Abomasal emptying defect (AED) is an idiopathic syndrome of abomasal distension and impaction described in Suffolk and Hampshire sheep primarily. No histological lesion has been consistently associated with this condition (Pruden et al 2004).
While the cause is unknown, it is suggested that it may be an acquired dysautonomia (degeneration and necrosis of neurons within autonomic ganglia), possibly toxic, requiring a genetic predisposition for expression (McGavin 2007).
In this case there were approximately 30 deaths, from a flock of 3000 Dohnes, from what appears to be an AED syndrome. The deaths occurred at the end of a drought, shortly after the sheep returned home from a few months out on the stock route, the deaths occurred over a period of 6-8 weeks.
AED is diagnosed in the absence of alternate findings and based on a history, of weak starving sheep, collapsing and dying with no response to any treatment, with clinical signs of starvation, a palpably large abomasums, in addition, some cases with a tachycardia. Autopsy findings, consistent with the diagnosis, are cachexia, a distended, impacted abomasum and the alimentary tract posterior to the abomasum empty.
On the 22nd July 2010, I was asked to investigate dying ewes on a property north of Hay. The owner had lost several ewes over the preceding few weeks, from a flock of approximately 3,000 Dohne ewes. I visited the property several times over the next 3 weeks, during which time, in excess of 20 ewes died.
The flock was on the Hay Travelling Stock Route until mid April 2010, came home to lamb, in Body Condition Score (BCS) 3-4, and were drenched back onto the property. They started lambing a week after they got home.
The property was still in drought (just starting to break), so the sheep came home to hard dry conditions with mainly shrubs and poverty bush (several types but predominantly Bassia intricata (Cunningham et al 1981), which is very spiny/prickly.
The owner found affected ewes in sternal recumbency, looking slightly bloated, with their head tucked back into their flank and dying after a few days. Deaths were predominantly confined to two mobs of 500 and 600 ewes.
The owner reported that he had a similar problem last year, (also a drought year), and was concerned about the possibility of a plant toxin.
Lamb's Tongue, also known as Purple Goosefoot, Scleroblitum atriplicinum (Cunningham et al 1981) reportedly caused deaths in the Hay district during the winter of 2009 (Sally Ware, I & I NSW, Hay and Greg Curran BVSc, I & I NSW, Broken Hill - personal communication).
On the initial visit I examined a six tooth (3-year-old) ewe which had been in sternal recumbency for at least 48 hours. The ewe was unable to stand had her head turned back into her flank and appeared dead. Her body condition score (BCS) was <1. Rectal temperature was 38.5 degrees Celsius and mucous membranes were pink, with normal capillary refill time. No abnormalities were detected on thoracic auscultation, though heart rate may have been slightly elevated.
Intravenous calcium borogluconate (Calcigol) was given with a slight response only. The ewe's demeanour did improve and she ate some hand fed salt bush but did not stand and died 2 days later.
A second ewe was also examined with similar findings however the second ewe had pale mucous membranes. Other ewes in the mob were in better condition with body condition scores of 2-3. All lambs in the mob appeared normal.
Blood and faecal samples were collected for laboratory analysis.
On a later visit, to examine another four ewes showing the same clinical signs, an autopsy was performed. These four ewes also had evidence of some black diarrhoea under their tails.
DPI Agronomist from Hay, Andrew Schipp, could not detect any potentially toxic plants. Plant identification was made difficult by the fact that many plants were just shooting after recent rainfall. There was no evidence of lambs tongue, Scleroblitum atriplicinum.
The ewe was very thin with no renal fat. The abomasum was enlarged, at least 60cm x 20cm x 20cm, and impacted with dry harsh fibrous material & sand - like cement (see figure 1). The abomasal contents were malodorous. The rumen contained fresh green feed, however the intestines were empty, except for a small amount of black fibrous prickly material in the descending colon. The liver appeared normal grossly. The gall bladder was distended and the bile duct was patent. There was a large amount of gelatinous oedema around the pancreas. Other organs appeared normal grossly.
Samples of liver, lung kidney, abomasal wall, abomasal contents, pancreas and mesenteric lymph nodes were collected and submitted to the State Veterinary Diagnostic Laboratory.
Faecal egg counts were low with 9 samples zero eggs per gram of faeces and one sample with 80 eggs per gram, suggesting that internal parasites were not a problem.
Biochemical changes in all animals were similar. There were marked elevations in glutamate dehydrogenase (GLDH) and gamma glutamyl transferase (GGT) consistent with bile duct and hepatocellular damage. Elevations in aspartate aminotransferase (AST) and creatinine kinase were also reported, likely to be secondary to recumbency. Urea was elevated in both animals and may be subsequent to dehydration or renal disease.
Histopathological changes included subacute abomasal ulceration, moderate pancreatitis, mild cholangitis and moderate suppurative lymphadenitis.
The pathologist concluded that the primary lesion is probably the abomasal impaction and ulceration due to the fibrous feed material. Inflammation in the pancreas and liver were probably secondary. There was no histological evidence of a toxic hepatopathy.
Abomasal Emptying Defect is rarely reported and is presumed to be a rare condition of sheep. It was first reported in Suffolk sheep and initially thought to be a genetic problem (Kline et al 1983). It has now been reported in other breeds and in goats (Smith et al 1992 and Edwards 2008), either individual cases or sporadic outbreaks, as occurred in this case. (Pruden et al 2004)
The defining feature of AED is a markedly distended and impacted abomasum. Despite this characteristic gross lesion, no consistent histological lesions have been described. The most frequently described clinical signs of AED are anorexia, progressive weight loss, and distension of the right ventral abdomen. Elevated ruminal chloride concentrations have been reported, presumably secondary to abomasal reflux. Tachycardia and atrial fibrillation have also been observed in cases of AED. The clinical duration of the disease ranges from days to months, and the prognosis is grave. (Pruden et al 2004)
Pruden et al (2004) report they found scattered chromatolytic and necrotic neurons within the celiacomesenteric ganglion, suggesting that AED may be caused by altered autonomic innervation. No evidence of inflammation was observed in affected celiacomesenteric ganglia, which is not typical of diseases that are caused by infectious agents. Therefore, AED may be triggered in susceptible sheep (primarily Suffolks) by an unknown toxin.
From the clinical symptoms, the history and the pathology it appears that this is most likely a case of abomasal emptying defect with impactions from harsh fibrous feed with low energy and protein levels. In this case it may be related to ingestion of poverty bush, although as the disease can develop over several months, it could well be a multifactorial. Both the drought, with increased soil ingestion and exposure of hungry sheep to a range of toxic plants and other materials of a haphazard nature could well have a role in this condition.
The syndrome continued over a 6-8 week period with losses totalling approximately 30 ewes. The syndrome has not returned this year, which has had nearly twice the average rainfall, and has been one of the best seasons in this area for many a year.