CASE NOTES

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An outbreak of crystal-associated cholangiohepatopathy in composite lambs grazing Tribulus terrestris

Bruce Watt, Central Tablelands Local Land Services, Bathurst, Will Clark-Dickson, farm manager and Angel Ngo, Elizabeth Macarthur Agricultural Institute, Menangle

Posted Flock and Herd March 2026

INTRODUCTION

Both caltrops or cathead (Tribulus terrestris) and some Panicum spp. of grasses contain steroidal saponins, the metabolites of which cause insoluble crystals to accumulate in bile ducts, leading to obstruction and hepatogenous photosensitisation. This condition can cause severe outbreaks of cholangiohepatopathy and photosensitisation, especially in young sheep, after summer and autumn rains have favoured the growth of these plants.

In this outbreak, which occurred in February 2025, lambs were grazed in a lucerne (Medicago sativa) paddock to defoliate it prior to spraying with the broadleaf herbicide fluroxypyr (Starane Advanced, Corteva Agriscience) so broadleaf weeds, including caltrops, could be targeted. Unfortunately, 250 lambs became sick and died due to hepatogenous photosensitisation. Approximately 140 lambs grew slower than expected suggesting residual organ damage.

HISTORY

On around 10 January 2025, a mob of 1600 mixed-sex August-2024-drop composite lambs was drenched (Abamec Dual) and vaccinated (5-in-1 clostridial booster) onto a lucerne paddock. The paddock also had an infestation of Bathurst burrs (Xanthium spinosum), caltrops and common heliotrope (Heliotropium europeaum). The aim was to graze the lucerne heavily to remove green leaf (rendering it less susceptible to the herbicide) and then remove the sheep and spray with fluroxypyr to remove weeds. On 21 January at least 80 dead lambs and 300-400 sick lambs were noticed in the paddock. The sick lambs were dull with swollen heads. The lambs were immediately moved to a paddock without caltrops.

Figure 1. Caltrops (Tribulus terrestris) and Bathurst burrs (Xanthium spinosum) in the pasture

CLINICAL FINDINGS

The mob was first examined in the paddock. Half the mob was grazing and seemed unaffected. However, numerous sick and dead lambs were seen under trees. The sick lambs were dull with black, necrotic eyelids, lips and ears. Three lambs were examined and then euthanased and necropsied.

Case 1. An approximately 30 kg composite ewe lamb. The lamb was dull, dehydrated, lethargic and sick with marked icterus and necrotic eyelids and ears.

Case 2. An approximately 30 kg composite ewe lamb. The lamb was dull, lethargic and sick but able to stand and walk. It had marked icterus and necrosis of the eyelids and ears.

Case 3. An approximately 35 kg composite ewe lamb. The lamb was dull, lethargic and sick with marked icterus and necrosis of the eyelids, which were black and sunken. The ears were dry and necrotic.

Figure 2. Case 1. Sick sheep with pale, jaundiced mucous membranes

Figure 3. Case 3. Moribund affected lamb with dry necrotic ears, eyelids and lips

NECROPSY FINDINGS

All cases were similar. All were composite ewe lambs with an estimated weight of 30-35 kg. All had black, necrotic eyelids, lips and ears. Each had jaundice of the subcutaneous tissues. The tissues were dry and there was little fluid in the abdominal contents. The liver was of normal size and shape but was olive coloured. The kidneys were brown and the lungs appeared normal.

Figure 4. Case 1 showing jaundiced, dehydrated carcase

LABORATORY FINDINGS

Biochemistry

Test	Normal values	Units		Results
Sample			1	2	3
GGT	0 - 55	U/L	184	163	102
GLDH	0 - 30	U/L	26	57	73
AST	0 - 30	U/L	1606	1266	1977
BIL	0.0 - 6.8	µmol/L	145.2	137.7	151.7
BIL-C		µmol/L	101.7	99.6	114.2
CK	0 - 300	U/L	301	315	1590
UREA	2.9 - 7.1	mmol/L	16.9	26.1	41.6
CREAT	0 - 265	µmol/L	128	186	436
PHOS	1.13 - 2.58	mmol/L	2.26	2.70	4.95
URE/CREA	0.00 - 0.07		0.13	0.14	0.10
PROTEIN	55.0 - 80.0	g/L	83.0	85.1	70.8
ALBUMIN	26.0 - 36.0	g/L	28.8	30.0	29.1
GLOB	30.0 - 57.0	g/L	54.2	55.1	41.7
ALB/GLOB	0.5 - 1.1		0.5	0.5	0.7
BHB	0.00 - 0.80	mmol/L	0.44	0.33	0.70
CA	2.12 - 2.87	mmol/L	2.42	2.29	1.88
MG	0.74 - 1.44	mmol/L	1.02	1.30	1.25
HAPTO	0.00 - 0.30	g/L	2.80	4.88	0.77
SERUM HB	0.00 - 0.20	g/dL	0.14	0.17	0.16

Figure 5. Table of biochemistry results

There was evidence of biliary injury in all animals (elevated GGT, hyperbilirubinaemia). The hyperbilirubinaemia mostly consisted of conjugated bilirubin, suggesting hepatic or post-hepatic/extra-hepatic causes were more likely. Two of three animals also had elevated GLDH and all had elevated AST, which additionally indicated hepatocellular injury. Haptoglobin was elevated in all animals indicating an acute inflammatory response. One animal was hypocalcaemic.

HISTOPATHOLOGY FINDINGS

Histopathology findings in the liver and kidney were consistent across all affected lambs at varying severity, with case 1 most severely affected. All lambs had evidence of cholangiohepatopathy, characterised by necrotising cholangitis, Kupffer cell hyperplasia, biliary hyperplasia, and occasional crystal ghosts/clefts within affected bile ducts (Figure 5). No crystals were observed under direct nor polarised light. Case 1 also had random single-cell necrosis within the liver. Tubulonephrosis was seen in cases 1 and 3, with case 3 also showing acute tubular degeneration and necrosis. No crystal ghosts/clefts were seen in the kidney.

Figure 5. Crystal ghost (arrow) within a bile duct with Kupffer cell hyperplasia and biliary hyperplasia. H&E, 10x

MANAGEMENT

Livestock should be removed from the affected paddock as soon as possible. Some sheep may be so severely affected with necrotic eyelids and lips that they should be euthanased. Less affected lambs should be sheltered from sunlight and provided with supportive treatment.

While cattle may also be intoxicated by steroidal saponins, in the experience of the first author they are less susceptible and have been successfully used to graze paddocks that are toxic to sheep.

As a result of this experience, one of us who manages this property (WC-D) would avoid putting lambs on paddocks with abundant fresh green caltrops. He would also monitor paddocks with high caltrop populations after rain. In this case, the lucerne stand was five years old with a declining plant population. He would consider bringing paddocks like this out of pasture a year earlier to reduce the caltrop population. After this event, the paddock was pulled out of lucerne rotation and was fallowed for a summer brassica crop.

DISCUSSION

Crystal-associated cholangiopathy is a well-known cause of photosensitisation and mortality, especially in young sheep. The disease was first reported in South Africa as 'geeldikkop' from the ingestion of Tribulus terrestris and 'dikoor' from the ingestion of Panicum species (Glastonbury et al. 1984, Button et al. 1987, Slattery 2022). While Tribulus and Panicum spp cause this disease in Australia, elsewhere a range of other plant species are implicated. However, Tribulus or Panicum spp are not always toxic and the contribution of sporadic environmental conditions such as wilting or the synergistic involvement of fungi has yet to be determined (Cullen et al. 2016).

REFERENCES

1. Glastonbury JRW, Doughty FR, Whitaker SJ and Sergeant E (1984) A syndrome of hepatogenous photosensitisation, resembling geeldikkop, in sheep grazing Tribulus terrestris Australian Veterinary Journal 61(10) pp 314-316
2. Button C, Paynter DI, Shiel MJ, Colson AR, Paterson PJ and Lyford RL (1987) Crystal-Associated cholangiohepatopathy and photosensitisation in lambs Australian Veterinary Journal 64(6) pp 176-180
3. Watt B, Hackney B and Bunker E (2013) Photosensitisation and cholangiopathy (Dikoor) in lambs grazing a forage brassica crop contaminated with Panicum gilvum www.flockandherd.net.au
4. Slattery SM (2022) Poisoning of lambs on mature Bambatsi panic www.flockandherd.net.au
5. Cullen JM and Stalker MJ (2016) Liver and Biliary System. Jubb, Kennedy and Palmer's Pathology of Domestic Animals: Vol 2, pp 258-352