Abomasal emptying defect (AED) primarily affects mature Suffolk sheep. It is characterised by progressive weight loss over days to months and distension and impaction of the abomasum. Damaged and necrotic neurons have been found within the celiacomesenteric ganglion suggesting that AED may be caused by altered autonomic innervation. The aetiology is unknown although given the breed predilection a genetic predisposition is presumed. However, pedigree analysis indicates that the condition is not inherited in a simple fashion (Pruden et al 2004).
In this case three of 60 Suffolk ewes were affected while none of the 3800 first cross ewes on the property showed symptoms.
This was the third ewe of a flock of 60 Suffolk ewes running on a large central tablelands grazing property to show weight loss, abdominal distension and death. The property runs over 3000 first cross ewes plus breeding cows on improved pastures.
A six year old Suffolk ewe was examined on the 14 November 2018 as she was the third that developed weight loss and abdominal distension. The previous two cases died. The ewe was in sternal recumbency and although bright, alert and responsive was emaciated, weak and unable to stand. The ewe had a markedly distended abdomen. On palpation of the abdomen, the digestive tract was firm and doughy on both sides. The ewe had a heart rate of 40 bpm, a respiration rate of 18 and a temperature measured at 35 degrees C.
The ewe was emaciated with little body fat. The abomasum was grossly distended and filled with green ingesta with small amount of clay ventrally. The pylorus was patent, with no abnormalities detected. There were scant intestinal contents. The liver, lungs and kidneys appeared normal.
The proximal duodenum, adjacent to the pyloric sphincter, contained an area of superficial erosion, overlain by small amounts of exudate comprised of fibrin and neutrophils. Scattered crypts of Lieberkuhn were dilated and lined by flattened epithelium. The mucosa contained mild to moderate infiltrates of lymphocytes and plasma cells. The cause of this mild duodenal erosion was not apparent. It was most probably a non-specific, secondary lesion. Neurons of the duodenal myenteric and submucosal plexus were normal. No lesions were seen within sections of pyloric abomasum, small intestine, ileocaecal valve, large intestine and mesenteric lymph node.
AED is predominantly a disease of Suffolk sheep (but has been reported in Hampshires, a Dorset and a Texel). Peake and Staples (2012) reported the condition causing 1% mortality in a mob of 3000 drought affected Dohne ewes in Australia. It is usually sporadic but outbreaks have occurred. Pedigree analysis indicates that the condition is not a strictly inherited trait.
As mentioned, Pruden et al (2004) found scattered necrotic and chromatolytic neurons in the celiacomesenteric ganglion (not examined in the ewe of this case report). They suggested that AED may be caused by altered autonomic innervation. They further speculated that an unknown excitotoxin may overstimulate parasympathetic neurons, causing immotility and subsequent impaction (and therefore AED) in susceptible sheep (primarily Suffolks). They added that increased sympathetic tone could also initiate the tachycardia that has been observed in cases of AED. Of interest, this ewe had bradycardia with a heart rate of 40 bpm.
Malfunction of the autonomic nervous system (dysautonomia) occurs both sporadically and familially in people, is seen in "grass sickness" of horses in Europe (characterized by gastrointestinal hypomotility and colic) and is reported in dogs, cats, hares and llamas. AED may be an acquired form of dysautonomia of sheep (Pruden et al 2004).