Matt73
Well-Known Member
I called Guelph two days ago for an update on Royal's autopsy (gosh that sounds odd and sad to me
) and got some good/bad news. He said that nothing has shown up so far in culture. No parasites, salmonella, clostrodium difficile, etc. But, reading on Wikipedia it can be hard to pin down a cause and we may never know...I said good and bad because he said it's nothing contagious, but I'd still like to know what caused it.
"To date, the precise causative factor has not been verified, and the disease has been attributed by various sources to viruses, parasites, bacteria, use of antibiotics and sulfonamides and heavy metal poisoning.[2][3][1] Other possible causes include peracute salmonellosis, clostridial enterocolitis, and endotoxemia.[1] Of interest is that Clostridium difficile toxins isolated in the horse have a genotype that is also that of the current human "epidemic strain," which is associated with human C. difficile-associated disease of greater than historical severity.[4] C.difficile can cause pseudomembranous colitis in humans,[5] and in hospitalized patients who develop it, fulminant C. difficile colitis is a significant and increasing cause of death.[6]
Horses under stress appear to be more susceptible to developing colitis X.[2] Disease onset is often closely associated with surgery or transport.[1] Excess protein and lack of cellulose content in the diet (a diet heavy on grain and lacking adequate hay or similar roughage) is thought to be the trigger for the multiplication of clostridial organisms.[3] A similar condition may be seen after administration of tetracycline or lincomycin to horses.[1] These factors may be one reason the condition often develops in race horses, having been responsible for the deaths of the Thoroughbred filly Landaluce,[7][8] the Quarter Horse stallion Lightning Bar,[9] and is one theory for the sudden death of Kentucky Derby winner Swale.[7]
The link to stress suggests that the condition may be brought on by changes in the microflora of the cecum and colon that lower the number of anaerobic bacteria, increase the number of gram-negative enteric bacteria, and decrease anaerobic fermentation of soluble carbohydrates, resulting in damage to the cecal and colonic mucosa and allowing increased absorption of endotoxins from the lumen of the gut.[10]" (Wikipedia)
"To date, the precise causative factor has not been verified, and the disease has been attributed by various sources to viruses, parasites, bacteria, use of antibiotics and sulfonamides and heavy metal poisoning.[2][3][1] Other possible causes include peracute salmonellosis, clostridial enterocolitis, and endotoxemia.[1] Of interest is that Clostridium difficile toxins isolated in the horse have a genotype that is also that of the current human "epidemic strain," which is associated with human C. difficile-associated disease of greater than historical severity.[4] C.difficile can cause pseudomembranous colitis in humans,[5] and in hospitalized patients who develop it, fulminant C. difficile colitis is a significant and increasing cause of death.[6]
Horses under stress appear to be more susceptible to developing colitis X.[2] Disease onset is often closely associated with surgery or transport.[1] Excess protein and lack of cellulose content in the diet (a diet heavy on grain and lacking adequate hay or similar roughage) is thought to be the trigger for the multiplication of clostridial organisms.[3] A similar condition may be seen after administration of tetracycline or lincomycin to horses.[1] These factors may be one reason the condition often develops in race horses, having been responsible for the deaths of the Thoroughbred filly Landaluce,[7][8] the Quarter Horse stallion Lightning Bar,[9] and is one theory for the sudden death of Kentucky Derby winner Swale.[7]
The link to stress suggests that the condition may be brought on by changes in the microflora of the cecum and colon that lower the number of anaerobic bacteria, increase the number of gram-negative enteric bacteria, and decrease anaerobic fermentation of soluble carbohydrates, resulting in damage to the cecal and colonic mucosa and allowing increased absorption of endotoxins from the lumen of the gut.[10]" (Wikipedia)
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