Update On Guillain-Barre Syndrome-Like Conditions In Animals

Abstract Disease conditions, including Coonhound paralysis,acute canine polyradiculoneuropathy (ACP), andcauda equina neuritis do occur in animals naturallyfrom time to time. The experimental induction ofparalysis in chickens with certain strains ofCampylobacter jejuni, and the recent observation ofToxoplasma-induced ACP raise the possibility thatperipheral nerve disease via immunologicmechanisms, induced by microorganisms, may occurin animals naturally. Experimental studies haveindicated that antigens responsible for production ofcross-reacting antibodies that cause neurologicalinjury may be present in unrelated bacterial pathogenssuch as C. jejuni and Brucella melitensis. Furtherstudies are required to determine if antibodies againstC. jejuni can damage human neural cells includingoligodnendroglial cells, the cell type responsible formyelin production in the central nervous system. Introduction Guillain-Barre syndrome (GBS) is an acute disease ofthe peripheral nervous system of humans,characterized by ascending paralysis, conductionblock with segmental demyelination of the nerves,macrophage and lymphocytic infiltration of the nerves,and elevated protein with no cells or very few cells inthe cerebrospinal fluid (Constantinescu et al. 1998). Descriptive accounts on GBS, including history,clinical, pathological, and epidemiological aspects aregiven by Hughes (1990), Ropper et al. (1991), andHughes et al. (1997). If full credit were to be given tothose clinicians who first recognized and describedthis paralytic disorder, then its name might properly beLandry-Guillain-Barre-Strohl syndrome (Steinberg1995). The diagnostic criteria for this idiopathicneuropathy have been outlined by Asbury et al (1978,1981, 1990), and these include more or lesssymmetrical paresis, and a loss of myotatic reflexes(Van der Meche et al. 1997). These symptoms may becaused by inflammatory demyelination, axonaldegeneration, or both (Hughes and Rees 1997). Motor,sensory and autonomic nerves supplying the limbs areaffected invariably, but respiratory muscles, facial,bulbar, and ocular motor nerves may be involved(Hughes and Rees 1997). GBS has been shown to beassociated with viral or bacterial infections, includingCampylobacter jejuni (Kaldor and Speed 1984,Hariharan et al 1996), Borrelia burgdorferi (Sigal andTatum 1988), Brucella melitensis (Namiduru et al.2003), or infection with the protozoan parasite,Toxoplasma gondii (Pascual et al. 1984, Bossi et al.1998), or following vaccinations, including rabies(Hemachudha et al 1988) and swine influenza(Langmuir et al 1984), or surgical procedures(Aranson and Asbury 1968). The present review is an attempt to update the onepublished 12 years ago by Hariharan et al. (1999) onnatural and experimental animal models of GBS, andincludes recent findings, including possible role ofToxoplasma gondii and Brucella melitensis in causingimmunologically mediated nerve injury in animals.Natural animal modelsSome naturally occurring animal diseases with varyingdegrees of resemblance to GBS have helped tounderstand immmunopathology and other aspects ofhuman disease. Coonhound paralysis (CHP), firstdescribed in 1954 is a neurological condition of dogsthat resembles GBS of humans, and it occurs incoonhounds in 1-2 weeks following a raccoon bite orscratch (Kingma and Catcott 1954). It was identifiedpathologically as acute canine polyradiculoneuritis byCummings and Haas (1967, 1972), who described theclinical and pathological features. The initial symptomsare weakness and hyporeflexia in the hind limbs.Paralysis progresses rapidly, resulting in flaccidsymmetric quadriplegia. The affected animals remainafebrile, and at the peak of their illness, there may becomplete absence of spinal reflexes, facial weaknessand labored respiration. Electromyographic findingsinclude evidence of denervation. Deaths haveoccurred due to respiratory failure. As in the case ofGBS, CHP is characterized by motor conduction delayand CSF albuminocytologic dissociation in affecteddogs. Affected roots and nerves containedmononuclear cell infiltrates, segmental myelin changesand axon degeneration. However, axon damage is amore consistent finding in CHP than in GBS(Cummings et al 1982). Idiopathic acute polyradiculoneuropathy (ACP) is themost commonly recognized peripheral neuropathy indogs, and it closely resembles the acute axonal or