Crofton weed (Ageratina adenophora) is a global and highly invasive weed, with ingestion causing severe respiratory disease in horses, leading to irreversible and untreatable pulmonary fibrosis and oedema. While reports of equine pneumotoxicity remain common in Australia and New Zealand, equine pneumotoxicity may be underdiagnosed in other countries where Crofton weed is endemic but poorly differentiated. The pathogenesis of Crofton weed toxicity following ingestion has been well described in a number of different animal models, including rodents, rabbits, and goats. However, induced toxicity is organ-selective across different animal species, and these vastly differ from the pathogenesis described in horses, both clinically and after experimental exposure. Sources of variation may include species-specific susceptibility to different toxins present in the plant, different mechanistic processes of toxicity, and species differences in toxin biotransformation and bioactivation across different organs. Considering disease severity and Crofton weed's invasiveness globally, assessing published toxicological and exposure data is necessary to advance research, identify specific toxins for horses, and possible prophylactic and therapeutic strategies. This review presents an overview of the available literature on equine toxicity, parallels between toxicity in horses and other animal species, and important aspects to be included in the future research agenda.
Keywords: Ageratina; Eupatorium; dyspnea; fibrosis; horse; lung; pneumonia; pulmonary fibrosis; toxic plant.