JPC SYSTEMIC PATHOLOGY
Signalment (JPC # 1803529): 2-month-old feeder pig
HISTORY: This pig was paralyzed. Three other pigs on the same farm as well as pigs on two nearby farms were similarly affected.
HISTOPATHOLOGIC DESCRIPTION: Spinal cord, cervical intumescence: Bilaterally and symmetrically, within the ventral gray horns, there are approximately 2 mm diameter circular foci of necrosis, characterized by rarefaction with loss of normal tissue architecture. Within these areas, there is moderate gliosis with few glial nodules and occasional neuronal satellitosis, central neuronal loss or degenerate neurons characterized by chromatolysis (mildly rounded perikaryon with pale eosinophilic cytoplasm with a ground glass appearance, an eccentric nucleus, and dispersal of Nissl substance), and moderate numbers of small caliber vessels lined by hypertrophied, reactive endothelial cells. Circumferentially, these areas are bounded by areas of spongiosis, characterized by numerous, variably sized, clear vacuoles within the parenchyma.
MORPHOLOGIC DIAGNOSIS: Spinal cord, cervical intumescence, ventral horns: Poliomyelomalacia, bilaterally symmetric, focally extensive, moderate with neuronal degeneration, necrosis, and loss, spongiosis, gliosis, breed unspecified, porcine.
ETIOLOGICAL DIAGNOSIS: Toxic poliomyelomalacia
CAUSE: Selenium toxicosis
CONDITION: Focal symmetrical poliomyelomalacia of pigs
CONDITION SYNONYM: Bilateral poliomyelomalacia, blind staggers, alkali disease, bob-tail disease
· Acute paralytic syndrome in feeder pigs associated with selenium intoxication
· Intoxication due to ration miscalculation with selenium (selenium-enriched yeast, sodium selenite/ate) or by ingestion of selenium (Se) accumulating plants
· Occurs in arid, alkaline soil in Wyoming and South Dakota, western Canada, parts of Australia, Ireland, Mexico and Israel
· Obligate accumulators/indicator plants (require high levels for growth, and can contain 5000 to 15,000 ppm of Se): Astragalus bisulcatus (two grooved milkvetch), Stanleya pinnata (prince’s plume), Aster parryi spp. (woody aster), and loco weed
· Facultative accumulators/secondary Se absorbers (do not require Se but will accumulate if available, contain up to 1000 ppm of Se): Acacia cana, Aster spp. (woody aster), Astragalus spp. (poison vetch), Atriplex canescens (saltbrush), Castilleja spp., Comandra pallida (bastard toadflax), Grindelia squarrosa (gumweeds), Machaeranthera ramosa Morinda reticulata, Neptunia amplexicaulis, Penstemon spp. Sideranthusspp. (ironweed)
· Unknown, but may be due to induction of a nicotinamide or niacin deficiency resulting in the generation of reactive oxygen species during reaction of thiols
TYPICAL CLINICAL FINDINGS:
· Acute form – Ataxia progressing to forelimb or hind limb paresis or quadriplegia
· Chronic form – Alopecia, coronitis, hoof separation at coronary band, deformed hooves, +/- sloughed hooves
· Elevated serum selenium and glutamic oxalo-acetic transaminase
· Elevated liver and kidney selenium levels
TYPICAL GROSS FINDINGS:
· There is edema and necrosis, or cavitation, of the ventral grey columns of cervical and lumbar enlargements of the spinal cord that is bilaterally symmetric
· Malacic foci are yellow-brown and soft or there are grayish areas of liquefaction
· Rough hair coat and partial alopecia
· Deformed hoof walls with multiple rings and cracks
· Coronary band inflammation which may progress to sloughing of hoof
TYPICAL LIGHT MICROSCOPIC FINDINGS:
· Focal, bilaterally symmetrical poliomyelomalacia in the ventral gray horns, primarily in the cervical and lumbar intumescences with marked neuronal loss, neuronal chromatolysis, status spongiosus, microcavitation and in chronic cases, endothelial and glial proliferation
· Wallerian degeneration in the ventral spinal nerve rootlets adjacent to affected areas
· Oligodendrocyte necrosis, gray matter astrocyte vacuolation, degenerate motor neurons, pyknotic nuclei, dilated cisternae in cytoplasm, and granular debris
ADDITIONAL DIAGNOSTIC TESTS:
· Chemical analysis of tissues (hair retains elevated levels well after clinical signs abate) and feeds
· Laminitis, swelling of coronary band and sloughed hooves: Frostbite, ergotism, fescue toxicosis
· Alopecia: Thallium toxicosis
· Staggering gait: Rabies
· Cattle: Myocardial necrosis, articular erosions of long bones, laminitis and/or sloughed hooves, loss of long hair from switch, death, atrophic and cirrhotic liver, toxic hepatitis, toxic tubular nephrosis and nephritis, hemorrhagic gastroenteritis, and passive congestion; alopecia and follicular atrophy on the base of tail and switch
· Sheep: Sudden death, respiratory and cardiac failure, gastroenteric disorders, laminitis, sloughed hooves, inapparent cutaneous lesions
· Horses, mules: Laminitis, deformed and/or sloughed hooves, loss of long hair from mane; alopecia and follicular atrophy on the base of tail and switch
· Poultry: Decreased egg weight and hatchability, embryo deformities of the eye, and head, low viability chicks, decreased egg production, vascular permeability changes, disturbances of lipid metabolism, cytoplasmic degeneration, and intra-epithelial hyaline formation affecting brain, heart, arteries, liver and kidneys, anemia, and stiff tibiotarsal joints
· Dogs: Convulsions, death, extreme hepatic periportal fibrosis, fatty degeneration, and multifocal cerebrocortical necrosis and malacia
· Goats: Alopecia of beard and flanks
· Aquatic birds: Accumulates in food chain leading to emaciation, hepatitis, ascites and embryo deformity
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