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  Discussion on Current Status of Founder Research
Author Message
Moderator:
DrO

Posted on Tuesday, Aug 15, 2006 - 11:22 am:

Here are two interesting summaries to articles that outline our current knowledge, or lack of, knowledge concerning the causes of founder with an emphasis on pasture associated founder. The first puts an emphasis on cecal derived vasoactive amines. However research has recently focused on the activation of metalloproteinase in the laminae by cecal bacteria toxins and possibility the influence of insulin resistance. There is still much we do not know and it still appears to me that we will find several different mechanisms or possible the interaction of these numerous factors.

J Nutr. 2006 Jul;136(7 Suppl):2103S-2107S.
Gastrointestinal derived factors are potential triggers for the development of acute equine laminitis.

Elliott J, Bailey SR.
Department of Veterinary Basic Sciences, The Royal Veterinary College, London, UK.

Equine laminitis is the painful and debilitating condition resulting from cellular damage and inflammation of the tissues comprising the bonds supporting the pedal bone within the hoof capsule. One of the reasons why this condition is so complicated and enigmatic is its association with gastrointestinal disturbances, particularly a diet of lush grass at certain times of the year. Determining the link between disturbances to the hindgut flora and pathophysiology in the foot is one of the keys to preventing this condition. Therefore, one of the biggest challenges in equine laminitis research is to determine those events that precede the onset of the classical clinical signs of lameness, bounding digital pulses, and warm feet. A main theory for the pathogenesis of acute laminitis involves the development of vasoconstriction within the foot, which leads to ischemic and/or inflammatory tissue damage. Serotonin is an important constrictor mediator controlling digital blood flow. Certain equine hindgut bacteria produce amino acid decarboxylase enzymes that convert free amino acids into monoamines. Therefore, amines formed and released from the gastrointestinal tract are hypothesized to act as the link between the ingestion of lush grass and the digital ischemia thought to precede laminitis. Equine cecal contents contain a range of amines that are present in micromolar concentrations. Tryptamine is the most potent cecum-derived amine, causing vasoconstriction in vitro and in vivo through direct activation of serotonin receptors and displacing serotonin from platelets. Monoamines found in the cecum of the horse could potentially induce hemodynamic disturbances in the digit that result in laminar ischaemia, and so trigger laminitis.


J Nutr. 2006 Jul;136(7 Suppl):2114S-2121S.
Countermeasures for pasture-associated laminitis in ponies and horses.

Harris P, Bailey SR, Elliott J, Longland A.
Equine Studies Group, WALTHAM Centre for Pet Nutrition, London, UK.

Laminitis occurs throughout the world in horses and ponies and has major welfare implications. It is obviously important to be able to recognize and treat the condition in its early stages so that pain and suffering are kept to a minimum. However, ideally it would be preferred to be able to recommend certain interventions/countermeasures that avoid or prevent the condition from occurring in the first place. Because pasture-associated laminitis occurs with grass consumption, one obvious way to avoid the condition is to prevent access to pasture and to feed forage alternatives that are known to be low in rapidly fermentable material. For the majority of horses, total restriction is not always a viable or desired option for financial, welfare, and health reasons. It also may not be necessary for those animals that are not predisposed to laminitis. This review discusses the possible countermeasures that could be considered now and in the future in the following 7 key areas:
1) Identifying animals predisposed to the condition;
2) Limiting development of insulin resistance;
3) Avoiding high intakes of rapidly fermentable material;
4) Preventing/reducing the formation and absorption of the various "triggering factors";
5) Reducing/preventing oxidative damage;
6) Preventing/reducing matrix metalloproteinase activity;
7) Preventing changes in blood flow.
It is unfortunate that little or no hard data exist at present on effective countermeasures, only mechanistic evidence for avoiding risk factors. However, there is much to gain, and research in this area is urgently required.

For specific recommendations on caring for the horse predisposed to founder see the article on Founder Overview and be sure to follow the links in that article to any relevant conditions that apply to your horse.
Member:
Erika

Posted on Tuesday, Aug 15, 2006 - 10:30 pm:

Thanks Dr. O, I am always interested in how to prevent and care for this devastating condition.

A couple of things came up tonight as I read other articles. One said that excessive fructans cause the proliferation of Streptococcus infantarius ssp. coli in the horse's gut, possibly releasing toxins that cause inflammation. If that is the case, could antibiotics possibly be of some use in the treatment of laminitis?

The second article discussed the success of removal of hoof wall to relieve further damage, since it usually heals very well. Again, do you foresee this possibly being a first-line treatment at any point in the future, or still a last ditch saving effort?
Erika
Member:
Paul303

Posted on Wednesday, Aug 16, 2006 - 1:45 am:

Mmmmm...yeah....what Erika said.
Moderator:
DrO

Posted on Wednesday, Aug 16, 2006 - 7:16 am:

Hello Erika,
Occasionally you see the suggestion of oral neomycin as a founder preventive measure for grain overload. It's efficacy has not been researched however. One problem with such therapy is that much of normal equine digestion depends on microbes and to specifically target those of the bowel will have adverse consequences on both digestion and nutrition. The balance of the good and bad of this procedure is what needs to be measured.

The toxins hypothesized released by Strep species are the same as those mentioned above that activate MMP's. There is much more on this in the article on founder.

There are several indications and techniques for removing wall from a foundered horse, I am uncertain to which one you are referring but these are discussed in the article. If after reading it you are still uncertain about the use of the procedure you read about, repost and give me some more details and I would be glad to comment.
DrO
Member:
Erika

Posted on Wednesday, Aug 16, 2006 - 7:55 am:

Thanks Doc. I don't have a current case of founder (thank God) but like to be prepared with the latest info.

I was speaking theoretically about hoof wall removal. I see that it does have it's place in severe cases. I was hypothesizing whether such a drastic move would prevent more severe damage, but I guess removing the wall would be considered pretty severe damage in itself, now that I think of it!

Thanks for the updates. We have a long way to go in understanding a lot about our horses' health. I am glad to see that there is so much research in this direction lately.

Erika
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