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szedlisa
Bronze Member
 Spain
124 Posts |
 Posted - 12 Jan 2007 : 8:16:38 PM
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CA is a defective genetic allele appearing in ALL Arabian Bloodlines. Please Read~
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Egbert
Gold Member
USA
1051 Posts |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 12 Jan 2007 : 8:21:13 PM
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Greetings to All Arabian Horse Breeders and Owners:
Cerebellar Abiotrophy is a neurological disease, most often noted in newborn foals of approximately 3 weeks to 4 months of age. The most notable symptoms are a palsey-like head shaking (called intention tremors), the lack of a normal blink response although vision is correct, and an awkward exaggerated form of action with the forelimbs often similar to a military goose-step or high elevation used to cross over a very low object called hypermetric action. As these affected foals will often run into things or fall down- sometimes causing head injuries, their condition can be mis-diagnosed as injuries from a blow to the head or neck, making the true neurological condition go unnoticed.
Cerebellar Abiotrophy (CA) is being recognized in all bloodlines of the arabian horse. Suspected to be an autosomal recessive defective allele, it can be passed forward through several generations without re-appearing. It is not a lethal gene. It does however make the horse generally unfit for riding or driving. Most affected horses are euthanized before they cause severe damage to themselves or to their handlers because of their inability to control their own balance.
More samples are needed to identify the specific allele or combination of alleles and develop a test for Carrier horses. All information is kept private to protect any of the horses and their owner/breeders respective breeding programs. Cases of actual affected CA have been the requirement in the past, but now they want samples from any related family members as well. It is in this realm where we could really be of help in pushing research on CA forward. If you have had a CA foal in the past, which has already been euthanized but still have what appears to be perfectly normal syblings or otherwise related family members, these too are important for this research.
It is my hope and goal for 2007 that with this concentrated effort of your welcomed participation that the markers for CA will be identified and a test will be developed.
Please help us obtain these goals.
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Spanish Arabians Photos
http://www.flickr.com/photos/szedlisa/collections/72157600851198212/
Cerebellar Abiotrophy (CA) Info:
http://www.cerebellar-abiotrophy.org/
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Edited by - szedlisa on 25 Feb 2009 3:09:10 PM |
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szedlisa
Bronze Member
Spain
124 Posts |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 12 Jan 2007 : 8:26:59 PM
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| see above post |
Edited by - szedlisa on 25 Feb 2009 3:12:44 PM |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 12 Jan 2007 : 8:28:04 PM
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| see above post |
Edited by - szedlisa on 25 Feb 2009 3:14:15 PM |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 12 Jan 2007 : 8:37:50 PM
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Geneticists at the Universities of Cornell, Michigan, Iowa and UC Davis in the USA and the Universities of Bern and Zurich in Swizerland, of Gent in Belgium and of Cordoba in Spain have been researching the CA problem since the early 60s. Similar studies are being explored in Australia as well under the auspices of Professors Dr. J D Baird and Dr. C D Mackensie.
This in depth description of Cerebellar Abiotrophy is available at Wikipedia:
Cerebellar abiotrophy
Cerebellar abiotrophy (CA) also referred to as cereballar cortical abiotrophy (CCA) is a genetic neurological disease in animals best known to affect certain breeds of horses and dogs. It develops when neurons known as Purkinje cells in the cerebellum of the brain begin die off. These cells affect balance and coordination. They have a critical role to play in the brain. The Purkinje layer allows communication between the cortical layers in the cerebellum. Put simply, without Purkinje cells, an animal loses its sense of space and distance, making balance and coordination difficult. In most cases, the neurons begin to die off shortly after the animal is born and the condition is noticable when the animal is less than six months old, though sometimes the onset of symptoms is gradual and the animal is much older before the owner or caretaker notices a problem.
CA cannot be prevented, other than by selective breeding to avoid the gene, and it cannot be cured. In addition to dogs and horses, there also have been cases of cerebellar abiotrophy in Siamese Cats; in Angus, Polled Hereford, Charlois and Holstein Friesian cattle; Merino and Wiltshire sheep; and Yorkshire pigs.
Other terms used
Cerebellar abiotrophy in horses was originally thought to be a form of cerebellar hypoplasia and was described as such in older research literature. The condition in Kerry Blue Terriers is sometimes called progressive neuronal abiotrophy (PNA). There are diseases that cause other types of cerebellar degeneration, but the loss of Purkinje cells is a clear way to diagnose CA.
Symptoms
A young Arabian horse with cerebellar abiotrophy, showing stiff awkward gait, and upper range of unnatural head bob. Symptoms of cerebellar abiotrophy include ataxia or lack of balance, an awkward wide-legged stance, a head tremor (intention tremor) (in dogs, body tremors also occur), hyperreactivity, lack of menace reflex, stiff or high-stepping gait, coarse or jerky head bob when in motion (or in very young animals, when attempting to nurse), apparent lack of awareness of where the feet are (sometimes standing or trying to walk with a foot knuckled over), poor depth perception, and a general inability to determine space and distance. The symptoms are, when taken as a group, fairly unique and not easily mimicked by other illnesses, though certain types of neurological injury and infection do need to be ruled out. However, verifying the diagnosis in terms of laboratory evidence is only possible by examining the brain post-mortem to determine if there has been a loss of Purkinje cells.
Most affected animals have normal intelligence and mildly affected animals can, in theory, live out a normal lifespan. However, affected animals are accident-prone, and for this reason many affected animals, particularly horses, are euthanized for humane reasons. Dogs may need lifetime assistance with tasks such as climbing stairs. Horses may experience difficulty stepping up and over objects, run into fences, fall easily, and even if allowed to mature to full growth, are generally considered unsafe to ride.
In horses, the symptoms may worsen from the time of onset for six to 12 months, but if not severe enough to mandate euthansia, they stabilize over time. In some dog breeds, symptoms appear to progressively worsen, but research is not consistent on this point. There also is some evidence that affected animals partially compensate for the condition by cognitively learning alternative methods for moving or to determine distance, and thus appear to improve because they become less accident-prone.
Cerebellar abiotrophy in horses
Cerebellar abiotrophy (CA) is best known as a condition affecting Arabian horses. It has also been observed in the Miniature horse, the Gotland Pony, and possibly the Oldenburg. Most foals appear normal at birth, with symptoms noticable at an average age of four months, though there have been cases where the condition is first observed shortly after birth and other cases where symptoms are first recognized in horses over one year of age.
In horses, CA is believed to be linked to an autosomal recessive gene. This means it is not sex-linked, and the gene has to be carried by both parents in order for an affected animal to be born. Horses that only carry one copy of the gene may pass it on to their offspring, but themselves are perfectly healthy--without symptoms of the disease.
There currently is no DNA test for CA in horses, though there is ongoing research at the Veterinary Genetics Laboratory at the UC Davis School of Veterinary Medicine.
Cerebellar abiotrophy in dogs
CA has been seen in the Australian Kelpie, the Gordon Setter, Border Collie, Labrador Retriever, Airedale, English Pointer, Scottish Terrier, Kerry Blue Terrier, Miniature Schnauzer, and other breeds. Onset varies by breed of dog. In a few breeds, Purkinje cells begin to die off shortly before birth, and pups are born with symptoms. Most dog breeds prone to the condition begin showing symptoms between 12 weeks and six months of age. In a very few breeds, symptoms do not appear until adulthood or even middle age.
In dogs, CA is also usually an autosomal recessive gene, but in a few breeds, such as the English Pointer, the gene is sex-linked.
References
Bibliography (available on line)
Baird JD, Mackenzie CD. "Cerebellar hypoplasia and degeneration in part-Arab horses." Aust Vet J. 1974 Jan;50(1):25-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4819469&dopt=Citation
Bjorck, G., Everz, K.E., Hansen, H.-J. and Henricson, B., 1973. Congenital cerebellar ataxia in the Gotland pony breed. Zbl. Vet. Med. [A] 20:341-354. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4199630&dopt=Citation
Blanco A, et. al. "Purkinje cell apoptosis in arabian horses with cerebellar abiotrophy." J Vet Med A Physiol Pathol Clin Med. 2006 Aug;53(6):286-7. http://www.blackwell-synergy.com/doi/abs/10.1111/j.1439-0442.2006.00836.x
DeBowes R.M., et. al. "Cerebellar abiotrophy." Vet Clin North Am Equine Pract. 1987 Aug;3(2):345-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3497695&dopt=Citation
de Lahunta, A. "Abiotrophy in domestic animals: a review." Can J Vet Res. 1990 January; 54(1): 65–76. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1255608
Fox, J., et. al. "Cerebello-Olivary and Lateral (Accessory) Cuneate Degeneration in a Juvenile American Miniature Horse."
http://www.vetpathology.org/cgi/content/full/37/3/271
Gerber H, Gaillard C, Fatzer R, Marti E, Pfistner B, Sustronck B, Ueltschi G, Meier HP, Herholz C, Straub R, Geissbuhler U, Gerber V. "Cerebellare Abiotrophie bei Vollblutaraber-Fohlen" (Cerebellar abiotrophy in pure-bred arabians) [German]. Pferdeheilkunde 1995;11:423-43; http://direct.bl.uk/bld/PlaceOrder.do?UIN=001143128&ETOC=RN&from=searchengine
Palmer, A.C., Blakemore, W.F., Cook, W.R., Platt, H. and Whitwell, K.E. "Cerebellar hypoplasia and degeneration in the young Arab horse: clinical and neuropathological features." Veterinary Record 93:62-66 (1973) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4748678&dopt=Citation
ADDITIONAL READING: (Sponseller & Gerber et al.are the most informative from a layperson's point of view ~ szedlisa)
Sponseller, Brett A.,"A pedigree analysis of cerebellar cortical abiotrophy in the Arabian horse", Cornell University:Seminar SF610.1 1994 no.9472; http://dspace.library.cornell.edu/handle/1813/3013
RO Waelchli and F Ehrensperger, "Two related cases of cerebellar abnormality in equine fetuses associated with hydrops of fetal membranes ", Veterinary College, University of Zurich, Switzerland. The Veterinary Record, Vol 123, Issue 20, 513-514 [1988] http://veterinaryrecord.bvapublications.com/cgi/content/abstract/123/20/513
F.O.A.L. Fight Off Arabian Lethals http://www.foal.org/
VetGen Veterinarian Genetic Services [New Site]
http://www.vetgen.com/equine-services.html
VGL - Veterinarian Genetics Laboratory - UC Davis (University of California at Davis) http://www.vgl.ucdavis.edu/research/equine/CA.html
Please note that the earlier studies in the 60s called CA 'cerebellar hypoplasia' until it was discovered that CH developed in the unborn fetus and CA developed starting at 2 or 3 weeks of age. Bret Sponseller based much of his study on his father's , Max Sponseller, extensive research in the mid 60s and published in 1967. They were working basically with a large east coast breeding herd which had lost 8 % of their foal crop and 6% the following year. Gerber et al in 1995 were working with the Finnish Registry as well as Belgium breeders, concentrating on Polish, Russian, Egyptian, Spanish, and Crabbet lines with 793 horses in their study with a 18.8 % foal loss in 1992 alone.
It is the son of the late Prof. Dr. H. Gerber, PD Dr. med. vet. Vincent Gerber, PhD, DACVIM, DECEIM, FVH, Head of Equine Internal Medicine of the Equine Clinic, Dept. of Veterinary Clinical Studies, Vetsuisse-Fakulty, University of Berne, who has initiated this present research project on Cerebellar Abiotrophy. Apparently research of this kind is adequately funded in Switzerland as there has been no hesitation whatsoever. They have already been recieving completed questionarries and samples and are extremely appreciative..
Keep them coming people!!
And please feel free to ask questions...
Lisa
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Spanish Arabians Photos
http://www.flickr.com/photos/szedlisa/collections/72157600851198212/
Cerebellar Abiotrophy (CA) Info:
http://www.cerebellar-abiotrophy.org/
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Edited by - szedlisa on 12 Jan 2007 9:12:11 PM |
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LYNDILOU
Platinum Member
United Kingdom
13976 Posts |
Posted - 13 Jan 2007 : 08:45:01 AM
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Looks like you haven't had many answers yet Lisa, I have just logged on, but I see this was posted yesterday.
I have yet to have heard of any cases of this nature, I have been a breeder of arabian horses for a long time now and can honestly say I have never experienced any of these symptoms, nor have I heard of any other breeders who have had them, I didn't know this condition exsisted till now and of course it is a worry ( one more thing to worry about) I do hope however anyone else who has, will help in the survey.  |
   
www.dreamfield-arabians.com |
Edited by - LYNDILOU on 13 Jan 2007 11:23:46 AM |
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Vygoda
Platinum Member
United Arab Emirates
1627 Posts |
Posted - 13 Jan 2007 : 11:19:13 AM
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Is this condition also or previously known as Cerebella Hypoplasia? Same 'symptoms'.
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 13 Jan 2007 : 3:06:29 PM
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Lyndilou - Nope not many answers..nor questions as yet :(
I also have been breeding arabians for some 45+ years, with some 150 foalings and only had one which I was not aware of at the time. A filly, born in July which is late in Spain, that was exported in November, saw no green grass until a long yearling and that was the reason the local US vets thought made her have head tremors. Given lots of vitamin E , she was used as a broodmare. Nobody knew much about CA back in the 70s. I only learned about it in 2000. I have seen over 80 since though. |
Edited by - szedlisa on 13 Jan 2007 3:06:57 PM |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 13 Jan 2007 : 3:14:40 PM
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| Vygoda - Exactly. For years CA and CH were used interchangeably, until it was discovered that one condition started during the development of the fetus prior to birth (CH) and the other started several weeks after birth (CA). Both involve the degeneration of the Purkenje Cells which govern mobility and balance. There is nothing more heartbreaking tha seing a CA horse trying to cope. Stress situations seem to bring on the head tremors and the poor soul tries to concentrate on getting a job done. Whether it be trying to get through a gate on her own, into a trailer or at a very young age, even trying to suckle properly. Cross ties are an absolute No-No. |
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szedlisa
Bronze Member
Spain
124 Posts |
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Montana
New Member
USA
9 Posts |
Posted - 15 Jan 2007 : 03:46:37 AM
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Hello from the states!
I currently own a filly affected with CA. Her case is mild enough that I have not chosen to put her down, even though she will never be ridable. But I want to encourage everyone to learn more about this genetic disease and to do what you can to help. It is appalling to watch a young horse repeatedly fall down, run into fences, run over people and have trouble with tasks as simple as eating a treat from your hand. With a DNA test for the gene, there would be no reason for a horse to ever again be born with this condition and that would be a wonderful thing.
There is no question that CA is a problem in the United States, though there is a need for a lot more education and information to be made available to Arabian owners there as well as elsewhere. It is often not recognized for what it is because veterinarians are more accustomed to seeing conditions like "wobbler's syndrome" or neurologic problems related to injury.
CA is a genetic recessive, which means both parents have to carry the gene for an affected foal to be born. Statistically a "generic" genetic recessive will crop up in about 3% of a given general population, but if two carriers are bred, there is a 25% probability of an affected foal being produced. So it is not surprising that people are not aware of the condition, especially because it is often first diagnosed after a foal has hurt itself due to incoordination, and thus the fall or injury is often thought to be the cause of the problem, without realizing that there was an underlying brain problem.
Also, it's an odd disease because it varies in severity and it not usually present at birth. My filly did not exhibit symptoms anyone noticed until she was a yearling, and this was also true of another filly I know of.
I simply encourage everyone here to help Lisa with her efforts and if you know of an affected foal, especially if the parents of the foal are still alive, please do what you can to help these research universities obtain the DNA samples they need. |
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Egbert
Gold Member
USA
1051 Posts |
Posted - 15 Jan 2007 : 07:46:27 AM
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Hi Lisa,
Many thanks, especially reading all 30 pages! No, I've never seen CA of which I am aware. On the other hand as a writer, interviewing various farm owners and as a breeder, don't think too many people would be eager to tell me about it.
One thing is that we really must try to learn if there are specific horses acting as carriers of the gene. Not using names for reasons that will be apparent, I KNOW from various interviews that horse X is always found in the pedigrees of SCID carriers. The question is, did carrier status occur as the result of a mutation in descendants of the horse OR did it come before X and X was a carrier as well. WHAT was it that created such a gene? Same with Lavander Foal? Hopefully that is what geneticists are striving to learn and determining a test that will determine carrier status as we have with SCID so people can make informed breeding decisions.
At least CA is not exclusive to Arabians.....
Lisa, I've known of you and admired you for all that you do for the Arabian for years and one day hope to visit you in Mallorca!
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justine
Gold Member
England
641 Posts |
Posted - 15 Jan 2007 : 1:01:03 PM
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Some years ago I bred a filly foal with CA.
The first thing I noticed, that when the mare was foaling, it was a very slow process although a normal birth. These small things I always take particular notice and make a note for future reference.
The filly was born, all looked ok.
Two hours later the foal was still on the floor with no attempt to move, I started to have suspicions this foal was not normal. We decided to help the foal up, from this time took 7 hours to find the milk (which can be normal). Suck reflex was normal.
The following morning I noticed the foal had a very slight wobble of the head when focusing on something. I called the vet, I think he thought I was just being paranoid at this early stage, it was probably the fact that the foals eyesight was not yet perfect.
I watched carefully over the next hours. Upon waking from a very deep sleep, the foal got up, not front end first but back end first!
Out comes my veterinary book.
It looked very much like CA. 3 vet opinions later, it was diagnosed.
Dr. Knottenbelt at Liverpool University (GB) was very interested in this case. We made videos and experimented with small tests, for example - throwing a carrot into the paddock to see what the response would be. In the beginning the reponse was more or less normal, look suprised, and investigate.
As weeks went on the front leg action was becoming very exagereted and balance was becoming more and more difficult. We already knew the fate of the foal and decided as long as she was sucking and not in danger of hurting herself we would keep her alive for the mothers sake.
At three months old she began to fall into fences, the carrot test was still a suprised look but she could not make her way to investigate, she wanted to but her legs would not go in the direction she wanted. This was sad, we named the day for her to go to sleep. Upon the request of Dr Knottenbelt we travelled the foal to the university in a trailer deep in straw so that she couldnt hurt herself, she stood all the way and loved her back stratching, she was not at all stressed about leaving her dam. Did she know? we cant tell.
On arrival at the university she hapilly walked out of the trailer with my arms around her body guiding her direction. We put her in a recovery stable with cushioned floor and walls, where vets watched her eat hay, drink water and study her reactions, again she was under no stress, she was a happy little soul.
A few hours later she was put to sleep. The post-mortem showed the cerebrem had not grown, the rest of the brain had. CA.
Her parents are now gone. The mother was polish, the father was russian. The breeding was never repeated but the mother bred other normal foals, the father sired many many great offspring.I did learn from other breeders that russian/polish have more CA than English/egyptian/spanish..... but this I dont no if it is true or proved. I only know its rare.
Forgot to say, her growth rate was normal.
Her name was `poppy`, bless her.
Justine (England)
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LYNDILOU
Platinum Member
United Kingdom
13976 Posts |
Posted - 15 Jan 2007 : 1:17:30 PM
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Oh poor little thing, it must have been very sad (and brave) for you to take her to her end but it was for the best, lets hope they can soon get to the bottom of this disorder and wipe it out |
www.dreamfield-arabians.com |
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Vygoda
Platinum Member
United Arab Emirates
1627 Posts |
Posted - 15 Jan 2007 : 7:23:36 PM
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Once you have seen a CA foal, and its progress, you can never mistake it for anything else.
Over many years but not recently, I have seen 5 foals with CA, the first one that I bred of all English lines that was diagnosed as a wobbler. This foal was perfect when born, and by 4 months old had a nodding head and leg disfunction that became increasingly worse rapidly leading it to have no control and banging into things as described. The diagnosis was queried with the vets and on autopsy was found to have CH, now known as CA.
The second one was of Russian lines and the colt evidenced it when it was 2 years old – not bred by me for what difference it makes – but nowhere as bad as the foal mentioned above.
The other 3 that I have seen were abroad and of English or American or French lines or combinations, all foals. How do you tell an owner what you feel is wrong with the foal - that was very difficult to do as they had not noticed it .
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Vygoda
Platinum Member
United Arab Emirates
1627 Posts |
Posted - 15 Jan 2007 : 7:40:07 PM
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I meant to say that it would be really great to have a test developed as has been done with SCID so that at least we breeders know the SCID status of our horses to help to eradicate it.
Unfortunately, none of the sires or dams are alive now of the horses I have been involved with, and sadly it would be impossible to ask the owners of the other ones I have seen to provide any information whatsoever.
CA is as devastating as having a SCID positve foal as the future is as bleak for them.
Very few 'everyday' vets are aware of CA so they need education too.
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tamila
Platinum Member
England
2532 Posts |
Posted - 16 Jan 2007 : 2:06:55 PM
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| ve spoken to my daughter, a vet in the states who is particularly interested in breeding, and she says it is not common but is slowly becoming more so. It needs to be controlled as does CID. |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 16 Jan 2007 : 2:54:01 PM
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"Lisa, I've known of you and admired you for all that you do for the Arabian for years and one day hope to visit you in Mallorca!"
Egbert ~ I gather you have spent some time here before and certainly would enjoy neeting you as well. Coffee pot is always on...so is the green tea.
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Edited by - szedlisa on 16 Jan 2007 5:02:56 PM |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 16 Jan 2007 : 3:09:43 PM
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"The question is, did carrier status occur as the result of a mutation in descendants of the horse OR did it come before X and X was a carrier as well. WHAT was it that created such a gene? "
Carrier status has been suspected back as far as the mid 1800s and even earlier. The Swiss worked out a trail back to Rymnik as stated in their published research. And further studies have picked up a Syrian Stallion imported in 1845 which appears in the backgound of ALL their horses studied. There are theories that the horse plagues in the Middle East and Egypt which occurred at that time could have caused a genetic mutation in the surviving animals. This is just a theory though. Genetic mutations are known to occur with or without visible cause. CA has been present, even if not expressed often, for a long, long time. It is felt that the ever diminishing genetic pool has allowed the more frequent expression in present day breeding. |
Edited by - szedlisa on 16 Jan 2007 3:37:46 PM |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 16 Jan 2007 : 5:01:07 PM
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Justine writes---"The post-mortem showed the cerebrem had not grown, the rest of the brain had. CA.
Her parents are now gone. The mother was polish, the father was russian. The breeding was never repeated but the mother bred other normal foals, the father sired many many great offspring.I did learn from other breeders that russian/polish have more CA than English/egyptian/spanish..... but this I dont no if it is true or proved. I only know its rare."
Justine ~ In actual fact it is more how the genes fall and pass through from generation to generation. CA is expressed in All bloodlines and not necessarily more than in one than another. I certainly imagine it was rare, or unrecognized, or simply overlooked; however it is becoming a problem now. Thankyou for sharing your experiences. CA needs to be talked about & it needs to have a TEST. |
Edited by - szedlisa on 16 Jan 2007 5:01:33 PM |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 16 Jan 2007 : 5:17:30 PM
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Justine,
Was that Dr. Derek Knottenbelt who in 2005 was awarded the British Equine Veterinary Association’s Welfare Award? It was for his outstanding contribution to national and international equine medicine – in recognition of pioneering treatments he has developed for sarcoid, ragwort poisoning and other equine diseases. If so I would like to get him in touch with Prof. Dr. Vinzent Gerber and Dr. Tosso Leeb on a profession level. Dr. Knottenbelt's research notes on your foal could be well appreciated.
And Tamila~
Anything that your daughter as a Vet in the states could contribute on the subject would be more than welcomed. Tomorrow the 17th is the last day of the Genome Horse Project World Conference and Workshops being held in San Diego and new information should be published shortly. I do know great strides have been done on HERDA and also the Y Chromazone and I believe the locus has been found for the CA allele but the actual allele has not yet been segregated. |
Edited by - szedlisa on 16 Jan 2007 5:25:52 PM |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 16 Jan 2007 : 5:54:06 PM
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Jane (Vygoda) ,
So right that "few everyday vets" are not fully aware of CA and its symptoms! Montana has had that scenario and I certainly have come across the same also, both in the states and here in Mallorca. I was very pleased to see that a team of 7 geneticists/reseachers at the University of Cordova had developed new methods of examining and preserving the Purkenje Cells, according to their published study last August. BTW, I enjoyed visiting your website. It seems as if we have shared similar interests in breeding selections in the past. <grin> I know I was pleased with my results and am sure you were as well. |
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Montana
New Member
USA
9 Posts |
Posted - 18 Jan 2007 : 12:07:07 AM
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Hi folks!
A couple of things for those of you who are most interested in this topic. I consulted with Dr. Alexander de LaHunta, a retired verterinary neurologist from Cornell University, about my filly. He told me a few interesting things. One is that the loss of of the purkinje cells the allow the granular and cortical layer of the cerebellum to communicate (which is basically what CA is...loss of purkinje cells...that's what they look for in an autopsy) will occur for about 6 to 12 months from onset but then stop and the horse will stabilize--if it lives that long and if the symptoms are not so severe that the horse is at risk of killing itself in an accident and needs to be euthanized for humane reasons!
This is true from my experience with my filly May. Severity of symptoms varies tremendously. She first had noticable symptoms as a yearling (though may have had symptoms that were not noticed sooner--she has a relatively mild case) and while it was so upsetting to see her repeatedly fall down and run into fences that I nearly put her down, my vet kept talking me out of it  and so I did notice what appeared to be an "improvement" over time...she didn't get better, but she DID learn to cognitively compensate for the fact that her cerebellum didn't fully communicate with the rest of her brain. She's now four.
The bottom line on bloodlines is that the suspect lines exist all over: in Crabbet, Polish, Russian, and Spanish breeding. (I think there have been cases in Egyptian lines, but I have no direct examples--however, the Egyptian lines have their own problems with Lavender foal syndrome and juvenile epilepsy anyway) So, no matter what horses turn out to be the progenitors, all the likely suspects are probably in 90-99% of all Arabian pedigrees today.
I also agree with Lisa that in places where the gene pool gets smaller, the prevalence is going to rise.
We must have a test because we simply cannot eliminate the suspect lines. We might on occasion be able to pinpoint a carrier, but even when you breed a carrier to a carrier, you have a 25% chance of a "clear" foal, and thus it is also important not to scapegoat a particular line. For example, I am virtually certain that a particular horse foaled prior to 1950 was a carrier. However, although people have helped me identify several of his sons and grandsons who are carriers too--they threw affected foals (including my filly)--I am also reasonably sure that his most famous son is probably NOT a carrier.
So, we have a dilemma: Without a test, we don't know who the carriers are until they produce an affected foal. But if we eliminate a bloodline without knowing if a horse is a carrier for sure, we risk throwing out the good with the bad.
I urge everyone to support Lisa's efforts and provide all the data you can. In the states, "wobblers" is a catchall term for horses with neurological problems. Any Arabian with neurological symptoms probably does NOT have true "wobbler's syndrome," but rather has CA or another genetic condition we know even less about called OAAM (occipital-atlantal-axial-myelopathy).
What IS important to remember is that this is a recessive condition, so it can "lurk" for generations, passed on as a carrier gene and yet a horse in between never throwing an affected offspring (this is particularly true of mares, even the most productive have relatively few foals compared to a stallion). In the case of my filly, a full sibling died mysteriously as a suckling...a massive onset of CA? We don't know, the breeders claim they found the foal dead in its stall one morning and the local agriculture college (no vet school) couldn't determine a cause of death--but didn't autopsy the brain! Other than that, May's sire has not, to my knowledge, sired other affected foals. But, it only takes one to identify a carrier. "Prepotency" has no effect...it's a flip of the coin, a 50-50 chance the carrier horse will pass on the gene every time (and, an affected foal will only occur if the horse is bred to another carrier who happens to pass on the gene as well).
In the total population, of random matings of carriers and non-carriers, the incidence will be about 3%. But if the gene pool shrinks, that incidence will rise. For example, there is documentation in the veterinary literature of a farm that closely bred certain bloodlines lost 8% of its foal crop to CA in a single year!
So, I encourage a twofold approach: 1) Education of veterinarians to recognize the disease when it appears; 2) Helping researchers obtain enough DNA samples to develop a test. To do this, we need owners who both recognize the condition and understand that it is to everyone's benefit to provide this critially needed data.
Sorry to go on so long about this, but the condition was first observed in the veterinary literature in 1966. I think 40+ years is plenty of time to educate vets and owners about the disease, and now that we have the technology, it's time to develop a test!
Thank you, everyone, for your interest and caring.
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Edited by - Montana on 18 Jan 2007 12:12:44 AM |
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szedlisa
Bronze Member
Spain
124 Posts |
Posted - 19 Jan 2007 : 03:14:10 AM
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Great post Montana. Thanks for stepping up to the plate and speaking out. According to the datasource the UK has 35149 registered arabians. 3% = 1054. The USA has 623602 which at 3% = 18708 and take Spain with their 12948 , 3% =388. Just as a random figure those are a lot of affected foals with CA expected to be born on an annual basis. It rounds out to aproximately 35-55% of ALL Arabians being from affected bloodlines. That breaks down to around 25% of the BREED is a carrier.
You may never see one in your lifetime and if so, consider yourselves very fortunate.
But it is with us. |
Edited by - szedlisa on 19 Jan 2007 03:14:55 AM |
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Cerebellar Abiotrophy (CA) , A Serious Concern
