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Animal Disease and Human Health Risk



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Difficulties in Containing the Disease

To contain the disease, some have suggested that we simply round up and slaughter all animals infected with prions. This may sound like a way to prevent human exposure. Unfortunately, it is not a viable option. There is currently no practical way to determine whether a cow or other animal has a prion infection until it enters the final stages of the disease. A long incubation period is typical; animals have the infection but have not yet shown any symptoms.

Most infectious illnesses--whether they are in humans or animals--have short incubation periods that range from a few days to a few weeks. Such diseases include measles, the common cold, and most intestinal infections. There are other human diseases, however, with long incubation periods; one example is AIDS. As many as ten or more years can elapse between the time of infection with HIV and the development of AIDS. Diseases with long incubation periods are especially worrisome because a person or animal can have the disease and transmit the infectious agent without ever showing any evidence of having the illness. This has been one of the worrisome features of AIDS. Thousands of healthy-looking HIV-infected individuals have passed the disease to others before they ever developed signs or symptoms of AIDS.

This same concern surfaces with BSE. Among cattle, the incubation period for this illness (time between infection with the disease-bearing agent and actual development of symptoms) ranges from two to eight years.33 When humans come down with a spongiform encephalopathy, they may never have eaten meat from a cow that was known to have BSE. However, it is conceivable that they ate meat from BSE-infected cattle that were in the incubation period and had not yet manifested the disease. We have already made reference to the incredible amount of human exposure to BSE. A minimum of nearly two million infected cows will have been consumed by the end of this decade. 34


No Laboratory Test For Prion Diseases

Further difficulty in diagnosing BSE in asymptomatic cattle comes from the fact that, unlike human HIV infection, there is no blood test for asymptomatic cows with the BSE prion. Infected animals' immune systems do not appear to mount any response against prions. It is for this reason that we cannot detect prion infection by measuring antibody levels as we do with HIV or hepatitis. Prions also cannot be grown in the laboratory because they are not, in the strictest sense, living organisms--they are merely proteins. In fact, until September of 1996, there was no readily available laboratory test that could identify BSE in a live animal. Now there is a test requiring a spinal tap (a long needle is inserted between the bone in the back to the spinal fluid) that can detect the prion protein itself and may be up to 95 percent accurate.35 The technical names for the special tests that look specifically for the abnormal prion proteins are immunohistochemistry and immunoblotting.36 The test can be falsely positive in people who have had a stroke or encephalitis.

Unfortunately, the test cannot detect the presence of prions in the spinal fluid until they have multiplied enough to cause symptoms to appear.37 Thus, the test cannot give a forewarning of the presence of the disease, but can only verify its presence when symptoms begin to be apparent. Furthermore, special post mortem microscopic brain studies are generally needed to make the diagnosis with more certainty, but even they may miss the detection of the disease. It is especially important to note that a cow may have BSE even if the telltale spongiform brain changes are not found on autopsy. The reason for this is that microscopic studies of animal brains at the time of their death may miss some of the disease's hallmarks.38 Thus, the actual prevalence of the disease may be grossly underestimated both in cattle and in humans. A summary of the difficulties in detecting or containing prion diseases is shown in Figure 9: Difficulties in Detecting Prion Diseases.


References
33 Pratt K. Bovine Spongiform Encephalopathy. Update. Animal and Plant Health Inspection Services (APHIS). U.S. Department of Agriculture, 1996 p. 1.

34 Dealler SF, Kent JT. BSE: an update on the statistical evidence. British Food Journal 1995;97(8):3-18.

35 Hsich G, Kenney K, et al. The 14-3-3 brain protein in cerebrospinal fluid as a marker for transmissible spongiform encephalopathies. N Engl J Med 1996 Sep 26;335(13):924-930.

36 Cutlip RC, Miller JM, et al. Intracerebral transmission of scrapie to cattle. J Infect Dis 1994 Apr;169(4):814-820.

37 Hsich G, Kenney K, et al. The 14-3-3 brain protein in cerebrospinal fluid as a marker for transmissible spongiform encephalopathies. N Engl J Med 1996 Sep 26;335(13):924-930.

38 Cutlip RC, Miller JM, et al. Intracerebral transmission of scrapie to cattle. J Infect Dis 1994 Apr;169(4):814-820.



Notice of Credit
The article above is compliments of the Uchee Pines Institute, Seale, Alabama, a teaching and treatment facility devoted to natural remedies. For mor information, call 334-855-4781,e-mail: ucheepine@csi.com, or visit their Website: http://www.ucheepines.org.



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