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normal range (mean = 83 (U/L), range 14–428 (U/L)). Serum alkaline phosphatase (ALP) and serum alanine transaminase (ALT) levels were also high (Table 2). Serum protein levels (mean 75.4 g/L) were slightly higher than the normal reference range and there was a low albumin/globulin ratio. Serum total bilirubin (mean 42.08 lmol/L) and conjugated bilirubin were higher than the normal ranges, but not high enough to show clinical signs of jaundice. However, a slight yellowish discolouration of body tissues was present in some cases. Serum levels of triglycerides (mean 1.51 mmol/L) were above than the normal range for horses. Serum cholesterol, blood urea nitrogen, creatinine, phosphorus, iron, iron binding capacity and transferrin saturation levels were in the normal ranges. On follow-up 2 years after discontinuation of the pearl millet
fodder, the mean serum GGT levels of 53 randomly selected clinically healthy horses on the farm averaged approximately 20 (U/L) (range, 5–51 (U/L)) (Table 3). However, serum GGT levels of the seven horses showing signs of chronic liver damage (CLD) were persistently high even after 2 years without pearl millet fodder (mean = 98 (U/L), range 50–169 (U/L)).
Treatment
The duration of the whole episode was long, and many animals were affected; therefore, all possible efforts (e.g. i.v. dextrose, antibiotics, NSAIDS, liver extracts, vitamin B complex, herbal liver tonics and low protein diets) to treat the horses were undertaken. There was no improvement in any animal, except several horses that were showing neurological signs exhibited a temporary improvement of those signs after i.v. dextrose therapy. After discontinuation of the pearl millet
a)
fodder, all the horses at the farm were treated with oral herbal liver tonics (Liv 52 of Himalaya Pvt. Ltd. at 50 mL daily for an adult horse) and jaggery at 250 g daily for an adult horse and were fed oats only as concentrate for 6 months.
Outcome
After discontinuation of pearl millet fodder, no new cases appeared at the farm, and most of the affected animals began to gain body weight. However, seven horses persistently showed signs of chronic liver damage and high serum GGT levels even after 2 years.
Post-mortem findings
Gross lesions A large amount of unclotted blood (Fig 2b) was seen during
post-mortem examination. Yellow-brown liver (Fig 2a) with firmness was common in all cases.
Microscopic lesions Liver cirrhosis was consistently observed. Hepatic architecture was completely lost and was instead characterised by massive mature connective tissue proliferation in the portal triads, extending to the liver parenchyma and leading to the formation of pseudo globules. Islands of hepatocytes could be seen in the proliferating fibrous tissue (Fig 3a and b).
Discussion
Claviceps invasion of the flowering heads of grasses produces ergot alkaloids. On ingestion, ergot produces a range of
b)
Fig 2: a) Liver: gross post-mortem finding. b) Gross post-mortem finding. a) b) A A
A
Fig 3: a) Liver section S&E stain. b) Liver section Masson’s trichrome stain. © 2017 EVJ Ltd
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