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Ill-thrift and wastage in ewes caused by urolithiasis and lupinosis

Katelyn Braine, District Veterinarian, Riverina Local Land Services, Gundagai

Posted Flock & Herd August 2020


Ill-thrift is the loss of body condition in the presence of ample feed. It can cause considerable production losses in sheep due to losses in weight gain and death. Differentials for ill-thrift in sheep include, but are not limited to, internal parasitism, Ovine Johne’s Disease, nutritional deficiencies and some infectious diseases. This case report describes the investigation of ill-thrift and wastage in a flock of adult composite ewes.

History and Clinical Findings

In August 2019, a sheep producer in the Riverina contacted the local District Veterinarian (DV) about ill-thrift and wastage in a flock of lactating ewes. The flock consisted of 400, mixed-aged, composite ewes. The ewes had been lambing from around 15 June 2019 to 20 July 2019. The ewes had been drenched for intestinal parasites and vaccinated against clostridial diseases pre-lambing. Since early May, the ewes had been grazing a wheat crop and they were fed supplementary barley grain up until the point of lambing. A calcium, magnesium and salt mineral lick was provided ad libitum for a couple of weeks prior to lambing and throughout lactation.

The producer reported that there were around six affected ewes. Apart from ill-thrift, loss of condition and lethargy, there were no other clinical signs noted by the producer. The average body condition score (BCS) of the flock was 2.5-3.0 out of 5. The clinically affected ewes had a BCS of 1.5 out of 5. At the time of the disease investigation the lambs had been marked and were in good condition.

Post-mortem Findings

Post-mortems were performed on two affected ewes. The first ewe that was post-mortemed was three years of age and had a set of twins at foot. A second post-mortem was completed, nine days following the first, on a ewe that was five years of age with a single lamb at foot. The second post-mortem was completed to verify if the laboratory findings from the first ewe were consistent, or an incidental finding. Both ewes were low in BCS and presented in sternal or lateral recumbency. The gross post-mortem findings were consistent between the two ewes, but relatively non-specific. Grossly the kidneys appeared mildly pale and there was mild thickening of the distal small intestine. The remainder of the post-mortem in both ewes was unremarkable.

Laboratory Findings

Samples were collected and sent to Laboratory Services at Elizabeth Macarthur Agricultural Institute (EMAI). Due to the age of the affected ewes and the loss of body condition, blood, ileocaecal and intestinal samples were submitted to test for the presence of Ovine Johne's Disease (OJD). Biochemistry and haematology profiles, as well as general histology, were also completed on samples from both the ewes.

In the first ewe, Johne's Disease serology (AGID) was negative. Histopathology of the small intestine and large intestine showed a mild, diffuse enteritis and colitis but no histological evidence of OJD. The histopathology of the kidney showed acute tubular injury, which was diffuse, moderate, sub-acute to chronic with intra-tubular protein and mineral deposits (urolithiasis). The mineral present was suspected to be struvite crystals.

The serum biochemistry profile for this ewe is shown in Table 1.

Ewe 1 Reference values
Urea 83.8 mmol/L 2.9-7.1 mmol/L
Creatinine 469 µmol/L 0-265 mmol/L
Phosphorus 6.58 mmol/L 1.13-2.58 mmol/L
Magnesium 1.75 mmol/L 0.74-1.44 mmol/L
Calcium 1.56 mmol/L 2.12-2.87 mmol/L
GLDH 33 U/L 0-30 U/L
GGT 381 U/L 0-55 U/L
AST 259 U/L 0-130 U/L
CK 1935 U/L 0-300 U/L
Table 1. Biochemistry results on ewe 1

The serum biochemistry profile reveals marked elevations in urea, as well as hyperphosphataemia, hypermagnesaemia, and hypocalcaemia, which is consistent with the histopathological findings from the kidney. The serum biochemistry also indicated some degree of hepatocellular injury due to a mild elevation in GLDH, and cholestasis due to a moderate increase in GGT. Other serum biochemistry findings included elevations in AST and CK. Histopathology of the liver was performed later, following the results from the second ewe, and showed changes that indicated a mild hepatocellular insult.

In the second ewe, Johne's Disease serology (AGID) was negative. On histopathology of the intestine, there was mild chronic enteritis but no histological evidence of OJD was seen at the ileocaecal junction. The most significant histopathological changes noted in this ewe were not seen in the samples of the kidney, as with the first ewe, but rather in the liver. Interestingly, there were both acute and chronic changes noted in the liver. The chronic changes to the liver included moderate-marked, diffuse biliary hyperplasia with a mild portal and centrilobular fibrosis. There was also mild-moderate, centrilobular vacuolar hepatopathy with multifocal single cell hepatocyte necrosis. The acute changes included a suppurative hepatitis from which Escherichia coli (E. coli) was cultured. The growth of E. coli in association with suppurative hepatitis was considered likely to be significant and indicative of a secondary septicemic process. The chronic changes, on the other hand, were considered likely to be from exposure to a hepatotoxin.

The serum biochemistry profile for this ewe is shown in Table 2.

Ewe 2 Reference values
GGT 196 U/L 0-55 U/L
GLDH 158 U/L 0-30 U/L
Urea 20.7 mmol/L 2.9-7.1 mmol/L
Phosphorus 3.0 mmol/L 1.13-2.58 mmol/L
AST 914 U/L 0-130 U/L
CK 1337 U/L 0-300 U/L
Calcium 1.84 mmol/L 2.12-2.87 mmol/L
Table 2. Biochemistry results on ewe 2

The serum biochemistry profile revealed elevations in GGT and GLDH, which is consistent with hepatocellular damage. Other biochemistry findings included elevations in urea, phosphorus, AST and CK, and a mild hypocalcaemia.


Johne’s disease (Paratuberculosis) is a notifiable disease in New South Wales. It is a mycobacterial infection that causes granulomatous enteritis, preventing the absorption of nutrients, therefore resulting in progressive wastage of clinically affected stock.1 This case occurred in an area where the herd-level prevalence of OJD is relatively high. Given that OJD is relatively common in the district, as well as no previous vaccination history against OJD in this flock, the presence of ill-thrift/wastage seen in ewes three years of age or older, and producer concern, it was important to exclude OJD as a cause of the clinical signs. Serology and histology in two of the affected ewes failed to produce any evidence of OJD, therefore excluding it as a cause of the ill-thrift observed in this case.

The most significant findings from the lab results were the presence of uroliths in the kidney sample from the first ewe, and histological changes to the liver in the second ewe. Liver changes were also seen in the first ewe but were much milder compared to those in the second ewe and were deemed to be not as noteworthy as the findings of the urolithiasis. The changes seen on histology in each ewe were consistent with the changes seen in their respective biochemistry.

Further discussion with the producer, following these results, revealed additional history of feeding 50 percent DDG sheep pellets and 50 percent barley grain in January, February and early March that year. The ewes were also fed lupin grain during the early summer and the producer commented that the lupin grain at the bottom of the silo was "wet and mouldy".

Uroliths are concentrated mineral deposits that can be found in the urinary tract. In Australia, urolithiasis usually occur as a consequence one of three different circumstances:
(1) feeding of high levels of cereal grains;
(2) grazing grass dominant or unimproved pastures, predisposing stock to the development of urinary calculi composed of silicates, oxalates or carbonates; and
(3) wethers grazing phyto-oestrogenic clovers.1

Sheep fed diets with high cereal grain or commercial pellets, as in this case, are predisposed to the development of uroliths composed of phosphate salts, such as magnesium ammonium phosphate (struvite) and calcium phosphate (apatite), due to an imbalance of the calcium and phosphorus dietary ratio. The low dietary calcium intake and low Ca:P ratio of diets containing highly concentrated grain or pellets cause increased urinary excretion of phosphorus. Decreased rumination and saliva production from diets containing highly digestible feedstuff also result in increased urinary excretion of phosphorus. Urinary crystals then develop from the interaction between the increase in urinary phosphorus excretion and an alkaline urine environment.1

In this case, the low dietary calcium and high dietary phosphorus content of the pellet and barley grain fed from January to March, along with a low nutritional plane of calcium while grazing cereal crops, as well as the demand on calcium requirements during lactation, is likely responsible for the development of urolithiasis seen in the first ewe, despite ad libitum access to mineral supplements.

Regarding the changes in the livers of both ewes, the lab suggested to consider possible exposure to a plant toxin as a likely cause of the changes seen. They suggested that whilst the morphological pattern of the liver was not consistent with toxins such as sporodesmin, saponins or phomopsin, they can cause biliary hyperplasia, as was seen in the liver sample of the second ewe, and should be considered as a possible differential diagnosis. There was no history of exposure to sporodesmin or saponins but given there was history of "wet and mouldy" lupin grain fed over early summer, it is suspected that the chronic changes seen in this case was due to lupinosis.

Lupinosis is caused by a toxin that is produced by the fungus Diaporthe toxica (formerly known as Phomopsis letostromiformis).1 Lupinosis in livestock can present in two different forms; acute or chronic. Acute lupinosis is most common in livestock grazing sandplain lupins following summer rains, whereas chronic lupinosis is more common in livestock grazing narrow leafed lupin stubbles or when being fed lupin grain.1

Acute lupinosis presents as severe depression and/or sudden death with marked jaundice. On post-mortem the liver is enlarged, golden yellow in colour, and fatty.2 Clinical signs of chronic lupinosis, on the other hand, include inappetence, gradual loss of condition and lethargy.1,2 Photosensitisation can also be seen in sheep with chronic lupinosis.1 On post-mortem of chronic lupinosis the liver is often tan coloured, small, firm and fibrotic.2 There were no signs of jaundice in either ewe in this case, making acute lupinosis less likely. The clinical signs of loss in condition and lethargy is consistent with the presentation of chronic lupinosis, however it is interesting to note that in this case the liver did not appear small, firm or fibrotic on gross post-mortem and there were no signs of photosensitisation.

Overall, it is likely that the ill-thrift and wastage seen in the tail end of the ewes in this flock was due to a combination of urolithiasis, chronic lupinosis, and the demands of peak lactation.


Thank you to Anne Jordan, John Bolton, and the Laboratory Services team at EMAI for their work on this case, as well as their guidance with testing and diagnosis during this disease investigation.


  1. Abbott K. The Practice of Sheep Veterinary Medicine. University of Adelaide Press, Adelaide, 2018
  2. Osweiler, G. Mycotoxic lupinosis. MSD Manual Veterinary Manual 2014 Retrieved 4 June 2020


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