Overview of Sorghum Poisoning

Sorghum species are drought-tolerant plants that may produce neuropathic and teratogenic manifestations. Sorghum poisoning has been seen primarily in the southwestern USA and Australia. The syndrome is reported almost exclusively in horses, although a similar disease has been reported in sheep and cattle. Lathyrogenic nitriles such as β-cyanoalanine, cyanogenic glycosides, and nitrates have been suggested as causative agents. The syndrome develops in horses after they have grazed hybrid Sudan pastures for weeks to months and produces axonal degeneration and myelomalacia in the spinal cord and cerebellum. (Also see Cyanide Poisoning.) Consumption of the seed will not produce the syndrome.

Sorghum poisoning is characterized by posterior ataxia or incoordination, cystitis, urinary incontinence (which predisposes both male and female horses to cystitis), and alopecia on the hindlegs due to urine scald. The loss of urinary bladder function is related to degeneration of spinal cord neurons. The incoordination may progress to irreversible flaccid paralysis. Deformities of the fetal musculoskeletal system (ankylosis or arthrogryposis) and abortion may occur during late pregnancy. The diagnosis is based on the analysis of urine for evidence of cystitis, characterization of spinal cord lesions, and analysis of forage for cyanide. Although fatal poisoning is infrequent, the impact on reproduction is the primary concern. Consumption of sorghum hybrids with low cyanogenic potential or restriction of access to sorghum grasses may limit the incidence. Dietary supplementation with sulfur may be beneficial. Affected horses often die from pyelonephritis. Treatment with antibiotics may be helpful, but a full recovery is rare if ataxia has developed. Consumption of pastures containing sorghum plant species is not recommended for horses.