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I p ulled this out of my vet book for you
Carol
Coonhound Paralysis -
Coonhound paralysis (CHP) is a sporadically-occurring neurological disease of dogs, occurring especially in raccoon-hunting breeds. The pathogenesis is unknown. A raccoon bite has been a consistent antecedent in CHP. The condition has been reproduced experimentally by injection of raccoon saliva into a dog that had recovered from two earlier spontaneous attacks. Results of this work suggested that raccoon saliva contains the etiologic factor for CHP and that only specifically susceptible dogs are at risk of developing CHP when exposed to this factor.
Interest has focused on CHP due to its resemblance to Guillain-Barre syndrome (GBS) in people and its potential as an elucidating model. Like the human syndrome, CHP may have an immunological pathogenesis, although results of one study of CHP did not conform with the evidence presented in GBS for an obligatory role of macrophages in initiating myelin damage. However, the observed changes do resemble those reported in immunological-mediated experimental allergic neuritis.
Pathological findings are associated with a polyradiculoneuritis, with both segmental demyelination and concurrent degeneration of myelin and axons. Leukocytic infiltration, consisting mostly of cells of the monocyte-macrophage series, and scattered aggregates of lymphocytes and plasma cells also are observed. Changes occur in peripheral nerves and nerve roots, especially in the latter and more consistently in ventral roots than dorsal roots. In one comprehensive study, lumbosacral roots and spinal nerves were more involved than thoracic and cervical roots and spinal nerves. Neutrophils may be present early in severely affected dogs. Chromatolytic changes in spinal motoneurons may occur secondary to severe axonal degeneration in peripheral nerves and nerve roots.
The disease affects dogs of any breed, both sexes, and usually of adult age. Clinical signs frequently appear 7 to 11 days after an encounter with a raccoon. Onset is marked by weakness and pelvic limb hyporeflexia, although thoracic limb involvement may sometimes be the initial and dominant clinical sign. Paralysis progresses rapidly, resulting in a flaccid symmetric tetraplegia; however, milder forms without paralysis can occur. The duration of paralysis varies from several weeks to 2 or 3 months. Motor impairment is more pronounced than sensory changes, although many dogs appear to be hyperesthetic to sensory stimuli. Bladder and rectal paralysis are not usually observed. In severely affected animals, there may be complete absence of spinal reflexes, facial weakness, loss of voice, inability to lift the head, and labored respiration. Motor nerve conduction velocities may be markedly reduced and EMG studies reveal widespread denervation 6 to 7 days after the onset. F-waves can be altered (e.g., prolonged F-wave latencies and F-wave dispersion, decreased F-wave amplitudes), depending on the clinical signs and duration of disease. In addition, increased F-ratios, and decreased CMAPs may be helpful EDX features. Note that in some cases, the EDX changes appear to have a distal distribution. Similar findings occur in people with GBS and it has been explained by the preferential involvement of longer nerves associated with their greater chance of being affected by a multifocal demyelinating process. Elevated protein with normal cell counts in CSF has been reported, especially in samples obtained from lumbar puncture. This protein is predominantly albumin and its origin is thought to be more consistent with protein transudation rather than intrathecal immunoglobulin production. Presence of circulating antibodies against raccoon saliva has been demonstrated using ELISA assays.
Prognosis is usually favorable, but dogs with severe axonal degeneration may die from respiratory paralysis or may have protracted, incomplete recoveries, and some animals may not show any clinical improvement. Protection from future attacks is short-lived or nonexistent. Affected dogs may have a greater chance of redeveloping paralysis on subsequent encounters with raccoons. Treatment is symptomatic. Corticosteroids in our experience have not been effective in expediting recovery. Good nursing care is essential, including physiotherapeutic rehabilitation.
In people, GBS (or acute inflammatory demyelinating polyradiculoneuropathy) appears to be an autoimmune disease, involving both cell-mediated and humoral factors (e.g., IgG and IgM antibodies) resulting from aberrant immune responses against various components of peripheral nerve fibers (the myelin sheath is the specific target structure) and is characterized by presence of inflammatory lesions (lymphocytes and macrophages) and localized demyelination throughout the PNS. Axonal lesions also occur but are usually less severe than the demyelinating lesions. However, two forms of axonal-GBS are recognized: acute motor-sensory axonal neuropathy and acute motor axonal neuropathy. Some forms of GBS appear to be related to Campylobacter jejuni infection (especially the axonal forms), while other antecedent events (or "triggers") include viral and spirochete infection, surgery, and vaccination (including some strains of rabies). While the existence of a primary axonal neuropathy in a small percentage of human patients having a poor prognosis has been reported, we found that the intensity and type of lesion in 13 GBS patients with severe clinical disease (all bed-ridden in an intensive care unit and most requiring assisted ventilation) had no predictive value for eventual clinical recovery, but was correlated with length of clinical course (axonal lesions dominated in 23% of patients, while axonal lesions in presence of the more classical demyelinating form of GBS was seen in a further 23% of patients). In people, supportive care is the cornerstone of treatment as the majority of patients recover once the acute stage is passed, while specific treatment includes plasmapheresis and intravenous immunoglobulins. Corticosteroids are usually ineffective.
Idiopathic Polyradiculoneuritis -
A condition that appears to be identical to Coonhound paralysis with respect to onset, clinical signs, clinical course, EDX findings, and pathology occurs in dogs that have had no possible exposure to raccoons. This condition has a world-wide distribution, occurs in countries where raccoon do not exist and may have an incidence much higher than the literature suggests. Mature dogs are typically affected; however, a suspected polyradiculoneuritis has also been reported in a 14 week old Rottweiler puppy in the UK. Note that mild forms of polyradiculoneuritis may occur in dogs in which flaccid paralysis does not develop fully in any muscle group and animals maintain ambulatory function. As with Coonhound paralysis, some dogs with idiopathic polyradiculoneuritis may require ventilatory support. In my experience, pathological findings in peripheral nerve biopsy samples (e.g., common peroneal nerve) reflect the clinical course of idiopathic polyradiculoneuritis: minimal changes are seen within the first 7 to 10 days of clinical signs. In chronic cases, the incidence of changes increases, usually reflecting a mixture of axonal degeneration, demyelination, and remyelination.
Idiopathic polyradiculoneuritis is clinically, but not pathologically, similar to distal denervating disease, reportedly the most common canine polyneuropathy in the UK. In a recent study examining the relationship between acute polyradiculoneuritis and prior infection or exposure to various infectious agents, affected dogs had significantly higher serum IgG titers against Toxoplasma gondii than controls, although a causal relationship was not established.
Despite the clinical prevalence of polyradiculoneuritis, demonstration of inflammatory cell infiltrates in peripheral nerve biopsies (e.g., common peroneal nerve or tibial nerve sampled at the level of the stifle) seems to be very uncommon, as least in my experience. Undoubtedly, inflammation would be more frequently observed in nerve root biopsy samples.
Cauda Equina Polyradiculoneuritis -
A polyradiculoneuritis has been reported in two dogs - a 9 year old female Labrador Retriever and an 8 month old female Yorkshire Terrier - that were presented with a lumbosacral syndrome (pelvic limb paraparesis, muscle hypotonia and atrophy, loss of patellar reflexes, and proprioceptive loss). Pain sensation, bladder function, and anal reflex were intact. Motor nerve conduction velocity was decreased in the sciatic-tibial nerves. Latency of F-waves was markedly increased following stimulation at the level of the greater trochanter and at the hock. Pathologically, lesions in both dogs were located in the lumbosacral nerve roots that comprise the cauda equina. Dorsal and ventral nerve roots, as well as dorsal root ganglia were involved. There was marked interstitial and perivascular infiltration of mononuclear cells (lymphocytes, plasma cells, and macrophages), axonal degeneration, demyelination, and remyelinating clusters. Milder changes were seen in nerve roots throughout the spinal cord, as well as in roots of the trigeminal nerve. Muscle changes reflected neurogenic atrophy. Intraneural injection of serum from an affected dog failed to induce demyelination in normal rat nerve. Serum levels of the myelin-specific protein, P2, were not elevated in either dog. Protein level in CSF was increased in one dog.
Chronic Inflammatory Demyelinating Polyneuropathy -
Over the past several years, we have accumulated data on a spontaneous demyelinating peripheral neuropathy that we have called chronic inflammatory demyelinating polyneuropathy (CIDP). Based on surveys of biopsies received from the Scott-Ritchey neuromuscular laboratory at Auburn University and from my private peripheral nerve laboratory, CIDP is one of the more common neuropathies seen in dogs and cats. This disorder occurs in dogs and cats of either gender and does not appear breed-related. Mature animals of any age may be affected (from 1 to 14 years). Onset of signs is usually insidious and the course is typically chronic, often relapsing, and frequently slowly progressive. Clinical signs are usually first noticed in the pelvic limbs and, in most animals, progress to involve the thoracic limbs. Clinical signs include tetraparesis, sometimes progressing to tetraplegia, stumbling gait, and hyporeflexia. Less commonly observed signs are muscle trembling (dogs), intermittent shifting limb lameness characterized by a plantigrade stance (cat), and ventroflexion of the head and neck (cat). Facial nerve paralysis or laryngeal paralysis are seen occasionally in dogs, while megaesophagus/regurgitation is found in some cats. Serological testing is normal, although one cat had an IgG monoclonal gammopathy. CSF analysis is usually normal, although occasional animals may show a moderate protein increase. Motor nerve conduction velocities (NCVs) are decreased, along with temporal dispersion, decreased amplitudes and prolonged latencies of the compound muscle action potentials. Slow sensory NCVs have also been noted. EMG studies in this report were either normal or revealed mild, patchy pattern of fibrillation potentials and positive sharp waves. Pathologically, changes in teased single fibers from peripheral nerves are dominated by multifocal paranodal demyelination, and sometimes segmental demyelination. Other changes include remyelination and variable numbers of fibers with internodal globules. Axonal degeneration is infrequently observed. Scattered, thinly myelinated fibers are seen on semithin sections. Severe changes may include presence of onion-bulbs and rarefaction of myelinated fibers. Ultrastructural studies reveal macrophages within myelinated fibers stripping the myelin sheaths, naked and remyelinating axons, and focal/multifocal endoneurial mononuclear cells, including lymphocytes, rare plasma cells, macrophages with myelin debris, and vacuolated fibroblasts. Indirect immunofluorescence revealed positive IgG staining in peripheral nerve myelin sheaths from two dogs. No fluorescence was seen using anti-dog or anti-cat C3 (positive immunofluorescence to anti-human IgM and C3d was observed in control dog and cat nerve sections incubated with serum from a human patient with an IgM monoclonal gammopathy). In skeletal muscle, minimal lesions are seen , apart from mild fiber size variation in some cases. Diagnosis is based on clinical signs, relapsing clinical history, and nerve biopsy studies. Prognosis is often favorable with treatment. The majority of dogs and cats (approximately 90%) were initially steroid-responsive (e.g., prednisolone at 1 - 2 mg/kg PO bid for at least a week followed by alternate day, reduced dosage for several weeks or several months), with many animals showing a return to normalcy following treatment. In some cases, the response to steroids is incomplete. Signs may relapse when treatment ceases (requiring addition treatment cycles) or upon reduction of the dose of steroids. Uncommonly, some animals with relapsing signs that are steroid-responsive may become steroid-resistant and deteriorate clinically.
The course of the disease, clinical signs, electrophysiology, and pathology have similarities to chronic inflammatory demyelinating polyneuropathy in people in whom weakness has a proximal distribution. Most human patients with CIDP respond to corticosteroids and other immunosuppressive agents (e.g., azathioprine and cyclophosphamide), plasma exchange, and intravenous immunoglobulin (therapies aimed at treating immune-mediated disorders).
Sporadic case reports of chronic relapsing polyradiculoneuritis in a dog and a cat, chronic relapsing polyneuropathy in a cat, and prednisolone-responsive neuropathy in a cat, also appear very similar to CIDP.
Infectious Polyradiculoneuritis -
A severe polyradiculoneuritis and/or polymyositis associated with either Toxoplasma gondii or Neospora caninum occurs commonly in dogs, especially those less than one year of age (see toxoplasmosis). In one dog with diskospondylitis due to Aspergillus terreus, multiple granulomas with fungal elements were found in the subarachnoid space associated with the nerve roots of the cauda equina.
Postvaccinal Polyradiculoneuritis
Post-vaccinal polyradiculoneuritis (e.g., multivalent vaccine, inactivated rabies vaccine) has been reported only sporadically in dogs with signs and clinical course similar to those in dogs with Coonhound paralysis. The condition, also known as postvaccinal inflammatory neuropathy (IPN), occurs rarely in people and is believed to be an autoimmune reaction triggered by the vaccine against some myelin, axonal or neuronal component.
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