CASE NOTES
Suspected Anagallis arvensis (syn. Lysimachia arvensis) intoxication in sheep
Erika Bunker, Veterinary Pathologist, Elizabeth Macarthur Agricultural Institute, Menangle, and Jess Cooke, District Veterinarian, Central Tablelands Local Land Services, Mudgee
Posted Flock and Herd September 2025
INTRODUCTION
Anagallis arvensis (syn. Lysimachia arvensis, scarlet pimpernel) is a weed of crops, fallow land and disturbed sites, and was introduced from Europe. There are two colour forms in Australia, the more common red (scarlet) or orange form, and the blue form. Flowering season is from August to November.
The weed contains an unidentified toxin that can potentially damage the kidneys. The whole plant is toxic and remains toxic when dried. Sheep and cattle can be affected (McKenzie, 2012). Nitrate has been detected in A. arvensis in New South Wales (NSW), however, no cases of nitrate-nitrite poisoning by this plant have been recorded in livestock.
Here we report an incidence of sheep dying from a toxic nephropathy after grazing a stubble paddock with abundant growth of A. arvensis.
Image 1. Anagallis arvensis, orange and blue flower versions, Menangle NSW, September 2022
HISTORY
In January 2021, eight of 128 Merino ewes with lambs at foot died on a property near Mudgee after grazing an oat stubble paddock for two weeks. Three died in the stubble paddock, and another two became weak and recumbent when moved out of the paddock, with one euthanised for necropsy. Another four were found dead the following day, having shown no prior clinical signs. There was minimal stubble in the paddock and a predominant growth of a plant presumptively identified as A. arvensis.
Image 2. Stubble paddock with A. arvensis
NECROPSY FINDINGS
On the first visit the Local Land Services District Veterinarian euthanised and necropsied one of the recumbent ewes and found seeds consistent with those of A. arvensis in the rumen. Other findings were large amounts of firm dry ingesta in the caecum and proximal large intestine. The following day two of the ewes that had died overnight were also necropsied. These had faecal staining around the breech and hocks and congestion of the abomasum and large intestine mucosa, with bloody contents.
Image 3. Rumen with seed (arrow) consistent with seeds found in the suspect plant
Image 4.Suspect plant, A. arvensis, with seeds (arrows)
Image 5. Congestion of abomasal mucosa
LABORATORY FINDINGS
Fresh and fixed samples from the three necropsies were submitted to the Veterinary Laboratory at Elizabeth Macarthur Agricultural Institute.
Aqueous humour analysis (performed by University of Sydney Veterinary Teaching Hospital Pathology Services, Camden) from the first ewe revealed a severe uraemia, as well as ketosis, hyperglycaemia and mild hypocalcaemia.
| Aqueous humour biochemistry | Reference values | |
|---|---|---|
| Calcium | - 1.35 | > 1.4 mmol/L |
| BOHB | + 1.98 | < 0.5 mmol/L |
| Magnesium | 2.30 | > 0.6 mmol/L |
| Urea | + 52.50 | (2.9 - 7.1) mmol/L |
| Glucose | + 8.72 | < 4.40 mmol/L |
| Nitrite (Semi qualitative) | Zero | mg/L |
| Nitrate (Semi qualitative) | Zero | mg/L |
On histopathology the most significant lesions were in the kidney samples. There was severe acute to subacute nephropathy with marked tubular injury, necrosis and degeneration of tubular epithelium and evidence of early regeneration and repair in all three ewes. Gastrointestinal congestion, as noted grossly, was confirmed with no evidence of bacterial enteritis. There were no significant liver lesions apart from non-specific degeneration.
Image 6. Kidney, first ewe, multifocal tubular necrosis and degeneration, H&E, 10x
DISCUSSION
Uraemia, in combination with the severity of histological kidney lesions, suggest that renal failure was the cause of illness and deaths in these ewes. The lesions, while not specific, were consistent with a toxic nephropathy and those reported in other cases of suspected poisoning by A. arvensis. Gastrointestinal irritation and diarrhoea could have been due to a primary irritant effect of the plant and/or secondary to uraemia or renal failure. Ketosis found in the first ewe necropsied would most likely have been secondary to renal failure.
Clinical, post-mortem and microscopic changes in this case were similar to Ross McKenzie's descriptions in his book in the chapter on A. arvensis: sheep are depressed, lose appetite, have no rumen movement, develop diarrhoea, drink large amounts of water, then become weak and staggery, collapse, become recumbent, comatose and die in 24-36 hrs. On post-mortem there is gastrointestinal congestion and haemorrhage and kidneys are pale and swollen with histological lesions of renal tubular necrosis and cortical fibrosis (McKenzie 2012).
Other nephrotoxic plants that may grow in the area were excluded. Amaranthus spp. were not present in the paddock. With Lythrum hyssopifolia, which grows under similar conditions as A. arvensis, you often also see liver lesions and it was not present in the paddock. There were no birefringent crystals in kidney sections suggestive of poisoning by oxalate-containing plants. There was no history of exposure to superphosphate, another nephrotoxic agent.
A. arvensis is usually unpalatable and intoxication is uncommon. A search of the NSW Department of Primary Industries laboratory information management system from 2007 to 2021 found only one previous case of suspected intoxication. This case occurred between late December 2008 and early January 2009 in sheep in the Young area. Thirty-five of 1500 Merino ewes that had grazed a stubble paddock died. In five ewes, small green berries were found in the rumen. Histology on the kidney of one affected ewe showed acute tubular necrosis. A plant sample from the paddock was identified as A. arvensis.
In the literature, reports of A. arvensis intoxication in sheep in Australia and elsewhere go back to early last century and are discussed below.
In February 1938 in Victoria 12 of 90 sheep died and many others were sick after grazing a fallow paddock with prolific growth of weeds, predominantly A. arvensis, following good summer rains. Clinical signs observed were diarrhoea, anorexia, suppressed rumination, weakness, staggering and recumbency. On post-mortem there was gross evidence of nephropathy. Feeding experiments with the weed collected from the offending paddock at intervals between February and July found that the first sample had the most toxic effect, with sheep dying after two days. Sheep fed with samples from subsequent harvests survived with symptoms becoming less pronounced with later harvest times, until sheep fed further along in the trial survived with no symptoms. Drying did not affect toxicity. Gross kidney lesions in the dead sheep necropsied suggested nephropathy. The author concluded that A. arvensis is only toxic for limited periods and under certain unknown conditions (Pullar 1939).
In NSW, during the summer of 1983/84 Merino ewes died from a toxic nephropathy on a wheat stubble paddock in the Riverina area. The authors noted that the summer had been unusually wet leading to exuberant growth of weeds in cereal stubble paddocks. A. arvensis grew amongst other weeds where the sheep died and had been moderately grazed. There was gross and microscopic evidence of nephropathy with coagulative tubular necrosis and some regeneration and fibrosis. While a feed trial failed to reproduce disease, it was suggested plant material may have been collected during a phase when it was no longer toxic (Rothwell et al., 1986)
A 1978 paper from South Africa described similar conditions under which poisonings occurred as in Australia. Unusually good summer rains for 17 days were recorded in a winter-rainfall area and sheep were grazing on previously fallow land with growth of A. arvensis amongst a range of other plants considered non-toxic. Both naturally and experimentally intoxicated sheep died from renal failure, with gross and microscopic evidence of kidney injury consisting of coagulative necrosis of tubules and variable evidence of regeneration and interstitial fibroplasia. With lower doses over a more prolonged period in the experimental cases it took longer for sheep to develop renal failure, with time for the more subacute changes of regeneration and fibroplasia to develop. The author suggested that with enhanced growth of A. arvensis after the summer rains the plant also became more palatable and so was readily eaten by the sheep (Schneider 1978).
Rivero et al., (2001) described several incidences of A. arvensis intoxication in both sheep and cattle grazing cereal stubble or fallow paddocks in Uruguay between 1994 and 1998 in December and January. During this time A. arvensis was in bloom and the predominant plant species, with both red and blue colour observed. In most outbreaks clinical signs occurred after 2–10 days exposure, with animals showing weakness, staggering, diarrhoea and death, azotaemia and gross and histological evidence of nephropathy and gastrointestinal tract irritation. The authors noted that all outbreaks occurred on farms located on basaltic or sandy-cretacic soils, with no cases on soils with better fertility where the plant was also present. Experimental feeding of the plant reproduced the disease.
While cattle are less commonly affected, likely due to the weed's tendency to grow as a flat mat making it more likely to be ingested by sheep rather than cattle, there is one report from Victoria in 2012 where 120 beef heifers grazed a wheat stubble paddock with weeds, predominantly A. arvensis, from mid-December to late January. During January rainfall occurred. Several cattle became sick and died, continuing for a few days after they were moved to another paddock. Affected animals were azotaemic and there was gross and microscopic evidence of nephropathy with tubular injury and early regeneration, as well as intestinal haemorrhages and ulcers. The authors thought that recent rainfall resulted in proliferation of A. arvensis, which became increasingly attractive to cattle in the absence of other palatable feed (Roche et al., 2012).
This case report, and review of other cases recorded, shows that A. arvensis intoxications occur rarely as stock usually try to avoid the plant, however, with unusual seasonal conditions animals can be poisoned. Such conditions when poisonings could be expected are good rains in summer after a drought favouring prolific growth of this weed, particularly in stubble paddocks, before other plants can grow and in the absence of much alternative feed. Access to large amounts of A. arvensis should be avoided.
REFERENCES
- McKenzie R (2012) Australia's Poisonous Plants, Fungi and Cyanobacteriae CSRIO Publishing, p 384-385
- Pullar EM (1939) Studies on five suspected poisonous plants Australian Veterinary Journal 15 19-23
- Rivero R, Zabala A, Gianneechini R, Gil J, Moraes J (2001) Anagallis arvensis poisoning in cattle and sheep in Uruguay Veterinary and Human Toxicology 43 27-30
- Roche MJ, McCowan CI, Kelly JC (2012) Suspected poisoning of cattle by scarlet pimpernel (Lysimachia arvensisL.) Australian Veterinary Journal 90(7) 269-271
- Rothwell JT, Marshall DJ (1986) Suspected poisoning of sheep by Anagallis arvensis (scarlet pimpernel) Australian Veterinary Journal 63 316
- Schneider DJ (1978) Fatal ovine nephrosis caused by Anagallis arvensis L. Journal of the South African Veterinary Association 49 321-324