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Congenital stationary night blindness (CSNB) can be inherited in an X-linked, autosomal dominant, or autosomal recessive pattern, depending on the genes involved. Two forms of CSNB can also affect horses, one linked to the leopard complex of equine coat colors and the other found in certain horse breeds. Both are autosomal recessives.
Congenital stationary night blindness has been linked with the leopard complex since the 1970s. [14] The presence of CSNB in non-leopard breeds and horses suggested that the two conditions might be located on close, but separate genes.
Nyctalopia (/ ˌ n ɪ k t ə ˈ l oʊ p i ə /; from Ancient Greek νύκτ-(núkt-) ' night ' ἀλαός (alaós) ' blind, invisible ' and ὄψ (óps) ' eye '), [1] also called night blindness, is a condition making it difficult or impossible to see in relatively low light. It is a symptom of several eye diseases.
A white horse has mostly pink skin under its hair coat, and may have brown, blue, or hazel eyes. "True white" horses, especially those that carry one of the dominant white (W) genes, are rare. Most horses that are commonly referred to as "white" are actually "gray" horses whose hair coats are completely white. Gray horses may be born of any ...
The complete form of congenital stationary night blindness is due to the absence of nyctalopin. [16] This absence is due to a mutation involving an 85 base pair deletion. [ 17 ] In humans, more than 30 mutations are found in the NYX gene and most of them have an impact either on the tertiary structure of the LRR domains of nyctalopin or to ...
The painful and inevitable death that follows usually prompts veterinarians and owners to euthanize foals suspected of having lethal white syndrome. [6] [7] Death is caused by an underdeveloped part of the digestive system. The large intestine of the horse comprises the cecum, the colon, and the rectum. [8]
Cattle, sheep, goat, and other ruminants that are diagnosed with PEM or pre-PEM suffer opisthotonus, cortical blindness, disoriented movement, and eventually fatality, if left untreated. [1] Current data shows that the onset of PEM can range from birth to late adulthood.
Individuals with this condition usually start showing signs of nyctalopia (also known as night-blindness) during their early childhood, increase in sensitivity to blue light, progressive decrease of visual acuity in both eyes, cataract, peripheral vision loss, vitreous liquefaction and detachment, clumped pigment deposits of the fundus, either peripheral or central retinoschisis, cystic ...