Acidosis, Lush Grass, and Laminitis
Though the exact mechanism of why spring/autumn grass causes laminitis isn’t known, there are many good explanations, theories, and published literature as to the why and how.
Despite not understanding the full reasons why, there are several known contributing factors, one of the most important is the altered or increased fermentation of rapidly digestible starch, sugar, and fructans contained in lush grass. The effect of such an increase produces an escalation in lactic acid production, a change in the microbial population, and a chronic or acute reduction in the pH of the hindgut that results in acidosis and laminitis.
Fig 1 How different foods affect the microbiome, high starch content makes the pH of the hindgut fall.
Acidosis Starch Overload
Acidosis is a particular state defined by a low pH in the hindgut, it can be also caused by high-starch meals given predominantly to sport/competition horses and is common in thoroughbred racehorse feeding practices. Though racehorses rarely get full-blown laminitis, acidosis causes increased digital pulses, sore feet, lethargy, weight loss, loss of appetite, hindgut ulceration, and poor performance syndrome.
In chronic cases of acidosis, the gut wall is weakened allowing for the leakage of toxins and pathogenic bacteria to translocate over the gut wall, creating other health problems in organs far away from the gut, and triggering a state of low-grade systemic inflammation and lactic acid buildup in muscles.
Acidosis caused by incomplete digestion of starch (from grains) rather than from lush grass, occurs frequently in racehorses (Richards et al., 2006), some grains such as maize and corn, digest quicker than others and cause a more rapid increase in lactic acid. Though not common outside of the thoroughbred industry both grains can be found in some sports and showing horse rations and for vulnerable horses these are best avoided.
Severe Acidosis (SIRS)
SIRS systemic inflammatory response syndrome, MODS or SRL (sepsis-related laminitis) is a type of laminitis caused by severe carbohydrate overload and alteration of the hindgut bacteria community.
The immune response to the bacterial infection is like the response in pleuropneumonia, enterocolitis, or endometritis.
Once triggered the innate immune system (Toll-Like Receptors) simply rage out of control through the body on a course of self-destruction from the gut/site of infection all the way down to the feet and continues unabated until another counter-response is triggered called CAR or compensatory anti-inflammatory response, the timing of this counter-response is absolutely make or break and decides whether the horse lives or dies. Both SIR and CAR have an equal set of signaling chemicals called cytokines and many animal studies have indicated that the balance of the response is entirely governed by the genetic/immune makeup of the individual and whether the timing of the SIR and CAR is in balance with each other.
This is the most extreme type of acidosis, with multiple symptoms affecting the feet, and respiratory systems, it can even cause blindness, the prognosis is guarded, and death is often the result.
Fig 2 Ulcers caused by SIRS/acidosis/laminitis.
As the image shows, the eyes of a mare affected by SIRS, can also be affected and involved in multiple organ failure, the eye membranes became red and inflamed by day 2 and an ulcer appeared in both eyes by day 6.
3 weeks on the mare is now fit, sound, and well and alongside the veterinary treatment of flunixin she was given 24 hour applications of ice to the feet, a four hourly 160 ml syringe of plant anti- oxidants (Pack of Polyphenols) mixed with omega 3 oil to mop up, buffer and protect the vital organs. Antioxidants are known to diminish and absorb circulating chemicals such as the IL cytokines
Though an episode of laminitis was inevitable as her heart rate was 88 bpm for 3 days, she was only lame for 1 week, with no rotation of the pedal bone.
Timeline of SIRS
SIRS previously known as ‘sepsis’ describes a cascade of inflammation and whilst the concentration is usually on the foot, (a digital pulse and paddling of the feet are usually the first symptoms) there is much more going on within the SIRS-afflicted horse. Research shows that, in these cases, subclinical inflammatory indicators are evident in the liver, lungs, and kidneys before the onset of clinical laminitis.
• A rectal temperature above 105°F or below 98°F (normal is 98.5-101.5);
• An elevated heart rate above 60 beats per minute (normal is around 30-40);
• Hyperventilation or abnormally rapid breathing.
A timeline of laminitis i.e. time to damage and expected damage to the structures of the foot.
Starch /Grain Overload Acodosis Laminitis
Undigested carbohydrates are pushed from the small stomach into the hindgut and cause a rapid change in the gut bacteria and a drop in pH, the lining of the gut disintegrates and toxins are absorbed into the bloodstream causing a massive inflammatory reaction.
Time to destruction/separation of the basement membrane is 24-40 hours
Time to the inflammatory response in the feet causing more damage is 72 hours, during this phase a chemical is released in the feet which is linked to the degeneration caused by arthritis.
Overload of Fructan Laminitis
Unknown mechanism of action but the time to destruction/separation of the basal membrane is 24-36 hours.
Toxaemia/Systemic Inflammatory Response Syndrome Laminitis
Caused by an infection or toxaemia
Time to destruction/separation of the basement membrane is 8-12 hours, there will also be a rapid loss of shape and arrangement of the sensitive lamellae.
Time to massive inflammatory response in the feet is 1.5 to 3 hours
Compare the above to endocrinopathic and mechanical onset laminitis.
Endocrinopathic (high insulin) laminitis- Unknown mechanism of action but insulin is thought to change the circulation to the foot causing vasoconstriction. There is a much slower onset of damage, no separation of the basement membrane, no massive inflammatory response either in the feet or in the gut. Lameness is due to the lengthening of the secondary epidermal lamellae, due to stretching rather than separation of the basement membrane, 28% of ponies are considered to have a higher than normal level of insulin and are said to be predisposed to this type of laminitis. Time to onset of laminitis from abnormally raised insulin levels is 36-48 hours
Mechanical onset laminitis, caused by uneven weight bearing or concussion-Is distinct from other forms of laminitis until the later stages, when there is evidence of secondary inflammation and vascular disruption, thought to be caused by inadequate blood flow to the tissues of the foot. Time to onset depends on the loading and level of concussion but within 20 hours.
First symptoms/warnings of acidosis
Symptoms of acidosis from overindulgence of grass and starch ingestion are-
Decreased appetite or loss of appetite,
Cribbing, weaving, anxious pawing the ground, obvious signs of discomfort.
Weight loss, lack of appetite, lethargy.
Anorexia (horse stops eating altogether)
Loss of performance, sometimes temporary but can cause chronic poor performance syndrome.
Mild Colic
Sore feet, digital pulses.
Inflamed joints
Diarrhoea
The role of fructans in the onset of acidosis caused by lush spring/autumn grass.
Laminitis has never been induced by the overfeeding of lush/spring grass, laboratory models use other methods and substances containing a type of fructan, hence there is a question as to whether fructans trigger laminitis at all, however as fructans are digested in the stomach and hindgut it’s worth taking a closer look at the mechanisms of breakdown.
Researchers first thought that fructans were indigestible in the stomach and that digestion could only occur by bacteria fermentation in the hindgut, however, more recent work has shown some fructans are broken down in the stomach by acidic hydrolysis or plant enzymes such as fibractase, alpha galactosidase and chitosan.
Digestion in the stomach starts with the release/secretion of hydrochloric acid (pH 2-5) causing the alteration/degradation of protein and the hydrolysis of polysaccharides including fructans. Fructans are more efficiently broken down at a pH 4 (Strauch et al., 2017)) however during a large meal such as the gorging of spring/autumn grass, the pH of the stomach becomes more acidic thus reducing the rate of fructan digestion and degradation, allowing a higher amount of fructans through to the hindgut where their rapid fermentation causes acidosis.
Bachmann et al. (2021) reported an increase in the relative abundance of lactic acid-producing Firmicutes and Bacteroides after feeding the horse a fructan supplement.
Some researchers identify fructans as being the number one cause of the drop in the pH of the hindgut, but there are studies that advocate adding a type of fructan (Jerusalem Artichoke Inulin) to the diet to improve the digestion of starch and sugars. The latter study indicated that adding a daily dose of fructans in the form of inulin to the diet conditioned the gut bacteria to be more active in the break- down of inulin fructan to lactic acid and SCFA. Priming the gut with a daily small dose of fructan (inulin) will increase the production of n-butyric acid.
Horses have gram-positive bacteria that contain fructokinase which can break down the fructan and convert it to fructose (Nocek et al 2011). The production or conversion of the fructan to fructose happens in the ileum (part of the small intestine) contributing to an increase in permeability of the gut wall otherwise known as leaky gut syndrome.
Recent studies suggest that this unusual and unique metabolism of fructose by fructokinase can lead to increased intestinal permeability and inflammation, plus the development of insulin resistance because of the effect of fruktokinase on liver function.
Previous work done by Kirsty Dougal et al has revealed that the predominant bacteria in the ileum (70%) belong to the largely gram-positive family and furthermore lactobacillaceae (gram positive) account for approximately 16.4% of this family.
Fructose triggers a change in metabolism more than any other nutrient, mainly because of its immediate influence on the endocrine system including leptin and insulin, and GLP-1, controlling intake and understanding the effect it has is paramount to controlling EMS and laminitis. For some owners who are constantly managing their horses diet to reduce/minimise or take out the fructose altogether, understanding the conversion of fructan to fructose by the gut bacteria might be the missing piece of the jigsaw.
Clearly, the horse is designed to break down and use fructans in a beneficial way, however, the regulatory/processing systems that exist may have been overwhelmed by the high levels of fructans arriving in the digestive system in grass consumed by horses turned out on lush pastures.
The role of histamine in the onset of acidosis
As the pH of the gut drops and pathogenic and lactic acid-producing bacteria increase, some of these bacteria produce lectins (Cohen et al., 2022). An abnormal increase in lectin increases the discharge of histamine from gastric mast cells and histamine-producing bacteria (Allisonella histaminiformans) identified in the faeces of cattle and the cecum of the horse from animals fed grain and grass but not from horses fed hay. The bacterium uses histamine to reproduce, it thrives in the acidic environment (acidosis).
Histamine production is part of an allergic reaction, foods containing high levels of lectins (grains), the allergic reaction to the lectin causes the gut wall to release even more histamine.
Histamine is a powerful inflammatory chemical that can cause the sudden inflammation of the gut wall and the dilation of blood vessels, it can also trigger the onset of laminitis either directly or because of a vasodilatory event.
Technological advances in the analysis of acidosis.
There are methods of testing for acidosis, including a kit to test the pH of faeces, and though quick, this method can't detect abnormal bacteria profile patterns which could help restore and rebalance the biome. The EquiBiome Analysis
provides a real-time snapshot of the microbial community, it is the most accurate test available as it is able to detect microbial profile patterns and can distinguish between dysbiosis (imbalances) of horses with endocrinopathic laminitis, EMS, and acidosis.
There are plans to develop a mobile biosensor that would continue to detect the abnormal bacteria community patterns initially identified by the EquiBiome analysis.
The mobile sensor would continue to help to monitor the health of the microbiome and management but if the gut as not all horses respond in the same way (see Fig 3) and those that are more vulnerable would benefit from being monitored more closely.
Fig 3. Horses respond differently to higher levels of rapidly digestible starch, different microbial fermentation patterns and the production of secondary metabolites are thought to be the reason.
Suitable targets would be Streptococcus equinus and Mitsuokella jalaludinii, post-concentrate feed makes them suitable targets for detection and subsequent indicators of equine hindgut acidosis (Fig 4).
Fig 4 from Davies, J., Thomas, C., Rizwan, M., & Gwenin, C. (2021). Development of electrochemical DNA biosensor for equine hindgut acidosis detection. Sensors, 21(7), 2319.
Comparing the feeding habits of wild/feral/freely grazing horses.
Large meals of cereal grains and access to high-sugar grasses/hay are not a natural part of an equine diet, horses have evolved as trickle feeders with high fibre content, and eating is also a social affair with a set pattern of social interactions.
Horses grazing naturally eat to maintain a high level of gut fill (Duncan. 2012), feeding consists of bouts of uninterrupted grazing separated by non-feeding intervals. Feeding doesn’t occur randomly but is divided into ‘meals’.
Feeding is part of being social and a herd activity, during mealtimes, horses take short (less than 10-minute breaks) to ‘look around’, stand guard or walk over to see what their neighbour is eating. There are longer periods between mealtimes for sleeping and resting and the feeding habits are similar to deer, i.e. food eaten includes grasses, sedges, leaves, tree shoots, and even bark, in the late summer/autumn fruit and berries are included.
Meal lengths are affected by the time of day, and herds prefer to eat duringn the day rather than the night.
Mealtimes in April are around 3 hours and 20 mins long, dropping to just 1 hour and 10 mins in October, the change in the length of the mealtime is due to the increase in the fibre content of the grass as the season goes on, suggesting that horses eat to fill their gut and to maintain a high gut fill level.
In April the nutritive value (glucose/starch/protein) of the green shoots is high whilst the biomass is low, meaning, horses must consume a greater quantity before the gut is full. Perhaps this partially explains why horses appear to gorge in spring, and why turning a horse out onto an unsuitable pasture ie containing high-sugar grasses causes a glut of carbohydrates to overflow into the hindgut instead of being digested in the stomach and small intestine.
One approach for horses prone to acidosis/laminitis might be to feed a hay net of low quality fodder before turning out and avoid a grazing mask which may cause a greater degree of stress to a hungry horse trying to fill his gut with fibre.
During times when flies are a nuisance, mealtimes are much shorter, horses stop feeding to rub themselves on each other and to groom each other, intervals between meals are longer and horses no longer feed until full and have longer periods of walking in between. The average feeding bout in between grooming and rubbing is around 25-45 seconds, literally snatching a bite to eat!
This change in routine coincides with mid- season when glucose/nutritive is still high and fibre content is also high enough to allow less time eating before gut fill level is achieved. Flies become a nuisance in the UK from the beginning to mid-June onwards, and in the fly season, feral horses graze for much longer periods between the hours of 4am and 8am.
Considering this information it may be a better regime to bring the horse in from the field through the day, to avoid the flies, provide a portion or two of low-quality hay to nibble and reduce the calorie intake through the day as nature intended.
Fertilised versus unfertilised pastures.
Fertilised pastures are reported to have a lower sugar content than unfertilised fields which could be a bonus, but they also have a higher nondigestible fibre content (Valk et al, 1996) meaning the horse will have to eat more to attain gut fill. Some native low-quality grass species contain less sugar and more fibre and in the autumn prior to the second flush of lush grass having an area of the field containing standing hay is of obvious benefit.
The benefits of ingesting fibre from standing hay
Standing hay is useful for horses to eat from the autumn through into the winter and has several benefits, (Fig 5) this is my own in February 23, almost grazed down, but still having a few seed heads to keep the horses happy and a second image of the same field currently (July 23). Note the plantain seed heads intact in the July image and all eaten by February. Plantain contains many secondary plant compounds, vitamins and antioxidants that support good gastric health.
Nutritive value of seed heads on the health of the microbiome.
Seeds stay longer in the gut of horses (up to 2 weeks) and go through many digestive actions, some of which provide remarkable benefits to horse health.
When ingested the seeds are abraded (the surface is worn away or damaged) and crushed by the grinding action of the teeth, they are then warmed up and made wet before being soaked in acid in the stomach and small intestine.
Finally, they are colonized by the gut bacteria in the cecum and large intestine. Proteolytic bacteria adhere to the surface of the seeds and excrete enzymes as they digest the hard, outer surface.
These enzymes have significant health benefits to the horse including the modulation of inflammation (gastric ulcers), reduction in swelling of the mucus membranes (helpful for gut wall integrity) and improving circulation.
Some examples of seeds that grow better after first being eaten, a great way to increase the biodiversity of your own equine pastures.
10,000 varieties of grass seed.
19,000 species of fabaceae (legumes)
4,400 species of sedges and rushes
1,265 species of flowering plants such as Cistaceae
2,500 species of small shrubs and herbs including the common nettle.
The microbiome profile of horses with acidosis.
Prior to the onset of laminitis, there is an increase in the species of bacteria that produce lactic acid (lactobacillus) and an increase in the bacteria that thrive in an acidic environment, plus a reduction in the bacteria that digest fibre, fibrobacteres (Jassim et al., 2005).
Fig 5. The onset of acidosis, showing a decrease in fibre digesting bacteria (Fibrobacteres and Firmicutes) and an increase in acid-producing bacteria Bacillota and Spirochaetes.
Lactobacilli were isolated from different gut sections in horses with laminitis caused by acidosis (Jassim et al., 2005) which indicates the ability of lactobacilli to adapt to changes in pH.
Lactobacillus salivarius adheres to the gut wall and has been isolated from the colon and rectum, it breaks down amino acids, possibly producing vasoactive amines such as histamine.
L. delbrueckii has been found in the gastrointestinal tract of horses and humans where it is identified as the main causative agent for the human form of gastrointestinal D-lactic acidosis.
Vasoactive is a term given to substances that are either vasoconstrictor (causing constriction or narrowing of the blood vessels) or have a dilator effect (causing dilation of the blood vessels.
In the case of horses with laminitis the effect of the histamine is hypothesised to contribute to the onset of laminitis by constricting the vessels to the hoof causing ischemia.
The increase of bacteria that thrive in an acidic gastric environment.
As the lactic acid bacteria increase and the pH of the gut drops, the bacteria that thrive in an acidic environment also increase. A low hindgut pH favours a particular group of bacteria called Spirochaetes. This family contains some of the most pathogenic disease-related bacteria such as Treponema pallidum (syphilis) and-
Leptospira (leptospirosis),
Borrelia (Lyme)
Treponema Pertenue (Yaws)
Spirochaetes are commonly found in the equine microbiome and are part of the core, common to all horses, (Dougal et al 2012) though the species listed below are not considered to be True Pathogens (always linked to disease). However, as all spirochaetes can translocate across the gut wall, high levels are thought to be detrimental to health and reduction is recommended. Spirochetes multiply in the blood and can survive in extravascular sites even when the bacteria in the blood have been eliminated.
The species found in the equine microbiome
Treponema_bryantii
Treponema_porcinum
Treponema_brennaborense
Treponema_saccharophilum
Treponema_amylovorum
Treponema_socranskii(
Treponema_parvum
Treponema_berlinense
The benefits of Treponema species listed above.
Treponema do have some benefits when present in the biome within a recommended average of 7-9%.
Treponema help and assist other members of the biome, such as Bacteriodes succinogens and Ruminococcus Alba in breaking down the woody, stemmy parts of plant material. Treponema consumes glucose and converts it into succinate, butyrate, acetate and formate. Succinate is an important antioxidant however when levels are too high inflammation and imbalance can occur within the gut.
Treponema needs vitamins and minerals to thrive, such are calcium, vitamin B1, vitamin B3, vitamin B5, vitamin B6, vitamin B9 and biotin. It also needs inulin and fructo-oligosaccharides, arabinoxylan and guar gum (found in many equine probiotics).
Horses with gastric ulcers have a different microbiome profile than healthy horses having levels of treponema higher than 9%, and a type of dysbiosis linked to ulceration.
Spirochetes are long, slender, and tightly coiled like a miniature spring, this shape together with an inbuilt motor and hook system enables them to cross connective tissues and the gut wall barrier, the speed of travel allows them to escape from the host’s immune system.
Fig 6 Spirochaete (Shutterstock)
Using the data from our own database of the analyses of 1,000’s of horses, the average percentage of Treponema within the microbiome of healthy horses is 9%, levels can increase in horses with laminitis, PSSM and acidosis to between 17-40% of the total biome.
Plant antimicrobials to reduce Treponema and the rationale for using them.
Treponema is a core member of the microbiome of horses at an average percent of 9%, however, when an imbalance or dysbiosis of the microbiome occurs, such as acidosis there is an increase and a rise in percentages of Treponema to 17% or above.
There is scientific evidence to support the use of antibiotics to reduce treponema species (Zeng et al., 2021, Dwivedi et al., 2015), infections responding to penicillin, erythromycin, and azithromycin with procaine penicillin G given intramuscularly to horses.
Recently there has been evidence of Treponema antibiotic resistance (Dwivedi et al., 2015). To combat antibiotic resistance there is a growing interest in the use of plant antimicrobial compounds such as terpenoids, either as an extract or by using the whole plant. There is a long history of ethnomedicinal use of plants to reduce Treponema infections (Vermani & Garg 2002, Soviati et al., 2020). Using evidence of before and after from our own database sarsaparilla (Smilax) and Acacia Catechu are both effective in reducing overgrowths of Treponema at a daily dose of 5g for sarsaparilla root and 2g of acacia catechu for 1 month.
Other plants include any member of the salvia family including Sage (Salvia officinalis) originates from the latin word salvere meaning be well! Is an important medicinal plant and just a daily dose of 6-7 fresh leaves can be used to help maintain a healthy gastrointestinal tract, sage will promote good bacteria and be effective against the over-proliferation of gram-negative bacteria (Treponema).
May also be used as a grooming tool for horses with long-term or chronic acidosis that have a build-up of lactate in the muscles.
List of other plants that contain terpenoids similar to salvicine.
Amaranthus spinosus (Amaranthaceae), Piper betle (Piperaceae), Pongamia pinnata (Leguminaceae), Sida cordifolia (Malvaceae), Ocimum tenuiflorum (Labiateae), Curcuma longa (Zingiberaceae), Swertia chirata (Gentianaceae), Phyllanthus niruri (Euphorbiaceae), Abrus precatorius (Leguminaceae), Aloe vera (Asphodelaceae), Senna alata (Leguminaceae), and Pistia stratiotes (Araceae). Plants used to treat syphilis include (with family name in parenthesis) include Cassia fistula (Leguminaceae), Mucuna pruriens (Leguminaceae), Solanum surattense (Solanaceae), Azadirachta indica (Meliaceae), Terminalia chebula (Combretaceae), Phyllanthus niruri (Euphorbiaceae), Gloriosa superba (Colchicaceae), Areca catechu (Arecaceae), and Gmelina arborea (Labiateae). The plant Phyllanthus niruri (Euphorbiaceae) was used as remedy for both syphilis and gonorrhea.
A timeline of laminitis- time to damage and expected damage to the structures of the foot.
Carbohydrate overload -Undigested carbohydrates pushed from the small stomach into the hindgut and cause a rapid change in the gut bacteria and a drop in pH, the lining of the gut disintegrates and toxins are absorbed into the bloodstream within 72 hours causing a massive inflammatory reaction.
Time to destruction/separation of the basement membrane is 24-40 hours
Time to the inflammatory response in the feet causing more damage is 72hours, during this phase a chemical is released in the feet which is linked to the degeneration caused by arthritis.
Overload of Fructan Laminitis- Unknown mechanism of action but time to destruction/separation of the basal membrane is 24-36 hours.
.Toxaemia/Systemic Inflammatory Response Syndrome Laminitis
Caused by an infection or toxaemia
Time to destruction/separation of the basement membrane is 8-12 hours, there will also be a rapid loss of shape and arrangement of the sensitive lamellae.
Time to massive inflammatory response in the feet is 1.5 to 3 hours
Compare the above to other types of laminitis with a different etiology.
Endocrinopathic (high insulin) laminitis- Unknown mechanism of action but insulin is thought to change the circulation to the foot causing vasoconstriction. There is a much slower onset of damage, no separation of the basement membrane, no massive inflammatory response either in the feet or in the gut. Lameness is due to the lengthening of the secondary epidermal lamellae, due to stretching rather than separation of the basement membrane, 28% of ponies are considered to have a higher than normal level of insulin and are said to be predisposed to this type of laminitis. Time to onset of laminitis from abnormally raised insulin levels is 36-48 hours
Mechanical onset laminitis- caused by uneven weight bearing or concussion-Is distinct from other forms of laminitis until the later stages, when there is evidence of secondary inflammation and vascular disruption, thought to be caused by inadequate blood flow to the tissues of the foot. Time to onset depends on the loading and level of concussion but within 20 hours.
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