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basbob Posted - 05 May 2010 : 6:09:33 PM
I've just read that SCID is one of six arabian prone diseases. What are the others and does anyone know why?
7   L A T E S T    R E P L I E S    (Newest First)
debs Posted - 06 May 2010 : 07:45:25 AM
I lost my horse of a lifetime a year last Jan to Equine Systemic Proteoglycan Accumulation.
My vets could not diagnose so we were sent to South Mimms vet hospital, where he was seen by an Israeli vet who recognised what it was immediatly. He told me that it seemed to be common in arabians and studies were taking place in the Middle East on Arabians in the army(?)Was absolutelt distraught at the time so bit of a hazy memory...
There does not seem to be any history in my boys family but he did say that it could present itself in many ways and if in an older horse would just be put down to old age.
(the body stops producing collagen so affects all ligaments, in legs, eyes aorta etc, lameness, blindness, heart attack)
My boy symptoms were so slight, i just noticed a change in his posture, looked a little hunched, had the vet up daily, took bloods etc but didnt know what it was, then on the 3rd day his fetlocks dropped so much they sent him off to hospital. He never had any lameness in his life, the change happened so quickly
Would be interested to hear if anyone has had to deal with this...
lisa rachel Posted - 06 May 2010 : 06:43:39 AM
Hi Lynda, was up on ovary -watch all night for frozen semen mares as well as having had a call to a horrible broken leg , so didn't see this, but Montikka's post covers the most important ones very well. There are others eg Arabian fading syndrome (not serious of course!), selective Igm deficiency etc, Also I just wanted to point out that while not limited to Arabs a lot of other diseases have a genetic basis eg ERS or tying up syndrome (genetic predisposition in some lines of Arab and TB which make episodes of tying up a real risk even with perfect management), sweet itch, susceptibility to sarcoids etc
For balance I would like to say that as far as many other common performance limiting conditions of wind and limb are concerned Arabs are remarkably sound and trouble free. To state the obvious just plain bad/good conformation and to an extent temperament are heritable, which is why careful selection of breeding stock is so important and why in my opinion testing for genetic diseases is important but should be viewed in context and EXCELLENT sires who happen to be carriers should not be excluded from the gene pool, simply never allowed to cover a carrier mare.
Right off to scan yet more mares then a castration-fest!
Cheers
Lisa
MinHe Posted - 05 May 2010 : 11:08:54 PM
You have to remember that Arabians have had the most study devoted to them - there are other genetic problems in other breeds but they have been subjected to as much scrutiny on the whole as the Arabian. And most of them have much smaller gene pools!

So no need for gloom and despondency the MORE we know, the better, as it allows us to make educated breeding decisions!

Keren
Montikka Posted - 05 May 2010 : 10:28:14 PM
Just copied the information below from Wikipedia:

Genetic diseases
There are six known genetic diseases in Arabian horses, two are inevitably fatal, two are not always fatal but usually result in euthanasia of the affected animal, the remaining conditions can be treated. Three are thought to be autosomal recessive conditions, which means that the flawed gene is not sex-linked and has to come from both parents for an affected foal to be born. The others currently lack sufficient research data to determine the precise mode of inheritance.[43] Arabians are not the only breed of horse to have problems with inherited diseases; fatal or disabling genetic conditions also exist in many other breeds, including the American Quarter Horse, American Paint Horse, American Saddlebred, Appaloosa, Miniature horse, and Belgian.[43]

Genetic diseases that can occur in purebred Arabians, or in partbreds with Arabian ancestry in both parents, are the following:

*Severe Combined Immunodeficiency (SCID). Similar to the "bubble boy" condition in humans, an affected foal is born with no immune system, and thus generally dies of an opportunistic infection, usually before the age of five months. There is a DNA test that can detect healthy horses who are carriers of the gene causing SCID, thus testing and careful, planned matings can now eliminate the possibility of an affected foal ever being born.[44]
*Cerebellar abiotrophy (CA or CCA). An affected foal is usually born without symptoms, but at some point, usually after six weeks of age, develops severe incoordination, a head tremor, wide-legged stance and other symptoms related to the death of the purkinje cells in the cerebellum. Such foals are frequently diagnosed only after they have crashed into a fence or fallen over backwards, and often are misdiagnosed as a head injury caused by an accident. Severity varies, with some foals having fast onset of severe coordination problems, others showing milder symptoms. Mildly affected horses can live a full lifespan, but most are euthanized before adulthood because they are so accident-prone as to be dangerous. Clinical signs are distinguishable from other neurological conditions, but a diagnosis of CA can also be verified by examining the brain after euthanasia.[45] As of 2008, there is also a genetic test that uses DNA markers associated with CA that can detect both carriers and affected animals.[46]
*Lavender Foal Syndrome (LFS), also called Coat Color Dilution Lethal (CCDL). The condition gets it name because most affected foals are born with a coat color dilution that lightens the tips of the coat hairs, or even the entire hair shaft. Foals with LFS are unable to stand at birth, often have seizures, and are usually euthanized within a few days of birth.[47][48] In November, 2009, Cornell University announced that a DNA test has been developed to detect carriers of LFS. Simultaneouly, the University of Pretoria also announced that they had also developed a DNA test.[49]
*Occipital Atlanto-Axial Malformation (OAAM). This is a condition where the cervical vertebrae fuse together in the neck and at the base of the skull. Symptoms range from mild incoordination to the paralysis of both front and rear legs. Some affected foals cannot stand to nurse, in others the symptoms may not be seen for several weeks. This is the only cervical spinal cord disease seen in horses less than 1 month of age, and a radiograph can diagnose the condition. There is no genetic test for OAAM, and the hereditary component of this condition is not well researched at present.[50]
*Equine juvenile epilepsy, or Juvenile Idiopathic Epilepsy, sometimes referred to as "benign" epilepsy, is not usually fatal. Foals are born normal and appear normal between epileptic seizures, and seizures usually stop occurring between 12 and 18 months.[48] Affected foals may show signs of epilepsy anywhere from two days to six months from birth.[51] Symptoms of the condition can be treated with traditional anti-seizure medications, which may reduce the severity of symptoms.[52] Though the condition has been studied since 1985 at the University of California, Davis, the genetic mode of inheritance is unclear, though the cases studied were all of one general bloodline group.[51] Recent research updates suggest that a dominant mode of inheritance is involved in transmission of this trait.[53] Some researchers have suggested that epilepsy may be linked in some fashion to Lavender Foal Syndrome due to the fact that it occurs in similar bloodlines and some horses have produced foals with both conditions.[48]
*Guttural Pouch Tympany (GPT) occurs in horses ranging from birth to 1 yr of age and is more common in fillies than in colts. It is thought to be genetic in Arabians, possibly polygenic in inheritance, but more study is needed.[54] Foals are born with a defect that causes the pharyngeal opening of the eustachian tube to act like a one-way valve. Air can get in, but it cannot get out. The affected guttural pouch is distended with air and forms a characteristic nonpainful swelling. Breathing is noisy in severely affected animals.[55] Diagnosis is based on clinical signs and radiographic examination of the skull. Medical management with NSAID and antimicrobial therapy can treat upper respiratory tract inflammation. Surgical intervention is needed to correct the malformation of the guttural pouch opening to provides a route for air in the abnormal guttural pouch to pass to the normal side and be expelled into the pharynx. Foals that are successfully treated may grow up to have fully useful lives.[56]
The Arabian Horse Association in the United States has created a foundation that supports research efforts to uncover the roots of genetic diseases.[57] The organization F.O.A.L. (Fight Off Arabian Lethals) is a clearinghouse for information on these conditions.[58] Additional information is available from the World Arabian Horse Association (WAHO).[59]



Pashon2001 Posted - 05 May 2010 : 7:13:37 PM
SCID - Severe combined immune deficiency
CA - Cerebullar Abiotrophy
Gutteral Pouch Tympany
Occipital Atlanto-Axial Malformation (OAAM) - A condition of the spine
Lavender Foal Syndrome
Equine Juvenile Epilepsy

I would imagine because the gene pool is so small that any genetic discrepancy has been allowed to breed on and magnify into large proportions.

Scary isnt it
LYNDILOU Posted - 05 May 2010 : 7:04:34 PM
I was also told this , there are supposed to be 6 lethal diseases associated with Arabian horses , perhaps we should ask our resident vet Lisa Rachel ?
BeckyBoodle Posted - 05 May 2010 : 6:36:20 PM
Can't say why other than there must have been some sort of gene mutation that has then gone down the bloodlines and only show up when a carrier meets a carrier. I am definitely no geneticist so may have it wrong.

I assume that Lavender Foal Syndrome and Cerebellar Abiotrophy are two of the others, which are reasonably well known.

Don't know what the other three are.

B


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