This article needs additional citations for verification. (May 2009) (Learn how and when to remove this template message)
The myotonic goat, otherwise known as the fainting goat, is a domestic goat that temporarily seizes when it feels panic. If startled by sudden movements or loud noises, they will attempt to escape from the disturbance, generally followed by a startle reaction. In more severe cases, this reaction results in strong tetanic contractions of the agonist and antagonist muscles, causing an uncontrolled stiffness that may cause the goat to remain “frozen” in the position that it was in previous to the attack, or cause it to fall to the ground on its side. During an attack, which may last from 5-20 seconds, the goat can often be picked up without any bending or movement occurring in its body. In the case of goats that are less severely affected with the condition, there may be some minor localized stiffness observed in the legs, however, they are still capable of running away. This behaviour is caused by a hereditary genetic disorder called myotonia congenita. The myotonic goat, similar to humans with congenital myotonia, exhibits no obvious muscle wasting, is rarely incapacitated by the condition, and lives a normal and healthy life span.
Slightly smaller than standard breeds of the goat, fainting goats are generally 43 to 64 cm (17 to 25 in) tall and can weigh anywhere from 27 to 79 kg (60 to 174 lb). Males, or billies, as they are often referred to, can be as heavy as 90 kilograms (200 lb). They have large, prominent eyes in high sockets. Their hair can be short or long, with certain individuals producing a great deal of cashmere during colder months. There appears to be no angora strain of the fainting goat. Common coat colors are black and white; however, most possible coat colors are found in this breed.
Terms previously used to refer to myotonic goats include “falling goats”, “stiff-legged goats”, “falling down goats”, “nervous goats”, "Tennessee goats", “epileptic goats”, and “fainting goats”. They are smaller and somewhat easier to care for and maintain than larger meat goat breeds, which makes the fainting goat desirable for smaller farms. They are also raised as pet or show animals as they can be friendly, intelligent, easy to keep, and amusing.
Fainting goats have a muscle condition called myotonia congenita. Myotonia congenita is a mutation in the genes that affects the skeletal muscles which causes a short term spasm of the muscles after you try to use them. This is a condition that occurs in many species, including humans. The goats do not truly "faint" in any sense of the word, as they never lose consciousness, just temporarily seize.
Classified as a meat goat as opposed to a dairy goat, it can be raised for chevon (goat meat). This breed is listed as threatened by The Livestock Conservancy, so the fainting goat is not used as often for chevon as other meat goat breeds; its rarity makes the live goat more valuable. The main reasons known for continuing to breed these goats has been for the observation of this behaviour as well as their ability to be kept in minimally fenced farms due to their lack of desire to jump over anything over 0.5m. Their size makes them easier to care for during chores such as foot trimming and administering medication. Smaller specimens of fainting goats are frequently kept as pets.
Besides the myotonia, another distinguishing feature of the fainting goat is its prominently set eyes. The eyes protrude from the eye sockets, as opposed to recessed eyes seen in other breeds. The profile is straight as opposed to the convex or "roman" profile.
Cause of "fainting" and additional informationEdit
Myotonia congenita is caused by an inherited disorder of a chloride channel in the muscles of the skeleton (skeletal muscle chloride channel 1, CLCN1). Congenital myotonia can be inherited as an autosomal dominant trait (with incomplete penetrance) or a recessive trait, resulting in the varying severity of the condition. In affected goats, the CLCN1 gene contains a missense mutation; the amino acid alanine is replaced with a proline residue. This small change causes the choride channel in the muscle fibres to have a reduced conductance of chloride ions. This missense mutation occurs in a sequence of seven amino acids that are included in a group of closely related channels including that of humans and rats. This causes a delay in the relaxation of the muscles after the goat has made an involuntary movement. A characterization of myotonia congenita is an increase in the tendency of the skeletal muscles to respond with repetitive action potentials and after discharges when stimulated. The increased muscle excitability has been shown to be largely accounted for by the lack of chloride permeability in these fibers. Myotonia congenita is also characterized by a significant increase in the fast isomyosins in each muscle type in the affected animals. The muscle fibers of the myotonic goat were found to be highly resistant, this was shown to be due to the blocking of chloride conductance. In a study, normal goat muscle fibers were able to be made myotonic by blocking the chloride conductance using myotonia inducing drugs, or by substituting in an anion that is unable to pass through a semi-permeable membrane.
Isolated intercostal muscle from goats with the condition were shown to be significantly different than that of normal goats in terms of temperature dependence of the resting membrane resistance and potassium efflux. These differences help to explain increases in the severity of myotonia in the whole animal that occurs upon decreasing the temperature of the involved muscles.
In a study testing the effect of hydration on myotonia in goats, it was found that upon depriving goats of water, the myotonic symptoms disappeared within 3 days and returned fully within 2-3 days of water being provided. If repeated attacks are precipitated in a goat with severe myotonia within 5-10 minutes of each other, the attacks become less severe, or completely stop altogether. After a period of rest of about 20-30 minutes, a severe attack can be induced again.
Observations were made regarding the development of myotonia congenita in kids. It was observed that there were no abnormalities in percussion responses or stiffness during the first 14 days of a newborn goat’s life. The first percussion responses were observed during days 18-143, and the stiffening and/or falling begins to occur during days 20-173.
Previous studies have reported that taurine, an amino sulphonic acid, when given to myotonic patients can reduce the symptoms of the condition. However, it has been shown that it does not antagonize the condition, nor prevent it.
The fainting was first described in scientific literature in 1904, and described as a "congenital myotonia" in 1939. The mutation in the goat gene that causes this muscle stiffness was discovered in 1996, several years after the equivalent gene had been discovered in humans and mice.
The experiments of Brown and Harvey in 1939 with the myotonic goat made a major contribution to the understanding of the physiological basis of this condition and influenced many other theories of myotonia and its causes.
Society and cultureEdit
- Bryant, S. H. (1979). Myotonia In The Goat. University of Cincinnati College of Medicine, 314-325
- Martin, A. F., Bryant, S. H., & Mandel, F. (1984). Isomyosin distribution in skeletal muscles of normal and myotonic goats. Muscle & Nerve, 7(2), 152-160. doi:10.1002/mus.880070212
- "Myotonic Goat Description". Retrieved 2005-01-01.
- myotonia congenita. (2015). In The Editors of the American Heritage Dictionaries (Ed.), The American Heritage Dictionary of Medicine (2nd ed.). Boston, MA: Houghton Mifflin. Retrieved from http://qe2a-proxy.mun.ca/login?url=https://search.credoreference.com/content/entry/hmmedicaldict/myotonia_congenita/0?institutionId=379
- ""Why Fainting Goats Do What They Do", D. Phillip Sponenberg". Retrieved 2004-03-01.
- "American Livestock Breeds Conservancy Watchlist". 2007-12-12. Retrieved 2006-07-11.
- Constable, PD; Hinchcliff, KW; Done, SH; Gruenberg, W. "Inherited diseases of muscle". Veterinary Medicine - A textbook of the diseases of cattle, horses, sheep, pigs and goats (11th ed.). Elsevier. pp. 1514–30. ISBN 9780702052460.
- Beck, C. L., Fahlke, C., & George, A. L. (1996). Molecular basis for decreased muscle chloride conductance in the myotonic goat. Proceedings of the National Academy of Sciences, 93(20), 11248-11252. doi:10.1073/pnas.93.20.11248
- Smith, BP, ed. (2015). "Chapter 42: Diseases of muscle. Myotonia". Large animal internal medicine (5th ed.). Mosby. p. 1281. ISBN 978-0-323-08839-8.
- Lorenz, Michael D.; Coates, Joan R.; Kent, Marc (2011). Handbook of veterinary neurology (5th ed.). St. Louis, Missouri: Elsevier/Saunders. p. 310. ISBN 978-1-4377-0651-2.
- Lipicky, R. J., & Bryant, S. H. (1972). Temperature effects on cable parameters and K efflux in normal and myotonic goats. American Journal of Physiology, 222(1), 213-215. doi:10.220.33.1
- Hegyeli, A., & Szent-Gyorgyi, A. (1961). Water and Myotonia in Goats. Science, 133(3457), 1011-1011. doi:10.1126/science.133.3457.1011
- C. (1990). The action of taurine on muscle fibers of normal and congenitally myotonic goats. Pharmacological Research, 22, 93-94. doi:10.1016/1043-6618(90)90824-w
- Kazek, K (2011). "The tale of the bulgy-eyed fainting goats". Forgotten tales of Tennessee. Charleston, SC: History Press. ISBN 9781625841483.
- Rüdel, R (2000). "Muscle chloride channelopathies: myotonia congenita". In Lehmann-Horn, Frank; Jurkat-Rott, Karin. Channelopathies. Burlington: Elsevier. pp. 44–46. ISBN 9780080528854.
- "Do Fainting Goats Really Exist?". Discovery. 11 April 2012. Retrieved 2017-08-20.