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Explaining Laminitis Part Two - What Causes Laminitis & Symptoms

Explaining Laminitis and Founder

Part Two
What Causes Laminitis?

What Causes Laminitis?
Though we have ample experience of how laminitis affects the horse during the acute painful stage, we know less about what causes things to go wrong in the first place. We know that laminitis occurs following a number of distinct occurrences in areas of the horses body often completely separate from the hooves:
• Following ingestion of large quantities of grain or fresh green pasture (carbohydrate overload)
• Following localized or systemic infection (e.g. retained placenta, respiratory infections)
• Following musculoskeletal problems (e.g. Rhabdomyolysis or ‘tying up’)
• Following periods of extended concussion (e.g. working on hard dry ground for long distances without rest)
• Severe, painful injury to one limb causes laminitis in the opposite supporting limb
• In response to an hormonal imbalance (e.g. Obesity, Equine Cushing’s Disease)
• Following prolonged antibiotic treatment (disrupting hind gut microflora)
• Following administration of excessive levels of corticosteroids

Disturbingly, there are a number of cases each year for which there is no obvious cause; sometimes laminitis seems to just ‘happen’ with no preceding occurrence or apparent risk factor to blame. For the non mechanical causes above, we assume that the triggering factor or factors are carried in the blood from wherever they originate and when they arrive at the hooves, begin their path of destruction. What we don’t know conclusively is what those triggering factors are, whether they are different depending on the initializing event and how they ultimately lead to the breakdown of the basement membrane. It’s likely that there is more than just one trigger factor involved, but singling out these substances will be the subject of research studies for some time to come.

‘Disturbingly, there are a number of cases each year for which there is no obvious cause; sometimes laminitis seems to just ‘happen’’

Carbohydrate Overload
This type of laminitis is the most common, is one of the most studied, and so is the type of laminitis that we know the most about. Recent research has suggested a couple of pathways. Current understanding outlines that after a large meal containing excessive levels of starch and sugar (i.e. a large grain meal), carbohydrates that are not fully digested in the small intestine pass back to the hindgut where they are fermented by certain sugar loving microbes. These microbes produce lactic acid as a by product, which in turn destroys many of the more sensitive microbes. As the balance is disturbed and the microbes continue to die, they release endotoxins which Dr. Chris Pollitt believes may alter the permeability (leakiness) of the hind gut lining. It is thought that this massive shift allows the release of one or more of the laminitis trigger factors into the bloodstream where they travel rapidly to the hooves and begin the process of laminitis. One of the sugar loving bacteria has been identified as a possible trigger factor for laminitis. During carbohydrate overload, Streptococcus bovis is the principal bacteria responsible for the fermentation of sugars to lactic acid. The numbers of S. bovis literally explode when sufficient carbohydrate is introduced to the hind gut. Laboratory models of laminitis have shown that S. bovis readily activates the MMP enzyme imbalance and experimentally causes laminitis. If it can be shown that S.bovis manages to escape the confines of the equine hind gut and reach the internal structures of the foot, this may answer one of the questions regarding trigger factors, at least for laminitis caused by grain overload.

Grass Founder
The modus operandi of grass founder is thought to be slightly different to grain founder, though usually leads to the same end result. In grass founder, research has concentrated on the presence of certain carbohydrates in grasses. In 1998 researchers Annette Longland and Andrew Cairns from the institute of Grassland and Environmental Research in Aberystwyth, Wales described the mechanism by which grasses store and use sugars as their energy source. Most plants store carbohydrate as starches (chains of the simple sugar glucose), but grasses store carbohydrate as fructan (chains of the simple sugar fructose). Grasses contain varying proportions of carbohydrates such as sucrose, glucose, fructose and fructans stored from the process of photosynthesis (the plants mechanism of making food for the energy to grow). Depending on climate and conditions, levels of sucrose and fructans fluctuate in grasses, and the researchers explained that variations in exposure to sunlight, day length, temperature and soil fertility etc. would drastically affect the levels of these carbohydrates in grass. They went on to explain that sugars are only produced during the day whilst there is light to power photosynthesis, and at night the plant uses the stores accumulated during the day. This means that the lowest levels of fructan would be present at first light, and the highest levels would be present in the evening. Some hays cut late in the afternoon in cool but sunny weather can contain high levels of fructan and the temperate grasses of southern regions are deemed to be more dangerous than the tropical species found further north.

‘…the lowest levels of fructan are present at first light,
 and the highest levels are present in the evening’

Fructans are stored in the lower part of the plant, so when grasses have been cropped close to the ground, the re-growth contains fructans as the primary storage unit. The more stressed the plant is, the slower it will grow, and the higher the concentration of fructans will become. For example, grasses that are exposed to stressful conditions such as frost will still produce fructan, but growth will be limited, so the fructan will be concentrated in the short grass. In Australia, where severe droughts are commonplace, the re-growth following drought breaking rain can contain dangerous levels of fructan. So in any of these conditions, a horse could be eating a diet that is very high in fructan – but what does this mean? Grass laminitis is a seasonal problem in most cases, brought on by the fresh growth of spring grass that is high in total sugar content (and presumably fructan). But laminitis has also been seen in horses that are restricted to ‘starvation paddocks’, where the short grass is stressed but still rich in fructans. Fructan cannot be digested in the small intestine, so passes through straight to the hind-gut.

‘In Australia, the re-growth following drought breaking rain
can contain dangerous levels of fructan’

Rapid consumption of these sugar rich grasses is thought to overwhelm the hind gut with fructan and other carbohydrates that escape digestion in the small intestine, similar to grain overload. But there, it is thought that the similarity ends. It has always been difficult for researchers to explain why the developmental stage of laminitis is not seen in grass foundered horses as it is in grain overload, with the horse or pony being discovered in severe pain, with no preceding signs. Perhaps the differences are a result of a difference in the way that fructans are fermented, and the way in which the trigger factor is released. Perhaps in the case of grass founder, the trigger factor is altogether different to that of grain overload, as yet, we just don’t know. This is the area of laminitis research currently being studied by Dr. Chris Pollitt New research could lead to the development of an analysis kit to assess the risk of certain pasture types and to indications about the best time of day for turnout in susceptible horses. It has already been accepted as common practice to limit turnout in susceptible horses during the day in the growing season, to beware of grazing stressed pastures and that feeding lucerne hay may be a good alternative as lucerne is relatively low in carbohydrates and fructan. We may in the future see special ‘laminitis proof’ pasture’s being developed with cultivars of grasses designed to have a low fructan content, but for now, we must observe the suggestions based on the facts that we have so far.

Concussion Laminitis
Though the feet of our equine friends are strong, they were never designed to take the kind of forces that we regularly thrust upon them. During the long hot summers, when the ground becomes extremely compacted, there is an increased risk of concussion laminitis. Pounding away on hard ground day after day affects the blood flow to the foot and may cause changes in the lamellar membrane. This in turn may lead to the mechanical tearing of the lamellar membrane leading to the partial or total breakdown of attachment to the pedal bone as previously described. This type of laminitis may affect only a portion of the lamellar surface, and so may not lead to a complete breakdown of the membrane, but can nevertheless be devastating for the horse involved.

Symptoms of Laminitis
The most disturbing thing about laminitis is that the initial developmental stages usually go undetected. It is only once the horse has begun to feel the pain of laminitis that the owner recognizes that something is amiss. Of course, by the time the pain is evident, much of the damage has already occurred, and the onus is then on damage control. Some of the symptoms currently recognized easily by the owner include:

• In the early stages, restlessness, warmth in the feet, shifting of weight from one foot to the other – if you notice these signs after a high risk incident, or your horse has had laminitis previously, it is wise to seek veterinary help immediately. Once the condition has become acute:
• Sore feet, usually in the front, but can also be apparent in the rear, especially in donkeys. The toe region is especially sensitive when tested with hoof testers.
• Throbbing digital pulse and heat in the feet
• Short, choppy strides and/or general reluctance to move, lameness in one or more limbs, especially when turning circles
• Characteristic ‘rocking horse’ stance with the hind legs tucked well under the body and the forelegs stretched out to allow weight transfer to the heel region.
• Bruising on the sole as a result of pedal rotation or sinking crushing the underlying capillaries, and bruising of the white line area

In chronic ongoing laminitis cases:
• Rings and ridges in the hoof wall
• Bruised soles or stone bruises
• Seedy toe (widening of the white line)
• Dropped soles

As we begin to learn more about laminitis, it is hoped that we will be able to pick up on some other early warning systems that can be recognized by the horse owner and used to begin treatment more rapidly.

Article reproduced courtesy of Kentucky Equine Research

Part One
Anatomy of the Horses Foot 
What Happens When a Horse Suffers a Laminitis Attack?

Part Three
Current Advice on Treating Laminitis

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