Neurotropic response of Spiroplasma mirum following peripheral inoculation in the rat

Bastian, Frank O.; Jennings, Roger A.; Hoff, Charles

doi:10.1016/0769-2609(87)90143-8

Cited by 17 publications

(6 citation statements)

References 5 publications

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“…Prion also recycles to the membrane surface. After transit through the epithelial cell, the Spiro- plasma may use the same entry mechanism to hitch a ride on dendritic cells and be distributed throughout the body, but with preference to lipid rich tissues such as brain, since they are neurotropic microbes (Bastian et al, 1987b).…”

Section: Nature Of the Agentmentioning

confidence: 99%

Slow virus disease: Deciphering conflicting data on the transmissible spongiform encephalopathies (TSE) also called prion diseases

Bastian

Fermin

2005

Microscopy Res & Technique

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The transmissible spongiform encephalopathies (TSE) that manifest as Creutzfeldt-Jakob disease in humans, as scrapie in sheep and goats, mad cow disease in cattle, or chronic wasting disease in cervids (deer) represent a serious human health crisis and a significant economical problem. Despite much research, the nature of the elusive pathogen directly involved with TSE is currently unresolved. This article reviews current pathogen-cell plasma membrane properties, showing that the primary biochemical marker of the prion disease is used as a receptor by the intracellular bacterium Brucella abortus. Such observation makes plausible the role for the prion in the pathogenesis of TSE, and supports the concept that Spiroplasma, a wall-less bacterium, may be a transmissible agent of TSE. Over the past three decades, we have published convincing evidence that Spiroplasma infection is associated with TSE. The bacterial-prion-receptor concept by other laboratories support a model for TSE wherein a Spiroplasma bacterium can bind to prion receptors (alone or with anchors) on the cell surface lipid raft, allowing entry of the microbe into the cell to initiate infection. The relevance of this new concept is that it offers a new window for future research involving a bacterium in the pathogenesis of TSE. Data from the bacterial-prion-receptor model will aid in the development diagnostic tests and/or treatment protocols for TSE.

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Section: Nature Of the Agentmentioning

confidence: 99%

Slow virus disease: Deciphering conflicting data on the transmissible spongiform encephalopathies (TSE) also called prion diseases

Bastian

Fermin

2005

Microscopy Res & Technique

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“…In the first, S. mirum has been shown to cause a persistent infection of the brain in the suckling rat. Furthermore, the tropism of this microorganism for the brain tissues was correlated to the presence of sterols, which are necessary for its growth [94]. In the second study, it was observed, by western blot, that antibodies to the fibrils associated with Scrapie interacted with either the brain tissue of patients with CJD either with fibrillar proteins resistant to proteases obtained from S. mirum [95].…”

Section: Spiroplasma and Transmissible Spongiform Encephalopathy (Tse)mentioning

confidence: 99%

Spiroplasma spp.: A Plant, Arthropod, Animal and Human Pathogen

Cacciola¹,

Bertaccini²,

Pane³

et al. 2017

Citrus Pathology

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Mollicutes is a class of smallest and free-living bacteria. They have no cell wall and their plasma membrane contains cholesterol; nevertheless, cellular organization does not differ from that of other prokaryotes. They are used as simple model systems for studying general biological problems, such as those concerning membrane structure and functions, symbiosis between arthropods and microrganisms, animal and plant pathogens. Mollicutes includes the family of Spiroplamataceae, which contains Spiroplasma genus, a group of species associated, in different manner, with arthropods (insects, mites, crustaceans). Spiroplasma species can be commensals or parasites and even be involved in more close symbiosis, such as synergism or mutualism. Out of 38 described Spiroplasma species, only three have been associated with plant diseases and three with arthropod diseases. Moreover, some species have been related to animal diseases, such as transmissible spongiform encephalopathy (TSE), and their role in human disease has been assessed.The chapter describes the taxonomic situation of the genus and reports the most important diseases due to the presence of Spiroplasma in different living organisms with special emphasis on citrus in which it causes one of the most economically damaging infectious diseases in a number of citrus growing areas worldwide.

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“…There are some avenues of support for spiroplasma being involved in hereditary CJD cases. Although we have shown spiroplasma to seek out brain and lymphoid tissues after peripheral inoculation (17), this may not necessarily be neurotropism but may instead be attraction to lipid-rich organs, which, in scrapie, may include endocrine glands and the ovary (79). Although we have shown spiroplasma to seek out brain and lymphoid tissues after peripheral inoculation (17), this may not necessarily be neurotropism but may instead be attraction to lipid-rich organs, which, in scrapie, may include endocrine glands and the ovary (79).…”

Section: Genetic Factors and Familial Cjdmentioning

confidence: 99%

The Case for Involvement of Spiroplasma in the Pathogenesis of Transmissible Spongiform Encephalopathies

Bastian

2014

Journal of Neuropathology & Experimental Neurology

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Spiroplasma biofilm formation explains the role of these wall-less bacteria in the pathogenesis of transmissible spongiform encephalopathies (TSEs). Spiroplasma embedded in the biofilm polysaccharide matrix are markedly resistant to physical and chemical treatment, simulating the biologic properties of the TSE agent. Microcolonies of spiroplasma embedded in biofilm bound to clay are the likely mechanism of lateral transmission of scrapie in sheep and chronic wasting disease in deer via soil ingestion. Spiroplasma in biofilm bound to the stainless steel of surgical instruments may also cause iatrogenic transmission of Creutzfeldt-Jakob disease. Sessile spiroplasma in biofilm attach to the surface by curli-like fibrils, a functional amyloid that is important for spiroplasma entering cells. Curli fibers have been shown to interact with host proteins and initiate formation of a potentially toxic amyloid that multiplies by self-assembly. In TSE, this mechanism may explain how spiroplasma trigger the formation of prion amyloid. This possibility is supported by experiments that show spiroplasma produce α-synuclein in mammalian tissue cultures. The data linking spiroplasma to neurodegenerative diseases provide a rationale for developing diagnostic tests for TSE based on the presence of spiroplasma-specific proteins or nucleic acid. Research efforts should focus on this bacterium for development of therapeutic regimens for Creutzfeldt-Jakob disease.

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Neurotropic response of Spiroplasma mirum following peripheral inoculation in the rat

Cited by 17 publications

References 5 publications

Slow virus disease: Deciphering conflicting data on the transmissible spongiform encephalopathies (TSE) also called prion diseases

Slow virus disease: Deciphering conflicting data on the transmissible spongiform encephalopathies (TSE) also called prion diseases

Spiroplasma spp.: A Plant, Arthropod, Animal and Human Pathogen

The Case for Involvement of Spiroplasma in the Pathogenesis of Transmissible Spongiform Encephalopathies

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