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Spiroplasma experimentally induce astrogliosis and retinopathy in ruminants characteristic of transmissible spongiform encephalopathies
Author(s) -
Bastian Frank O.,
Todd William J.,
French Hilari M.,
Boudreaux Charles M.,
Enright Fred M.,
Elzer Philip H.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.173.5
Subject(s) - spiroplasma , astrogliosis , embryonated , chronic wasting disease , biology , transmissible spongiform encephalopathy , pathology , virology , scrapie , medicine , disease , mollicutes , microbiology and biotechnology , virus , central nervous system , mycoplasma , prion protein , neuroscience
Spiroplasma mirum, tiny motile wall‐less bacterium, is a candidate causal agent of transmissible spongiform encephalopathy (TSE), which includes scrapie in sheep, chronic wasting disease in deer and Creutzfeldt‐Jakob disease (CJD) in humans. Spiroplasma spp. have been cultured from TSE‐affected brains via passage in embryonated eggs into cell‐free media. When inoculated into ruminants, spiroplasma induced spongiform encephalopathy with clinical signs of TSE. Here, brain tissues and eyes from the reported study (Bastian et al., JMM, 2007) were examined by immunohistochemistry for glial fibers and distribution of the organisms. Spiroplasma induced a striking astrogliosis with hypertrophic astrocytes and retinopathy characteristic of TSE. Spiroplasma were demonstrated in neurons throughout the brain tissues and retina. Cell‐free spiroplasma were seen within the vitreous and organisms immunostained within vacuolated corneal endothelia. The infected corneal endothelia may be the source for iatrogenic transmission of CJD via corneal transplants, and the presence cell‐free organisms within the vitreous may account for contamination of instruments secondary to ophthalmic surgical procedures involving the posterior eye. Supported in part by NIH grant R01‐NS044003, donations from CJD‐affected families and LSU Agricultural Center Research funds.