53:. JEB is the result of a genetic mutation that inhibits protein production that is essential for skin adhesion. Therefore, tissues, such as skin and mouth epithelia, are affected. Blisters form over the entire body causing pain and discomfort, and open sores leave newborn foals highly susceptible to secondary infection. The condition can be categorized into two types of mutations: JEB1 and JEB2. JEB1 is found in Belgian Draft horses, as well as other related Draft breeds. In contrast, JEB2 is found in American Saddlebred horses.
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Currently, there are no treatments available for JEB. However, the disorder can be prevented through good breeding management. Horses that are carriers of JEB should not be incorporated into breeding programs. Although, if breeders are insistent on breeding a carrier, precautions need to be taken
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Mutations in the genes LAMB3, LAMC2, and COL17A1, are the cause of JEB. These genes are associated with the protein responsible for skin attachment to the underlying layers, laminin 332. When the genes undergo mutations, the protein is altered, making it dysfunctional. As a result, the skin is
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Biopsies of the skin may be performed to identify the cleavage that takes place at the dermal-epidermal junction. Another test that can aid in a diagnosis of JEB is the positive
Nikolsky’s sign. By applying pressure to the skin, transverse movements can indicate slipping between the dermal and
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JEB is an autosomal recessive trait; both parents must carry the recessive gene in order to have an affected offspring. If N represents a normal individual and J represents an affected individual, the following crosses indicate the rate of occurrence among related horses.
186:(PCR). This method allows mane and tail samples to be genetically tested for the mutated genes that cause the condition. Hair samples must be pulled, not cut, with roots attached. The test can detect both JEB1 and JEB2. Testing costs around $ 35.00 US per sample.
100:(hair loss), abnormalities of fingernails and toenails, and joint deformities. Children born with JEB may not live past the first year of age if the condition is severe enough. Other children that have a less severe case of JEB may live a normal lifespan.
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and tongue after the first attempt at nursing. Within the next few days, the foal develops lesions all over the body, especially over pressure points. The proteins affected by the gene mutations are also present in the hooves, causing hooves to slough.
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JEB also affects the human population. Symptoms are closely related to those that are seen in horses. Blisters occur over a large portion of the body and are very susceptible to agitation. There are other symptoms associated, such as
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One of the biggest risks factors faced by the affected foals is susceptibility to secondary infection. Within three to eight days after birth, the foal may die from infection or is euthanized for welfare reasons.
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Foals which are homozygous recessive (J/J) do not make it to reproductive age, so cannot be a parent. Carriers (N/J) do not display symptoms and have normal skin.
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Another protein, called type XVII collagen, is affected by a mutation in COL17A1. Due to this mutation, the defective protein is not able to produce
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for the disorder is highly recommended among breeding programs for the Draft horse and
Saddlebred breeds to determine their carrier status.
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Foals appear normal immediately after birth. JEB affects tissues including
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Lloyd, D.H.; Littlewood, J.D.; Craig, J.M.; Thomsett, L.R. (2003).
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epidermal layers. An easier and more definitive test is through
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to ensure that the other mate is not a carrier as well.
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The
Belgian Draft Horse is one breed in which JEB occurs
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very fragile and may be damaged by even minor trauma.
376:Color Atlas of Diseases and Disorders of the Foal
374:McAuliffe, Siobhan B.; Slovis, Nathan M. (2008).
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145:, so one of the first signs is blistering of the
41:) is an inherited disorder that is also known as
338:Floyd, Andrea E.; Mansmann, Richard A. (2007).
325:"Junctional Epidermolysis Bullosa (JEB) Test"
113:(N/J) x (N/J) = 50% N/J, 25% N/N, and 25% J/J
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356:Higgins, Andrew J.; Snyder, Jack R. (2006).
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91:Junctional epidermolysis bullosa (medicine)
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235:"Junctional Epidermolysis Bullosa (JEB)"
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310:. U.S. National Library of Medicine.
306:Berman, Kevin (November 20, 2012).
255:Illustrated Guide to Equine Disease
118:(N/N) x (N/J) = 50% N/N and 50% N/J
308:"Junctional Epidermolysis Bullosa"
273:Current Therapy in Equine Medicine
153:Other symptoms that occur in JEB:
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285:"Testing for Genetic Diseases."
35:Junctional epidermolysis bullosa
21:Junctional epidermolysis bullosa
342:. St. Louis: Elsevier Science.
275:. St. Louis: Elsevier Science.
253:Abuterbush, Sameeh M. (2009).
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391:Practical Equine Dermatology
271:Robinson, N. Edward (2003).
61:JEB has been documented in
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393:. Ames: Blackwell Science.
257:. Ames: Blackwell Science.
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16:Genetic disorder of horses
184:polymerase chain reaction
172:Incisors present at birth
199:Treatment and prevention
378:. St. Louis: Elseiver.
360:. St. Louis: Elsevier.
50:hairless foal syndrome
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177:Diagnosis and testing
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79:American Saddlebreds
67:American Cream Draft
19:For other uses, see
169:Suppressed appetite
237:. Animal Genetics.
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358:The Equine Manual
327:. UC Davis. 2012.
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289:. pp 42–43.
166:Oral ulcers
212:References
163:Depression
287:Equus 353
190:Prognosis
405:Category
137:Symptoms
131:collagen
104:Genetics
98:alopecia
147:gingiva
75:Comtois
85:Humans
77:, and
47:or
39:JEB
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366:^
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