JPC SYSTEMIC PATHOLOGY

NERVOUS SYSTEM

March 2023

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: The gray matter of the ventral horns is replaced by two bilaterally symmetric, 2 mm diameter, circular foci of liquefactive necrosis characterized by increased pallor (rarefaction) with loss of normal tissue architecture.  Within these foci there is moderate gliosis, few glial nodules, occasional neuronal satellitosis, and moderate numbers of small caliber blood vessels lined by hypertrophied, reactive endothelial cells. Within the center of these necrotic foci there is neuronal loss, and remaining neurons within the necrotic foci are often degenerate characterized by chromatolysis (rounded perikaryon with pale eosinophilic cytoplasm with a ground glass appearance, an eccentric nucleus, and dispersal of Nissl substance). These necrotic foci are circumferentially bounded by areas of spongiosis characterized by numerous, variably sized, clear vacuoles within the parenchyma. 

 

MORPHOLOGIC DIAGNOSIS: Spinal cord, cervical intumescence, ventral horn grey matter: Necrosis and rarefaction (poliomyelomalacia), bilaterally symmetric, focally extensive, moderate, with neuronal degeneration and loss, spongiosis, and gliosis, breed unspecified, porcine.

 

ETIOLOGICAL DIAGNOSIS: Toxic poliomyelomalacia 

 

CAUSE: Selenium toxicosis 

 

CONDITION: Focal symmetrical poliomyelomalacia of pigs

 

CONDITION SYNONYM: Bilateral poliomyelomalacia, selenosis, blind staggers, alkali disease, bobtail disease

 

GENERAL DISCUSSION:

• Acute paralytic syndrome in feeder pigs associated with chronic selenium (Se) intoxication

• Intoxication due to ration miscalculation with selenium (e.g. selenium-enriched yeast, sodium selenite/ate) or by ingestion of Se-accumulating (seleniferous) plants
• Acute toxicity results in severe gastrointestinal, cardiovascular signs, and death

• Selenium- a metalloid and essential element that acts as an antioxidant with a narrow margin of safety and potential for toxicosis

• Toxic potential varies by chemical form, rate of consumption, nature of diet, and by species and individual animal
• Widely distributed in soils at concentrations ranging from <0.01 parts per million (ppm) to >500 ppm; areas of high soil concentration particularly extensive in parts of the United States (Montana, Utah, Wyoming, Colorado, North and South Dakota, Kansas, Arizona, and Nebraska), as well as western Canada, and parts of China, Ireland, Mexico, Australia, New Zealand, and Israel, among others

• Many nonseleniferous plants, grasses, and weeds can passively accumulate selenium if growing in soils with high selenium content

• Seleniferous plants:  Occur in arid, alkaline soil; typically not palatable and ingested by newly introduced animals or in times of food scarcity 

• Obligate accumulators/indicator plants (require high levels for growth, and can     contain >1,000 ppm of Se): Astragalus bisulcatus (two grooved milkvetch), members of the genus Astragalus, Machaeranthera, and Stanleya
• Facultative accumulators/secondary Se absorbers (do not require Se but will accumulate if available, contain up to 1,000 ppm of Se): Members of the genus Aster, Atriplex, Castilleja, and Gutierrezia

 

PATHOGENESIS:

 

TYPICAL CLINICAL FINDINGS:

• Ataxia progressing to forelimb or hind limb paresis or quadriplegia
• Alopecia, coronitis, hoof separation at coronary band, deformed hooves, +/- sloughed hooves

 

TYPICAL GROSS FINDINGS:  

• Central nervous system lesions:
  • Bilaterally symmetric edema and necrosis or cavitation of the ventral grey columns of cervical and lumbar enlargements (intumescences) of the spinal cord
  • Malacic foci are yellow-brown and soft or there are grayish areas of liquefaction
• Other lesions: 
  • 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 symmetric necrosis (poliomyelomalacia) in the spinal cord ventral gray horns, primarily in the cervical and lumbar intumescences, with marked neuronal loss, neuronal chromatolysis, status spongiosus, microcavitation, and in more chronic cases, endothelial and glial proliferation, astrocytosis, and accumulation of gitter cells
• Wallerian degeneration in the ventral spinal nerve rootlets adjacent to affected areas
• Identical lesions can occur in the brainstem

 

ULTRASTRUCTURAL FINDINGS:

 

ADDITIONAL DIAGNOSTIC TESTS:  

• Diagnosis requires demonstration of clinical signs + identification of a dietary source of selenium with a concentration of >5 ppm selenium in the feed sample
• Chemical analysis of tissues (ie, hair) 

 

DIFFERENTIAL DIAGNOSIS:

• Laminitis, swelling of coronary band, and sloughed hooves: Frostbite, ergotism, fescue toxicosis  
• Alopecia: Thallium toxicosis (I-T01)
• Staggering gait (clinical localization to spinal cord lesion without intracranial involvement): Rabies (N-V06, relatively uncommon in swine)

 

COMPARATIVE PATHOLOGY:  

Selenium toxicosis in other animals:

• Cattle: Myocardial necrosis; sloughed hooves; cirrhotic liver; alopecia and follicular atrophy on the base of tail; emaciation; roughness of coat; focal symmetric poliomyelomalacia of the ventral horns, limited to the sacral and lumbar enlargements in Ayrshire calves
• Horses: Laminitis; deformed and/or sloughed hooves; loss of long hair from mane; alopecia and follicular atrophy on the base of tail (“bobtail disease"); emaciation; roughness of coat
• Sheep: Sudden death, myocardial necrosis, pulmonary edema and hemorrhage (due to vasculitis of alveolar septa); sloughed hooves; inapparent cutaneous lesions 
• Goats: Alopecia of beard and flanks in the western United States
• Wild birds and poultry: Severe lymphocytic depletion and lymphocytolysis of the bursa of Fabricius; congenital long-bone deformities
• Aquatic birds: Accumulates in food chain leading to emaciation, cardiac flaccidity, ascites, limb deformities, brachygnathia, fluid accumulation in skull, feather and claw abnormalities, and embryonic death
• Rainbow trout:  Selenium toxicity can induce nephrocalcinosis
• Yellow-bellied slider turtles (experimentally induced): Kidneys- acute tubular degeneration and regeneration; claws- epidermal hyperplasia with disorganization and intercellular edema to ulceration, and accumulation of seroheterophilic exudate between epidermis and cornified layer (Haskins, Vet Pathol, 2018)

 

References:  

1. Cantile C, Youssef S. Nervous system. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 1. 6^th ed. Philadelphia, PA: Elsevier Ltd; 2016:308.
2. Caswell JL, Williams KJ. Respiratory System. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 2. 6^th ed. Philadelphia, PA: Elsevier Ltd; 2016:520.
3. Fenton H, McManamon R, Howerth EW. Anseriformes, ciconiiformes, charadriiformes, and gruiformes. In:   Terio, KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Academic Press Elsevier; 2018:705, 717.e3.
4. Frasca Jr. S, Wolf JC, et al. Osteichthyes. In:  Terio, KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Academic Press Elsevier; 2018:955.
5. Haskins DL, Howerth EW, Tuberville TD. Experimentally Induced Selenosis in Yellow-Bellied Slider Turtles (Trachemys scripta scripta). Vet Pathol. 2018; 55(3): 473-477.
6. Mauldin EA, Peters-Kennedy J. Integumentary System. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 1. 6^th ed. Philadelphia, PA: Elsevier Ltd; 2016:570-571.
7. Miller AD, Porter BF. Nervous system. In: Zachary JF,ed. Pathologic Basis of Veterinary Disease. 7th ed.  St. Louis, MO: Elsevier; 2022:938.
8. Schmidt RE, Reavill DR, Phalen DN. Pathology of Pet and Aviary Birds. 2^nd ed. Ames, IA: John Wiley & Sons; 2015: 181, 207.
9. Welle MM, Linder KE. The Integument. In: Zachary JF,ed. Pathologic Basis of Veterinary Disease. 7th ed.  St. Louis, MO: Elsevier; 2022:1159.

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