Research
Acute paretic syndrome in juvenile White Leghorn chickens resembles late stages of acute inflammatory demyelinating polyneuropathies in humans
1 Chair of General Pathology & Neuropathology, Institute of Veterinary Pathology, Ludwig-Maximilians-University, Munich, Germany
2 Institute of Veterinary Physiology, Ludwig-Maximilians-University, Munich, Germany
3 Institute for Medical Microbiology, Infectious and Epidemic Diseases, Ludwig-Maximilians-University, Munich, Germany
4 Lohmann Tierzucht, Cuxhaven, Germany
5 Institute of Farm Animal Genetics, Friedrich-Loeffler-Institute, Neustadt, Germany
6 Institute of Animal Breeding and Genetics, Georg-August-University, Göttingen, Germany
Journal of Neuroinflammation 2010, 7:7 doi:10.1186/1742-2094-7-7
Published: 28 January 2010Abstract
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.
