Spiroplasma, small motile wall-less bacteria, are linked by molecular and serological studies to the transmissible spongiform encephalopathies (TSEs), which include scrapie in sheep, chronic wasting disease (CWD) in deer and Creutzfeldt–Jakob disease in humans. In this study, two experiments were undertaken to determine the role of spiroplasma in the pathogenesis of TSE. In experiment 1, Spiroplasma mirum, a rabbit tick isolate that had previously been shown to experimentally induce spongiform encephalopathy in rodents, was inoculated intracranially (IC) into ruminants. S. mirum-inoculated deer manifested clinical signs of TSE after 1.5 to 5.5 months incubation. The deer, as well as sheep and goats, inoculated with S. mirum developed spongiform encephalopathy in a dose-dependent manner. In experiment 2, spiroplasma closely related to S. mirum were isolated from TSE-affected brains via passage in embryonated eggs, and propagated in cell-free M1D media. Spiroplasma spp. isolates from scrapie-affected sheep brain and from CWD-affected deer brain inoculated IC into sheep and goats induced spongiform encephalopathy closely resembling natural TSE in these animals. These data show spiroplasma to be consistently associated with TSE, and able experimentally to cause TSE in ruminant animal models, therein questioning the validity of studies that have concluded the prion, a miss-folded protease-resistant protein that builds up in TSE brains during the course of the disease, to be the sole causal agent. The spiroplasma infection models reported here will be important for investigating factors involved in the pathogenesis of TSE since ruminants are the natural hosts.

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Spiroplasma spp. from transmissible spongiform encephalopathy brains or ticks induce spongiform encephalopathy in ruminants

The transmissible spongiform encephalopathies (TSEs) are caused by infectious agents whose structures have not been fully characterized but include abnormal forms of the host protein PrP, designated PrPSc, which are deposited in infected tissues. The transmission routes of scrapie and chronic wasting disease (CWD) seem to include environmental spread in their epidemiology, yet the fate of TSE agents in the environment is poorly understood. There are concerns that, for example, buried carcasses may remain a potential reservoir of infectivity for many years. Experimental determination of the environmental fate requires methods for assessing binding/elution of TSE infectivity, or its surrogate marker PrPSc, to and from materials with which it might interact. We report a method using Sarkosyl for the extraction of murine PrPSc, and its application to soils containing recombinant ovine PrP (recPrP). Elution properties suggest that PrP binds strongly to one or more soil components. Elution from a clay soil also...

Fate of prions in soil: detergent extraction of PrP from soils.

Introduction: Human prion diseases (PrDs) are transmissible fatal nervous system disorders with public health implications. They are characterized by the presence of a disease-associated form of the physiological cellular prion protein. Development of diagnostic procedures is important to avoid transmission, including through blood products. Methods used for the detection of disease-associated PrP have implications for other neurodegenerative diseases. Areas covered: In this review, the authors discuss recent progress in the understanding of the molecular background of phenotypic variability of human PrDs, and the current concepts of molecular diagnosis. Also, the authors provide a critical summary of the diagnostic methods with regard to the molecular subtypes. Expert opinion: In spite of a lack of specific tests to detect disease-associated PrP in body fluids, the constellation of clinical symptoms, detection of protein 14-3-3 in cerebrospinal fluid, electroencephalogram, cranial MRI and prion protein g...

Molecular diagnosis of human prion disease.

The recovery of a novel Spiroplasma sp. from brain tissues from sheep with scrapie, cervids with chronic wasting disease, and from patients with Creutzfeldt-Jakob disease through passage through embryonated eggs has raised the issue of the role of Spiroplasma in the transmissible spongiform encephalopathies (TSE). In this review, we have inserted into an epidemiologic infection model evidence accumulated over the past 30 years showing involvement of Spiroplasma infection in TSE. These data support our hypothesis that a Spiroplasma sp. is the causal agent of TSE, although Koch's postulates must be fulfilled to definitively answer that question.

Spiroplasma as a candidate agent for the transmissible spongiform encephalopathies.

An overview of prion biology and the role of blood filtration in reducing the risk of transfusion-transmitted variant Creutzfeldt-Jakob disease.

Safe method for isolation of prion protein and diagnosis of Creutzfeldt-Jakob disease.

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Safe method for isolation of prion protein and diagnosis of Creutzfeldt-Jakob disease.