Ileocolonic aganglionosis in an overo foal (abstract)

Authors: Julian AF
Publication: New Zealand Veterinary Journal, Volume 42, Issue 2, pp 75-76, Apr 1994
Publisher: Taylor and Francis

Animal type: Horse, Livestock
Subject Terms: Abdomen, Alimentary system/gastroenterology, Congenital disease, Integument/skin/wool/hair/fur/feather, Pathology
Article class: Abstract

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Abstract: The American paint horse or pinto (Spanish for painted) has two different types within the breed: the overo, which has white patches on a dark coat and the tobiano, which has black patches on a white coat. Within the overo type the amount of white may be quite small or a horse may be almost entirely white, but the basic pattern is that the ventral abdomen is spotted white whilst dorsal aspects are dark. The overo is considered to be recessive.
The mating of two overos can produce white, overo-spotted or solid-pigmented foals. The white overo foals may have small pigmented areas on the head or rump regions. White overo foals will appear normal at birth but no meconium will be passed. They develop colic within the first day and die between 23 and 132 hours.
A white overo foal about 60 hours old was presented for post-mortem examination. The foal was seen to feed normally on the first day but on the second day it developed colic and the mare was dripping milk that evening. On the third day, the foal was more distressed and frequently lying down. It was humanely killed that morning.
The foal was white, apart from small patches of brown hair on the rump and in the forelock. The irides were blue.
The proximal small intestine was grossly normal while the distal portion was mildly dilated and fluid filled. The ileum was about 2 cm in diameter. The caecum and large colon were distended with meconium and gas. The right ventral colon was about 5 cm in diameter. In this part of the colon, the meconium was about 1 cm thick and adherent to the wall of the colon with a large gas filled space in the centre of the lumen. The left dorsal colon and the right dorsal colon were each about 4-5 cm in diameter and contained meconium.
The small colon was about 1 cm in diameter and serpiginous. The rectum was also about 1 cm in diameter. Both the small colon and the rectum contained tenacious mucus only in the lumen; no meconium was present.
Histological examination of sections of the intestinal tract revealed normal myenteric ganglia in the duodenum, decreasing numbers in the jejunum and an absence of ganglia in the ileum, caecum and entire colon. Hypertrophied nerve bundles were seen in some aganglionic sections. This confirmed the diagnosis of ileocolonic aganglionosis.
Congenital aganglionosis and the resulting megacolon is seen in man (Hirschsprung’s disease) and in particular colour-coated strains of mice and rats.
The reason for the association between congenital aganglionosis and skin colour is because the ganglionic cells in the myenteric plexus and the melanocytes in the skin originate from the embryonic neural crest. A failure in development or migration of these cells from the neural crest will affect both coat colour and ganglion cells.
Megacolon in association with hypoganglionosis of the myenteric plexus has been reported in Clydesdale foals in the United States and Australia. The age of onset of signs has been between 4 and 9 months so this may not be a congenital problem.

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