion, have been described to total dietary calcium content evaluated to ensure adequate be more severe with glandular as compared to squamous le- intake and balance relative to total dietary phosphorus. Di- sions. Concurrent disease and other stress factors, such as etary calcium supplementation may be achieved by increas- prolonged transportation, may predispose to development of ing or substituting legume for grass forages. Alfalfa hay can glandular ulceration. Experimentally high doses of non- provide an excellent source of calcium (Lewis, 1995). Di- steroidal anti-inflammatory drugs induce ulceration of the etary calcium can also be increased with addition of calcium glandular mucosa. carbonate in a mineral or grain supplement. Dietary Ca:P The remainder of this discussion deals with gastric ulcer- ratio greater than 2.5:1 is not warranted unless dietary fac- ation in mature horses. tors impeding calcium availability (i.e., oxalates) are docu- mented. Removal of feed containing high amounts of ox- Epidemiology and Risk Factors alates would be desired; however, feeding supplemental dietary calcium and phosphorus has been shown to control Squamous mucosal ulceration is common in perfor- the disease in grazing horses where alternative feed re- mance horses, with prevalence ranging from approximately sources were not available (McKenzie et al., 1981b). 40–90 percent in various studies (Murray et al., 1996; Mc- Clure et al., 1999; Vatistas et al., 1999b; Rabuffo et al., 2002; Dionne et al., 2003; Andrews et al., 2005). The preva- Gastric Ulcer Syndrome lence and severity of gastric ulceration appears to be de- Equine gastric ulcer syndrome (EGUS) refers to a group pendent on several factors, including feeding and housing of distinct disorders that includes neonatal gastric ulcera- management, and the form and level of physical activity. tion, gastroduodenal ulcer disease of suckling foals, gastric However, intense exercise appears to play a major role in glandular ulceration, and squamous mucosal ulceration (An- the development of squamous gastric ulcers. In an epidemi- drews and Nadeau, 1999; Lester, 2004). The neonatal con- ological study of Thoroughbreds, the prevalence of gastric dition generally occurs in foals with concurrent severe ill- ulcers was 100 percent in actively racing horses and 91 per- ness such as generalized sepsis or peripartum asphyxia cent for horses in race training (Murray et al., 1996). A high syndrome, and it may be clinically inapparent or result in prevalence (67 percent) was also reported in one study of perforation and fatal peritonitis. Gastroduodenal ulcer dis- endurance horses after 50- and 80-km races (Nieto et al., ease in suckling foals is characterized by ulceration of the 2004). In an experimental study, gastric ulceration devel- proximal duodenum, pylorus, stomach, and/or distal esoph- oped soon after the start of simulated race training and was

UNIQUE ASPECTS OF EQUINE NUTRITION 253 maintained during the period of active training (Vatistas et tion might result in enhanced acid secretion and lower stom- al., 1999a). In contrast, there is low prevalence of gastric le- ach pH. sions in horses given limited controlled exercise and kept at pasture (Andrews et al., 2005). In a study of 275 Standard- Stall Confinement breds, horses in race training were nine times more likely to have gastric ulcers than horses not in training (Dionne et al., Confinement housing has been implicated in the devel- 2003). opment of gastric ulcer disease. In one study, squamous mu- Exposure of the squamous mucosa to gastric acid is cosal lesions were apparent 7 days after relocating horses thought to be the primary cause of ulceration, although other from pasture to a stall environment (Murray and Eichorn, acids (short-chain or volatile fatty acids produced by fer- 1996). It has been proposed that lack of socialization with mentation in the stomach or reflux of bile acids from the other horses, changes in dietary composition, and intermit- duodenum) and pepsin also may play a role (Andrews et al., tent rather than continuous feeding could contribute to the 2005). In vitro experiments using strips of nonglandular increased risk of gastric ulceration after confinement squamous mucosa have shown that hydrochloric acid, alone (Lester, 2004). and in combination with volatile fatty acids, cause dose- dependent inhibition of cellular sodium transport, cell swell- Temperament ing, and ulceration (Nadeau et al., 2003a,b). Therefore, fac- tors that alter gastric acid secretion, production of volatile Some studies have reported a higher prevalence of ulcer- fatty acids in the stomach, and exposure of the squamous ation in horses with nervous temperaments. One unproven mucosa to these organic acids may alter risk for develop- hypothesis is that horses with nervous dispositions maintain ment of mucosal injury and ulceration. reduced gastric volume in response to persistent tension of Repeated oral administration of hypertonic electrolyte the abdominal muscles, forcing acidic gastric fluid to the solutions, a common practice in horses during endurance dorsal (squamous) region of the stomach (Lester, 2004). competitions, may be another risk factor for ulceration of the squamous mucosa in horses. In a study of 14 horses, oral Putative Nutritional Factors administration of 56.7 g of commercial electrolyte supple- ment mixed with 60 ml of water once an hour for 8 hours There is no definitive evidence implicating diet in the (approximately 11 g sodium, 24 g chloride, 7.5 g potassium, development of squamous ulcer disease. Possible dietary 1.5 g calcium, and 300 mg magnesium per dose) resulted in influences include the effects of diet composition, meal a significant increase in mean ulcer number (P = 0.017) and size, and feeding frequency on saliva production; the rate severity (P = 0.0006) scores in the nonglandular stomach and extent of intragastric fermentation; and gastric empty- (Holbrook et al., 2005). ing rate (Andrews et al., 2005). Saliva production during the consumption of a hay meal is approximately double that produced during intake of the equivalent DM as grain, in Nonnutritional Factors part due to the longer period of mastication required for in- gestion of forage (Meyer et al., 1985). As the flow of sali- Exercise vary fluid and masticated feed into the stomach may buffer Exercise may favor prolonged exposure of the squamous the acidity of gastric contents, the lower volume of salivary mucosa to gastric glandular secretions (hydrochloric acid, fluid with ingestion of grain may favor mucosal injury due pepsin) and bile acids due to alterations in gastric volume. In to exposure to hydrochloric acid. Another consideration is a study of horses exercising on a treadmill, there was a sud- the potentially ulcerogenic effects of volatile fatty acids den and marked decrease in gastric volume after the onset of (VFA) produced by the fermentation of starch and other trotting in concert with an increase in intra-abdominal pres- readily fermentable substrate in the nonglandular region of sure (Lorenzo-Figueras and Merritt, 2002). The authors sur- the stomach (Nadeau et al., 2003a,b; Andrews et al., 2005). mised that the exercise-induced increase in intra- In studies of harvested equine gastric squamous mucosa, abdominal pressure was responsible for the decrease in gas- the addition of 60 nmol/L VFA (butyric, propionic, acetic, tric volume. Furthermore, the decrease in volume resulted in and valeric acids) resulted in decreased chloride-dependent exposure of the squamous mucosa to the acidic contents sodium transport, cell swelling, and tissue damage (Nadeau (pH 1–2) of the dependent area of the gastric lumen. It also et al., 2003a). In the acidic conditions of the equine stom- has been suggested that an exercise-associated decrease in ach (pH ≤ 4), these organic acids will be predominantly in gastric emptying rate increases exposure of the squamous nonionized forms and therefore able to penetrate and dam- mucosa to acidic gastric fluid (Lester, 2004). Other re- age squamous epithelial cells. In a previous study (Nadeau searchers have reported that exercise training results in an et al., 2000), this research group compared the effects of a increase in the serum gastrin response to meal feeding (Furr grass hay (bromegrass) diet vs. a combination of legume et al., 1994). Such an increase in serum gastrin concentra- hay (alfalfa) and grain on gastric squamous epithelial ul-

254 NUTRIENT REQUIREMENTS OF HORSES ceration and the pH and VFA contents of gastric juice in Colic horses with surgically implanted gastric cannulae. Surpris- ingly, the number and severity of squamous ulcers were Colic is defined as abdominal pain and is used to describe greater in horses that received the grass hay-only diet. In symptoms resulting from intestinal ileus or inflammation this group, postprandial pH was lower and butyric acid con- (White, 1999). Worldwide, colic is one of the most frequent centration higher when compared to the alfalfa/grain diet, causes of emergency treatment of horses (White, 1990; whereas acetic, propionic, valeric, and isovaleric acid con- Proudman, 1991; Traub-Dargatz et al., 2001) and is reported centrations were higher in the alfalfa/grain diet group, con- as a leading cause of equine mortality in the United States sistent with a higher rate of intragastric fermentation in (Tinker et al., 1997a; USDA, 2001). Estimates of the annual grain-fed horses. In a subsequent analysis of these data, incidence of colic range from 3.5 to 10.6 colic cases per 100 the presence of VFA (butyric, propionic, and valeric acids) horses (Kaneene et al., 1997; Tinker et al., 1997a; USDA, and low stomach pH (gastric acidity) were found to be 2001). Mortality rate among horses with colic has been esti- significant predictors of ulcer severity (Andrews et al., mated in two large-scale studies at 6.6 percent (Tinker et al., 2005). 1997a) and 11 percent (Traub-Dargatz et al., 2001). The size of grain meals may affect the extent of intragas- Colic can be classified according to the disease causing tric fermentation and thus VFA production (Metayer et al., it. These classifications include ileus (e.g., spasm, intralu- 2004; Lorenzo-Figueras et al., 2005). Metayer et al. (2004) minal obstruction, paralytic ileus, displacement/strangula- compared gastric emptying rate in horses fed a small (300 tion); inflammation (e.g., enteritis); ulcer (e.g., gastric ul- g/100 BW) vs. large (700 g/100 kg BW) high-starch con- cers, intestinal ulcers, dorsal colitis); and false colic (e.g., centrate. Although the calculated rate of gastric emptying pregnancy, rhabdomyolitis, liver disease, renal/bladder dis- (g/min) was higher with the large meal, gastric emptying in ease) (White, 1999). However, in many cases, the cause of terms of percent of the total meal was much slower. Thus, colic is unknown (Kaneene et al., 1997; Tinker et al., 1997a; with large starch-rich meals, intragastric fermentation and White, 1999). volatile fatty production may be favored due to the large Several factors have been reported to influence the risk of load of fermentable substrate and longer residence time in colic. These risk factors include diet and feeding character- the stomach. istics, internal parasitism, intrinsic factors (e.g., sex, age, Feeding frequency also may affect the risk of gastric and breed), medical history (e.g., previously affected by squamous ulceration (Murray and Schusser, 1993; Lester, colic), management (e.g., housing, activity level), and 2004). In grazing horses, the continuous flow of saliva and weather-related factors (Goncalves et al., 2002). It should be ingesta may provide a buffering effect such that gastric pH noted that risk factors do not imply a direct cause-and-effect remains above 4 for most of the day. On the other hand, relationship and that the relationship between risk factors given that horses are continuous secretors of gastric acid, and colic is not always clear (Cohen, 1997; Goncalves et al., stomach pH falls when feed is withheld and the nonglandu- 2002). Among the various risk factors identified, diet and lar mucosa is exposed to an acid environment. In healthy feeding characteristics are often associated with the greatest horses, squamous ulceration was induced by alternating 24- risk for colic (Tinker et al., 1997b; Cohen et al., 1999; Hud- hour periods of feed deprivation and ad libitum access to son et al., 2001). The diet and feeding characteristics asso- hay over an 8-day period (Murray and Schusser, 1993). Ul- ciated with the risk of colic include changes in feeding pro- ceration developed after 24 hours of cumulative feed depri- gram, amount of concentrate fed, access to pasture, type of vation. The median intragastric pH during a 24-hour period forage, and characteristics of water delivery. with ad libitum access to grass hay was 3.1, whereas me- Diet change and change of hay were reported to increase dian pH was 1.6 during feed deprivation. These findings the risk of colic by 5 and 9.8 times, respectively, according to confirm that gastric acidity is the primary mechanism of the results of a prospective matched case-control study in- squamous mucosal ulceration and suggest that the typical volving 2,060 horses (Cohen et al., 1999); however, no practice of twice daily meal feeding may be a contributing specifics describing the change were provided (e.g., increase, factor. decrease, change in type, or change in source). In a follow-up Further studies are needed to better elucidate the role of study, the same group reported that a recent change in batch diet composition in ulcer development and to identify feeds of hay (i.e., different source), but not type of hay (e.g., legume and feeding methods that reduce risk of squamous ulcer dis- vs. grass), increased the risk of colic by 4.9 times (Hudson et ease. For example, it has been suggested that the feeding of al., 2001). Additionally, a recent change in type (e.g., pelleted lower starch and higher oil and fiber concentrates is benefi- vs. textured) of grain or concentrate fed increased the risk of cial, but this hypothesis remains unproven. Interestingly, colic 2.6 times. The authors of these studies noted that both corn oil supplementation (45 ml/d) in ponies was associated experiments were conducted during drought conditions, with a significant decrease in gastric acid production and in- which may have influenced the outcome. However, others creased prostaglandin E2 concentration in gastric juice (Car- have also reported increased risk of colic associated with a gile et al., 2004). change in concentrate or hay feeding (Tinker et al., 1997b).

UNIQUE ASPECTS OF EQUINE NUTRITION 255 Concentrate intakes between 2.5 and 5 kg/d and those can result in colic due to inflammation (Jones, 2004) and/or greater than 5 kg/d increased the risk of colic 4.8 and 6.3 blockage (Blikslager and Jones, 2004) of the intestine. times compared to horses on pasture receiving no concen- trate (Tinker et al., 1997b). Concentrate intake of less than Enterolithiasis 2.5 kg/d was not significantly associated with the incidence of colic compared to horses on pasture receiving no con- Enteroliths (intestinal calculi) are found in the large in- centrate. However, the association between amounts of testine, where they may cause obstruction and varying de- grain fed per day and colic is not always clear. Hudson et grees of abdominal pain (colic). Enteroliths are composed of al. (2001) reported that feeding greater than 2.7 kg/d of oats struvite, a mixture of magnesium ammonium phosphate increased the risk of colic 5.9 times, but noted that this fac- (Hassel et al., 2001). The struvite crystals are laid down in tor may not be causative, but only a marker for some other concentric rings, typically surrounding a dense nidus or for- factor (e.g,. level of exercise). Reeves et al. (1996) reported eign body (e.g., cloth, metal, hair, or pebbles). Enteroliths an increased risk of colic associated with feeding increased may form singly or in large groups of small calculi. Large amounts of whole corn grain, but a decreased risk associ- calculi tend to be located in the right dorsal colon, while ated with increased amounts of nonroughage concentrate smaller calculi may enter the transverse colon and descend- feed. Interestingly, the amount of whole corn grain fed was ing colon. Clinical signs of abdominal pain can occur when relatively low (i.e., colic affected and nonaffected horses calculi become lodged in a segment of large intestine, re- consumed 1.3 ± 0.18 and 0.7 ± 0.13 kg/d, respectively), as sulting in variable amounts of distention with gas and in- was the difference in amount of nonroughage concentrate. gesta proximal to the obstruction. Alternatively, multiple Colic affected and nonaffected horses consumed 3.4 ± 0.10 small calculi may cause abdominal pain without obstruc- and 3.9 ± 0.11 kg/d, respectively (Reeves et al., 1996). tion, perhaps due to irritation of the bowel wall. Hudson et al. (2001) reported that a recent decrease in The occurrence of enterolithiasis has been reported over pasture availability (i.e., either no pasture time or a decrease a wide geographic area. However, there is a high prevalence in pasture acreage or time at pasture) increased colic risk of enterolithiasis in certain geographic regions, such as Cal- three times compared to horses in which no change in pas- ifornia and in the southeastern United States (Florida, ture was made. However, the association between colic Louisiana) (Hassel et al., 1999). In one study, horses with risk and pasture access is not always clear (Reeves et al., enterolithiasis represented approximately 15 percent of 1996). horses admitted to the Large Animal Clinic at the University Based on an observation of a small group of horses, Pugh of California–Davis for evaluation of colic and 27.5 percent and Thompson (1992) suggested that feeding Coastal of patients undergoing celiotomy for treatment of colic Bermudagrass hay was a factor in the development of im- (Hassel et al., 1999). In contrast, enterolithiasis was an un- paction colic. However, this association has not been sub- common (< 2 percent of cases) cause of colic at a referral stantiated (Cohen et al., 1999). In addition, results of epi- clinic in Texas (Cohen et al., 2000). All breeds of horses can demiological studies implicated water source (e.g., bucket, be affected. However, in one report, Arabian and Arabian pond, automatic waterer) as a colic risk factor, but the rela- crosses, Morgans, American Saddlebreds, and donkeys were tionship is unclear (Reeves et al., 1996; Kaneene et al., significantly overrepresented in the study population (Has- 1997; Cohen et al., 1999). sel et al., 1999), while in another study, Arabian and minia- Mechanisms by which various factors contribute to the ture breeds were at increased risk for development of en- development of colic are not clearly defined. Clarke et al. teroliths (Cohen et al., 2000). A high prevalence in siblings (1990) provided evidence supporting the hypothesis that also has been reported (Hassel et al., 1999), raising the pos- meal feeding of concentrated diets leads to exaggerated fer- sibility of a heritable component to the disease. In a study of mentation characteristics in both the foregut and hindgut 900 equids, the mean age of occurrence was 11.4 years and altered fluid balance in the hindgut. Exaggerated fer- (Hassel et al., 1999). However, colonic obstruction due to an mentation, specifically that resulting in decreased pH, could enterolith has been recognized in horses less than 1 year of result in damage to the intestinal mucosa and/or excess gas age (Lloyd et al., 1987), suggesting that intestinal calculi production leading to intestinal distention (Clarke et al., can grow to sufficient size to cause intestinal obstruction 1990). Rate of passage was increased with increased meal within a short time period. size when high-starch diets were fed to horses (Metayer et al., 2004). Feeding meals containing greater than 2 to 4 g Nutritional Factors starch/kg BW has been reported to increase postileal diges- tion of starch (Potter et al., 1992), which has been reported Several studies have identified increased alkalinity in the to decrease hindgut pH leading to mucosal damage (Garner colonic contents of horses with enteroliths compared with a et al., 1977). Meal feeding of concentrated meals may alter control population (Hintz et al., 1988, 1989; Hassel et al., fluid balance in the hindgut, which could predispose horses 2004). Hassel et al. (2004) measured the pH and mineral to impaction colic (Clarke et al., 1990). Ingestion of sand contents of colonic ingesta in 43 horses with enterolithiasis

256 NUTRIENT REQUIREMENTS OF HORSES and 19 horses with surgical colic due to nonstrangulating cent of the day outdoors were at increased risk (OR = 4.5; obstruction of the colon without enteroliths. Mean pH of 95 percent CI, 1.4–13.9) for enterolithiasis, while Hassel et colonic contents for horses with enteroliths (pH 7.32 ± 0.07) al. (2004) found that horses with enteroliths were one-tenth was significantly higher than for control horses (pH 6.93 ± as likely (OR = 0.11; 95 percent CI, 0.03–0.45) to have daily 0.13), while percent colonic dry matter was lower in the access to pasture than horses without enterolithiasis. It was horses with enteroliths (13.6 percent ± 0.7 percent vs. 20.9 suggested that ingestion of grass might dilute the effects of percent ± 2.1 percent). Horses with enterolithiasis also had alfalfa on the chemical composition of colonic contents, a higher percent nitrogen and concentrations of magnesium, speculation in part supported by observations of higher phosphorus, sulfur, sodium, calcium, and potassium in colonic mineral contents in horses without daily access to colonic ingesta (Hassel et al., 2004). The mechanisms of pasture grazing (Hassel et al., 2004). Alternatively, in- these differences in colonic pH and chemical composition creased physical activity by horses at pasture might lower are not known, but contributing factors might include diet risk of enterolith formation via alterations in intestinal tran- composition, mineral content of water supply, and genetic sit, colonic ion exchange, or diet digestibility (Orton et al., differences in mechanisms for colonic luminal ion ex- 1985; Pearson and Merritt, 1991; Hassel et al., 2004). change. Alternatively, the observed differences in mineral The feeding of wheat bran also has been proposed as a risk content and dry matter of colonic ingesta may be attributa- factor for the development of enteroliths because of its rela- ble to the presence of enteroliths rather than the predispos- tively high protein (CP 16–17 percent), phosphorus (1.2 per- ing cause (Hassel et al., 2004). Nonetheless, the higher pH cent–1.3 percent), and magnesium (0.6 percent–0.7 percent) and mineral content of colonic ingesta might favor deposi- content (Lloyd et al., 1987). However, in the study by Cohen tion of struvite. This hypothesis is consistent with findings et al. (2000), only 1 of 26 horses with enterolithiasis had been in dogs and cats with struvite urolithiasis, wherein formation fed wheat bran. There are no published reports of the rela- of calculi is promoted by alkaline conditions and high min- tionship between mineral content of the water supply and eral concentrations in urine (Osborne et al., 1989). enterolithiasis. An association between the feeding of alfalfa hay and de- velopment of enterolithiasis has been reported (Blue and Nutritional Management Wittkopp, 1981; Lloyd et al., 1987; Murray et al., 1992; Cohen et al., 2000; Hassel et al., 2004). When compared to Studies in dogs and cats have demonstrated that a diet grass forages, alfalfa has both high protein and magnesium with low magnesium, phosphorus, and protein that results in content, which could result in higher levels of ammonium maintenance of low urine pH is effective for prevention or nitrogen and magnesium in the large intestine. In addition, even dissolution of struvite calculi in the urinary tract. The because alfalfa has high buffering capacity (Fadel, 1992), results of epidemiologic and case-control studies (Hassel et high-alfalfa diets could favor alkalinization of colonic con- al., 1999; Cohen et al., 2000; Hassel et al., 2004) that iden- tents and struvite deposition. In support of these considera- tified alkaline pH and higher mineral concentrations in sam- tions, Hassel et al. (2004) reported that horses with en- ples of colonic fluid in horses with enterolithiasis also sug- terolithiasis were fed a higher proportion of alfalfa in their gested that dietary modifications promoting acidification of diet (91.9 percent ± 2.6 percent) compared with control colonic contents might be beneficial for prevention of en- horses (62.1 percent ± 7.7 percent). From univariate regres- terolithiasis in horses. Specific dietary recommendations sion analysis, it was shown that horses on a diet of more than have included the exclusion of alfalfa and wheat bran from 70 percent alfalfa were at greater risk for enterolithiasis the diet, an increase in the grain:hay ratio, and supplemen- (odds ratio [OR] = 13; 95 percent confidence interval [CI], tation with apple cider vinegar (Hintz et al., 1989; Murray et 3.5–48.7) than horses on a lower alfalfa (< 70 percent) diet al., 1992; Lewis, 1995; Stratton-Phelps and Fascetti, 2003). (Hassel et al., 2004). In addition, the mean concentrations of However, there are limited data on the effectiveness of these magnesium, phosphorus, sulfur, sodium, calcium, and approaches for modification of the colonic environment and potassium in colonic contents of horses fed more than 70 no information regarding efficacy for prevention of en- percent alfalfa were 1.5–2 times higher than of horses on the terolith formation. In laboratory experiments, a colonic pH lower alfalfa diet (Hassel et al., 2004). However, because of less than 6.6 reduced the weight of implanted enteroliths most horses fed an alfalfa diet do not develop enteroliths, it (Hintz et al., 1989). Daily supplementation of ponies with is clear that alfalfa is not the only factor involved in en- apple cider vinegar (one-half cup or 110 ml per day) also re- terolith formation. Indeed, in the report of Cohen et al. sulted in a modest decrease in the pH of colonic contents but (2000), 14 of the 26 horses with enterolithiasis were not fed did not appear to reduce the size of enteroliths (Hintz et al., alfalfa. 1989). In epidemiologic studies, stall confinement and/or lack of Based on current knowledge, grass rather than legume access to pasture have been identified as risk factors for en- (alfalfa) forage, should be fed to horses with a history of en- terolithiasis (Cohen et al., 2000; Hassel et al., 2004). In one terolithiasis to reduce intake of nutrients that may promote study (Cohen et al., 2000), horses that spent less than 50 per- struvite deposition. Wheat bran also should be avoided.

UNIQUE ASPECTS OF EQUINE NUTRITION 257 Feeding grain (e.g., 0.5 kg/100 kg BW) and about 1 cup spores, small fungal spores, and dust mites. The role of dust (220 ml) of apple cider vinegar twice daily may be benefi- mites in exacerbating the allergenicity of molds is unclear. cial in promoting mild acidification of colonic contents. Fi- Storage mites infest many feedstuffs and were linked to the nally, daily pasture turnout may reduce risk of enterolith spread and growth of molds within those infected feeds. In formation. addition to these usual allergens, endotoxins (lipopolysac- charides) can amplify the symptoms of RAO (Pirie et al., 2003). The small size of respirable particles allows escape Recurrent Airway Obstruction from the turbinate trap in the upper respiratory tract (Art et Recurrent airway obstruction (RAO) is the accepted ter- al., 2002). If not captured by the bronchial mucociliary minology for the disease entity in mature horses formerly mechanism, these particles can traverse to the alveoli. The known as chronic obstructive pulmonary disease (COPD) or threshold limiting value (TLV) is the level of exposure of an heaves (Robinson, 2001). Approximately 9.2 percent of agent above which disease or organic dysfunction can occur. clinical cases referred to North American veterinary teach- The TLV of spores for horse stables has been calculated at 33 ing hospitals have RAO (Ward and Couetil, 2005). Epi- particles/cm3 (Webster et al., 1987). demiologic studies indicate that affected horses were typi- Thermotolerant and thermophilic fungal species (As- cally 4 years or older and symptoms occurred more often in pergillus, Rhizomucor, Penicillium, and Stachybotrys spp.) winter and spring and occurred more often in the southern produce the majority of small respirable, fungal spores in than northern hemisphere (Couetil and Ward, 2003; Ward hays, straw, and shavings (Clarke and Madelin, 1987). The and Couetil, 2005). The monthly prevalence of RAO was high temperature conditions (> 38°C) preferred by these significantly correlated to total pollen counts measured 3 fungi most often occur in poorly cured hay, which heats dur- months before clinical symptoms and to total mold counts ing storage. Fungal invasion was shown to occur in the occurring 1 month before or during the same month of clinic stand-ing crop, during curing, and during storage, but admission (Ward and Couetil, 2005). A genetic predisposi- growth during storage was enhanced in square alfalfa hay tion has been reported with exacerbation by environmental bales when moisture content of the hay was high (29 percent contaminants in stables and age of horse (Marti, 2001; Marti ) at baling (Wittenberg et al., 1989). For horses with heaves, and Ohnesorge, 2002). The incidence of RAO in German hay should contain few mold and fungi. Hay has been Warmblood horses was 17, 48, and 69 percent when neither, graded at levels I through III based on numbers of mold and one, or both parents, respectively, were affected by RAO fungi type. Grade I hay had less than 999 particles/mg symptoms. Using a relative risk analysis, Marti and Ohne- source material, grade II ranged from 1,000–4,999 parti- sorge (2002) reported that the relative risk of RAO is low in cles/mg source material, and grade III contained more than offspring (13 percent) if neither dam nor sire is affected, but 5,000 particles/ mg source material (Clarke and Madelin, increased 3.2-fold (P < 0.05) if either parent was affected 1987). Hays and bedding with a grade III score are undesir- and 4.6-fold (P < 0.05) if both parents were affected. able for horses because millions of spores can be inhaled Environmental pollutants, generically labeled as “stable from these materials by a horse. dust,” include airborne fungi, thermophilic actinomycetes, Bedding has also been shown to contribute to horse sta- dust mites, endotoxins, and inorganic compounds (Clarke ble dust. Harvesting conditions often determine the quality and Madelin, 1987; McGorum et al., 1998; Art et al., 2002) of the straw for bedding. Based on their mold content, and typically enter the microenvironment (stall) and straws used to bed horse stalls were generally classified as macroenvironment (stable) through feed and bedding. RAO good or poor quality (Clarke and Madelin, 1987; Vandenput symptoms are not exclusive to indoor-stabled horses. A et al., 1997). Straws and shavings had a similar complement condition known as “summer-pasture-associated obstructive of molds as contaminated hays, whereas peat harbored few pulmonary disease” (SPAOPD; also known as “summer- potential allergenic molds (Clarke and Madelin, 1987). By pasture associated allergy”) has been recorded in horses on contrast, good-quality wheat and flax straw had fewer res- pasture (Seahorn and Beadle, 1993; Costa et al., 2000). pirable particles and allergenic spores than wood shavings (Vandenput et al., 1997). All-natural bedding materials were inferior to cardboard bedding, which had low levels of res- Nutritional Factors pirable dust and spores (Kirschvink et al., 2002c). Pelleted Stable dusts have been classified as nonrespirable (> 10 newspaper may be an alternative to straw and shavings as mm) or respirable (large or small) particles (Clarke and bedding, although particle mass less than 10 µm was ini- Madelin, 1987). Large respirable particles are 5–10 mm and tially higher in the newspaper product than either natural include particles such as plant structures, large pollen grains, bedding material when spread in the stall (Ward et al., and “fair weather” spores (Alternaria, Cladosporium spp). 2001). This study also confirmed that microbial numbers in These particles typically are not inhaled because of rapid the breathing zone and on the legs of horses were greater in sedimentation to the stable floor. Small respirable particles autumn than in summer. When bedding down the stall, are 0.1–5 mm and are typically comprised of actinomycetes horses should be removed from the barn. In one study, the

258 NUTRIENT REQUIREMENTS OF HORSES high exposure to respirable dust particles during “bedding idized and reduced glutathione, glutathione redox ratio, and down” increased airborne particles in the breathing zone of ascorbic acid have been characterized in normal horses un- the horse 3- to 6-fold (Webster et al., 1987). Good stable dergoing RAO episodes and those in remission (Art et al., ventilation is indispensable in the control of respirable par- 1999; Kirschvink et al., 2002a; Deaton et al., 2004). Horses ticles in the breathing zone of the horse, yet many stables with an induced RAO or clinical RAO crisis have increased were inadequately ventilated to accomplish this objective production of elastase, decreased ascorbic acid concentra- (Webster et al., 1987). tion in bronchoalveolar lavage fluid, and epithelial lining fluid (Deaton et al., 2004, 2005a,b) and increased total glu- tathione and oxidized glutathione (Art et al., 1999). Al- Pathogenesis and Clinical Symptoms though these data would indicate an increased production of Exposure of a sensitized horse to excessive amounts of free radicals or reactive oxygen species and that ascorbate respirable dust particles or organic dust in hay and moldy might be protective, the acute neutrophilic episode did not bedding has been shown to initiate neutrophilic inflamma- result in a marked pulmonary oxidative stress (Deaton et al., tion of the small airway (bronchioles) and/or the entire tra- 2005b; Deaton, 2006). When healthy horses were given an- cheobronchial tree (Robinson et al., 1996). Altered re- tioxidant supplements including ascorbic acid, there was no sponses by the mucociliary system result in increased mucus effect on ascorbic acid concentrations in pulmonary epithe- and/or mucopus production in the bronchial and bronchiolar lial lining fluid (Deaton et al., 2002), yet an antioxidant sup- tree (Gerber et al., 2004), mucosal edema, and broncho- plement containing vitamins C and E plus selenium given to spasm, eventually followed by varying degrees of fibrosis heaves-affected horses in remission resulted in improved ex- and fibroplasia of the submucosa. These pathologies reduce ercise tolerance and lower airway inflammation (Kirschvink oxygen exchange and a progressively reduced exercise tol- et al., 2002b). Further data will be required to determine if erance of the horse. Other symptoms, which can be mild to dietary ascorbic acid supplementation ameliorates or pro- severe, include coughing, respiratory distress, mucus or mu- tects the equine airway from pathology associated with the copurulent nasal discharge, abnormal lung sounds, in- inflammatory responses seen in RAO. creased work in breathing, and an abdominal “heave” line after chronic and sustained respiratory impairment (Robin- Nutritional Management and Prevention son et al., 2003). Importantly, the symptoms of RAO can be induced by a moldy hay/straw challenge in affected horses The best environment for RAO-prone horses has been to (McGorum et al., 1993). house them outdoors on pasture (Art et al., 2002). Horses The hypothesized causes for the airway hyperresponsive- with symptoms of heaves become asymptomatic within 4–6 ness seen in RAO-affected, RAO-prone horses, and SPAOD- days of being turned outdoors (Vandenput et al., 1998). Im- affected horses are numerous. Airway inflammation seen in provement in respiratory function was observed within 3 RAO has been suggested to originate at a cellular level, in days after pasture turnout in horses who were induced into a part from increased activity of transcription factors such as RAO episode by environmental modification (Jackson et al., nuclear factor-KB and activator protein-1 (Bureau et al., 2000). However, every precaution must be taken to mini- 2000). The profound neutrophilia seen in RAO may promote mize respiratory allergens even when the heaves-prone the continued production of mucus by the mucociliary ap- horses are kept outdoors. Supplementary hays and grains, if paratus (Gerber et al., 2004), perhaps through upregulation fed, should have minimal organic dust content. Despite the of equine MUC5AC mucin mRNA (Gerber et al., 2003). apparent benefit of housing RAO horses outside, the outdoor Other pathologic indicators in RAO horses include an in- environment may not be acceptable for horses prone to creased expression of IL-4 mRNA and IL-13 mRNA and a SPAOPD. decreased expression of IFN-γ mRNA indicative of an IgE- Unfortunately, horse athletes, including RAO-affected mediated response (Robinson, 2001; Bowles et al., 2002), horses, must often be stabled. If bedded and fed with feeds increased IL-1 β mRNA (Matera et al., 2005), higher sys- with low allergenicity, even RAO-affected horses appear to temic levels of endothelin-1 (Benamou et al., 1998), and re- be able to stay asymptomatic indoors. Thompson and duced densities of the β-adrenergic receptors of the lung and McPherson (1984) showed that horses with symptoms of bronchi particularly of the β-1 subtype, which may increase RAO became asymptomatic within 4–24 days after mea- airway smooth muscle sensitivity (Abraham et al., 2006). sures were taken to control dust in the stable by bedding The upregulation of the inflammatory genes has been with shredded paper and feeding a complete pelleted diet. linked to the redox conditions initiated by the increase in re- Similar observations were observed in heaves-affected active oxidant species (ROS) or free radicals during inflam- horses bedded with cardboard or good-quality straw and fed mation (Kirschvink and Lekeux, 2005). The overabundance a completed pelleted diet (Vandenput et al., 1998; of ROS in airway inflammation relative to the level of neu- Kirschvink et al., 2002c). tralizing oxidants has been speculated to exacerbate airway Good-quality hay for RAO-affected horses has low num- pathology. The concentrations of antioxidant indicators, ox- bers of thermophilic and thermotolerant molds and fungi

UNIQUE ASPECTS OF EQUINE NUTRITION 259 and dust mite allergens, but, contrary to popular belief, sta- Annandale, E. J., S. J. Valberg, J. R. Mickelsen, and E. R. Seaquist. 2004. ble operators were less able to detect mold through smell or Insulin sensitivity and skeletal muscle glucose transport in horses with polysaccharide storage myopathy. Neuromusc. Dis. 14:666– 674. appearance than expected (Clarke and Madelin, 1987). Árnason, T., and Bjarnason, T. 1994. Growth, development and size of Ice- Moreover, feed quality, based on allergenicity, cannot be landic toelter horses. Búvísindi 8:73–83. guaranteed because weather conditions at the time of har- Art, T., N. Kirschvink, N. Smith, and P. Lekeux. 1999. Indices of oxidative vest, methods of harvest, and storage all profoundly influ- stress in blood and pulmonary epithelium lining fluid in horses suffer- ence mold growth in hays, straws, silage, and grains. Al- ing from recurrent airway obstruction. Equine Vet. J. 31:397–401. Art, T., B. C. McGorum, and P. Lekeux. 2002. Environmental control of though pelleted or cubed alfalfa and grass silage can have respiratory diseases. In Equine Respiratory Diseases, P. Lekeux, ed. low levels of aeroallergens and dust and have been effec- Document No. B0334.0302. Ithaca, NY: International Veterinary Infor- tively used in diets of stabled, heaves-affected horses (Ray- mation Services. mond et al., 1994; Vandenput et al., 1997), these observa- Bailey, S. R., C. M. Marr, and J. Elliott. 2004. Current research and theo- tions may not apply universally to similar feeds produced in ries on the pathogenesis of acute laminitis in the horse. Vet. J. 167:129–142. other geographic areas. Poor-quality meals and uncoated Barneveld, A., and P. R. van Weeren, 1999. Conclusions regarding the in- pellets can expose animals to a large number of respirable fluence of exercise on the development of the equine musculoskeletal particles (Li et al., 1993), so quality of these products should system with special reference to osteochondrosis. Equine Vet. J. Suppl. also be evaluated. 31:112–119. Management to prevent and control symptoms of RAO Barneveld A., R. van Weeren, J. Knaap. 1999. Influence of early exercise on the locomotion system. 50th Annual Meeting of the European Asso- involves medical treatment, as well as eliminating or mini- ciation for Animal Production, Zurich. mizing the respiratory tract allergens (stable dust, especially Bell, R. A., B. D. Neilsen, K. Waite, D. Rosenstein, and M. Orth. 2001. respirable particles) in the horse’s macroenvironment (barn) Daily access to pasture turnout prevents loss of mineral in the third and microenvironment (stall). There are several ways to re- metacarpus of Arabian weanlings. J. Anim. Sci. 79:1142–1150. duce exposure of the horse to respirable dust: keep the horse Benamou, A. E., T. Art, D. J. Marlin, C. A. Roberts, and P. Lekeux. 1998. Variations in systemic and pulmonary endothelin-1 in horses with re- outdoors, use only dust and mold-free feeds, moisten feeds, current airway obstruction (heaves). Pulm. Pharmacol. Therap. use nondusty bedding, wash stalls regularly to remove dust, 11:231–235. and provide effective and sufficient ventilation to remove Benders, N. A., K. Junker, T. H. Wensing, S. G. A. M. van den Ingh, and J. dust particles in barn and stall air (Thompson and McPher- H. van der Kolk. 2001. Diagnosis of secondary hyperparathyroidism in son, 1984; Webster et al., 1987; Raymond et al., 1994; Van- a pony using intact parathyroid hormone radioimmunoassay. Vet. Rec. 149:185–187. denput et al., 1998). Soaking or steaming can reduce res- Beneus, L. 2005. Lokalisation av osteochondrosforandrengar hos Svenska pirable particles in hay. The major impact of soaking hay to havhodshastar. Ph.D. Thesis. Uppsala University, Sweden. reduce respirable particles was realized within 30 minutes; Bertone, J. J. 1992. Nutritional secondary hyperparathyroidism. Pp. no further benefit was observed in soaking hay for 12 hours 119–122 in Current Therapy in Equine Medicine, 3rd ed., N. E. Robin- (Moore-Colyer, 1996). Although soaking hay up to 30 min- son, ed. Philadelphia: W. B. Saunders. Beynen, A. C., and J. M. Hallebeek 2002. High-fat diets for horses. Pp 1–13 utes or steaming for 80 minutes reduced 93 percent of res- in Proc. 1st Europ. Equine Nutr. Health Cong., Antwerp Zoo, Belgium. pirable particles, steaming had no effect on nutrient loss Available at http://www.equine-congress.com. Accessed April 15, 2006. whereas soaking reduced phosphorus, potassium, magne- Blackman, M., and M. J. S. Moore-Colyer. 1998. 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Nutrient Requirements of Horses: Sixth Revised Edition Get This Book
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Proper formulation of diets for horses depends on adequate knowledge of their nutrient requirements. These requirements depend on the breed and age of the horse and whether it is exercising, pregnant, or lactating.

A great deal of new information has been accumulated since the publication 17 years ago of the last edition of Nutrient Requirements of Horses. This new edition features a detailed review of scientific literature, summarizing all the latest information, and provides a new set of requirements based on revised data. Also included is updated information on the composition of feeds, feed additives, and other compounds routinely fed to horses. The effects of physiological factors, such as exercise, and environmental factors, such as temperature and humidity, are covered, as well. Nutrient Requirements of Horses also contains information on several nutritional and metabolic diseases that horses often have.

Designed primarily as a reference, both practical and technical, Nutrient Requirements of Horses is intended to ensure that the diets of horses and other equids contain adequate amounts of nutrients and that the intakes of certain nutrients are not so excessive that they inhibit performance or impair health. This book is primarily intended for animal nutritionists, veterinarians, and other scientists; however, individual horse owners and managers will also find some of this material useful. Professors who teach graduate courses in animal nutrition will find Nutrient Requirements of Horses beneficial as a textbook.

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