Dr. Judith L. Mulholland

The horse has evolved to eat a large volume of low quality roughage which is passed through the digestive tract at a faster rate than most other herbivores. Horses prefer a different part of the plants than other grazers, this is a way of encountering less competition for food. Ruminants (cattle, sheep, goats etc.) have a large fore stomach, which is populated by bacteria and protozoa which allows them to digest cellulose (the fibrous part of plants), and they are 30% more efficient than equines at digesting it. However, once the rumen is full, they must stop eating and ruminate (re-chew) the feed. The poorer the quality of the feed the longer it takes to digest. This limits how much a ruminant can eat. When horses encounter poor quality feed their survival strategy is to eat more. They digest cellulose in their caecum (hind gut), which is also populated by bacteria. Therefore, they cannot, and do not need to re-chew their food. By eating a lot more of what is available, horses will survive where cattle will not because, they eat constantly and digest quickly.

This evolutionary fact is why domesticated horses encounter so many problems when we try to feed them on high carbohydrate diets. The carbohydrate (starches, sugars etc.) which are not digested in the small intestine reach the caecum, where the bacteria which are there to digest the fibre cause energy rich feed to ferment, and this is the first step towards acidosis and feed induced laminitis.

Equines are also subjected to feed grown on poor quality soils which are low in essential minerals and elements. They graze many toxic plants, and different types of grasses to those which they evolved to eat.

Sugar and starch levels in growing grass vary by the hour, depending on the time of day and amount of sunshine. Fructan is a soluble sugar which occurs in high concentrations in the stem of grass. Mammals do not make the enzyme required to digest fructans, and they go through the small intestines undigested to the hind gut, where the microorganisms can ferment and digest it. The Streptococci bacteria, which favour its digestion, undergo a population explosion which precedes acidosis (refer below). Therefore a warm, sunny afternoon in late spring is more likely to cause D-lactic acidosis and laminitis than a cool morning in autumn because the pasture plants have been photosynthesising all day and accumulating fructan. Ponies can get laminitis in hours, or overnight.

• The horse eats a lot of grain, or a different type of grain, or spring grass rich in carbohydrate (starch and/or sugars).

• Some digestion of sugars and starches occurs in the small intestine, but much of the grain or grass and all of the fructan will get to the large intestine. This is where all cellulose (the fibrous part of plants) is digested. Bacteria in the large caecum (hind gut) secrete the enzymes which digest the fibre but, when there is a lot of carbohydrate present as well, this is fermented via Lactobacillus species and Streptococcus equinus and bovis bacteria to the D and L isoforms of lactic acid. The host can use the L form but the D form persists in the hind gut and leads to D-lactic acidosis.

• A venous blood test can confirm the presence of D-lactic acid.

• The increasing acidity causes the pH to drop from normal 6.8 - 7.0 down to 4.0-5.0 which kills most of the normal bacterial flora of the caecum, including gram negative enterobacteriaceae species which release the lipopolysacharide component of their cell wall as an endotoxin.

• The endotoxins are absorbed during the developmental phase of laminitis leading to endotoxaemia. This may lead to watery diarrhoea and fever. However, giving endotoxin alone in experimental models has not been able to cause laminitis.

• By 24 hours after carbohydrate overload the epithelial cells which line the caecum begin to degenerate, and the damaged large bowel becomes leaky. By 49-72 hours, the cells have sloughed off, which allows the lactic acid and endotoxin to be absorbed straight into the blood stream where they act as laminitis trigger factors. About 10 - 15% of horses can die from accidental ingestion of large amounts of grain, leading to cardiovascular shock. These horses appear severely ill, with a high heart and respiration rate, fever, colic, diarrhoea etc.

• When these severe cases begin to respond and recover from the primary digestive insult, they have reached the time frame for the clinical signs of the second stage of laminitis to appear.

• The rate of fermentation in the hind gut depends upon the type of grain and starch content. High risk grains are wheat, sorghum, corn, barley and bread. Oats are considered low risk.

• A few species of bacteria prefer the low pH, and these acid loving bacteria proliferate rapidly and go on to produce more acid as they ferment the carbohydrate and further lower the pH. The result is the whole population of micro flora in the caecum has been changed in a matter of hours.

• Streptococcus bovis is a bacteria which proliferates during fermentation and acid production. It is suspected that not only does it like an acidic environment and produces acid itself, it also releases an exotoxin that is implicated in the activation of the MMP enzymes which dissolve the basement membrane leading to laminitis.

• The horse has now absorbed the toxins from the bacteria, the acid from fermentation and the caecum and the large intestines have become inflamed.

• Inflammation and the low pH attracts water so that fluid is lost into the large intestines from the body. The effect of this is an acidic and dehydrated animal. Dehydration leads to decreased perfusion of tissues. Local tissue effects begin to occur to counteract this which can eventually lead to vasoconstriction. This short term attempt at raising blood pressure leaves the peripheral tissues depleted of blood flow and cellular waste products being to increase in a low oxygen environment so that eventually the vasoconstrictive effects are overcome and this is followed by vasodilation and systemic shock.

• Laminitis results from the effect of the toxins and acidity which lead to inflammation of the tissues, localised circulatory changes, and derangement of the normal activities of the enzymes which regulate the chemical bonds which adhere the basement membrane and laminae to each other within the hoof.

• The basement membranes of organs and tissues throughout the body are being affected. In the hoof this is marked by the dissolving of the normal chemical bonds which keep the sensitive and insensitive laminae tightly bound to each other.

• The laminae separate and the laminitis progresses.