Related Experiment Video
Updated: Jul 23, 2025

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids
Published on: April 25, 2016
Equine Crofton Weed (Ageratina spp.) Pneumotoxicity: What Do We Know and What Do We Need to Know?
Frances Marie Shapter1, José Luis Granados-Soler1, Allison J Stewart1
1School of Veterinary Science, University of Queensland Gatton, 5391 Warrego Highway, Gatton, QLD 4343, Australia.
Abstract:
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.
Related Concept Videos
Fungal Phylum Ascomycota
Physical Properties of Amines
Anticholinesterase Agents: Poisoning and Treatment
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is...
Direct-Acting Cholinergic Agonists: Therapeutic Uses

