Coonhound Paralysis (CHP) and Acute Idiopathic Canine Polyradiculoneuritis (AICP) are the most common causes of acquired polyneuropathy in dogs. These are the canine equivalent of Guillain-Barré Syndrome (GBS) in humans. This neuropathy has been frequently associated with dogs that hunt raccoons, thus the colloquial name of Coonhound Paralysis. Contact with raccoon saliva appears to have an etiologic role in the development of polyneuropathy. The disorder is most commonly reported in North America, as well as Central and parts of South America and other countries around the world with an indigenous population of raccoons. AICP is an identical disorder reported in dogs with no exposure to raccoons, including countries with no indigenous raccoon population.
AICP and CHP are inflammatory disorders that primarily affect the ventral nerve roots and to a much lesser extent the dorsal nerve roots. The lumbar and sacral nerve roots are often more affected than the thoracic and cervical nerve roots. Histologic analysis typically demonstrates axonal degeneration, paranodal and segmental demyelination, and infiltration of inflammatory cells. Early in the course of the disease, neutrophils predominate, but lymphocytes, plasma cells, and macrophages become more common with chronic disease.
The inciting cause of AICP is unknown, but theories include recent illness or vaccination, immune-mediated disease, and viral infection. In human GBS, Campylobacter infection is considered one of the major triggers and has been reported in up to 40% of GBS patients. One study conducted in Australia recently identified an association between AICP and Campylobacter spp. infection in dogs that were fed raw chicken as part of their diet. Other infectious agents associated with GBS include Haemophilus influenza, Mycloplasma pneumoniae, Epstein-Barr virus, cytomegalovirus, Borrelia burgdorferi, Toxoplasma gondii, and Zika virus. GBS has also been reported following vaccination again rabies and swine influenza.
Young adult Coonhound and hunting dogs are at the highest risk of Coonhound Paralysis, but dogs of any age/breed can be affected by either disorder.
Clinical signs usually begin 1-2 weeks after exposure to the inciting trigger and can progress for up to 4-5 days after onset. In both diseases, the history typically reflects a sudden onset of pelvic limb weakness that rapidly progresses to nonambulatory tetraparesis within 48–72 hours.
Golden Retriever puppy with acute idiopathic polyradiculoneuritis.
Neurologic examination reveals typical LMN signs as described above in the affected limbs with flaccid tetraparesis or tetraplegia, decreased to absent reflexes, and decreased to absent withdrawal. Dysphonia is common and some patients have facial weakness. Urinary and anal sphincter tone usually remain normal, so these patients typically do not become incontinent. Sensory function remains intact in the limbs; some patients appear hyperesthetic when the limbs are manipulated. Postural reactions may be normal if sufficient muscle strength remains, but they often are absent.
A presumptive diagnosis can be made via a combination of history, potential exposure to raccoons or other potentially inciting triggers, and neurologic exam findings.
Electrodiagnostics can help differentiate this disease from other causes of acute, rapidly ascending lower motor neuron paresis (e.g., Tick Paralysis, botulism, acute fulminating myasthenia gravis). Electromyography (EMG) may reveal spontaneous electrical activity, especially after day 4 of disease. Decreased compound muscle action potential (CMAP) amplitude may be recorded on motor nerve conduction studies. Measurement of the F wave, which measures transmission through the ventral roots, is usually abnormal. The F-wave latency may be prolonged or absent, the F-wave amplitude may be decreased, and there may be increased F ratios.
Lumbar cerebrospinal fluid (CSF) analysis often demonstrates albuminocytologic dissociation (elevated protein content with normal white blood cell count). It’s possible that the increased protein content is likely due to a breakdown of the blood-nerve barrier in the proximal nerve roots that are still surrounded by the subarachnoid space. The protein level is normal in CSF collected from the cisterna magna.
An ELISA test using pooled raccoon saliva (1:2000 dilution) has demonstrated high sensitivity and specificity for detecting circulating antibodies to raccoon saliva in dogs with CHP, but the test is not commercially available. Dogs with ACP without exposure to raccoons do not have circulating antibodies to raccoon saliva and the ELISA test is negative.
There is no specific treatment for this condition other than time, nursing care (e.g., hydration, nutritional support, prevention of pressure sores) and intense physical therapy. It is very important to monitor the patient’s respiratory status, especially during the progressive stage of disease (first 4-5 days) as some patients develop severe, potentially life-threatening, respiratory muscle weakness due to the involvement of the phrenic and intercostal nerves. These patients may need to be mechanically ventilated. Most dogs are still able to voluntarily urinate, but catheterization can be considered to maintain hygiene.
Glucocorticoids have not been shown to shorten the duration of disease or improve the degree of recovery so they are not routinely used in this condition. At higher doses, glucocorticoids cause neuromuscular weakness, which can exacerbate the patient’s weakness and make it difficult to assess the patient’s degree of recovery.
Treatment with human intravenous immunoglobulin (IVIg) and plasmapheresis has been shown to speed recovery in human patients with GBS. IVIg has been reported to shorten the duration of clinical signs in dogs, but it can be difficult to obtain and may be cost prohibitive. Plasmapheresis is only available at a limited number of veterinary specialty hospitals and universities.
The prognosis for most patients is good to excellent as long as the patient does not experience respiratory impairment requiring mechanical ventilation. However, recovery may take several weeks to months (up to 4-6 months). Patients that require mechanical ventilation still have a fair to good prognosis barring development of aspiration pneumonia, but prolonged ventilation may be required.
After recovery, avoid exposure to raccoons or other factors that may have triggered the clinical signs as survival does not confer immunity. This author treated the same German Shepherd for CHP on three separate occasions. The dog was a guard dog at a junkyard and would frequently encounter raccoons “on the job.” The dog’s owner refused to keep the dog inside and the dog developed respiratory paralysis during the third incident and was euthanized.
- Baker M, Kvalsvig A, Zhanget J, et al. Declining Guillain-Barre syndrome after campylobacteriosis control, New-Zealand, 1988–2010. Emerg Infect Dis 2012;18:226-33.
- Bossi P, Caumes E, Paris L, et al. Toxoplasma gondii-associated Guillain-Barre syndrome in an immunocompetent patient. J Clin Microbiol 1998;36:3724-5.
- Cao-Lormeau VM, Blake A, Mons S, et al. Guillain-Barre syndrome outbreak associated with Zika virus infection in French Polynesia: A case-control study. Lancet 2016;387:1531–9.
- Cuddon P. Acquired canine peripheral neuropathies. Vet Clin N Am 2002;32:207-49.
- Cuddon PA. Electrophysiological and immunological evaluation in coonhound paralysis. Proc Am Coll Vet Intern Med 1990;8:1009-12.
- Cummings JF, deLahunta A, Holmes DF, et al. Coonhound paralysis: further clinical studies and electron microscopic observations. Acta Neuropathol (Berl) 1982;56:167-78.
- Cummings JF, Haas DC. Coonhound paralysis, an acute idiopathic polyradiculoneuritis in dogs resembling the Landry-Guillain-Barre syndrome. J Neurol Sci 1967;4:51-81.
- Cummings JF, Haas DC. Idiopathic polyneuritis. Animal model: coonhound paralysis, idiopathic polyradiculoneuritis of coonhounds. Am J Pathol 1972;66:189-92.
- Fischer A, Steinberg TA, Jurina K, et al: Observational investigation of the clinical course of polyradiculitis after treatment with human intravenous immunoglobulins. Proc Am Coll Vet Intern Med
- Gehring R, Eggars B: Suspected post-vaccinal acute polyradiculoneuritis in a puppy. J S Afr Vet Assoc 2001;72:96.
- Hemachudha T, Griffin DE, Chen WW, et al. Immunologic studies of rabies vaccination-induced Guillain-Barre syndrome. Neurology 1988;38:375–8.
- Holmes DF, Schultz RD, Cummings JF, et al: Experimental coonhound paralysis: Animal model of Guillain-Barré syndrome. Neurology 1979;29:1186-7.
- Holt N, Murray M, Cuddon PA, et al: Seroprevalence of various infectious agents in dogs with suspected acute canine polyradiculoneuritis. J Vet Intern Med 2011;25:261-6.
- Jacobs BC, Rothbarth PH, van der Meche FG, et al. The spectrum of antecedent infections in Guillain-Barre syndrome: A case-control study. Neurology 1998;51:1110–5.
- Kusunoki S, Chiba A, Hitoshi S, et al. Anti-Gal-C antibody in autoimmune neuropathies subsequent to mycoplasma infection. Muscle Nerve 1995;18:409–13.
- Langmuir AD, Bregman DJ, Kurland LT, et al. An epidemiologic and clinical evaluation of Guillain-Barre syndrome reported in association with the administration of swine influenza vaccines. Am J Epidemiol 1984;119:841–79.
- Lastovica AJ, Goddard EA, Argent AC. Guillain-Barre syndrome in South Africa associated with Campylobacter jejuni O: 41 strains. J Infect Dis 1997;176:139–43.
- Mancardi GL, Del Sette M, Primavera A, et al. Borrelia burgdorferi and Guillain-Barre syndrome. Lancet 1989;2:985-6.
- Mishu B, Blaser MJ. Role of Campylobacter jejuni in the initiation of Guillain-Barre syndrome. Clin Infect Dis 1993;17:104-8.
- Mori M, Kuwabara S, Miyake M, et al. Haemophilus infection and Guillain-Barre syndrome. Brain 2000;123:2171-8.
- Nyati KK, Nyati R. Role of Campylobacter jejuni infection in the pathogenesis of Guillain-Barre syndrome: An update. Biomed Res Int 2013;2013:852195.
- Prasad KN, Pradhan S, Nag VL. Guillain-Barre syndrome and Campylobacter infection. Southeast Asian J Trop Med Public Health 2001;32:3.
- Rupp A, Galban-Horcajo F, Bianchi E, et al. Anti-GM2 ganglioside antibodies are a biomarker for acute canine polyradiculoneuritis. J Peripher Nerv Syst 2013;18:75-88.
- Schrauwen E, Van Ham L. Postvaccinal acute polyradiculoneuritis in a young dog. Prog Vet Neurol 1995;6:68-70.
- Tremblay ME, Closon A, D’Anjou G, et al. Guillain-Barre syndrome following H1N1 immunization in a pediatric patient. Ann Pharmacother 2010;44:1330-3.
- Visser LH, van der Meche FG, Meulstee J, et al. Cytomegalovirus infection and Guillain-Barre syndrome: The clinical, electrophysiologic, and prognostic features. Dutch Guillain-Barre Study Group. Neurology 1996;47:668-73.
Last updated: February 3, 2019
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