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Equine Degenerative Myeloencephalopathy (EDM)


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#1 phanilah

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Posted 01 May 2009 - 05:35 PM

Another carry over from the CA thread. Also from Understanding Equine Neurological Disorders by Dr. Bradford Bentz (and I again apologize for any typos).

Beth
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Equine Degenerative Myeloencephalopathy (EDM):

EDM is a disease that affects the spinal cord, primarily in young horses. A familial tendency has been suggested in the Paso Fino, Arabian, Appaloosa and Thoroughbred breeds; however, no pattern of inheritance has been identified. Clinical signs of EDM are often noticed in horses less than a year old, but also are seen in horses several years of age. The onset of symptoms may be abrupt or slow.

Clinical signs of EDM include ataxia, proprioceptive deficits, weakness and spasticity of all four limbs, with the hind limbs often being the most affected. An affected horse may exhibit a "stabbing" gait and may drag its toes. It resists backing and may drag its feet or assume a "dog-sitting" position. When turned in a tight circle, it will pivot on the inside limb and swing the outside limb out away from its body. It is also prone to falling.

The cause of EDM is poorly defined. The disease has often been associated with vitamin E deficiency. Hereditary factors and toxic compounds also may play a role in the development of EDM.

EDM is diagnosed through microscopic examination of the spinal cord. The ante-mortem diagnosis relies on history, clinical signs, and the elimination of other diseases as possible causes. Low-serum vitamin E levels in horses with compatible clinical signs and good diagnostic evaluations are supportive of an EDM diagnosis.

Treatment of EDM is nonspecific. Affected horses have been reported to benefit from vitamin E supplements. Earlier tratment with vitamin E is more likely to be helpful. Horses kept on sand or dirt lots may be at greater risk for this disease. High-quality forage and vitamin E supplementation may be advisable for horses with low viamin E levels or vitamin E-poor diets.
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#2 phanilah

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Posted 01 May 2009 - 05:36 PM

J Vet Intern Med. 1987 Jan-Mar;1(1):45-50.

Equine degenerative myeloencephalopathy: a vitamin E deficiency that may be familial.
Some additional info:

Mayhew IG, Brown CM, Stowe HD, Trapp AL, Derksen FJ, Clement SF.
Department of Medical Sciences, College of Veterinary Medicine, University of Florida, Gainesville 32610.


Two horse farms, on which there was a high incidence of proven and suspected equine degenerative myeloencephalopathy (EDM), were studied. Symmetric ataxia and paresis, along with laryngeal adductor, cervicofacial, local cervical, and cutaneous trunci hyporeflexia, characterized the syndrome. Serum vitamin E concentration reflected a deficient state in affected and unaffected horses on both farms when compared with selected reference groups and with published values. A high incidence of the disease was evident in offspring of two particular sires on one farm. Vitamin E supplementation resulted in correction of the deficient state in most horses and was associated with a drastic reduction in the incidence of EDM on one farm from 40% to less than 10% the year following vitamin E supplementation. In addition, during the last year, the severity of signs in the few cases was dramatically reduced. This information substantiates the hypothesis that EDM is a vitamin E-responsive disorder of Equidae with a possible familial predisposition.

PMID: 3506620 [PubMed - indexed for MEDLINE]
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#3 phanilah

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Posted 01 May 2009 - 05:39 PM

And another that may be of interest. When I previously posted this abstract in another discussion, I was going to try to get the full paper. I was bad and didn't follow through. But, since I need to forward some information to Dr. deLahunta, I will ask him if he has a copy of the paper he can send me.

Beth
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Am J Vet Res. 1990 Aug;51(8):1300-5.

Factors associated with the development of equine degenerative myeloencephalopathy.

Dill SG, Correa MT, Erb HN, deLahunta A, Kallfelz FA, Waldron C.

Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca 14853.


A case-control study was done to identify factors associated with the development of equine degenerative myeloencephalopathy (EDM). Questionnaires were mailed to the owners of 146 horses admitted to the New York State College of Veterinary Medicine between November 1978 and June 1987 and diagnosed as having EDM by histologic examination. Questionnaires also were sent to owners of 402 clinically normal horses admitted to the college during the same period. Data were compared between the EDM-affected and control groups (56 and 179 questionnaires returned, respectively). Risk factors identified included the use of insecticide applied to foals, exposure of foals to wood preservatives, and foals frequently spending time on dirt lots while outside. Foals spending time outside on green pastures was a protective factor. Foals from dams that had had an EDM-affected foal were at higher risk of developing EDM than were foals from other dams.

Publication Types:
Research Support, Non-U.S. Gov't
PMID: 2386332 [PubMed - indexed for MEDLINE]
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#4 phanilah

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Posted 01 May 2009 - 05:50 PM

From TheHorse.com

Studies on Vitamin E
by: Marcia King
October 09 2001, Article # 657


Researchers at Oregon State University and elsewhere are continuing to examine the role of vitamin E in horse health, including disease prevention and therapy. In particular, vitamin E deficiencies and/or supplementation could be important factors in equine degenerative myeloencephalopathy, equine motor neuron disease, and equine protozoal myeloencephalitis.

Equine degenerative myeloencephalopathy (EDM) is a disease of the spinal cord and brain stem. EDM is one cause of wobbler disease, and it affects young horses of all breeds. Clinical signs of ataxia (incoordination) usually appear by age one, and the signs can be acute in onset or progress slowly from clumsiness to visible ataxia. If the horse does not deteriorate to the point where euthanasia is recommended, progression of EDM usually arrests by age two or three.

The relationship between vitamin E and EDM began to surface 13 years ago when Linda L. Blythe, DVM, PhD, a professor of neurology at Oregon State University, and colleague Morrie Craig, PhD, professor of biophysics/toxicology, observed that a family of Appaloosa horses had a high incidence of EDM.

"In the family, two half-brothers initially had the disease," said Blythe. "Their dam had produced four foals, all wobblers. One of the affected stallions had sired seven offspring, and of those, four were ataxic."

Using one of the Appaloosa foals, a moderately ataxic horse, as a foundation stallion, Blythe and Craig bred him to a number of mares, studied the offspring, and compared them to foals from non-EDM-affected horses on the same pasture.

"We found that the EDM stallion sired nine foals that from ages six weeks to ten months had vitamin E levels that fell far below their control counterparts on the same pasture," said Blythe. "That gave a pretty good indication that vitamin E was involved. It wasn't simply what they were eating in the pasture, because the control foals were eating the same thing."

Blythe also wanted to know if EDM had a nutritional and/or developmental cause.

"We didn't know if the foals had any disease before they started eating food, or if
it was a nutritional problem after birth," she said.

Examining the vitamin E levels in both blood and tissues of foals near the time of birth, Blythe concluded that although EDM has a genetic predisposition, this disease is not something with which foals are born.

In another study, Joe Mayhew, DVM, when he was at the University of Florida, worked with the foals of two Standardbred stallions which had produced EDM in 40% of their offspring. The mares bred to these two stallions and their foals were supplemented with approximately 1,500 IU per day of vitamin E, and the following year, only 10% of their offspring were affected. In subsequent years, none of the offspring of those stallions had EDM.

Subsequently, the OSU researchers designed a treatment study of wobbler and control foals grazing on the same pasture. As the wobbler foals started developing incoordination and their vitamin E levels dropped at about six months of age, Blythe supplemented them with 6,000 IU per day of vitamin E. By the time the horses were two years old, their coordination appeared normal. "All markedly improved, while one or two had some residual neurological deficits," she said.

While massive vitamin E supplements given to EDM foals can halt disease progression and often can return a horse to usefulness, Blythe emphasizes that preventing EDM by supplementing foals, especially those from families known to have a history of this disease, is a far better option.

Equine motor neuron disease (EMND) is a rare, naturally occurring disease of the nerve cells that control the skeletal muscles. EMND is similar to Lou Gehrig's disease in humans, and the affected horse can suffer from weight loss, excessive recumbency, trembling, muscle atrophy, constant weight shifting of the rear limbs, and abnormally low head carriage.

Discovered and studied at Cornell University, EMND has no known cause. However, the most commonly identifiable environmental risk factor for EMND is an absence of grazing for more than a year and poor-quality hay. EMND horses also have low levels of vitamin E in tissues or blood.

Cornell researchers placed five EMND horses on pasture for periods ranging from nine months to more than two years, and vitamin E was administered to two of the affected five. The researchers noted dramatic clinical improvement in four of the five affected horses. Comments Blythe, "They don't know whether the disease caused reduced vitamin E, i.e., used it up, or if low vitamin E was a causative factor. They don't think vitamin E deficiency alone will cause the disease, but they think it will set the stage or make the horse more likely to get this disease when exposed to something, and nobody knows what that something is."

Equine protozoal myeloencephalitis (EPM) is a disease of the central nervous system, brain, and spinal cord, and it is caused by a protozoal parasite. Onset can be extremely rapid, slow and insidious, or subtle. Clinical signs vary and can include weakness, lameness, incoordination, inability to move correctly (especially in the hindquarters), persistent recumbency, seizures, weight loss, blindness, loss of balance, and disuse of a single limb.

Treatment is aimed at killing the protozoa via oral anti-protozoal medications. With treatment, many horses can become useful again, but some will continue to exhibit signs of neurologic disease. Untreated, horses either will stay the same (showing non-life-threatening neurological signs) or, more likely, the central nervous system damage will worsen and the horse will become incapacitated or die.

In addition to using anti-protozoal medications, some experts recommend supplementing with 6,000-9,000 IU per day of vitamin E. Although no control trials have been done to support this, Blythe points out that, "Vitamin E has been shown in people and horses to augment or make the immune system work better. Vitamin E may help the immune system do the final killing (of the parasite) where antibiotics don't destroy all of it."

How Much, and When to Measure

Another OSU study identified normal levels of vitamin E, and when blood samples measuring those levels should be taken. Explained Blythe, "We found that at one time of the day levels would be adequate, but at another time, they'd be marginal. There's an inherent variation of about 12% in these horses."

This means two or three blood samples should be taken over a single day and pooled for the vitamin E analysis in order to get an averaged value.

Additional studies are underway using radiolabelled (deuterated) vitamin E. Lori Walker, a graduate student and a PhD candidate studying with Blythe and Craig, is researching whether horses sired by EDM-affected stallions and normal horses absorb vitamin E at the same rate, and to ascertain if natural vitamin E is different or better than synthetic vitamin E. The data collection is completed, and it is awaiting statistical analysis.

While research continues into vitamin E's potential, one thing is already clear: Sufficient levels of vitamin E are critical when dealing with specific equine health needs, especially in the young, growing horse from one month to two years of age.

The Role of Vitamin E

Vitamin E generally is supplied through green forage, with little added to most concentrate feeds. Storage can destroy some of the vitamin E in foods.

The metabolic role of Vitamin E is not completely understood. It appears to prevent free radical damage to tissues or lipid peroxidation, a process which can result in harmful effects in the body. It also is important for the proper function of nerves and muscles. Deficiencies may impair neuromuscular function.

Who Needs Vitamin E?

Not every horse needs vitamin E supplementation. Blythe says that studies show horses most at risk for vitamin E deficiency include the following:

Horses without access to green pastures;
Horses fed old hay or pelleted feed;
Horses kept where winters are severe and kept in the barn for long periods of time;
Horses exposed to creosote-painted fences;
Horses sprayed with excessive insecticide;
Horses with EDM, EMND, EPM, and foals of EDM horses;
Foals up to two years of age;
Ill horses, especially those with diseases affecting the immune system;
Older horses which might not have the gastrointestinal efficiency for absorbing vitamin E from grasses;
Heavily exercised or raced horses.

Says Blythe: "Our research shows you need about 2,000 IU a day to prevent neurologic dysfunction, and 6,000-9,000 IU a day for treating a disease process that damages the nervous system such as EPM, EMND, or EDM."--Marcia King
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#5 phanilah

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Posted 13 January 2010 - 06:58 PM

Bouncing this back up, given current discussions.

Beth
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#6 H Fillmore

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Posted 13 January 2010 - 07:51 PM

MICHAEL BOWLING - - COME BACK - - Please provide your Professional Opinions on the following
important subject

KNOWN FACTS : From papers above & Myhorse.com/health/supplements

1. Vitamin E Deficiencies & / or Supplementation could be important Factors in Equine
Degenerative Myeloencephalophy (EDM), Equine Motor Neuron Disease (EMND), &
Equine Protozoal Myeloencephalitis (EPM).

2. - EDM = Disease of Spinal Cord & Brain Stem affecting young horses (< 3 yrs old)
Symptoms = Wobbling & Poor Coordination.

- EMND = Progressive Degeneration of Nerves that Control Skeletal Muscles.
Symptoms = Coordination Problems, Muscle Atrophy with GAIT Changes,
Weakness, Lying Down Frequently, Constant Weight Shifting
of Rear Legs, Low Head Carriage.

- EPM = Disease of Cntrl Nervous Sys, Brain, & Spinal Cord Caused by Protozoal Parasite.
While Antibiotics is needed to fight this ailment, Vit. E which also builds the IMMUNE
System Appears to "Do the final Killing of the Parasite" - - OSU.
Symptoms = Rapid or Slow - Weakness, Coordination Problems (esp in Rear-end),
Loss of Balance, Lying Down Freq., Weight Loss, Blindness, Seizures.

3. Horses with Highest Risk of Vit. E Deficiency include the Following:
- Horses with No Access to Green Pasture
- Horses Fed Old / Stored Hay
- Horses Living where Winters are Severe
- Older Horses with Poor Gastrointestinal Efficiency for Absorbing Vit E
- Horses Families with Historys of EDM, EMND, & EPM Affliction.

4. Lori Walker / OSU is Researching whiether METABOLISM of Vit. E Plays a Role in above
Illnesses, - With Analysis of collected Data Due Soon !

5. Medallela Tail-Line Horses (Mostly Bint El Bataa), have been Affected for many Generations
with Neuorological Disorders, with symptoms similiar to those described above.

MY HYPOTHESIS :

1. In Light of the Myhorse.com/ Acta Vet Scandinavia Report on EMND Describing Rear-End
Muscle Atrophy with GAIT Changes, & Many U.S. Reports of Bint El Bataa Horses exhibiting
"Hopping" or "Paddling" Actions when Running - I Believe the Problem is One & the Same.
I also Believe B. E. Bataa Mares (like Grete and Ebocenta), Who Layed-Down most of the time
and needed help Rising suffered from EPM.

2. In Concurrence with OSU Suspicions of Poor Metabolism and / or Gastrointestinal Processing
of Vit. E, - I Believe the mtDNA (Whose Function is to Metabolize Food Neutrients & Feed Body
Cells), - Is Functioning a Little Poorer in the Bint El Bataa T-L Horses than the mtDNA of others.

3. I also Believe that - Since the Bint El Bataa mtDNA Genetics is Passed-On from One
Generation to the next - This Explains Why these horses continue to be More At-Risk
of Vitamine E Deficiency than other Lines!


THANKS IN ADVANCE, MIKE - - - - HUGH

#7 Demelza

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Posted 13 January 2010 - 10:07 PM

I don't have a problem with your theory regrading Vitamin E Hugh - it definitely sounds like it helps. However it would be great if owners can get their "affected" horses seen by a vet, to try and figure out if the "hop" is EDM or something different. A proper diagnosis would go a long way to helping these horses - if we can figure out how to breed them then this would save on $$$ with vitamin E supplementation.

Here in mid Canterbury, NZ, I feed out stored meadow hay for more than half the year. I have some horses with BeB lines and I am assuming they are "clear" as I haven't noticed any "hop", BUT then again I might not recognise it if I saw it anyway.

Hope you can participate in the research that is starting Hugh, we'd all be grateful for any progress made in this area. None of us want to throw out the bloodlines (especially when some great endurance horses descend from the likes of Shiko Ibn Sheikh, Sankt Georg, Rafter G Charisma etc), we just want to know what is happening and how to avoid it (preferably by breeding it our rather than excessive supplementation).

#8 DJ Sheldon

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Posted 13 January 2010 - 10:37 PM

Hugh,

I don't have a dog in this fight, but it seems to me you are consistently ignoring the fact that these conditions RUN IN FAMILIES. Yes, perhaps vitamin E supplimentation will prevent or improve symptoms, but it does not alter the genetic component that underlies these conditions. As has been mentioned over and over, what happens when the supplemented horse that has the symptoms masked is passed on to an owner or breeder that does not continue to supplement? Because of that genetic component, the symptoms will again be apparent.

I am just baffled by your resistence to the fact that there is something in the BeB line that causes a problem, whether it is an inability to utilize normal amounts of vitamin E, or some other genetic glitch. It's there. You may be able to lessen the symtoms with supplimentation, but as Hansi stated, why would you breed horses that couldn't sustain themselves normally?

DJ

#9 Angella

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Posted 13 January 2010 - 10:53 PM

Hugh,

I don't have a dog in this fight, but it seems to me you are consistently ignoring the fact that these conditions RUN IN FAMILIES. Yes, perhaps vitamin E supplimentation will prevent or improve symptoms, but it does not alter the genetic component that underlies these conditions. As has been mentioned over and over, what happens when the supplemented horse that has the symptoms masked is passed on to an owner or breeder that does not continue to supplement? Because of that genetic component, the symptoms will again be apparent.

I am just baffled by your resistence to the fact that there is something in the BeB line that causes a problem, whether it is an inability to utilize normal amounts of vitamin E, or some other genetic glitch. It's there. You may be able to lessen the symtoms with supplimentation, but as Hansi stated, why would you breed horses that couldn't sustain themselves normally?

DJ


If a treatment... or even a supplement concoction... can eliminate the symptoms of the disorder, I'm not necessarily against careful breeding of these horses. BEB and her sisters were incredible horses with a lot to offer... and losing their line would be a loss to the breed, imo. By carefully breeding, we should be able to continue the line and hopefully getting clear horses... so long as we can find a way to successfully treat the others. However, I am dead set against breeding two affected horses together and other such irresponsible breeding practices.

Hopefully the study turns up something to help us breed around any BEB issues.

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#10 DJ Sheldon

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Posted 14 January 2010 - 12:59 AM

Angella,

I didn't mean to imply that this line should be allowed to be lost, just that breeding should be undertaken cautiously, which I believe is what you are saying.

DJ

#11 Ray

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Posted 14 January 2010 - 03:31 AM

Oh well, everytime Beth puts up a new illness, I think I've got it... :) :poop:

#12 Angella

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Posted 14 January 2010 - 03:34 AM

[quote name='DJ Sheldon' date='Jan 14 2010, 12:59 AM' post='47282']
Angella,

I didn't mean to imply that this line should be allowed to be lost, just that breeding should be undertaken cautiously, which I believe is what you are saying.

DJ
Yup... that's exctly what I'm saying. :)

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#13 H Fillmore

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Posted 14 January 2010 - 11:23 AM

- - - DE NAHED (Snowlion x RG JOYE)
* Only living Grand-Son of Pritzlaffs- Bint Nefisa
* Only Heirloom / S.O. Son of Snowlion
* Perfect Conformation / High Perfectly placed Neck / Wide Hip & Body

Nahed Trotted Perfectly Normal today! - A little Stiff in the Hocks, but No "Hopping" or "Paddling" Motion.

Attached Files



#14 DJ Sheldon

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Posted 14 January 2010 - 11:54 AM

SHELDON - - RE-READ POST 4 ABOVE !! Not every horse needs Vit E Supplementation - - Just those
with no access to Green Pastures, Horses fed old Hay, & horses where winters are Severe,(AS I POINTED OUT BEFORE), and horses Prone to EDM, EMND, & EDP (BINT EL BATAA LINES).
If your Mother had Diabitus - Would you say "Give her insulin for the rest of her life" or would you say - "If she can't live on her own without help - just let her die" ???


- - - - HUGH

SIGH. :) What you have just said changes nothing in my post. There are few areas of the world where horses are not fed stored hay, and all horses fed stored hay and without access to green pastures and in severe climates do NOT have ataxia problems. It only appears to be a nutritional problem in those horses who are genetically predisposed to have a problem.

The example you use about my mother does just not apply. Livestock are NOT people, and you cannot apply the same rules to both. People are not bred the way livestock are. When you visit a doctor and he takes a medical history, one of the questions they always ask is if any family members have certain conditions. That is because certain conditions run in families. If people were bred as livestock, then we should avoid "breeding" people with conditions that are inherited. But people, being a little higher up the food chain, have the ability to talk and tell us what hurts, and what makes it better. People (or most of them) are capable of doing much more than a horse, contributing much to society. A horse that can't be ridden really has limited usefulness.

And what is with SHOUTING at me and addressing me by my last name only? The last person that addressed me like that was a biology professor who yelled at everyone all the time and had the reputation of being a rude, cranky, old man. If you feel you must address me by my last name and in capital letters, it is MRS. SHELDON to you.

DJ

#15 Ray

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Posted 14 January 2010 - 04:19 PM

SHELDON!! Give yo momma some Vit E and she be fine!!! :36_1_29:

#16 DJ Sheldon

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Posted 14 January 2010 - 04:22 PM

SHELDON!! Give yo momma some Vit E and she be fine!!! :36_1_29:

:)

#17 Angella

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Posted 14 January 2010 - 04:36 PM

BEB phenomena...??? I thought there was no problem with the BEB lines? That's what you claim on the thread you have declared "dead"...

mtDNA, you claim... not genetic. Given that mtDNA is only traced from mother to foal, would you care to explain how (was it Chiron's?) stallion "Babi" passed it on? Oh wait... that doesn't fit your theory... it must be disregarded... just as every piece of information that doesn't fit is.

It's not difficult, Hugh, to "prove" any theory you want when any piece of information that doesn't support your theory is tossed out as irrelevant and unrelated.

Hell, if I wanted to do that, I could prove the earth was flat and the center of our solar system...

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#18 Ray

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Posted 14 January 2010 - 11:49 PM

OPINIONS CENSURED






- - - DE NAHED (Snowlion x RG JOYE)
* Only living Grand-Son of Pritzlaffs- Bint Nefisa
* Only Heirloom / S.O. Son of Snowlion
* Perfect Conformation / High Perfectly placed Neck / Wide Hip & Body

- - - - TO BE PUT-DOWN - BY POPULAR DEMAND


Hugh, this is a terrible thing to say!! Why would you say something like this, when all people are trying to do is convince you to see another side of this problem?

Communications can be rough out here, but no one wishes you bad luck, nor do they think badly of your horses. The condition El Bataa seems to have bequeathed us is not anyone's fault - least of all yours. Just think about pitching in to help resolve this bugger. If a test can be developed, it could very well be that other lines will find they might need it, too. Because it is late onset, in many cases, I would test my horses for it.

#19 Jill Erisman

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Posted 15 January 2010 - 01:13 AM

As a side note to this,
I must add that Richard Pritzlaff found
a way around the El Bataa hop first by
using a son
>Shiko Ibn Sheikh
<then Umi (x Bint Dahma)
>then Almoniet (x Monieta)
who sired Sonietas Solar RSI
and Sonimoniet RSI among others.

All of the Solar and Sonimoniet get I
have observed loose trotting in a
pasture have not exhibited the hop
at all if they aren't out of El Bataa
tail-female mares. I guess my point
here is that Pritzlaff has perhaps provided
us an example of how to keep the
blood without throwing the baby out
with the bath water.

Jill

#20 Angella

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Posted 15 January 2010 - 02:53 AM

OPINIONS CENSURED






- - - DE NAHED (Snowlion x RG JOYE)
* Only living Grand-Son of Pritzlaffs- Bint Nefisa
* Only Heirloom / S.O. Son of Snowlion
* Perfect Conformation / High Perfectly placed Neck / Wide Hip & Body

- - - - TO BE PUT-DOWN - BY POPULAR DEMAND



Yup... that's exactly what we're saying :5298_orcspash:

Or, perhaps, you could even try breeding more responsibly by not breeding an affected mare to him... perhaps... possibly... and maybe even contributing samples from your affected horses to the study so a person can find a way to test these lines and breed around any issues...

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