AFIP SYSTEMIC PATHOLOGY

JPC SYSTEMIC PATHOLOGY

NERVOUS SYSTEM

April 2017

N-T06

 

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

 

GENERAL DISCUSSION:

·       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)

 

PATHOGENESIS:

·       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

 

ULTRASTRUCTURAL FINDINGS:

·       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

 

DIFFERENTIAL DIAGNOSIS:

·       Laminitis, swelling of coronary band and sloughed hooves: Frostbite, ergotism, fescue toxicosis

·       Alopecia: Thallium toxicosis

·       Staggering gait: Rabies

 

COMPARATIVE PATHOLOGY: 

·       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

 

References: 

1.      Brue RN. Nutrition. In: Ritchie BW, Harrison GJ, Harrison LR, eds. Avian Medicine: Principles and Application. Lake Worth, FL: Wingers Publishing, Inc; 1994:75.

2.      Cantile C, Youssef S. Nervous system. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. Philadelphia, PA: Elsevier Ltd; 2016:308.

3.      Carson TL. Toxic minerals, chemicals, plants, and gases. In: Straw BE, D’Allaire S, Mengeling WL, Taylor DJ eds. Diseases of Swine. 10th ed. Ames, IA: Iowa State University Press; 2012:309,954.

4.      Davis TZ, Stegelmeier BL, Panter KE, Cook D, Gardner DR, Hall JO. Toxicokinetics and pathology of plant-associated acute selenium toxicosis in steers. J Vet Diagn Invest. 2012; 24: 319.

5.      Desta B, Maldonado G, Reid H, et al. Acute selenium toxicosis in polo ponies. Journal of Veterinary Diagnostic Investigation. 2011;23(3):623-628.

6.      Hovda LR. Disorders caused by toxicants. In: Smith BP, ed. Large Animal Internal Medicine. 5th ed. St. Louis, MO: Mosby, Inc; 2015:1593-1594.

7.      Humphreys DJ. Veterinary Toxicology. 3rd ed. London, England: Bailliere Tindall; 1988:69-71.

8.      Jones TC, Hunt RD, King NW. Veterinary Pathology. 6th ed. Baltimore, MD: Williams & Wilkins; 1997:729-731.

9.      Julian RJ, Brown TP. Poisons and toxins/other toxins and poisons. In: Saif YM, ed. Diseases of Poultry. 13th ed. Ames, IA: Iowa State University Press; 2013:1294.

10.   Miller AD, Zachary JF. Nervous system. In: McGavin MD,ed. Pathologic basis of Veterinary Disease. 6th ed.  St. Louis, MO: Elsevier Mosby; 2017:853.

11.   Radostits OM. Diseases caused by inorganic and farm chemicals. In: Radostits OM, Gay CC, Constable PD, Hinchcliff KW, eds. Veterinary Medicine A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. 11th ed. London, England: Saunders, Ltd.; 2017:1474-1475,1478.

12.   Strugnell BW, Payne JH, Matthews R. Selenium toxocosis in sheep associated with excessive sodium selenite in a commercial supplement. Veterinary Record. 2010;167:707-708.

13.   Summers BA. Degenerative diseases of the central nervous system. In: Summers BA, Cummings JF, de Lahunta A, eds. Veterinary Neuropathology. St. Louis, MO: Mosby, Inc.; 1995:258-261. 


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