Introduction:
Recurrent Seasonal Pruritus ("Sweet Itch") in horses is a common complaint with horse-owners, and may indeed represent a significant cost to the equine industry. Approximately 20% of all Icelandic ponies exported from Iceland suffer from sweet itch. The condition is caused by the serum of biting insects, specifically the Culicoides or biting midge (also known as 'no-see-ums' and 'punkies'). These insects are not found on their native island so the horses have built up no immunity to the serum. Sweet itch is not restricted to Icelandics, and has been reported in many breeds around the world since the summer of 1840. It is known as 'Queensland Itch' in Australia, 'Kasen' in Japan, 'Sommerekzem' in Germany, and the condition has been reported in many other countries across the world. The condition has affected many horses across several U.S. states and Canadian provinces.

Flaxseed is the highest vegetable source of omega-3 fatty acids, and is fed routinely to affected horses by many stable managers. Although research has been conducted, confirming the practice of feeding omega-3 fatty acids to dogs as an effective treatment for atopic skin disease, limited data exist to validate this practice in horses. By demonstrating the efficacy of flaxseed supplementation in reducing the intra-dermal skin-test response of affected horses, new information will be made available to horse-owners about a relatively inexpensive alternative to standard corticosteroid therapy.

Materials and Methods:
Six Icelandic horses with a history of sweet itch, confirmed by an intradermal skin test with Culicoides extract, were transported to and housed at the Equine Research Centre for the duration of the 14 week, double-blind, placebo-controlled, cross-over trial. Each horse was randomly allocated to receive either flaxseed or placebo (3 horses per group) in their daily ration for a period of 42 days, after which horses received no supplements for a further 14 days. After a 14-day break, the groups were reversed, and the trial was repeated. In this way, each horse could act as its own control.

Results:
There was a significant improvement in the average skin test response of horses to Culicoides when they were receiving flaxseed. This was evidenced by a smaller area of the wheal that was created in response to the intradermal injection of Culicoides (see Figure 1).

There were no significant differences in the surface temperature of the skin test sites in either treatment or placebo groups.

Figure 1: Changes in the Area of Reaction from Culicoides

There were no significant changes in the fatty acid profile of skin or blood in either treatment or control horses. However, when horses were receiving flaxseed, there was a significant reduction in the concentration of some of the long-chain saturated fatty acids in the hair. As hair is composed mainly of protein and minerals, any changes in fatty acids must reflect changes in secretions that come from the skin and are deposited into the hair. These secretions form a waterproof coating that supports many bacteria (called "dermal microflora"), and some skin bacteria are known to metabolise compounds (trans-urocanic acid and histidine) that are involved in immune function. By altering the fatty acids of the skin secretions, it is possible that, in this study, certain populations of bacteria were affected, thereby changing the ability of these bacteria to metabolise these compounds, and reducing the immune response to Culicoides injection. Although it is not possible to confirm that this was the case with our current data, previous research does provide intriguing possibilities for a mechanism of action of the components of flaxseed.

Conclusions:
In this study, Flaxseed had the following effects:

• improved the average response of atopic horses to a common
  skin allergen
• no adverse effects, as determined by complete blood screens
• reduced concentration of the long-chain saturated fatty acids in the skin secretions, suggesting a possible mechanism of altered microbial metabolism leading to reduced immune response

Further studies with a larger sample size are required to confirm the possible mechanism described here.

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