title: Acute paretic syndrome in juvenile White Leghorn chickens resembles late stages of acute inflammatory demyelinating polyneuropathies in humans.
abstract: BACKGROUND
  Sudden limb paresis is a common problem in White Leghorn flocks, affecting about 1% of the chicken population before achievement of sexual maturity. Previously, a similar clinical syndrome has been reported as being caused by inflammatory demyelination of peripheral nerve fibres. Here, we investigated in detail the immunopathology of this paretic syndrome and its possible resemblance to human neuropathies.
  
  
  METHODS
  Neurologically affected chickens and control animals from one single flock underwent clinical and neuropathological examination. Peripheral nervous system (PNS) alterations were characterised using standard morphological techniques, including nerve fibre teasing and transmission electron microscopy. Infiltrating cells were phenotyped immunohistologically and quantified by flow cytometry. The cytokine expression pattern was assessed by quantitative real-time PCR (qRT-PCR). These investigations were accomplished by MHC genotyping and a PCR screen for Marek's disease virus (MDV).
  
  
  RESULTS
  Spontaneous paresis of White Leghorns is caused by cell-mediated, inflammatory demyelination affecting multiple cranial and spinal nerves and nerve roots with a proximodistal tapering. Clinical manifestation coincides with the employment of humoral immune mechanisms, enrolling plasma cell recruitment, deposition of myelin-bound IgG and antibody-dependent macrophageal myelin-stripping. Disease development was significantly linked to a 539 bp microsatellite in MHC locus LEI0258. An aetiological role for MDV was excluded.
  
  
  CONCLUSIONS
  The paretic phase of avian inflammatory demyelinating polyradiculoneuritis immunobiologically resembles the late-acute disease stages of human acute inflammatory demyelinating polyneuropathy, and is characterised by a Th1-to-Th2 shift.
authors.affiliation: Chair of General Pathology & Neuropathology, Institute of Veterinary Pathology, Ludwig-Maximilians-University, Munich, Germany.
authors.forename: Sophie R
authors.initials: SR
authors.lastname: Bader
authors.forename: Sonja
authors.initials: S
authors.lastname: Kothlow
authors.forename: Sascha
authors.initials: S
authors.lastname: Trapp
authors.forename: Susanne Cn
authors.initials: SC
authors.lastname: Schwarz
authors.forename: Hans-Christian
authors.initials: HC
authors.lastname: Philipp
authors.forename: Steffen
authors.initials: S
authors.lastname: Weigend
authors.forename: Ahmad R
authors.initials: AR
authors.lastname: Sharifi
authors.forename: Rudolf
authors.initials: R
authors.lastname: Preisinger
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schmahl
authors.forename: Bernd
authors.initials: B
authors.lastname: Kaspers
authors.forename: Kaspar
authors.initials: K
authors.lastname: Matiasek
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D002645:Chickens; D004195:Disease Models, Animal; D005260:Female; D005434:Flow Cytometry; D005727:Ganglia, Spinal / Q000473:pathology / Q000648:ultrastructure; D005838:Genotype; D020275:Guillain-Barre Syndrome / Q000473:pathology* / Q000503:physiopathology* / Q000662:veterinary* / Q000821:virology; D006801:Humans; D016015:Logistic Models; D008285:Major Histocompatibility Complex / Q000235:genetics; D046529:Microscopy, Electron, Transmission / Q000379:methods; D009494:Neurosyphilis; D037121:Plant Lectins; D013116:Spinal Cord / Q000473:pathology / Q000648:ultrastructure; D013127:Spinal Nerves / Q000473:pathology / Q000648:ultrastructure; D014759:Viral Envelope Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D037121:Plant Lectins; C017707:Ricinus communis agglutinin-1; D014759:Viral Envelope Proteins