Diseases / Miscellaneous / Multi-factorial / Metabolic Diseases / Chronic Wasting Disease of Deer and Elk / Detailed Disease Description:

< > Literature Reports of PROPHYLACTIC TREATMENT (OTHER THAN VACCINES) for CWD of Deer and Elk:

Prophylactic Treatment

Editorial Summary (Editorial Overview Text Replicated on Overall Disease page - CWD of Deer and Elk)
  • At present no prophylactic treatment is available against CWD.
  • Several compounds have been shown to inhibit PrPres production in cell-free systems and/or in scrapie-infected neuroblastoma cells and some of these compounds have been shown to prolong the incubation period in hamsters if given starting prior to, or at the same time as, peripheral inoculation of scrapie agent. However at this time no compounds are considered effective for treatment of the TSE diseases.

Limited data on other TSE diseases is provided in literature reports below the information on CWD. Information on these diseases within the "Chronic Wasting Disease of Deer and Elk" volume of Wildpro is provided for comparative purposes and is not intended to be comprehensive.

Data Source Notes
  • There is at present [2002] no treatment available for CWD. (N8.18.w8)

Other TSE Diseases

Drugs which have been shown to have some protective effect in vivo or in vitro:

  • Congo red, given prior to inoculation with scrapie, has been shown to prolong the incubation period in hamsters following either intraperitoneal or intracerebral inoculation. The greatest prolongation was seen following treatment with 10 mg per hamster once per week following intraperitoneal inoculation of scrapie (134.6 +/- 11.0 days, versus 100.9 +/- 4.2 days in control animals, a delay of 33.7 days). In animals infected intracerebrally, prolongation by 13.7 days (from control of 58.3 days) was produced by doses of 75 mg/wk, in six doses of 12.5 mg per dose; doses of 10 mg/wk delayed the onset of clinical illness by 10.1 days. (J80.69.w1)
  • Congo red has been shown to potently inhibit the accumulation of PrP-res in scrapie-infected neuroblastoma cells, with a greater than 90% reduction in detected PrP-res following five days treatment of the cells with Congo red. Metabolism of normal PrP in the cells was not affected. (J253.59.w1)
  • Congo red inhibited the replication of PrP-res accumulation and scrapie infectivity in scrapie-infected neuroblastoma cells. (J80.67.w2)
  • Curcumin at 10uM resulted in partial mean inhibition of up to 41% in the cell-free conversion reaction mixture using purified PrP-res (263K strain) to induce the conversion of hamster 35S-PrP-sen to 35S-PrP-res. Curcumin was shown also to cause a concentration-dependant reduction in PrP-res accumulation in scrapie agent infected murine neuroblastoma (ScNB) cells with a concentration of about 10nM giving half maximal inhibition. It was noted that this concentration was 2,500 times lower than the concentration at which curcumin first produces cytotoxic effects in cells. However oral administration of curcumin to hamsters in food did not have a protective effect against high-dose intracerebrally inoculated with material containing 253K strain scrapie agent. (J80.77.w2)
  • In a cell-free system, the compounds Tryptan Blue, Evans Blue, Sirius Red F3B, Primuline and Thioflavin-S, all related to Congo Red, all inhibited production of PrP-res in a cell-free system; Sirius Red F3B also blocked formation of PrP-res in scrapie-infected mouse neuroblastoma cells (IC50 of 32 nM) to a similar extent as that seen with Congo Red. (J71.S16.w1)
  • Pentosal polysulphate has been shown to potently inhibit the accumulation of PrP-res in scrapie-infected neuroblastoma cells, primarily by prevention of accumulation of new PrP-res rather than by destabilisation of preexisting PrP-res. Metabolism of normal PrP in the cells was not affected.(J80.67.w1)
  • A peptide containing a conserved PrP sequence (corresponding to hamster PrP residues 119 to 136) has been demonstrated to be capable of inhibiting the formation of PrP-res in both mouse and hamster cell-free systems and in scrapie-infected mouse neuroblastoma cells. (J80.73.w1)
  • Postexposure, repeated (initially at seven hours post-exposure, then daily for 20 days), treatment with CpG oligodeoxynucleotide 1826, a strong inducer of innate immunity, following intraperitoneal inoculation of mice with brain material from terminally infected mice with RML scrapie, resulted in no clinical disease being seen after more than 330 days. In contrast inoculation without such treatment resulted in infection at about 181-183 days in all mice. Treatment at 0 or 7 hours and daily for four days prolonged the incubation period to approximately 250-253 days but did not prevent the development of disease. (J98.360.w1)
Technique Descriptions, if available
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Authors & Referees

Authors Dr Debra Bourne MA VetMB PhD MRCVS (V.w5)
Referee Suzanne I Boardman BVMS MRCVS (V.w6)

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