Dr. Cecilia Penedo is of the firm opinion that stallions affected with CA will not be able to perform a live cover for breeding. This comes from their own experience when they maintained a test herd at UC Davis and the difficulties they had to deal with normal breeding proceedures. I have in fact seen the get of an affected stallion and the stallion himself. The stallion shows only slight symptoms of ataxia but does have the intention head tremors and a notable lack of menace responce (slow blink). Although he did sire one foal , he has not been used for breeding since. I only relate this to show that a stallion whose condition is unrecognized and certainly any carrier stallion ( no symptoms) can and have been used for breeding.
I think I can top that. I have a friend who somehow trained her stud to "ground collect." She will only do AI. I'm not asking the details, and I haven't witnessed it, but he's apparently never live covered a mare in his life! And I bought one of his babies, so obviously something's working!
Certainly with AI dummies and such, collection of a mildly affected stud wouldn't be totally impossible--however, on the other hand, I have heard talk from people who worked at Davis back when they had the herd of affected horses and apparently they really did have a pretty incredible circus going on there
Chuckle!!! I also know of a stallion with basically 3 legs that had to be "ground" collected, because an accident pretty much mangled his right hind leg. He was the well-known Galero son, *Makorr, who was born at and stood at Dr.Peter Hautappel's Rodania Stud in the Netherlands before being exported to the states. A highly intelligent horse ( and with a very perceptive owner!), *Makorr has a large block of wood in his turnout run, which he used to rest his hind leg on. And yes...*Makorr would move the block to where he wanted to stand so he could see "his" mares. Clever Boy!!
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.
Presumably - given the date - this second horse was, like Rymnik, also part of a central European breeding programme?
In the 17th century, Polish noblemen sent emissaries out to search for the noblest desert horses from the Middle East. Prince Sanguszko at Slawuta, Count Branicki at Bialocerkiew, Count Dzieduszycki at Jarczowce, and Count Potocki at Antoniny were some of the best known breeders. The studs at Gumniska and Antoniny were founded with mares from Slawuta . Most of Poland's original oriental light horse stock came as a result of spoils of war from the Ottoman Empire and came from the Negeb with a number from Syria, and the arabian desert. Many were purchased through Nicolas Gliocchio, the horse trader/buyer for many european breeders. Exports and some purchases were made through Constantinople (Istambul).
The stallion Seglavi Ardżebi db. imported in 1858 to Sławuta established the line that lasted till 1908. Rymnik (born 1876) – the sire of Jaskółka (dam of famous: Skowronek, Parada and Bakszysz) belonged to this line. Rymnik's dam line was Caramba d.b. 1863, bred by ks. Roman Snguszko, at Gumniska.
One ancestor was imported from Syria: Abu Cheil d.b. (SY) 1845 grey stallion to Jarczowce (PL)and is found in the dam line of BARCELONA (Slawuta) and in Rymnik's sire line. Rymnik's descendants are so extensive and have been so interbred during the successive generations down to present day breeding programs that Abu Cheil d.b. does indeed appear in the background of many of our Arabians. This stallion is also called Abu Hejl d.b. The El Masri Database has this to say about him: "Imported to Poland in 1845 by Count Juliusz Dzieduszycki's to his Jarczowce Stud. In 1854 Abu-Helj went to Count Potocki's Antoniny Stud Farm. Then in 1867, he bred 2 mares at Gumniska.His dam was said to be descended directly from a mare belonging to the Prophet Mohammed and on his sire's side, he was a 1/2 brother to Batran-Aga. He sired 50 foals, all very typical Arabians and of strong build."
Some researchers have the theory that possibly a genetic mutation was caused at some point in history. The plagues of Egypt and the Middle East come to mind. Besides the early plagues mentioned in the Bible, an outbreak of African horse sickness in Egypt in 1880 and then another one in the 1920's (see Lady Wentoworth) reduced the equine population to a mere handful of arabians. Another in 1959-60 killed between 200,000 - 300,000 head alone in the Middle East. And there were ten major horse plagues in Egypt between 1819 and 1953 which killed off thousands of horses.(http://www.bpeah.com/ArabiaToEgypt.htm). The Ali Pasha Sherif breeding program (also with descendants of the sought after Syrian lines) of aproximately 400 head lost over half of his stock with the AHS plagues in Egypt during the 1860s. Only by moving horses to Upper Egypt was he able to save what remained.
As a very promenient present day geneticist has said the defective gene of CA "is in the breed". It is really not a question of pinpointing specific progenators, but a question of supplying enough information to identify the allele and develop a test.
The other probable progenitor horse I am aware of, one foaled in the 1840s (I think the same horse Lisa is thinking of), is NOT linked directly to any central European breeding program. He is an ancestor of the Blunt imports. And, it doesn't matter...he's everywhere. I am willing to bet money that 98% or more of all Arabians alive today carry multiple lines to him. I stopped counting the number of times he shows up in my filly's pedigree at 93...!
The only studies in the USA that even hint at pedigree issues both point at Crabbet-bred horses in the USA, partly because both studies were based on horses who threw affected foals in the early-to-mid 1960's, well before the USA's "Polish invasion" and at a time when Russian and most Spanish horses couldn't be registered in the US.
Crabbet horses sold worldwide...they are in almost everything--Egyptian, Spanish, Russian, Polish, you name it...we must remember that the Blunts did in fact do much to help save the breed from extinction in its native lands. But this means we also have a gene pool that is small enough that we have to be a little careful--and sometimes have not been...One veterinary journal stated, with considerable disapproval, that Arabian breeders (at least in the USA) qualified for membership in a society for the promotion of incest in horses! The farm that was the target of the study had lost 8% of its foal crop to CA in one year, they had something of a point.
So far, I do not believe we have identified a carrier who we KNOW was the parent of an affected foal who does not carry lines to BOTH of the suspected progenitor horses discussed here. If the gene did come out of Syria, then it's everywhere. If the mutation occurred later, say in Egypt during the mid-1800's, it's still everywhere.
At this point in time, any horse in the western world is apt to have some suspect lines. We are all at risk. I believe the statistics Lisa stated are accurate...
So bottom line is that this gene is definitely "in the population," we must focus our energies on the development of a DNA test, as there is no way we can eliminate it by eliminating lines to the progenitors.
To rely too much on pedigree lines, we would paint clear horses as carriers and falsely assume horses who just never got bit by the statistical roll of the dice were clear when they were not...only a DNA test, just like we have for SCID, will work. That's why we need samples from both affected horses and, when possible, their unaffected relatives.
(As an earlier poster stated, we may know that almost every SCID carrier traced to Horse X. If Horse X is who I think it is, again, we are talking an animal in over 90% of all Arabian pedigrees today, so while it's good trivia, it's no help in eliminating the disease because some of his offspring also had to be clear...a recessive doesn't hit every time!)
If you have an affected horse put down, consider trying to get a brain histopathology report done to see if the brain has the purkinje cell loss typical of CA...this info will also be invaluable. Many Universities can perform this type of test. If you ask them ahead of time, they can provide detailed instructions for autopsy to your veterinarian.
Please help, even if you don't have an affected horse, help increase awareness.
Just bumping up this thread... Foal season has started so keep a close eye on those newborns during the next few moths to see if you see any head tremors. Especially when the foal is trying to suckle. Remember that CA can (but not always) be seen about two to three weeks after birth.
Foals diagnosed with Cerebellar Abiotrophy with a histopathic neocropsy have shown a 65% loss of Purkinje Cells. See U of Cordoba study. Depending on the % of PK cells degenerated affects the symptoms and how lightly or heavily the condition appears and when it appears.
Some interesting information here. Hope this helps for anyone to understand the degeneration process. Here is a very good link on mutations as well: scroll down to FREQUENCY of MUTATIONS and Males Contribute More Mutations Than Females. Mutations: http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/M/Mutations.html
Remember hair samples are easy to collect. 30 to 40 pulled strands with hair follicle attached. Place in a Labeled clean plastic bag and mail off. Be sure to identify each sample separately.
Finally, some real press! This month's issue (March 2007) of Arabian Horse World carries a major article in their feature "Stud Farm Diaries" on Genetic Diseases in Arabians and especially CA!
Check it out! What a wonderful thing to finally be getting some ink in the "mainstream" press.
Thanks go out to everyone who has been shaking the trees about this disease. This is the type of publicity we have been hoping for!
This is really a great article on page 277!! Cindy Reich is a well-known Arabian horse judge in the states besides being an author with amonthly feature article in the Arabian Horse World and the stud and breeding manager at the University of Colorado. She has many many years of experience behind her and has written of her experience with Cerebellar Abiotrophy and the symptoms seen.
This is a big help for anyone whois seeing the symptoms for the first time. The severe cases are easy to spot by both owner and vet alike. The slight cases area different story and as so often the foal has crashed into some hard unyielding object, most people think it is the accident which has caused the head tremors. Not so. Tis the other way around.
Some hair samples are trickling in but we do desparately need more owner/breeder participation. So even if you have only a normal family related member, please consider sending hair samples and/or blood samples.
Cindy Reich was raised on a small family-owned Arabian horse breeding operation in Boulder, Colorado. She began showing when she was eight-years-old and showed in all competitive disciplines from equitation to halter, native costume to working cow horse and reining for over 25 years. Cindy graduated from Colorado State University with a degree in Bio-Agricultural Science. She worked as the breeding manger and artificial insemination technician for numerous breeding farms over the past 25 years including Paramont Farm, Lasma East, Varian Arabians, Aries Arabians, Fidelis International, BARA Farms, Wrigley Arabians, KEG Arabians and Wolf Springs Ranch. Cindy did post graduate work in equine reproduction at University College in Dublin, Ireland.
Some of the stallions Cindy has managed include Tornado, *Marsianin, *Aladdinn, *Eukaliptus, *Menes, Bey el Bay, Bay Abi, *Posjenik, Promotion, Wisdom, Cal-O-Bask, *Nilo, High Jack and Legacy of Gold among others. When Cindy was based in Holland for one year and Belgium for one year managing the breeding of *Menes, she took the opportunity to visit many European farms and shows. Currently, Cindy is managing all client mares and stallions for the Equine Reproduction Laboratory at Colorado State University.
Cindy has been a licensed judge in the Arabian division for 29 years and has judged Arabian national shows in the U.S., Canada, Sweden, Brazil, Australia and Venezuela. Livestock in the 4-H program was Cindy’s first judging assignment when she was just nine-years-old. She judged livestock and horses through the 4-H program for 10 years. Later, she was on both the equine and livestock judging teams for Colorado State University. She was named High Senior Individual at the U.S. National Arabian Youth Judging contest twice. She was a member of National Champion Sr. Judging Team at the U.S. Arabian Nationals, and she coached two National Champion youth judging teams and one Reserve National Champion Youth judging team.
Cindy Reich has also published a part two to her earlier article, this month's article is on non-genetic foal diseases, but as some mimic those that ARE genetic, it is worth a read in order to differentiate between conditions.
I have been recently asked on how I would handle dealing with the potenial CA carriers? Should they not be bred at all (both mares & stallions), should all stallions deemed carriers be gelded? As of right now without testing one must have produced an affected foal to know if the parents are carriers. So how to handle this both before and after testing?
In my opinion good breeding practices consist of a program based on quality Foundation Mares for which individual stallions are used ( in the plural) to complement the mare's phenotype and genotype.
Within the Spanish bloodlines (with which I am most familiar), it has been a long accepted axiom to avoid doubling up on the mare lines. Whereas it is common to find line breeding to a specific stallion and in many cases an inbred factor to an individual stallion, repetitive usage of inbreeding or line breeding to a specifc mare is not recommended. There are many reasons for this approach. The major one being that the stallion lines have already been reduced to three in direct male descent. Further reduction of an already small genetic pool by reducing the female lines with inbreeding would reduce the genetic variation even more and jeopardize the future of the Spanish Arabian. Reducing the genetic variation not only enhances and sets the positive desired traits; it also does the same for those not so desirable traits. This applies to physical attributes as well as temperment and any hidden neurological disorders such as SCIDS and CA.
This selective form of line breeding ( ie. avoiding it in the female lines) would be a wise approach to breeding in any of the Arabian bloodlines.
Not always, but in general, Cerebellar Abiotrophy is found in Arabians with repetitive crosses to one or more carriers. Obviously the more confirmed and suspected carriers in the background of a horse, the more likely the odds are that it also will be a carrier and/or affected if bred to another carrier. At this point in time a confirmed carrier is a mare or a stallion which has produced/sired a foal with clinical signs of Cerebellar Abiotrophy and has had a histopathic diagnosis completed on the status of the Purkenje cells.
As all affected horses will produce 100 % carriers no matter if bred to a clear or carrier mate, no affected horse should be used for breeding at all. Confirmed Carrier mares should not be bred to known carrier stallions or even stallions with suspected carriers in their background. Confirmed Carrier stallions should be stated as such and bred only to non-carrier mares whenever possible. These breeding practices will not eradicate CA from the genetic pool but they will reduce the occurrance of CA and provide some sort of protection for future generations.
SCID testing has had a beneficial effect on lowering the rate of scid foals produced. Keep in mind that the owner of a scid foal knows that it will die. In order to avoid financial loss and time loss, mare owners have become more selective in their choice of stallions and in testing their own mares. With CA, even when there is a test, affected foals do not die. If only slightly affected many will not be recognized and may be used for breeding as is the case at present. A normal looking foal will mature to breeding age and will usually be bred, even if a carrier. Testing will only provide guide lines for the responcible breeder.
What is happening now, is that confirmed carrier horses are being used as breeding stock. Any affected foals are quietly euthanized. The carrier mare is rebred; produces a normal looking foal and both are sold onwards. Or, in some more responcible establishments, because carrier mares can also produce clear foals, selected daughters are kept , bred and if no affected foal is produced, will be retained in the breeding herd and the original dam sold onwards or simply retired from breeding. Testing will eliminate such a long drawn out and expensive process of identifying carrier progeny. However, at the moment that is the only way to ascertain if a mare line is a CA Carrier line or not.
Short term breeders are the cause of much of the spread of undesirable genetic conditions. They tend to breed for a quick turn over. These breeders can have very few or numerous breeding stock. Numbers are not a qualification of the description. Short term breeders do not test their own progeny's bloodlines through breeding before selling. Far too often they will continue to breed their carrier mare for a number of years before keeping a "replacement" daughter, without ever having bred any of the previous daughters themselves or test any of the sons..
A concientious breeder will want to see how the progeny breed onwards and if the correct breeding selections are being made to further their breeding goals. The short term breeders are also the ones who usually sell off their confirmed carrier stock without a word to an unsuspecting buyer that the mare or the stallion has had wierd head shaking foals. It comes down to keeping the profit/loss margin in favor for the breeder. A horse with a neurological condition is pretty hard to sweep under the rug.
It will all be up to the breeders themselves, but I do feel that horses with suspected genetic defects should be required to have a disclosure clause in any breeding or sales contract. That is just my opinion to be sure.
I would largely concur with much of what Lisa says; never breed an affected horse, even if the horse can reproduce, you are knowingly introducing more carriers into the gene pool every time. If you have a known carrier, you need to remember that there is no test yet; just because another horse is so far "clear," that may just be luck. Likewise, just because the parent of a horse threw affected foals does not necessarily mean the horse happened to get the carrier gene--a carrier has a 50-50 probability of passing on the gene, and even in carrier to carrier matings, the statistical probability is that 25% of the offspring will be clear--and 25% will be affected.
This is why I urge people to send in DNA and support the development of a test. You can take precautions and avoid known carriers, but it's still a crapshoot!
The Quarter Horse world just got a test for HERDA announced within the past month. All it takes is time, money and DNA samples to get these genes identified and a test developed.
In the meantime, Lisa's reasoning is good. I personally would seriously limit linebreeding on BOTH sides. With a limited gene pool and few stallions, you sometimes have no choice, but when you are not breeding a limited group (like straight -anythings) these genes are autosomal, meaning that they are not sex-linked. Therefore, a carrier stallion can spread more little carriers far and wide. In short, if you are a big breeder and have a few horses to play with, AND are willing to geld or spay your experiments that don't work out, that's one thing. But please don't sell breedable animals on (at least, not without full disclosure) if you know they have thrown affected offspring. And if you are a small breeder with only a very few mares, for heaven's sake, don't breed too closely! The people who have to breed closely (such as the straight Davenport breeders) actually try to maximize the genetic diversity within their population.
Now, that said, avoiding linebreeding is no guarantee. My affected filly appears at first glance to be about as complete an outcross as you are going to see, with no common ancestors in her first four generations. She has Russian, Polish, Crabbet and Egyptian breeding. Yet, she has several different stallions who appear on both sides of her pedigree (from four different and major sire lines), and she also goes back over 90 times to one particular stallion who might be one of the historic carriers of the gene. So in theory, her breeders did everything right (except buy a stud colt who was sired by a known carrier; but they may not have known the horse was a carrier at the time.)
I personally would encourage honesty. I know I'm on a fool's quest for that, but it can't hurt to ask stallion owners if they will put a genetic diseases clause in their contracts (full refund of stud fee, NOT a free re-breeding) and ask if the stud has ever thrown offspring that were put down it their first year, and why, possibly request names of the mare owners and so on. Yes, I know I'm dreaming, but hey, I'm not the only one...
For those of you who get the AHA magazine, The Modern Arabian Horse, keep an eye out for the August/September issue. There is an extensive article on genetic diseases in the Arabian horse. This is the first recognition by the American Arabian Registry of the status of inherited genetic conditions in the arabian breed. It will be followed up by extended articles on each of the genetic diseases posted on the AHA website on their Education Health Pages for public viewing.
It has taken a lot of hard work, many hours of research and the dedicated efforts of a 6 member team to get this accomplished. Hats off to all of them !!
ESRE has come thru and the American Arabian Horse Registry has recognised the need to define and describe the 5 genetic diseases which can be found in the Arabian breed.
Dr. Cecilia Penedo from UC Davis has identified the chromosomal region, which harbors the causative muation and is now analyzing the genes within this region. She and her team of researchers have sufficient "markers" in their database and with their knowledge of carrier lineage are offering 'predictions' as to the status of the presenc of CA in owner/breeders horses.
This is not a genetic DNA test like scid but is an indirect preliminary genetic test based on markers. But for those who wish to know if their horses are predicted carriers or not , please send a request to her at [EMAIL]mctorrespenedo@ucdavis.edu [/EMAIL] with full name, registration number if applicable and parentage of each individual horse. A link to a full pedigree at AllBreedPedigree Database will facilitate matters and assure a more speedy responce.
If you wish to contribute Hair Follicle samples at the same time, include the date sent in your email send them to: Cecilia Penedo Horse Research - CA Veterinary Genetics Laboratory University of California One Shields Avenue (For Overnight or 2-Day Delivery use: 980 Old Davis Road) Davis, CA 95616-8744
Needle nose pliers makes pulling 30-40 hairs with the follicle bulb attached fairly easy (so do a lot of carrots ~grin). Each sample should be identified separately to avoid confusion, ( with multiple horses, lite-weight sandwich baggies are handy), airmail to UC Davis in a normal letter envelope and mark the outside "For Cerebellar Abiotrophy Research".
Dr Penedo is out of her office until September 15, however the Lab is open and the rest of the research team available.
This an excellent opportunity to obtain a "predicted" status of all your horses. There will be some surprises to be sure; however better to have the knowledge in order to make careful breeding selections in the future, than to go through the costly and heartbreaking saga that some of us have had to experience.
Recently a 6 year old mare which was well under saddle (with no previous symptoms)has shown clinical signs and after extensive tests for EPM, Wobblers, (all of which were negative) was euthanized and had a histopathic diagnosis of her Purkenje Cells done at UC Davis. The mare was positive for CA.
Get your horses analysized and avoid a costly experience such as this mare's owner. Far better to be prepared and to breed selectively than to risk the occurrance of CA.
Keep in mind that this is a "rule in" not a "rule out" determination. Until we locate the actual allele, we can't be certain if the horse truly is "clear" for CA. The research to date can only suggest if there is a high probability that a horse is a carrier. To ever promote a horse as "clear" based on this data would be a bad idea, as they have not in fact developed a test.
Cerebellar Abiotrophy (CA) , A Serious Concern
Posted - 20 Jan 2007 : 9:49:59 PM
And I bought one of his babies, so obviously something's working!
