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whether the horse continues to be fed high NSC-containing feedstuffs may be greater determining factors (Luthersson et al. 2009; Malmkvist et al. 2012). In some situations, changes, such as moving horses from pasture to stall housing, might be effective in reducing squamous ulcer scores in some horses (Woodward et al. 2014).
Diet
Pasture grazing, high forage (dry matter [DM] intake, ≥1.5% bodyweight) and low concentrate (≤0.5% bodyweight) diets, a diet low in NSC, feeding smaller more frequent meals and providing ad libitum forages might reduce the risk of squamous ulceration as discussed below.
Eliminate bolus feeding and increase forage/fibre intake One management practice that may help decrease squamous ulcers is to feed a forage based diet ad libitum or at least ensure that forage is provided every few hours and before exercise (even in small amounts). Along with hay, stabled horses should be fed (if required) 3 or 4 smaller meals (not to exceed 0.5 kg/100 kg bodyweight every 6 h and containing 20% NSC or lower) per day. Smaller low NSC meals will decrease intragastric fermentation, reduce production of VFAs and improve gastric emptying rate. Providing alfalfa hay and good quality grass hay as the
forage and/or adding alfalfa chaff to any complementary feed may be advantageous, although the total ration needs to be balanced to account for the alfalfa inclusion rate. However, straw as the only or main forage should be avoided as it was found to be at least 4.4 times more likely to increase squamous gastric ulcer severity scores (Luthersson et al. 2009). Although absolute requirements have not been
determined for horses, current recommended levels of forage (grass and preserved forages) are ideally ≥1.5 kg DM/100 kg bwt for all horses including those with high energy requirements (in which case young, less mature, high energy forages should be considered) (Harris et al. 2013). A target minimum, even for race horses, is 1.25 kg DM/100 kg bwt (Harris et al. 2013). Lower levels may be required for those horses on a strict veterinary monitored weight loss programme (but not less than 1 kg DM/100 kg bwt) in which case appropriate measures need to be put into place to maximise the time spent chewing the restricted forage intake (Bruynsteen et al. 2014; Ellis et al. 2015). Appropriate protein, vitamin and mineral balancers will be required to nutritionally balance the ration especially if fortified concentrate feeds are not required to be fed.
Reduce the intake of nonstructural carbohydrate Smaller grain diets should be fed. Larger grain meals, 700 g/ 100 kg bwt, resulted in slower gastric emptying compared to a smaller, 300 g/100 kg bwt grain meal (Metayer et al. 2004). Increased gastric retention time will increase the fermentation by resident bacteria, resulting in higher VFA production and a greater potential for squamous injury. The intake of nonstarch carbohydrates and particularly grains should therefore be restricted through the use of lower NSC complementary feeds. Based on previous studies, feeding <0.5 kg grain-based (‘sweet feed’)/100 kg bwt (NSC = 20%) should help keep stomach VFA concentration of acetic acid below threshold (20 mmol/l) and minimise the effect on squamous ulcers
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(Andrews et al. 2006). Feeding <2 g NSC/day or <1 g NSC/ meal has also been recommended (Luthersson et al. 2009). This can be a challenge for some trainers of high intensity exercising horses to achieve without an apparent (real or perceived) loss in performance, often resulting in the inclusion of various supplements as discussed below.
Antibiotics vs. probiotics Helicobacter pylori and other Helicobacter spp. have not been shown to cause squamous or glandular ulcers in horses, although Helicobacter DNA has been isolated from the squamous and glandular mucosa of horses (Scott et al. 2001; Contreras et al. 2007). Instead, other resident, acid-tolerant bacteria (Escherichia coli, Lactobacillus and Streptococcus) are suspected to contribute to the worsening of squamous ulcers (Al Jassim et al. 2008). A large population of these bacteria was isolated from the gastric contents of horses fed various diets in one study (Al Jassim et al. 2008). In rats, which have a compound stomach similar to horses, bacteria (E. coli) rapidly colonised acetic acid-induced glandular stomach ulcers and impaired glandular ulcer healing (Elliott et al. 1998). In that study, oral antibiotic treatment with streptomycin or penicillin suppressed bacterial colonisation of the ulcer and markedly accelerated glandular ulcer healing compared with placebo-treated controls. In addition, oral administration of lactulose resulted in increased Lactobacillus growth and colonisation of the ulcer bed, which may facilitate glandular ulcer healing. These studies in rats only looked at healing of ulcers in the glandular mucosa. In a study evaluating horses with spontaneously occurring squamous ulcers, an antibiotic (trimethoprim sulfadimidine) or a probiotic preparation containing Lactobacillus agilis, Lactobacillus salivarius, Lactobacillus equi, Streptococcus equinus and Streptococcus bovis administered orally decreased ulcer number and severity compared with untreated controls (Al Jassim et al. 2008). These data suggest that resident stomach bacteria are important in maintenance and progression of squamous ulcers in horses. Treatment with antibiotic or probiotic preparations may facilitate squamous ulcer healing after 2 weeks of treatment, but a full effect was not seen until after 4 weeks of treatment (Al Jassim et al. 2008). Antibiotic treatment may be indicated in horses with chronic nonresponsive squamous ulcers. However, antibiotic administration did not improve healing of glandular gastric ulceration in horses receiving omeprazole (Sykes et al. 2014a, b). In any case, antibiotics should be used responsibly and only when acid suppressive therapy and dietary management changes are not effective.
Dietary supplements
A plethora of equine dietary ‘supplements’ or feed additives are available on the market for gastric ulcers. Many of these products have not been tested in horses, and this is a controversial area for many reasons, not least that in many parts of the world legislation restricts the claims that can be made for such products, which perhaps reduces the likelihood of studies being undertaken to support efficacy (Harris et al. 2013). In addition, even if a product is shown to work under precise experimental conditions, there is no way to know if it works under real field conditions where multifactorial risk factors may be present (Sutton 2014). Alternatively, if it does not work under experimental
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