Neuroaxonal Degeneration in Sheep GrazingSorghumPastures

Abstract

Abstract. During the fall of 1992, 250 (10%) of 2,500 Rambouilet cross feeder lambs grazing Sorghum bicolor developed neurologic signs including weakness, ataxia, head shaking, knuckling of the fetlocks, inability to rise, and opisthotonos. One hundred fifteen (46%) of the affected lambs died. Twenty of the surviving lambs exhibited residual neurologic signs of ataxia when stressed. At the same time, 275 (25%) of 1,100 ewes grazing a nearby sudex pasture (S. sudanese x S. bicolor) gave birth to lambs that were weak and unable to rise. Newborn lambs exhibited extensor rigidity and opisthotonos when assisted to a standing position. The dystocias that occurred were due to lambs with contracted limbs (arthrogryposis). All affected lambs died or were euthanized. Histologic examination of the brains of 3 feeder lambs and 9 newborn lambs revealed similar microscopic lesions. The predominant change was the presence of focal axonal enlargements (spheroids) in the proximal segments of axons, which were restricted to the nuclei of the medulla, cerebellum, and midbrain. In addition, the spinal cord contained spheroids in the ventral horn gray matter of the 6 newborns examined. Ultrastructurally, the spheroids were composed of aggregates of neurofilaments, mitochondria, vesicular bodies, and dense bodies bounded by a thin myelin sheath. There was mild gliosis in the more severely affected animals of both groups. There was minimal Wallerian degeneration in the white matter adjacent to affected nuclei in the brain and the ventromedial and dorsolateral funiculi of the spinal cord. This is the first detailed report of Sorghum toxicity in sheep.Ataxia, recumbency, and the birth of weak cystitis, urinary incontinence, or malformed offspring have been reported in pastures.

Axonal Degeneration in Sheep Caused by the Ingestion of Halimium Brasiliense

“…These lesions differ from other previous reports of axonopathy [2][3][4][5]7,11,12,[15][16][17] and apparently represent a novel morphologic manifestation of toxic axonopathy. Axonal changes are classified as reactive, degenerative, regenerative, and dystrophic.…”

“…Ultrastructurally, the spheroids contain collections of mitochondria, irregular bundles of neurofilaments, tubulovesicular structures, and electron-dense granules bordered by a thin myelin sheath. 3 Axonal spheroids occur in a variety of circumstances and vary with each syndrome by their distribution in the neuraxis and by ultrastructural composition. 15,17,18 In H. brasiliense toxicosis, secondary Wallerian degeneration is suggested by the presence of a few ellipsoids, rare Gitter cells, axonal spheroids containing membranous bodies, vesiculo-membranous bodies, dense bodies, and small vesicles.…”

Nodding syndrome in Mundri county, South Sudan: Environmental, nutritional and infectious factors

“…Neuropathological examination reveals focal neurofilamentous swellings in proximal regions of axons restricted to the nuclei of the medulla oblongata, cerebellum, and midbrain, with additional axonal spheroids in the ventral horn gray matter. 37 Whether this pattern of neurological damage is strictly associated with repeated exposure to sorghum cyanogens is unclear, since mycotoxin endophytes associated with grasses also have potential neurotoxicity, as discussed below.…”

Effects of Long-Term Low-Dose Cyanide Administration to Rats

“…Furthermore, prolonged cyanide exposure through both tobacco smoke and cassava consumption may be implicated in the pathogenesis of ocular pathologies such as tobacco}alcohol amblyopia (Solberg et al, 1998), retrobulbar neuropathy of pernicious anemia (Freeman, 1988), Leber's hereditary optic neuropathy (Tsao et al, 1999), and Cuban optic neuropathy (Tucker and Hedges, 1993). Horses, cattle, and sheep grazing on cyanogenic Sorghum pastures developed neuronal disorders, especially ataxia (Adams et al, 1969;McKenzie and McMicking, 1977;Bradley et al, 1995).…”