JPC SYSTEMIC PATHOLOGY

NERVOUS SYSTEM

January 2023

N-M20 (NP)

 

SIGNALMENT (JPC #1491862): Unknown age and gender coonhound   

 

HISTORY: This animal was used frequently for hunting raccoons. The onset of illness was marked by weakness and hyperreflexia in the hind limbs. Paralysis progressed rapidly and resulted in flaccid symmetric quadriplegia. The animal died of respiratory failure.

 

HISTOPATHOLOGIC DESCRIPTION: Peripheral nerve: Multifocally, myelin sheaths are segmentally dilated up to 30 µm in diameter and contain either swollen axons (spheroids) or pale, eosinophilic, fibrillar debris and few foamy macrophages (digestion chambers/Wallerian degeneration). Multifocally separating nerve fibers are predominantly perivascular inflammatory infiltrates composed of few lymphocytes, plasma cells, fewer macrophages, and rare neutrophils.   

 

MORPHOLOGIC DIAGNOSIS: Peripheral nerve: Neuritis, lymphoplasmacytic, subacute, multifocal, moderate, with mild Wallerian degeneration, coonhound, canine.

 

ETIOLOGIC DIAGNOSIS: Idiopathic neuritis and axonal degeneration

 

CONDITION: Acute idiopathic polyradiculoneuritis

 

SYNONYM: Coonhound paralysis (CHP), acute canine polyradiculoneuritis (ACP)

 

GENERAL DISCUSSION: 

• The most common inflammatory condition of peripheral nerves in dogs; occurs less commonly in cats and rarely horses
• Rare sporadic inflammatory condition of spinal nerve roots and peripheral nerves
• Historically associated with raccoon bites and scratches; may occur without history of exposure

• Likely multiple other etiologies including vaccination, trauma, toxins

• Most commonly hunting hounds:  Black and tan, blue tick, walker, redbone
• Both sensory and motor nerves can be involved

 

PATHOGENESIS:

• Unknown pathogenesis; immune-mediated disorder affecting myelin, axons, or both 
• Experimentally reproduced following inoculation of pooled raccoon saliva into a dog; no agent isolated
• Anti-GM₂ ganglioside antibodies have been found in affected dogs (similar to Guillain-Barré syndrome in humans) 
• Recovered dogs may be more susceptible; certain hounds may be predisposed

 

TYPICAL CLINICAL FINDINGS:

• Signs typically occur 7-10 days post exposure
• Hyperethesia and ascending hindlimb weakness that progresses to flaccid symmetric tetraplegia/tetraparesis; rapid atrophy of muscle that may last from weeks to months
• Dysphonia, facial weakness, labored respirations 
• No cerebral signs
• Most dogs recover; some may die due to respiratory paralysis
• Recovery may be delayed with residual muscular atrophy

 

TYPICAL GROSS FINDINGS:

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Affects primarily ventral roots of spinal nerves and peripheral nerves
• Lymphocytes, plasma cells, and histiocytes infiltrate nerves/perivascular tissue
• Segmental primary demyelination and Wallerian degeneration, retrograde chromatolysis
• Axonal degeneration is variable
• Schwann cell proliferation and remyelination occur with Büngner’s bands and axonal sprouting during recovery

 

ULTRASTRUCTURAL FINDINGS:

 

ADDITIONAL DIAGNOSTIC TESTS:

• Electrodiagnostics suggest motor denervation
• CSF: May have mildly increased protein

 

DIFFERENTIAL DIAGNOSIS:

Histologic differentials:  

Clinical differentials: 

• Botulism (type C neurotoxin)
• Tick paralysis (neurotoxin secreted by female Dermacentor spp.; interferes with ACH release)
• Infectious polyradiculoneuritis (Toxoplasma gondii, Neospora caninum)

 

COMPARATIVE PATHOLOGY:

• Humans: Guillain-Barré syndrome (GBS, acute ascending inflammatory paralysis)

• Thought to be due to autoantibodies to peripheral nerve protein
• Can be induced by infectious agents (e.g. Campylobacter jejuni, Coxsackie B virus, cytomegalovirus, Epstein-Barr virus, Mycoplasma spp, vaccinations i.e. Influenza A)

• Equine: Cauda equina neuritis (N-M18); idiopathic granulomatous inflammation
• Rats: Experimental auto-immune (formerly allergic) neuritis (EAN) via inoculation with peripheral nerve proteins emulsified with adjuvant is used as an animal model for human GBS (Tomikawa, Tox Pathol. 2019)

 

REFERENCES:

1. Cantile C, Youssef S. The nervous system. In: Maxie MG ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed.  Philadelphia, PA: Saunders; 2016:394.
2. Miller AD, Porter, BF. Nervous System. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:991.
3. Tomikawa E, Mutsuga M, Hara K, Kaneko C, Togashi Y, Miyamoto Y. Time Course of Axon and Myelin Degeneration in Peripheral Nerves in Experimental Autoimmune Neuritis Rats. Tox Pathol. 2019;47(4):542-552.
4. Valentine BA. Skeletal Muscle. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:1034-5.

 

 

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