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Mycotoxic Lupinosis


Gary D. Osweiler

, DVM, MS, PhD, Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University

Last full review/revision Dec 2014 | Content last modified Jun 2016

Lupines (Lupinus spp) cause two distinct forms of poisoning in livestock: lupine poisoning and lupinosis. The former is a nervous syndrome caused by alkaloids present in bitter lupines; the latter is a mycotoxic disease characterized by liver injury and jaundice, which results mainly from the feeding of sweet lupines. Lupinosis is important in Australia and South Africa and also has been reported from New Zealand and Europe. There is increasing use of sweet lupines, either as forage crops or through feeding of their residues after grain harvest, as strategic feed for sheep in Mediterranean climate zones. Sheep, and occasionally cattle and horses, are affected, and pigs are also susceptible.

Etiology and Pathogenesis:

The causal fungus is Phomopsis leptostromiformis, which causes Phomopsis stem-blight, especially in white and yellow lupines; blue varieties are resistant. It produces sunken, linear stem lesions that contain black, stromatic masses, and it also affects the pods and seeds. The fungus is also a saprophyte and grows well on dead lupine material (eg, haulm, pods, stubble) under favorable conditions. It produces phomopsins as secondary metabolites on infected lupine material, especially after rain.

Clinical Findings, Lesions, and Diagnosis:

Clinical changes are mainly attributable to toxic hepatocyte injury, which causes mitotic arrest in metaphase, isolated cell necrosis, and hepatic enzyme leakage, with loss of metabolic and excretory function.

Early signs in sheep and cattle are inappetence and listlessness. Complete anorexia and jaundice follow, and ketosis is common. Cattle may show lacrimation and salivation. Ketosis is a common sequela in pregnant cattle or recently calved cows. Survivors may develop hepatic cirrhosis. Sheep may become photosensitive, and a skeletal muscle myopathy can develop. As disease progresses, liver failure may cause hepatoencephalopathy characterized by stumbling, disorientation, and recumbency before death. In acute outbreaks, deaths occur in 2–14 days.

In acute disease, icterus is marked. Livers are enlarged, orange-yellow, and fatty. More chronic cases show bronze- or tan-colored livers that are firm, contracted in size, and fibrotic. Copious amounts of transudates may be found in the abdominal and thoracic cavities and in the pericardial sac. Some animals may have spongiform lesions in the brain.

Feeding of moldy lupine material, together with clinical signs and increased levels of serum liver enzymes, strongly indicate lupinosis.


Frequent surveillance of sheep and of lupine fodder material for characteristic black spot fungal infestation, especially after rains, is advised. The utilization of lupine cultivars, bred and developed for resistance to P leptostromiformis, is advocated. Oral doses of zinc (≥0.5 g/day) have protected sheep against liver injury induced by phomopsins.

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