Lavender foal syndrome (LFS), also called coat color dilution lethal (CCDL), is an autosomal recessive genetic disease that affects newborn foals of certain Arabian horse bloodlines. Affected LFS foals have severe neurological abnormalities, cannot stand, and require euthanasia shortly after birth. The popular name originates due to a diluted color of the foal's coat, that in some cases appears to have a purple or lavender hue. However, not all foals possess the lavender coat colour, and colouring can range from silver to light chestnut to a pale pink. Carrier horses have no clinical signs and DNA testing can determine if a horse carries the gene.
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Newborn Horse Syndrome Suggests Links to Childhood Autism
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My name is Ellen Jackson, I'm the sole proprietor of Victory Rose thoroughbreds here in Vacaville. We raise about 70 to 80 foals a year. We also race them. The investment to raise a racehorse is quite large. So that's why we put in so much to making sure the foal can be just as healthy as possible. We want to see the foal bright and alert, aware of the environment, sticking close to the mare, nursing, but the important thing is that it moves away from you. That's the normal response because they're prey animals. When we don't see that, then we know there's something wrong with the foal. So, when you see the behavior change, could be an infection, but it also could be this syndrome that's been described for about 100 years: maladjusted -- nicknamed "dummy foal" -- it could be that. Well it used to be just a nightmare. You go oh, great. We're going to have to bottle feed this baby or tube feed this baby for the next ten days or however long until it grows out of it. But it was pretty much a waiting game. It was really quite frustrating. It would take 24 hour micromanagement, and lots of bodies and no sleep, until that baby came out of the syndrome. Our research showed the cause of that is not low oxygen, but actually a persistence of the hormones that keep them asleep in the womb. And we also found that the birth canal pressures, which we now mimic with a procedure with these foals that come into the clinic, they're maladjusted. We create birth canal pressures, it lowers the neurosteroids, and they wake up. Often very, very quickly, very similar to what happens when they're born. You put on the, the harness, we've built sort of a little harness that just snaps on, doesn't affect the foal in any way, and then as soon as you go and tighten it up a little bit, they just drop. And go to sleep. And then you unsnap it while they're out, you unsnap it, and they jump up, and nicker! It's amazing. We had one that was trying to climb in the feeder, cause it couldn't figure out how to get out of that corner. We squeezed it, and it got up and nickered to the mom for the first time. Immediately. It was just astounding. They have identified a group of chemicals that modulate neurodevelopment in the foal that may be very relevant to autism. And so it certainly caught my interest. Well, this all started when John Madigan and Monica Auman(?) came to talk to me and suggested that I should be thinking about a connection between these two completely unrelated disorders. And I really knew nothing about fetal transition in consciousness until they sort of forced me to think about it. We believe our research has brought some new understanding that could be applicable to some conditions in children. One of the things we'd like to look at is autism spectrum disorder. In order to pursue that and apply what we've learned, we're looking for some support and help to get that done.
Impacted bloodlines
Arabians of "Egyptian" bloodlines have the most documented cases of the disorder, with 10.3% of Egyptian Arabians being carriers, but only 1.8% of non-Egyptian Arabians.[1] Cases reported in peer-reviewed veterinary literature are mostly of foals descended from a number of "Egyptian Arabian" or Egyptian-related bloodline groups, in Australia, a few breeders of Crabbet-related lines have also had foals affected by LFS.[citation needed] Lavender foal syndrome should be considered in any weak newborn Arabian or part-Arabian foal, particularly if it has some degree of "Egyptian" breeding, if the foal cannot stand, if other signs of neurological problems are present, and especially if it has an abnormally light coat color.[2]
History and research
The condition has been recognized since the mid- to late-1950s.[2]
Research into the genetics of LFS has been conducted at the University of California, Davis and Cornell University in the United States, the University of Queensland in Australia, and the University of Pretoria in South Africa. In November, 2009, Cornell University announced a DNA test has been developed to detect carriers of LFS. Simultaneously, the University of Pretoria also announced they had developed a DNA test.[3] Testing is now available at Cornell, Pretoria, and Queensland, Australia.
Clinical signs
The condition gets its name because most, though not all, affected foals are born with a unique coat color dilution that lightens the tips of the coat hairs, or even the entire hair shaft. The color has variously been described as a silver sheen, a dull lavender, a pale, dull pinkish-gray, or pale chestnut.[4] This dilution differs from gray foals because grays are born a dark color and lighten with age. It is also different from roan, because the hair is of a uniform shade, not of intermingled light and dark hairs.
Foals with LFS are unable to stand, and sometimes cannot even attain sternal recumbency (to roll from their side to lie upright, resting on the sternum, a precursor position to standing). They may lie with their necks arched back (opisthotonus) and legs stiff (extensor rigidity); generalised tonic-clonic seizures or seizure activity such as 'paddling' leg movements are also common.[5][6] Apparent blindness may also be a clinical sign of the disorder, but is not seen in every case.[7] Although they do have a sucking reflex, they cannot stand to nurse,[1] and affected foals are usually euthanized within a few days of birth. There is no cure.[5] In some cases, the mare may also have difficulty foaling, though foaling difficulties are not the cause of the condition.[8] In some cases, LFS-affected foals may be larger than usual.[9]
LFS is different from neonatal maladjustment syndrome, but may be confused with it if the distinctive coat color is overlooked.[10]
Inheritance
Lavender foal syndrome is thought to be created by an autosomal recessive gene[8][1] at MYO5A.[11] When a horse is heterozygous for the gene, it is a carrier, but healthy and has no clinical signs of the condition. If two carriers are bred together, however, classic Mendelian genetics indicate a 25% chance of any given mating producing a homozygous foal, hence affected by the disease. Carrier horses can be bred and produce non-affected foals, as long as they are bred with a non-carrier for the LFS gene.[6] It is hypothesized, though untested, that LFS may be linked to another genetic disease that affects Egyptian-related Arabians, juvenile epilepsy. This theory has been raised because of a small number of horses that have produced both LFS and epileptic foals.[8]
LFS is one of six genetic diseases known to affect horses of Arabian bloodlines.[4]
References
- ^ a b c Brooks, Samantha; Gabreski, Nicole; Miller, Donald; Brisbin, Abra; Brown, Helen; Streeter, Cassandra; Mezey, Jason; Cook, Deborah; Antczac, Douglas (2010-04-05). "Whole-Genome SNP Association in the Horse: Identification of a Deletion in Myosin Va Responsible for Lavender Foal Syndrome". PLOS Genetics. 6 (4): e1000909. doi:10.1371/journal.pgen.1000909. PMC 2855325. PMID 20419149.
- ^ a b "01 Lavender Foal Syndrome - VeterinaryPartner.com - a VIN company!". VeterinaryPartner.com. Retrieved 2011-11-06.
- ^ "The Onderstepoort Veterinary Genetics Laboratory > University of Pretoria". Web.up.ac.za. 2009-11-04. Archived from the original on 2011-10-01. Retrieved 2011-11-06.
- ^ a b Goodwin-Campiglio, Lisa, Beth Minnich and Brenda Wahler, et al. AHA Equine Stress, Research and Education Committee (August–September 2007). "Caution and Knowledge" (PDF). 'Modern Arabian Horse. Arabian Horse Association. pp. 100–105. Archived from the original (PDF) on 2009-03-03. Retrieved 2008-10-01.
{{cite web}}: CS1 maint: multiple names: authors list (link) - ^ a b "Lavender Foal Syndrome Fact Sheet". James A Baker Institute for Animal Health, Cornell University. Archived from the original on 2008-05-09.
- ^ a b Tarr, CJ; Thompson, PN; Guthrie, AJ; Harper, CK (2013-08-22). "The carrier prevalence of severe combined immunodeficiency, lavender foal syndrome and cerebellar abiotrophy in Arabian horses in South Africa" (PDF). NA. 46 (4): 512–514. doi:10.1111/evj.12177. hdl:2263/49153. PMID 24033554. Retrieved 2017-04-04.
- ^ Schott, HC; Peterson, AD (December 2005). "Cutaneous Markers of Disorders Affecting Young Horses". Clinical Techniques in Equine Practice. 4 (4): 314–323. doi:10.1053/j.ctep.2005.10.006.
- ^ a b c Fanelli, H.H. (2005). "Coat Color Dilution Lethal ("lavender foal syndrome"): A Tetany Condition of Arabian Foals" (PDF). Equine Veterinary Education. 17 (5): 260–263. doi:10.1111/j.2042-3292.2005.tb00386.x. Archived from the original (PDF) on 2009-09-17.
- ^ "Lavender Foal Syndrome (LFS)/Coat Color Dilution Lethal (CCDL)" (PDF). Arabian Horse Association. Retrieved 2017-04-05.
- ^ Bierman, A; Guthrie, AJ; Harper, CK (2010-04-13). "Lavender foal syndrome in Arabian horses is caused by a single-base deletion in the MYO5A gene". Animal Genetics. 41 (2): 199–201. doi:10.1111/j.1365-2052.2010.02086.x. Retrieved 2017-04-05.
- ^ Bellone RR (10 November 2010). "Pleiotropic effects of pigmentation genes in horses". Animal Genetics. 41 (s2): 100–110. doi:10.1111/j.1365-2052.2010.02116.x. PMID 21070283.
Additional information
- Goodwin-Camplglio, Lisa. "Genetic Disorders in Arabian Horses" Current Research Projects. 'World Arabian Horse Organization, September 2008.
- Page, P; Parker, R; Harper, C; Guthrie, A; Neser, J (2006). "Clinical, clinicopathologic, postmortem examination findings and familial history of 3 Arabians with lavender foal syndrome". J. Vet. Intern. Med. 20 (6): 1491–4. doi:10.1111/j.1939-1676.2006.tb00772.x. PMID 17186871.
This page was last edited on 14 April 2024, at 00:13