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There appears to be an increasing consciousness over the concept of microbiome. Derived from microbiotica – classified as an ecological community of microorganisms found in or on around multicellular organisms (plants or animals). The microbiome describes the microorganisms themselves; despite the range of the definition, microbiome is generally recognised as those microorganisms inhabiting the mammalian gut. Microorganism is a deliberate term as it includes bacteria, viruses, fungi, protozoa and other single cell organisms – across three of the five kingdoms (plants and animals make up the other two kingdoms).

The microbiome is increasingly recognised as a potent influencer of its hosts health, function and wellbeing. Where, in the past, the gut microflora were responsible for affecting digestion, preventing the adhesion of pathogens to the gut wall and, in the case of herbivores releasing energy from fibre, the microbiome is now known to have a far greater interaction with the host, is probably unique to the host and will vary with the environment, both internal and external.

Animals are born (or hatched) with no microbiome but immediately ingest microorganisms. In the case of mammals this is mainly through maternal contact – suckling and faecal contamination – but also through soil contamination and latterly, creep feeding. The microbiome changes through weaning and then takes on its adult characteristics. In the case of the horse this will include a shift from mainly sugar fermenting bacteria – lactobacilli, bifidobacter – to those that can utilise fibre, such as ruminococcacea and lachnospiracea, mirroring the change in diet.

The microbiome also varies along the length of the gut. As the acidity of the environment changes from acidic to neutral, those microbes that are best suited dominate, and their interactions have important consequences. For example, there are lactic acid producing bacteria (streptococcus e.g.) along the length of the gut. However, in the small intestine lactic utilising bacteria, such as veilonella, reduce lactic to acetic and propionic. In the large intestine veilonella do not thrive and so any lactic generated is not utilised. It is this characteristic that can impact on hind gut integrity – by negatively affecting absorption – that can increase the risk of laminitis. In the case of laminitics, it has been shown that they have greater variation in their microbiome than non-laminitics, including the presence of specific clostridium species. The implication is that laminitics will have a more “volatile” inter-relationship, and so more susceptible to changes in the gut environment.

It is not just variations in the hindgut that can impact on wellbeing, but the stomach and small intestine too; it is the interaction between the microbiome and the gut wall, the gut barrier and the immunological sites (Peyers Patches).

Lining the gut and providing a physical barrier between it and the gut contents is a layer of mucin, embedded with phospholipids. This layer protects the gut wall from mechanical erosion and also inhibits microbial adhesion. This means that the gut populations move along the intestine with the food (collectively known as chyme) and change as the environment changes. Entering the lower gut results in a drop in the acid loving bacteria and rise in fibre fermenters. The microbiome is an ever- shifting spread of organisms, influenced in part by diet.

Although the barrier prevents adhesion, it is permeable to both feed nutrients, digesta and the by-products of the fermentation of the microbiome. However, this is not a straightforward and quantifiable resource. The fermentation end products of one bacterium can be a nutrient for another and so a microbial end product may be the result of a number of fermentations, an example of which can be the breakdown of cellulose: Figure 1. Bacterial breakdown of cellulose by various () bacteria.

The various nutrients etc. are then presented to the gut membrane where they cross into body by a number of mechanisms. Primary is the transcellular route – this means across the cell, either by active or passive transport – but secondary is the paracellular route. The paracellular route is the permeation of components between the cells of the gut wall and is governed by a complex of actin and myosin (the same biochemicals as a contracting muscle) regulated by a number of factors. This entire complex is known as a Tight Junction and has the capacity to expand and contract, allowing different sized nutrients to pass across the gut barrier into the lymph system. And, critically, many of the regulatory mechanisms are derived from the microbiome. As an example, lactate – derived from glucose fermentation, loosens the tight junction, whilst butyrate tightens it. In an optimal scenario, the small intestine can absorb larger molecules as more lactate is fermented there, although mediated by lactate utilizing bacteria. The hindgut, where fibre fermentation is greatest, generates less lactate and more butyrate, so absorption is limited to smaller molecules (such as the slow release VFA’s themselves). Changing the diet to starch-rich means more starch – glucose – to enter the hindgut which releases more lactate; there being less lactate utilising bacteria, the increased lactate loosens the tight junctions allowing the absorption of larger molecules. As these are generally endotoxins from other fermentation pathways (amines, pathogenic antigens), their absorption can cause problems. Keeping the tight junctions at optimal function is down to a well-balanced microbiome. Also, butyrate is essential in energising the cells of the gut themselves, where acetate and propionate are the major components of slow release energy and energise every cell in the body.

This leads to the final characteristic of the microbiome; it is influenced by the diet, both indirectly and directly.

Indirectly, as various nutrients have a direct impact on the gut barrier. Pectins – the soluble fibre faction, particularly rich in beet products – can be incorporated into the mucus layer, especially the gastric barrier, and stimulate mucus production of the small intestine; other components such as plant bioactives can support antioxidative control of the barrier integrity, and so help maintain its function and permeability.

Directly, dietary profiles will affect the population dynamics of the microbiome and so the quantities and proportions of fermentation end products, both useful (slow release energy), less so (nitrite a vasoconstrictor) or toxic (amines, for example). Feeding beyond a horse’s ability to digest nutrients sufficiently (diets too high in protein, starch etc. will result in microbiome disruption), causes undigested nutrients being fermented in the hindgut, changing the environment and disrupting the normal balance. By feeding within the parameters of what the horse is capable of digesting in the upper gut, the subsequent environment of the hindgut is not compromised. In the case of the horse, this is best achieved by ensuring that protein, oil and sugar/starch are kept at modest levels (oil has a specific role in the absorption of nutrients, but too much can lead to endogenous problems) and that fibre is the main energy source. Certainly, high energy diets can be achieved by choosing the right fibre sources, and the fibre profile is also a tool in maintaining an optimal microbiome.

In animals and plants, the microbiota has evolved alongside the host species. The modern horse has, through selective breeding, changed remarkably over the past few thousand years; however, its gut has not and is still suited to the microbiome of the nomadic species of the Asian steppes. Modern feeding practices need to recognise the central role of the microbiome and match it to the different lifestyles that the horse can achieve.