Sorghum Toxicity
Robert J. MacKay • Mary O. Smith
■ Definition and Etiology A syndrome of ataxia and cystitis in horses, cattle, and sheep has been linked to the consumption of annual grasses of the genus Sorghum.1-4 Incriminated species have included Sorghum bicolor (sorghum), Sorghum sudanense (sudangrass), sorghum-sudan hybrids, and Sorghum halepense (Johnson grass, oxgrass).
The causative toxin is not known, although there is evidence that chronic cyanide toxicity has a role.5 This disease does not appear to be linked to the breed, gender, or age of an animal.3■ Clinical Signs The first sign observed is usually ataxia of the pelvic limbs, followed by urinary incontinence. Affected animals have a swaying pelvic limb gait and a tendency to knuckle in the fetlocks. Occasional affected horses may walk with a hopping gait, in which both pelvic limbs are lifted off the ground simultaneously. Signs in horses tend to worsen on backing, and animals may fall or even become recumbent.3 During an outbreak of the disease in cattle, 3 of 54 affected cows became recumbent, and 2 died.6 The perineal muscles are relaxed, and urine dribbles from a flaccid, distended bladder.4,6 In mares the vulva opens and closes repeatedly; in stallions and geldings the penis is relaxed and protrudes from the prepuce.7 There may be paresis of the tail in affected horses and cattle. Loss of skin sensation over the hindquarters has been described in a cow, which suggests involvement of both sensory and motor nervous pathways.6 Headshaking, ataxia, weakness, recumbency, opisthotonos, and death have been reported in affected sheep, and the rate of mortality can approach 50%.8
Cystitis in affected animals may be severe and occurs secondary to urine retention. Dribbling of urine onto the skin of the perineum and pelvic limbs results in scalding of the skin and dermatitis.
Pyelonephritis is a common sequela to chronic cystitis and may be fatal.2,3 Sometimes the clinical signs may be chronic; in one outbreak, horses had been showing signs for as long as 3 years.3Abortion in mares, arthrogryposis as a congenital deformity of foals and lambs, and neurologic abnormalities in newborn lambs have also been linked to the feeding of Sorghum plants.3,8
■ Clinical Pathology Diagnosis of sorghum toxicity is based on the presence of typical clinical signs in association with a history of feeding on Sorghum plants. No specific diagnostic test is available. Cystitis and pyelonephritis are identified by typical findings on routine urinalysis, serum biochemistry, and urine culture.
■ Pathophysiology The precise nature of the toxic substance in Sorghum plants that causes this syndrome is unknown. Most Sorghum spp. are cyanogenic plants that contain the cyanogenic glycoside surrina, which, when hydrolyzed, releases hydrocyanic acid at potentially toxic concentrations.1 Acute, sometime fatal cyanide toxicosis has been described in cattle that ingest large amounts of rapidly growing sorghum.9,10 Chronic exposure to cyanide has been suggested as the cause of the neuropathologic changes found in animals with ataxiacystitis syndrome.3 Experimental long-term dosing of potassium cyanide to goats caused histologic changes in the CNS that were comparable with those of the natural disease.5 It has also been suggested that the toxic principle in Sorghum plants may be a lathyrogen-like substance.2
■ Epidemiology The cyanide content of Sorghum plants is increased by rain after drought and higher in new shoots and wet plants.1 In one survey of the disease in horses, most cases occurred during the wet season and involved young, growing plants.3 The period of grazing before the onset of signs ranges from 1 week to many months.3,6
■ Necropsy Findings Wallerian degeneration, swelling of axons and myelin sheaths, and demyelination in a small number of nerve fibers throughout the length of the spinal cord and in the cerebellum, cerebellar peduncles, and pons have all been described, together with the presence of phagocytic gitter cells.
In lambs grazing on sorghum, there were also lesions in the ventral horn gray matter of the spinal cord.3,6,8 These changes are not associated with specific tracts. Ultrastructural studies of brains and spinal cords of affected sheep have revealed that the axonal swelling (spheroids) are composed of aggregates of neurofilaments, mitochondria, vesicular bodies, and dense bodies, enclosed within a thin myelin sheath.8■ Treatment and Prognosis Withdrawal of Sorghum plants from the diet of affected animals results in a gradual improvement in the clinical signs over weeks to months, although recovery may not be complete.6,8 Death is a potential outcome, however, and mortality rates can be high in some cases.8 There is no specific treatment for affected animals. Supportive therapy includes antibiotics for treatment of bacterial urinary tract infections.
■ Control Avoidance of feeding Sorghum plants as a predominant part of the diet or the sole diet is the only method of control. This plant has considerable feed value and does not present a major hazard when used as part of a diversified feeding regimen.