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Pimelea poisoning of cattle, historically known as St. George Disease or Marree Disease, is a prevailing issue in arid grazing regions of inland Australia. Ingestion of the toxic native Pimelea species that contain the secondary metabolite simplexin, a diterpene orthoester with potent protein kinase C activity, induces diarrhoea, characteristic oedema and potentially fatal right-sided heart failure in cattle. Outbreaks of toxic Pimelea in the grazing field depend on seasonal prevalence. However, all stages of the plant carry the toxin, from seeds, juvenile plants to dead plant material. Livestock generally avoid consuming green Pimelea plants and only consume toxic Pimelea when pasture is minimal or where Pimelea growing through grass tussocks results in inadvertent ingestion. Our knowledge base of Pimelea poisoning has greatly improved with past research, yet the health hazards for livestock grazing in Pimelea affected pastures remains a significant issue whilst the ongoing search to develop effective strategies to mitigate poisoning continues. The goal of this review is to collate historical and recent research giving an overview of the current understandings of Pimelea poisoning, the toxin, its toxic effects and progress made towards remedies to alleviate the effects of Pimelea intoxication.

Pimelea poisoning affects cattle grazing arid rangelands of Australia, has no known remedy and significant outbreaks can cost the industry $50 million per annum. Poisoning is attributable to consumption of native Pimelea plants containing the toxin simplexin. Charcoal, bentonite and other adsorbents are currently used by the livestock industry to mitigate the effects of mycotoxins. The efficacy of such adsorbents to mitigate Pimelea poisoning warrants investigation. Through a series of in vitro experiments, different adsorbents were evaluated for their effectiveness to bind simplexin using a simple single concentration, dispersive adsorbent rapid screening method. Initial experiments were conducted in a rumen fluid based medium, with increasing quantities of each adsorbent: sodium bentonite (Trufeed®, Sibelco Australia), biochar (Nutralick®Australia) and Elitox® (Impextraco, Belgium). Data showed the unbound concentration of simplexin decreased with increasing quantities of each adsorbent tested. Sodium bentonite performed best, removing ~95% simplexin at 12 mg/mL. A second experiment using a single amount of adsorbent included two additional adsorbents: calcium bentonite (Bentonite Resources, Australia) and a synthetic adsorbent (Waters, USA). The concentration of simplexin remaining in the solution after 1 h, the amount able to be desorbed off the adsorbent-toxin matrix with replacement fresh fluid, and the amount remaining bound to the adsorbent were measured. All samples containing an adsorbent were statistically different compared to the blank (p < 0.05), indicating some binding activity. Future work will explore the binding mechanisms and behaviour of the toxin-adsorbent complex in the lower gastrointestinal tract.