Over the several years I've been breeding dalmatians, I've always been asked what is LWS (Lethal White Syndrome).

So to help answer this I want and compiled this list of explanations, Now every animal can get LWS, Cats, Dogs, Horses, even people weirdly enough ( Called *** Waardenburg Syndrome).. but it all boils down to one thing.. if an animal is born with LWS it is 9 out of 10 times deadly and the animal either dies or is put down. Rats can have several babies with LWS in a dalmatian litter but I most stress that the LWS is not hereditary and can not be passed on to any offspring. 

*** Of course people are  not put down, only animals are, but humans due tend to suffer a bit more then our animal counter parts.. 

 Please follow the following link
Lethal White Syndrome

Waardenburg syndrome (WS) is named after the Dutch ophthalmologist who, in 1947, first described a patient with hearing loss, dystopia canthorum (ie, lateral displacement of the inner canthi of the eyes), and retinal pigmentary differences. In 1951, after identifying other patients with similar symptoms, Waardenburg defined the syndrome now classified as Waardenburg syndrome type 1 (WS1).¹ Findings in WS1 include hearing loss, dystopia canthorum, and pigmentary abnormalities of the hair, skin, and eyes.

In 1971, Arias defined the phenotype of Waardenburg syndrome type 2 (WS2), which includes all of the WS1 features except dystopia canthorum.² Both WS1 and WS2 are transmitted as autosomal dominant conditions with interfamilial and intrafamilial variability.

Two far rarer variant forms of WS have also been identified. Waardenburg syndrome type 3 (WS3), or Klein-Waardenburg syndrome, includes features of WS in association with severe contractures. Waardenburg syndrome type 4 (WS4), or Waardenburg-Shah syndrome, has features of WS in association with Hirschsprung disease. WS4 is a heterogeneous disorder with either autosomal recessive or autosomal dominant inheritance.

A frequently asked question is why megacolon in rats appears to be associated with patches of white pigment. I did a bit of reading on the subject and have found out why. It has to do with a common develomental pathway going awry.

In the embryo, neural cells originate in a strip along the back (called the neural crest) and migrate from there to the rest of the body during development (fig. 1). Pigment cells are actually a subset of these neural cells. Lots of neural cells do this migration, such as the ones that ennervate the colon, and ones that go into the inner ear.

If this cell migration is delayed, then these cells may not reach their destination. So, you can end up with depigmented (white) areas on the body, particularly the areas far away from the back, such as the face, irises, feet, belly, tail tip and so forth (fig. 2) though the depigmentation can be widespread too.

A delay in migration of the neural cells means that the end of the colon may not get ennervated, which means the animal cannot control the colon properly, resulting in megacolon.

Neural crest cells also migrate into the inner ear, where they are important for hearing. This is why a mutation in cell migration can sometimes result in white splotches and deafness (e.g. in cats and dogs).

Cell migration is a complex process with many steps, and there are many different ways it can go wrong. For example, migrating cells follow molecular "signposts" which tell them where to go in the body. A mutation in these signposts, or in the migrating cells' receptors which are supposed to "read" these signposts, can affect migration.

Rats aren't the only animals with mutations in cell migration resulting in white pigment and colon and hearing problems. Many other animals have these mutations too, and each mutation results in a different constellation of related symptoms... from blazed rats or odd-eyed rats with megacolon, to white foals with megacolon (called lethal white foal syndrome), to humans with a white forelock, odd-eyes, deafness, and megacolon (called Waardenburg Type 4 or Waardenburg-Shah Syndrome), to white-faced deaf ferrets (also called Waardenburg), to dogs and cats with a white coat and deafness (like many dalmatians). All are mutations in the process of cell migration from the neural crest during embryogenesis.

The mutations found in these different species may not be the identical mutation, and the same species may have different kinds of mutations that affect this developmental pathway, but they all affect the same, common, underlying process.

Note, however, that megacolon may be caused by other factors (e.g. Lipman et al. 1998). Not all blazed rats have megacolon, and megacolon can be found in non-blazed rats as well.

If you enjoyed this piece and would like to know more, here's more depth on mutations in pigment cell migration.

This usually acures in dogs that are from Merled line like the australian shepards, Dalmatains, white Shepards and etc.

 When careless breeders put merles together to get stronger merling the resulting puppies can be born deaf, blind and with digestianal problems.. 9-10 times these dogs are put down shortly after birth or the breeder will keep them around to rebred again for a profit for the rear color.

Dalmatians seem to be more prone to getting LWS being that the dalmatain strand in its self seems to be a by product of over whiting dogs. Most dalmatains that are deemed unshowable, breedable because of huge spotting thier faces walk away clean of any defect.

 White Shepards if bred carelessly will produce a whole litter of blind and deaf puppies, with just a small precent of puppies healhty enough to live a half way decent life without any defects. 

 LWS in dogs in more seen when a certain bred of dog is or has become more popular through tv shows such as 101 Dalmatains.

When dogs are born with LWS they don't die immediately after birth but sometimes are made to linger on for days even weeks to see the outcome of the breeding and to find our more about this defect. A handful of good breeders will have dogs that suffer from LWS put down , the other handful such as in puppy mills and careless breeders will let the dogs suffer their entire lifes just to reproduce with no concern about the outcome of future litters and etc. 

The lethal white syndrome, intestinal aganglionosis, is an autosomal recessive defect seen in foals from two overo paint parents. The color pattern for overo paints can be confusing, but generally these horses have white coloring under their belly and on the sides of the neck and abdomen. White does not generally cross the back but there are exceptions.

Lethal white foals are characterized by an unpigmented (white) hair coat and light blue eyes (irises), and show intestinal colic in the first few days of life. These foals experience colic because they lack the proper nervous supply (myenteric ganglia) in the terminal portions of the ileum (end of the small intestine), cecum and entire colon (large intestine).

This is due to a defect in the genes that regulate the development of a certain line of embryonic cells that later mature into two types of cells: cells that produce skin pigment (melanocytes) and cells that become the nerves to the end of the small intestine, the cecum and the large intestine. The common genetic link between pigmentation and nerve supply to the intestine explain the lethal white syndrome. Carriers of this gene have also been found in some tobiano and solid colored horses especially if they have overo color patterns in their ancestors.

Affected foals are born with a mostly white coat color, light blue irises and pigmented retinas. Occasionally, small pigmented areas may be present. Foals appear normal at birth, standing and nursing normally. Though some fecal staining may be present at the anus, affected foals do not pass meconium. Colic (abdominal pain) is the primary problem that develops within the first 12 hours of life and becomes progressively worse over the first 24 hours of life. The foal's abdomen is distended with gas because of its inability to pass feces. It is seen with equal frequency in both males and females.

This is a genetic disease. The risk factor for the disease is the breeding of two overo paint horses to each other or the breeding of overo paint to a non-overo that has overo breeding in its pedigree. If two carriers (heterozygotes) for the mutant lethal white gene are bred, there is 25 percent chance of getting a lethal white, 50 percent chance of getting an overo colored offspring and 25 percent chance of having a solid colored off spring.

The white hair coat and the parentage are fairly strong indicators that you may be dealing with a lethal white foal. Signs of colic in the first day of life accompanied by a distended abdomen also point toward the diagnosis of a lethal white. Small intestinal distention can be seen on radiographs of the abdomen. Other problems that may present with similar colic signs include meconium retention and atresia ani, which is the failure of an anus to form. Your veterinarian will try to eliminate these other causes during the physical examination.

Meconium is the first feces or manure that a foal passes after birth. It is often hard for foals to pass and results in abdominal distention and colic. Meconium impactions can usually be diagnosed and treated with a gentle, soapy water enema. Radiographs of the abdomen may show meconium in the rectum. Intestinal atresia can be diagnosed easily by lifting the foal's tail and looking for an anal opening. It is usually discovered when trying to take the foals temperature. It is unlikely that foals with these other problems would be unpigmented.

Recently genetic testing has been developed to identify the mutation site of the DNA sequence responsible for the lethal white overo foal. The test can be performed on either whole blood or hair samples with roots. Plucked mane and tail hairs are the easiest to obtain. This test can be used to detect carriers, non-carriers and affected animals. Labs currently performing the test include the veterinary schools at University of California, Davis and University of Minnesota.

The prognosis is grave; there is no treatment for this genetic disease. Euthanasia is recommended and if not euthanized, they will die naturally within 2 to 3 days. Necropsy (examination after death) of affected foals may show meconium in the colons, gas in the small intestine and contraction of the small colon.