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TSEs in humans include kuru , fatal familial insomnia , Gerstmann-Straussler-Scheinker disease , and Creutzfeldt-Jakob disease (see [link] ). TSEs in animals include mad cow disease , scrapie (in sheep and goats), and chronic wasting disease (in elk and deer). TSEs can be transmitted between animals and from animals to humans by eating contaminated meat or animal feed. Transmission between humans can occur through heredity (as is often the case with GSS and CJD) or by contact with contaminated tissue, as might occur during a blood transfusion or organ transplant. There is no evidence for transmission via casual contact with an infected person. [link] lists TSEs that affect humans and their modes of transmission.
| Transmissible Spongiform Encephalopathies (TSEs) in Humans | |
|---|---|
| Disease | Mechanism(s) of Transmission National Institute of Neurological Disorders and Stroke. “Creutzfeldt-Jakob Disease Fact Sheet.” http://www.ninds.nih.gov/disorders/cjd/detail_cjd.htm (accessed December 31, 2015). |
| Sporadic CJD (sCJD) | Not known; possibly by alteration of normal prior protein (PrP) to rogue form due to somatic mutation |
| Variant CJD (vCJD) | Eating contaminated cattle products and by secondary bloodborne transmission |
| Familial CJD (fCJD) | Mutation in germline PrP gene |
| Iatrogenic CJD (iCJD) | Contaminated neurosurgical instruments, corneal graft, gonadotrophic hormone, and, secondarily, by blood transfusion |
| Kuru | Eating infected meat through ritualistic cannibalism |
| Gerstmann-Straussler-Scheinker disease (GSS) | Mutation in germline PrP gene |
| Fatal familial insomnia (FFI) | Mutation in germline PrP gene |
Prions are extremely difficult to destroy because they are resistant to heat, chemicals, and radiation. Even standard sterilization procedures do not ensure the destruction of these particles. Currently, there is no treatment or cure for TSE disease, and contaminated meats or infected animals must be handled according to federal guidelines to prevent transmission.
For more information on the handling of animals and prion-contaminated materials, visit the guidelines published on the CDC and WHO websites.
A few days later, David’s doctor receives the results of the immunofluorescence test on his skin sample. The test is negative for rabies antigen. A second viral antigen test on his saliva sample also comes back negative. Despite these results, the doctor decides to continue David’s current course of treatment. Given the positive RT-PCR test, it is best not to rule out a possible rabies infection.
Near the site of the bite, David receives an injection of rabies immunoglobulin, which attaches to and inactivates any rabies virus that may be present in his tissues. Over the next 14 days, he receives a series of four rabies-specific vaccinations in the arm. These vaccines activate David’s immune response and help his body recognize and fight the virus. Thankfully, with treatment, David symptoms improve and he makes a full recovery.
Not all rabies cases have such a fortunate outcome. In fact, rabies is usually fatal once the patient starts to exhibit symptoms, and postbite treatments are mainly palliative (i.e., sedation and pain management).
Go back to the previous Clinical Focus box.
Both viroids and virusoids have a(n) _________ genome, but virusoids require a(n) _________ to reproduce.
RNA, helper virus
Describe the disease symptoms observed in animals infected with prions.
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