Laminitis, like many conditions, is a description of the effect rather than its cause. That is the condition is an inflammation of the lamellar and may be caused by a number of factors including physical damage, bacterial toxins (disease), metabolic conditions – EMS, IR & Cushing’s Disease - and diet.
In the case of diet, nutritional imbalance can trigger an effect, but the best-known “culprit” is probably the feeding of excess non-structural carbohydrates, such as starch or fructans. This generates high levels of lactic acid, which increases the absorption of negative factors from the hindgut.
What is a common factor is the inundation of tissues with oxidative, inflammatory, toxic and vaso-constrictive parameters in the extremities (limbs) due to – in part - reduced circulation, compared to the body core.
Why then are non-structural carbohydrates particularly implicated whilst structural ones (fibres) are not? The answer is relatively simple. It depends on the microbes in the gut.
The gut of the horse has three major areas; the stomach, the foregut or small intestine and the hindgut. In order to process the fibrous food that is its natural diet, the hindgut is disproportionately large compared with the rest of the gastro-intestinal tract and acts as a fermentation chamber. The stomach produces acid to condition feed – especially to denature protein and initiate the breakdown of starch, while the small intestine bombards feed with enzymes and absorbs the resultant nutrients. This means that the large intestine deals with those nutrients that aren’t absorbed or cannot be broken down by the horse’s enzymes.
It is a combination of the available nutrients and the acidity along different portions of the gut, that dictate the populations of microbes, from acid loving lactobacilli in the stomach, to more basic preferring cellulytic bacteria in the hindgut. In conjunction with recent research, that 15% of starch, 10% of oil, up to 70% of protein and 95% of fibre leave the small intestine undigested, the hindgut is major area of fibre fermentation. Whilst there are 100’s of cellulytic bacteria per ml in the stomach and small intestine, there are millions per ml in the large intestine. However the numbers of lactic producing bacteria and lactic utilising bacteria do not change significantly along the length of the intestine.
This means that, in a normal horse, whilst the starch and sugars that are not digested are broken down to lactic acid along the length of the gut, the lactic utilising bacteria take this lactic acid and convert it to volatile fatty acids, or slow release energy. Even when the starch level of a diet increases, the relative numbers of the lactic producers and lactic utilisers remains relatively constant and so there does not appear to be a nett increase in lactic acid in the hindgut. Obviously this is a fairly simplistic explanation, as there are many species of bacteria and other micro-organisms in the hindgut but the overall effect holds true: nett lactic acid production, irrespective of the diet (as long as it remains within reasonable limits) remains constant and so there is no “cue” to initiate the process of endotoxin absorption, vaso-constriction and inflammation. Meanwhile the cellulytic bacteria (and those that utilise other fibre structures) carry on generating slow release energy.
So why is the laminitic different, and why is it that individuals come down with laminitis whilst their pasture mates seem immune?
Recent research has shown that there are two major effects at work. Firstly, dietary change. In intestinally diseased horses there is a concomitant decrease of fibre utilisers (Fibrobacter, Ruminococcaceae) and a rise in lactic producers (Lactobacilli, Bacilli, Streptococci) in the hindgut, whilst lactic utilisers (Veillonellaceae) remain constant. Nett result is increasing lactic acid and endotoxins from the destruction of the fibre users.
The second factor is probably the decider, in that it appears to be that which determines whether a horse will be laminitic or not.
Laminitic horses have a higher diversity of hindgut microbes than “normal” horses. Researchers publishing their work in BMC Veterinary Research discovered that, using the diversity index of OTU, that laminitic horses had around 20% greater diversity of species. Because of the complexity of microbial systems it is not possible to identify them all but the research concluded that not only were there were large differences in the numbers of microbes common to laminitic and normal horses, but laminitics also had far greater populations of two Clostridiales genera.
This research is in early stages, the authors pointing out that many species are uncharacterised and future investigation is warranted, but identification of species such as some similar to Mitsuokella jalaluinii – which has been shown to generate massive amounts of lactic acid (22.6 mM compared to 3.7 mM from Lactobacillus delbrueckii) – indicates how diversity may upset the lactic producing/lactic utilising balance.
We are still some way from being able to identify laminitis potential from hindgut microbial proportions, but we are moving in the right direction.
For more information on Fibre-Beet or Speedi-Beet please contact British Horse Feeds on 01765 680300 or visit www.britishhorsefeeds.com