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Journal of Clinical Microbiology, January 2006, p. 91-97, Vol. 44, No. 1
0095-1137/06/$08.00+0     doi:10.1128/JCM.44.1.91-97.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Absence of Spiroplasma or Other Bacterial 16S rRNA Genes in Brain Tissue of Hamsters with Scrapie

Irina Alexeeva,1 Ellen J. Elliott,1,2 Sandra Rollins,1,{dagger} Gail E. Gasparich,3 Jozef Lazar,1,{ddagger} and Robert G. Rohwer1,2*

VA Maryland Health Care System, Medical Research Service, Baltimore, Maryland 21201,1 University of Maryland School of Medicine, Department of Neurology, Baltimore, Maryland 21201,2 Towson University, Department of Biological Sciences, Towson, Maryland 212523

Received 22 June 2005/ Returned for modification 24 August 2005/ Accepted 11 October 2005

Spiroplasma spp. have been proposed to be the etiological agents of the transmissible spongiform encephalopathies (TSEs). In a blind study, a panel of 20 DNA samples was prepared from the brains of uninfected hamsters or hamsters infected with the 263K strain of scrapie. The brains of the infected hamsters contained ≥1010 infectious doses/g. The coded panel was searched for bacterial 16S rRNA gene sequences, using primers selective for spiroplasma sequences, primers selective for mollicutes in general, and universal bacterial primers. After 35 PCR cycles, no samples were positive for spiroplasma or any other bacterial DNA, while control Spiroplasma mirum genomic DNA, spiked at 1% of the concentration required to account for the scrapie infectivity present, was readily detected. After 70 PCR cycles, nearly all samples yielded amplified products which were homologous to various bacterial 16S rRNA gene sequences, including those of frequent environmental contaminants. These sequences were seen in uninfected as well as infected samples. Because the concentration of scrapie infectivity was at a known high level, it is very unlikely that a bacterial infection at the same concentration could have escaped detection. We conclude that the infectious agent responsible for TSE disease cannot be a spiroplasma or any other eubacterial species.

* Corresponding author. Mailing address: Research Service, Mail Code 151, VA Medical Center, 10 N. Greene Street, Baltimore, MD 21201. Phone: (410) 605-7000, ext. 6462. Fax: (410) 605-7959. E-mail: rrohwer{at}umaryland.edu.

{dagger} Present address: Greenbaum Cancer Center, University of Maryland, Baltimore, MD 21201.

{ddagger} Present address: Department of Dermatology and Human Molecular Genetics Center, Medical College of Wisconsin (MCW), 8701 W. Watertown Plank Rd., Milwaukee, WI 53226.

Journal of Clinical Microbiology, January 2006, p. 91-97, Vol. 44, No. 1
0095-1137/06/$08.00+0     doi:10.1128/JCM.44.1.91-97.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Brenner, S. R., Brown, P. W. (2009). TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY IN THE 21st CENTURY: NEUROSCIENCE FOR THE CLINICAL NEUROLOGIST. Neurology 72: 292-292 [Full Text]  


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