Lethal white overo syndrome

LWO prevents the foal’s intestine from moving its contents normally

The intestine relies on a network of nerve cells to help move its contents. In a foal with LWO, an essential part of that network fails to develop properly. Aganglionosis means that affected intestinal areas lack the nerve-cell groups required for normal function.

The variant affects EDNRB, a gene involved in the embryonic development of pigment cells and certain nerve cells. This shared developmental role explains the link between coat pattern and intestinal disease. The foal does not die because its coat is white; the fatal problem is the failure of intestinal function.

References [3] · [4] · [1]

Signs of LWO can appear in the first hours after birth

Affected foals are usually white or nearly white, with pink skin and often blue eyes. They may initially seem normal, but intestinal contents cannot move properly. Abdominal pain often becomes apparent within the first twelve hours and worsens quickly.

Colic may involve restlessness, rolling, sweating or a swollen abdomen. These observations cannot diagnose a foal remotely: a painful newborn needs prompt veterinary assessment whatever its coat color. A photograph cannot show whether its intestine is functioning normally.

References [2]

A white coat does not prove that a foal has LWO

A horse with one copy of the frame overo variant in EDNRB can show the coat pattern of that name. Colored areas often frame white patches, but expression varies widely. A carrier may have very little white or appear solid-colored. A visual coat name therefore cannot replace a laboratory result.

Other mechanisms can produce very pale or extensively white foals without LWO. A cremello, for example, does not have this syndrome simply because of its color. Combined patterns can make appearance harder to interpret. The relevant variant and the foal’s clinical findings need to be assessed together.

References [1] · [2]

The frame overo variant has been documented in Paint Horses and other breeds

LWO is mainly reported in Paint Horses and related populations. The variant has also been identified in Quarter Horses, Appaloosas, Thoroughbreds and American Miniature Horses. This does not mean every horse in those populations is a carrier, or that every other ancestry is excluded.

A pedigree, registry entry or lack of striking markings does not establish the two copies a horse carries. For a breeding decision, the informative evidence is each parent’s own result rather than population membership alone.

References [2] · [1] · [3]

One copy of the frame overo variant can affect coat pattern; two copies cause LWO

The intestinal syndrome has autosomal recessive inheritance: two copies are required, inherited one from each parent. One copy does not cause that syndrome but can change the coat. Some catalogs therefore describe incomplete dominance when considering the combined coat and health effects; they are describing a different effect.

A one-copy horse is not affected by the intestinal syndrome, but that result is not a guarantee of overall health. Deafness may also occur in some carriers. Presenting the finding as a complete health clearance would therefore be misleading.

References [1] · [2] · [4]

Diagnosing LWO through examination of the foal and frame overo DNA testing

For a white foal with colic, the veterinarian investigates the digestive problem and uses DNA testing within that assessment. Coat color alone cannot identify LWO: a pale foal may be free of this syndrome and have another problem.

Testing targets the frame overo variant in EDNRB. Reports often use N/N, N/O and O/O. The symbol N means the tested variant was not detected on that copy, not that the EDNRB gene is absent. The result helps distinguish possible diagnoses but does not test every white-coat mechanism or intestinal disease.

References [1] · [2]

What care is possible for a foal with LWO?

There is no cure for the LWO intestinal syndrome. Affected foals die within their first days or are euthanized to prevent worsening suffering. Symptomatic treatment for colic cannot restore the nerve network that failed to develop.

That prognosis applies to two-copy foals with the syndrome. It should not be applied to every frame overo horse or white foal. Veterinary assessment distinguishes the different situations and supports welfare decisions without confusing appearance with diagnosis.

References [2] · [1]

Testing the mare and stallion to prevent a foal with LWO

If the mare and stallion each have one copy of the frame overo variant in EDNRB, every conception has a 25% chance of a foal with two copies and LWO, a 50% chance of a foal carrying one copy and a 25% chance of a foal without that variant. These are probabilities for each pregnancy, not a guaranteed distribution across four births.

A carrier paired with a confirmed non-carrier cannot produce a foal with two copies of this variant. It still has a 50% chance of transmitting its copy. Testing both parents, including one that looks solid-colored, provides better information than selecting a pairing from the amount of white desired.

References [1] · [2] · [3]

Questions about the condition: Lethal white overo syndrome

Scientific sources about the condition: Lethal white overo syndrome

This article brings together the research and the university and laboratory resources listed below. Numbers after each section link to the references used. Sources consulted in November 2026.

1. 1.
   Lethal White Overo (LWO): DNA testing and interpretation

   UC Davis — Veterinary Genetics Laboratory · Test documentation

2. 2.
   Lethal White Overo Syndrome (LWO): clinical signs, diagnosis and prognosis

   UC Davis — Center for Equine Health · University resource

3. 3.
   Santschi et al. (1998) — Endothelin receptor B polymorphism associated with lethal white foal syndrome in horses

   Mammalian Genome — University of Minnesota research · Research

4. 4.
   Metallinos, Bowling & Rine (1998) — A missense mutation in the endothelin-B receptor gene is associated with Lethal White Foal Syndrome

   Mammalian Genome — University of California, Berkeley research · Research