eCureMe LIFE
  eCureMe home eCureMe log In Sign Up! go to eCureMe.com
Health Topics     April 25, 2013
      Men’s Forum
      Women’s Forum
      Diet and Exercise Forum
      Open Forum
       Calorie Count
       Health O-Matic Meter
       Health Guru Weblog
       Natural Medicines
       Vitamins & Minerals
       Alternative Living
       Restaurant Review
       Healthy Teas
       Fitness
 






Healthy Living June Issue
ANIMAL DISEASES AND HUMAN HEALTH RISK


Prions: Frightening Carriers of Disease

One might think that processed meat and bone meal from sheep or cows could not carry any kind of serious infection. After all, carcasses are boiled as part of the process of "rendering" that ultimately converts the dead animals into feed for living creatures. It is true that the high temperatures typical in that rendering process would be sufficient to kill most disease-bearing organisms. However, the type of infectious agent that is responsible for BSE is very unusual. Unlike most illnesses that are caused by bacteria or viruses, BSE is caused by something called a prion (pronounced "pree-on"). The destructive powers of prions are outlined in Figure 3: Destructive Power of Prions.

Prions are very resilient proteins that are particularly worrisome because they are resistant to most forms of disinfection. They retain their infectivity even after normal sterilization procedures such as those using heat and ionizing radiation. In fact, prions are not even destroyed by temperatures well above the boiling point. In a laboratory test of the scrapie prion, some infectivity still remained after a full hour of exposure to dry heat at 680 degrees Farenheit. (360 degrees Celsius.).9 Prions are also impervious to freezing and drying.10 Much of the reason for their hardiness is no doubt related to their unusual composition. Prions have no genetic material and consist entirely of protein.11 They are composed of a complex combination of thousands of amino acids. Since some sterilization processes-like ionizing radiation-work by destroying an organism’s genetic material, prions can not be harmed by these measures.



How Do Prions Cause Disease?

One of the most perplexing questions about prions is how an agent with no genetic material can cause disease. The renowned prion researcher, Dr. Stanley Prusiner has come up with a likely explanation based on his years of research. In an excellent article in Scientific American, Prusiner explained the current understanding of how prions do their dirty work.12 Research suggests that these prion proteins are similar in structure to proteins that occur naturally in the brains of humans and animals. The prions differ from those similar normal proteins, however, in slight differences in their three dimensional shape.13 The subtle differences allow these proteins to combine into abnormal aggregates that are responsible for the brain changes produced by a malady called Creutzfeldt-Jakob disease (CJD) and other related diseases.14 Furthermore, when abnormal prion proteins come into contact with normal brain proteins, they can influence the normal proteins to take on the prion protein’s three dimensional shape. This change in shape appears to set up a chain reaction in which the changed proteins later influence neighboring proteins to do the same. The result is a progressively devastating and ultimately fatal disease that has no known treatment.

The characteristics of prions are summarized in Figure 4: Characteristics of Prions.



Ten Young Infected Britons Awakened Public Health Officials

It was Creutzfeldt-Jakob statistics that really got the medical community’s attention in March 1996. By that time 10 young Britons and several farmers had become victims of this devastating illness, as described in Figure 6: Britons Died of Creutzfeldt-Jacob Disease.

The fact that the disease affected a group of individuals whose average age at death was less than 28 (and who were all younger than 42 when diagnosed)22 was extremely unusual. As we have already pointed out, CJD is typically a disease of older adults. Furthermore, all 10 of these individuals had similar symptoms-but those symptoms were different from those that usually accompanied CJD. For example, instead of causing death within 6 months, this apparent CJD variant lingered for up to 23 months. The brain wave patterns of the diseased individuals differed from the usual CJD patient, as did the type of mental impairment they suffered as the disease progressed.23

These unusual disease features prompted a group of leading British scientists to raise the concern that a new variant of CJD had emerged. They felt the most likely source of this variant was BSE,24 meaning that this form of CJD was transmitted from the meat of cows infected with BSE. Further thickening the plot was the occurrence of a worrisome cluster of CJD-infected British dairy farmers. Four such farmers had died with CJD in the past three years. Statisticians said that such a cluster would be very unlikely to occur simply by chance.25 According to the microbiologist Dr. Jeffrey Almond, a researcher and spokesman (at the Conference on Emerging Infections at Harvard University) for the British government’s BSE advisory committee, as of June 1997 there had been 19 confirmed cases of this new CJD causing death, one of which occurred each in France and Italy.



CJD Cases in the U.S.

There are CJD cases in our country among young adults,26 but at this writing they are not thought to be directly related to mad cow disease. However, the symptoms are not unlike the British form of CJD. It is always fatal, and is especially heart wrenching when family members watch such a young victim die. The symptoms are listed in Figure 7: Progression of Symptoms of CJD in Cases in the U.S..27, 28 The disease typically begins with mild symptoms that advance within a few weeks. The disease can then progress to the point where the patient can no longer function alone.



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.



What Animal Products are Free of Prions?

Many consumers have become aware of at least some of these compelling statistics regarding prion-related diseases. This has naturally prompted questions as to which animal products present risk to humans. Most of the focus of late has been on beef, which is warranted. Although organ tissue carries the greatest risk, animal studies do suggest that meat (from animal muscle alone) can transmit prion-related diseases.47 This is not surprising since muscle is interlaced with lymph and nervous tissue-two tissues known to be infected with BSE.48 However, we cannot exclude the possibility that milk may also carry disease-inducing prions. Many may recall how some years ago assurances were given that a mother could not pass HIV to her child by nursing.49 Of course, we now know that HIV can be transmitted in breast milk.50

Granted, prion diseases are vastly different from HIV. The risk from milk does appear to be much smaller than from eating beef or cattle organ tissues. Nonetheless, a British BSE expert has pointed out that at least one human case suggests passage of prions in milk. A Japanese woman dying of CJD was found to have the infectious agent in her colostrum (the type of breast milk made in the initial days following delivery).51 Milk has been under suspicion in established medical circles. It was one of the products targeted when the United Kingdom was beginning to recognize the magnitude of the mad cow problem. The action taken against milk by the British government is explained in Figure 11: Milk from BSE Infected Cattle is Banned.52

Both humans and animals were banned from consuming an infected cow’s milk. Unfortunately, as we have already noted, animals are infected with the BSE prion long before they manifest any symptoms. When infected symptom-free cows are milked, their milk is mixed in collection tanks with milk from healthy cows. If the prion is present in milk, it could theoretically contaminate the whole collection tank. Pasteurization cannot destroy prions, so that process provides no consolation. Although at this time it cannot be stated for certain that milk can transmit a prion-related disease, many are wondering: is it worth taking the chance?

Eating the flesh of animals other than cows or drinking their milk may not be safe either. These other animals may also be infected with prion-related diseases. As already mentioned, some 20 animal species, including sheep and goats, can become infected with the transmissible spongiform encephalopathies.

Suspicions are also raised concerning products made from animal glands. Health food stores often feature a variety of supplements that include glandular extracts. These agents appear to have a higher risk of prion contamination and thus I think it is prudent to avoid them. Is There Risk of Mad Cow Disease in the U.S. or Other Non-European Countries? Even in the U.S., a country that officially states that there is no evidence of BSE, there have been reports that are less than comforting. One piece of evidence comes from American cases of Transmissible Mink Encephalopathy. Five outbreaks of this disease affecting thousands of mink have been documented in the U.S. The disease bears a striking similarity to both BSE and CJD, causing rapid dementia and death with spongiform brain changes.

Three of these five outbreaks occurred in large mink farms that had a practice of feeding their mink "downer" or "non-ambulatory" cattle. These synonymous terms refer to cows that die in the field or fall down and are unable to rise and stand up without support. Deemed unfit for human consumption, such cows have been used as a food source for mink and other livestock. (Of note, diseased cattle may have been food sources for the mink in the other two outbreaks as well).53 In one outbreak, the only animal protein that had been consumed by the mink had come from a U.S. downer cow and almost the entire mink herd died from a spongiform encephalopathy.54

Dr. Mark Robinson and colleagues at Washington State University have demonstrated that mink can get a spongiform encephalopathy by eating BSE-infected cattle tissue.55 The original research report describes the transmission as occurring with "relative ease" even by the oral route. In contrast to this, it has not been possible to infect mink by feeding them scrapie-infected sheep tissue. One chilling possibility is that U.S. cows are harboring the BSE prion and that the mink had then contracted the disease from this source.



Prion Diseases Have Long Incubation Periods

There is one other very important aspect that needs to be reemphasized. These transmissible spongiform encephalopathies have extremely long incubation periods. As already mentioned regarding humans, there is evidence that kuru can take up to 30 years to manifest itself. This is likely to be the same with CJD. As we have seen with BSE, it may take up to six or eight years or more before infected cows show signs of the disease. Again, the important implication is that thousands of animals and humans may now be infected but may not develop symptoms for many years. However, an infected cow can theoretically transmit the illness whether or not it has yet developed symptomatic disease. The widely publicized ban on feeding dead animal parts to British cattle has not stopped the epidemic, although it has appeared to slow it down. When the statistics were reviewed in a 1997 report, 31,903 British cattle that had developed BSE were born after the ban was implemented.59 The important message is that young cows may be infected and may be able to transmit disease to humans.



What Should We Do?

The Consumers’ Association, an independent British "watchdog group," has been quoted as saying that the only way to avoid BSE risk would be to stop eating beef altogether. This concurs with the recommendation of the esteemed BSE researcher and Professor of Microbiology at Leeds University, Dr. Richard Lacey. His simple answer to the problem is stated in Figure 12: Eating Meat Should be Avoided.64

Many people in Great Britain have taken his advice to heart. At this writing, 47 percent of homes do not purchase beef in the United Kingdom.65 Others are saying even more. Some are suggesting that the time has come to recognize that disease in animals has become so rampant worldwide that we all need to seriously consider becoming vegetarians. They point out that BSE is just one of many fatal diseases linked to animals. Literally hundreds of deaths have been documented in the U.S. alone from a host of animal-related infections. Some of the most significant causative agents may not yet be household words; however, most will recognize at least one of them, as listed in Figure 13: Other Disease Causing Agents in Meat and Meat Products .

Adding to all of the foregoing, we cannot forget that the risk of dying prematurely from the Western World’s two leading killers, cancer and heart disease, rises with increasing consumption of animal products.



Beyond Mad Cow Disease

It was in 1996 that mad cow disease captured world headlines. However, in that same year, other diseases linked with animals were claiming thousands of human lives even though they did not garner front page coverage.

Few Americans are aware of the host of potentially fatal diseases that are caused by germs that lie no further away than the local grocery store, or even their own refrigerator. Some of these bacteria and viruses cause illnesses that are well understood by public health professionals as posing a threat to human health. The links between other germs and human risks are more speculative. However, almost all of these diseases are largely linked to animal products.

Infectious illnesses have again become a high priority in the public health arena. Of particular concern are growing threats to our food safety. A recent editorial in the New England Journal of Medicine put it this way, "The microbiologic hazards of food present an issue of increasing concern."69 In view of this, we need to determine if dietary choices could minimize our personal risk from these distressing and sometimes lethal infectious diseases.

Despite the high level of sanitation in the United States, our food is responsible for virtually thousands of infectious disease cases each year. Roughly 60,000 cases of food-related illness are reported annually to the Centers for Disease Control.70 These 60,000 reported cases considerably underestimate the true number of cases. Current estimates are a staggering 80 million cases each year of intestinal illness due to contaminated foods in the U.S. alone.71



Now Is Decision Time

Most of us put off any decision about changing our lifestyle until we are forced to. However, when it comes to dietary changes, often those "must change" situations come too late. Changes in diet will not help much if you are diagnosed with Creutzfeldt Jakob disease. When Salmonella, Listeria, Campylobacter, or another food-borne acute infection strikes, you could be one of the "unlucky ones" and not live to choose a better diet. Even survivors can develop irreversible physical problems that no nutritional program can resolve. The documented information in this chapter calls for a decision. The decision time is now. In light of the evidence of the numerous and serious diseases in animals, choosing the safest diet is certainly reasonable. It makes sense. Focus not on what you are giving up, but rather on the wide variety of fruits, grains, nuts and vegetables that can be heartily enjoyed on this optimal diet.



References

  1. The British The Spongiform Encephalopathy Advisory Committee. Report to Parliament on March 22, 1996 (printed report downloaded from Microsoft Network’s BSE forum).
  2. Pratt K. Bovine Spongiform Encephalopathy. Update. Animal and Plant Health Inspection Services (APHIS). U.S. Department of Agriculture, 1996 p. 1.
  3. Ministry of Agriculture, Fisheries, and Food (MAFF), United Kingdom (UK): BSE: 12-month summary of developments. Http://www.maff.gov.uk.animalh/bse/bseanni.htm. Updated to Feb. 28, 1997.
  4. Patterson WJ, Dealler S. Bovine spongiform encephalopathy and the public health. J Public Health Med 1995 Sep;17(3):261-268.
  5. World Health Organization Press Release (WHO/28). International Experts Propose Measures To Limit Spread Of BSE And Reduce Possible Human Risks From Disease; 3 April 1996. (printed report downloaded from Microsoft Network’s BSE forum).
  6. Pratt K. Bovine Spongiform Encephalopathy. Update. Animal and Plant Health Inspection Services (APHIS). U.S. Department of Agriculture, 1996 p. 1.
  7. Wilesmith JW. An epidemiologist’s view of bovine spongiform encephalopathy. Philos Trans R Soc Lond B Biol Sci 1994 Mar 29;343(1306):357-361.
  8. World Health Organization Press Release (WHO/28). International Experts Propose Measures To Limit Spread Of BSE And Reduce Possible Human Risks From Disease; 3 April 1996. (printed report downloaded from Microsoft Network’s BSE forum).
  9. Brown P, Liberski PP, et al. Resistance of scrapie infectivity to steam autoclaving after formaldehyde fixation and limited survival after ashing at 360 degrees C: practical and theoretical implications. J Infect Dis 1990 Mar;161(3):467-472.
  10. World Health Organization Fact sheet: Bovine Spongiform Encephalopathy (BSE); Fact sheet N113; March 1996 (available via Internet at http://www.who.ch)
  11. Prusiner SB. The prion diseases. Sci Am 1995 Jan;272(1):48-51, 54-57.
  12. Prusiner SB. The prion diseases. Sci Am 1995 Jan;272(1):48-51, 54-57.
  13. Prusiner SB. The prion diseases. Sci Am 1995 Jan;272(1):48-51, 54-57.
  14. Taubes G. Misfolding the way to disease. Science 1996 Mar 15;271(5255):1493-1495.
  15. Pratt K. Bovine Spongiform Encephalopathy. Update. Animal and Plant Health Inspection Services (APHIS). U.S. Department of Agriculture, 1996 p. 1.
  16. Feinberg MB. Slow Virus And Retrovirus Infections. In: Scientific American Medicine (CD-ROM), 1995.
  17. Feinberg, M.B. Slow Virus And Retrovirus Infections. In: Scientific American Medicine (CD-ROM), 1995.
  18. Dillner L. BSE linked to new variant of CJD in humans. BMJ 1996 Mar 30;312(7034):795.
  19. Creutzfeldt-Jakob disease in patients who received a cadaveric dura mater graft-Spain, 1985-1992. MMWR Morb Mortal Wkly Rep 1993 Jul 23;42(28):560-563.
  20. Creutzfeldt-Jakob disease in patients who received a cadaveric dura mater graft-Spain, 1985-1992. MMWR Morb Mortal Wkly Rep 1993 Jul 23;42(28):560-563.
  21. Gibbs CJ Jr, Asher DM, et al. Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-758.
  22. Will RG. (National Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital), Letter to British neurologists on March 21, 1996: (printed report downloaded from Microsoft Network’s BSE forum).
  23. Sir Kenneth Calman, Chief Medical Officer of Britain, "A new variant of CJD" (a message to British physicians); 3-22-96 (printed report downloaded from Microsoft Network’s BSE forum).
  24. The British The Spongiform Encephalopathy Advisory Committee. Report to Parliament on March 22, 1996 (printed report downloaded from Microsoft Network’s BSE forum).
  25. USDA: APHIS (Animal and Plant Health Inspection Service). Bovine Spongiform Encephalopathy: Implications for the United States. A Follow Up. February 1996. Centers for Epidemiology and Animal Health. Fort Collins, Colorado. p. 4.
  26. World Health Organization consultation on public health issues related to bovine spongiform encephalopathy and the emergence of a new variant of Creutzfeldt-Jakob disease. MMWR Morb Mortal Wkly Rep 1996 Apr 12;45(14):295-6, 303.
  27. Transmissible Spongiform Encephalopathies. In: Lederberg J, editor. Encylcopaedia of Microbiology Volume 4. Rockefeller University; New York, NY:Academic Press, 1992 p. 299-309.
  28. Isselbacher KJ, Braunwald E, et al, editors. Harrison’s Principles of Internal Medicine-13th edition (CD-ROM version). New York, NY: McGraw-Hill, Inc. Health Professions Division, 1994.
  29. Dealler SF, Kent JT. BSE: an update on the statistical evidence. British Food Journal 1995;97(8):3-18.
  30. Pratt K. Bovine Spongiform Encephalopathy. Update. Animal and Plant Health Inspection Services (APHIS). U.S. Department of Agriculture, 1996 p. 1.
  31. Conference on Emerging Infections at Harvard University. June, 1997.
  32. USDA: APHIS (Animal and Plant Health Inspection Service). Bovine Spongiform Encephalopathy: Implications for the United States. A Follow Up. February 1996. Centers for Epidemiology and Animal Health. Fort Collins, Colorado. p. 4-5.
  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.
  39. Lopez OL, Larumbe MR, et al, Difficulties in differential diagnosis of long-term Creutzfeldt- Jakob disease. Neurologia 1995 Jan;10(1):37-40.
  40. DJD personal communication with Dr. Ron Hamilton (412-647-6615) at the University of Pittsburgh (had 1 case in 60 who had CJD and had no suggestion on very sketchy clinical data of a prion disease being suspected) and Dr. Larry Hansen (619-534-6212) at UC San Diego who recalled 3 CJDs in some 500 Alzheimer’s autopsies. From Hamilton, if a patient is suspected of CJD they are not supposed to go through the path eval that they are doing for Alzheimer’s in their registry.
  41. Taubes G. Misfolding the way to disease. Science 1996 Mar 15;271(5255):1493-1495.
  42. Evans DA. Estimated prevalence of Alzheimer’s disease in the United States. Milbank Q 1990;68(2):267-289.
  43. Barcikowska M, Kwiecinski H, et al. Creutzfeldt-Jakob disease with Alzheimer-type A beta-reactive amyloid plaques. Histopathology 1995 May;26(5):445-50.
  44. Liberski PP, Papierz W, Alwasiak J. Creutzfeldt-Jakob disease with plaques and paired helical filaments. Acta Neurol Scand 1987 Dec;76(6):428-432.
  45. Collinge J, Owen F, et al. Prion dementia without characteristic pathology. Lancet 1990 Jul 7;336(8706):7-9.
  46. Smith TW, Anwer U, et al. Vacuolar change in Alzheimer’s disease. Arch Neurol 1987 Dec;44(12):1225-1228.
  47. Dealler S, Lacey R. Beef and bovine spongiform encephalopathy: the risk persists. Nutr Health 1991;7(3):117-133.
  48. Groschup MH, Weiland F, Pfaff E "Detection of scrapie agent in the peripheral nervous system of diseased sheep." Goettingen prion meeting November 1995 http://www.airtime.co.uk/bse/intm.htm
  49. Jelliffe DB, Jelliffe EF. HIV and breastmilk: non-proven alarmism. J Trop Pediatr 1988 Aug;34(4):142.
  50. US Dept. Of Health and Human Services. Managing Early HIV Infection Quick Reference Guide for Clinicians: Number 7. AHCPR Publication No. 94-0573, January 1994 p. 14.
  51. Tamai Y, Kojima H, et al. Demonstration of the transmissible agent in tissue from a pregnant woman with Creutzfeldt-Jakob disease. N Engl J Med 1992 Aug 27;327(9):649.
  52. Pratt K. Bovine Spongiform Encephalopathy. Fact sheet. Animal and Plant Health Inspection Services (APHIS). U.S. Department of Agriculture, 1991Jul p. 1.
  53. Robinson MM, Hadlow WJ, et al. Experimental infection of mink with bovine spongiform encephalopathy. J Gen Virol 1994 Sep;75 ():2151-2155.
  54. Marsh RF, Bessen RA, et al. Epidemiological and experimental studies on a new incident of transmissible mink encephalopathy. J Gen Virol 1991 Mar;72 ( Pt 3):589-594.
  55. Robinson MM, Hadlow WJ, et al. Experimental infection of mink with bovine spongiform encephalopathy. J Gen Virol 1994 Sep;75 ( Pt 9)():2151-2155.
  56. USDA: APHIS (Animal and Plant Health Inspection Service). Bovine Spongiform Encephalopathy: Implications for the United States. A Follow Up. February 1996. Centers for Epidemiology and Animal Health. Fort Collins, Colorado. p. 13.
  57. Cutlip RC, Miller JM, et al. Intracerebral transmission of scrapie to cattle. J Infect Dis 1994 Apr;169(4):814-820.
  58. Prusiner SB. The prion diseases. Sci Am 1995 Jan;272(1):48-51, 54-57.
  59. Ministry of Agriculture, Fisheries, and Food (MAFF), United Kingdom (UK): BSE Enforcement Bulletin Issue 8: BSE status report to March 17, 1997. From Internet at http://www.maff.gov.uk/animalh/bse/enforce8/statrep8.htm
  60. Rodney Scale personal communication with Kendra Pratt at Animal and Plant Health Inspection Services (APHIS). U.S. Department of Agriculture, 1996.
  61. Bovine Alliance on Management & Nutrition (BAMN). Undated. A Guide to Modern Calf Milk Replacers. USDA. Animal and Plant Health Inspection Agency (APHIS), 1996 p. 3.
  62. (21 CFR Part 589) Substances prohibited from use in animal food or feed; Animal proteins prohibited in ruminant feeds. Food and Drug Administration. Department of Health and Human Services. Federal Register 1997 Jun 5;62(108):30936-30978.
  63. Lopez-Abente G, Morales-Piga A, et al. Cattle, pets, and Paget’s disease of bone. Epidemiology 1997 May;8(3):247-251.
  64. Lacey RW. "It’s a Mad, Mad, Mad, MAFF World." The Vegetarian (published by The Vegetarian Society UK) Autumn 1993.
  65. Ministry of Agriculture, Fisheries, and Food (MAFF), United Kingdom (UK): BSE: 12-month summary of developments. http://www.maff.gov.uk.animalh/bse/bseanni.htm. Updated to Feb. 28, 1997.
  66. Cousens SN, Vynnycky E, et al. Predicting the CJD epidemic in humans. Nature 1997 Jan 16;385(6613):197-198.
  67. Lacey RW. Creutzfeldt-Jakob disease and bovine spongiform encephalopathy. Bovine spongiform encephalopathy is being maintained by vertical and horizontal transmission. BMJ 1996 Jan;312(7024):180-181.
  68. Dealler SF, Lacey RW. Transmissible spongiform encephalopathies: the threat of BSE to man. Food Microbiology 1990;7: 253-279.
  69. Blaser MJ. How safe is our food? Lessons from an outbreak of salmonellosis N Engl J Med 1996 May 16;334(20):1324-1325.
  70. Ten leading nationally notifiable infectious diseases-United States, 1995. MMWR Morb Mortal Wkly Rep 1996 Oct 18;45(41):883-884.
  71. Craig WJ. Are You Safe at the Plate. In: Nutrition for the Nineties. Eau Claire, MI: Golden Harvest Books, 1992 p. 267-279.
  72. Update: multistate outbreak of Escherichia Coli O157:H7 infections from hamburgers-western United States. MMWR Morb Mortal Wkly Rep 1993 Apr 16;42(14):258-263.
  73. Badr, KF, Brenner BM. Vascular Injury to the Kidney: Hemolytic Uremic Syndrome (HUS) And Thrombotic Thrombocytopenic Purpura (TTP). In: Isselbacher KJ, Braunwald E, editors, et al. Harrison’s Principles of Internal Medicine-13th edition (CD-ROM). New York, NY: McGRAW-HILL, Inc. Health Professions Division, 1994.
  74. MacDonald KL, Osterholm MT. The emergence of Escherichia Coli O157:H7 infection in the United States. The changing epidemiology of foodborne disease. JAMA 1993 May 5;269(17):2264-2266.
  75. USDA:APHIS:VS. Escherichia Coli O157:H7: Issues and Ramifications. March 1994. Centers for Epidemiology and Animal Health. Fort Collins, Colorado. P. S-1.
  76. Notice to Readers: Final reports of notifiable diseases. MMWR Morb Mortal Wkly Rep 1996 Aug 30;45(34):724-754.
  77. Outbreak of acute gastroenteritis attributable to Escherichia Coli serotype O104:H21-Helena, Montana, 1994. MMWR Morb Mortal Wkly Rep 1995 Jul 14;44(27):501-503.
  78. Community outbreak of hemolytic uremic syndrome attributable to Escherichia Coli O111:NM-South Australia 1995. MMWR Morb Mortal Wkly Rep 1995 Jul 28;44(29):550-1, 557-558.
  79. Outbreaks of Escherichia Coli O157:H7 infection and cryptosporidiosis associated with drinking unpasteurized apple cider-Connecticut and New York, October 1996. MMWR Morb Mortal Wkly Rep 1997 Jan 10;46(1):4-8.
  80. Keene WE, Sazie E, et al. An outbreak of Escherichia Coli O157:H7 infections traced to jerky made from deer meat. JAMA 1997 Apr 16;277(15):1229-1231.
  81. Outbreak of Escherichia Coli O157:H7 infection-Georgia and Tennessee, June 1995. MMWR Morb Mortal Wkly Rep 1996 Mar 29;45(12):249-251.
  82. Outbreak of Escherichia Coli O157:H7 infection-Georgia and Tennessee, June 1995. MMWR Morb Mortal Wkly Rep 1996 Mar 29;45(12):249-251.
  83. Notice to Readers: Final reports of notifiable diseases. MMWR Morb Mortal Wkly Rep 1996 Aug 30;45(34):724-754.
  84. Outbreak of Escherichia Coli O157:H7 infection-Georgia and Tennessee, June 1995. MMWR Morb Mortal Wkly Rep 1996 Mar 29;45(12):249-251.
  85. Outbreak of Escherichia Coli O157:H7 infection-Georgia and Tennessee, June 1995. MMWR Morb Mortal Wkly Rep 1996 Mar 29;45(12):249-251.
  86. Tappero JW, Schuchat A, et al. Reduction in the incidence of human listeriosis in the United States. Effectiveness of prevention efforts? The Listeriosis Study Group. JAMA 1995 Apr 12;273(14):1118-1122.
  87. Update: foodborne listeriosis-United States, 1988-1990. MMWR Morb Mortal Wkly Rep 1992 Apr 17;41(15):251, 257-258.
  88. Update: foodborne listeriosis-United States, 1988-1990. MMWR Morb Mortal Wkly Rep 1992 Apr 17;41(15):251, 257-258.
  89. Schwartz B, Ciesielski CA, et al. Association of sporadic listeriosis with consumption of uncooked hot dogs and undercooked chicken. Lancet 1988 Oct 1;2(8614):779-782.
  90. Craig WJ. Are You Safe at the Plate. In: Nutrition for the Nineties. Eau Claire, MI: Golden Harvest Books, 1992 p. 267-279.
  91. Rees JH, Soudain SE, et al. Campylobacter jejuni infection and Guillain-Barre syndrome. N Engl J Med 1995 Nov 23;333(21):1374-1379.
  92. Haas LF, Sumner AJ. Acute Inflammatory Demyelinating Polyradiculoneuropathies (Landry’s or Guillain-Barre syndrome). In: Kelley WN, DeVitaVT JR, et al, editors. Textbook of Internal Medicine-2nd edition. Philadelphia, PA: JP. Lippincott Company, 1992 p. 2235-2236.
  93. Rees JH, Soudain SE, et al. Campylobacter jejuni infection and Guillain-Barre syndrome. N Engl J Med 1995 Nov 23;333(21):1374-1379.
  94. Jacobson MF, Lefferts LY, Garland AW. Meat, Poultry, and Eggs. In: Safe Food: Eating Wisely in a Risky World. Venice, CA: Living Planet Press, 1991 p. 91-92.
  95. Craig WJ. Are You Safe at the Plate. In: Nutrition for the Nineties. EauClaire, MI: Golden Harvest Books, 1992 p. 267-279.
  96. Outbreak of Salmonella enteritidis associated with nationally distributed ice cream products-Minnesota, South Dakota, and Wisconsin, 1994. MMWR Morb Mortal Wkly Rep 1994 Oct 14;43(40):740-741.
  97. Hennessy TW, Hedberg CW, et al. A national outbreak of Salmonella enteritidis infections from ice cream. The Investigation Team. N Engl J Med 1996 May 16;334(20):1281-1286.
  98. Outbreak of Salmonella enteritidis associated with nationally distributed ice cream products-Minnesota, South Dakota, and Wisconsin, 1994. MMWR Morb Mortal Wkly Rep 1994 Oct 14;43(40):740-741.
  99. Outbreak of Salmonella enteritidis associated with nationally distributed ice cream products-Minnesota, South Dakota, and Wisconsin, 1994. MMWR Morb Mortal Wkly Rep 1994 Oct 14;43(40):740-741.
  100. Outbreak of Salmonella enteritidis associated with nationally distributed ice cream products-Minnesota, South Dakota, and Wisconsin, 1994. MMWR Morb Mortal Wkly Rep 1994 Oct 14;43(40):740-741.
  101. Hennessy TW, Hedberg CW, et al. A national outbreak of Salmonella enteritidis infections from ice cream. The Investigation Team. N Engl J Med 1996 May 16;334(20):1281-1286.
  102. Hennessy TW, Hedberg CW, et al. A national outbreak of Salmonella enteritidis infections from ice cream. The Investigation Team. N Engl J Med 1996 May 16;334(20):1281-1286.
  103. Salmonella enteritidis infection. (pamphlet) Centers for Disease Control/National Center for Infectious Diseases; US Dept of HHS; November 1992.
  104. Salmonella enteritidis infection. (pamphlet) Centers for Disease Control/National Center for Infectious Diseases; US Dept of HHS; November 1992.
  105. Outbreak of Salmonellosis associated with beef jerky-New Mexico, 1995. MMWR Morb Mortal Wkly Rep 1995 Oct 27;44(42):785-788.
  106. Craig WJ. Are You Safe at the Plate. In: Nutrition for the Nineties. EauClaire, MI: Golden Harvest Books, 1992 p. 267-279.
  107. Cobb, LL. Findings presented at 97th General Meeting of the American Society for Microbiology, Miami, 1997.
  108. Surveillance for foodborne-disease outbreaks-United States, 1988-1992. MMWR Morb Mortal Wkly Rep 1996 Oct 25;45 No.SS-5: 18-19.
  109. Clostridium perfringens gastroenteritis associated with corned beef served at St. Patrick’s Day meals-Ohio and Virginia, 1993. MMWR Morb Mortal Wkly Rep 1994 Mar 4;43(8):137, 143-144.
  110. Cho SN, Brennan PJ, et al. Mycobacterial aetiology of Crohn’s disease: serologic study using common mycobacterial antigens and a species-specific glyColipid antigen from Mycobacterium paratuberculosis. Gut 1986 Nov;27(11):1353-1356.
  111. Mycobacterium paratuberculosis implicated in Crohn’s Disease. Gastroenterology Observer 1995 Nov/Dec;14(6):4-5.
  112. Mycobacterium paratuberculosis implicated in Crohn’s Disease. Gastroenterology Observer 1995 Nov/Dec;14(6):4-5.
  113. Streeter RN, Hoffsis GF, et al. Isolation of Mycobacterium paratuberculosis from colostrum and milk of subclinically infected cows. Am J Vet Res 1995 Oct;56(10):1322-1324.
  114. Grant IR, Ball HJ, et al.. Inactivation of Mycobacterium paratuberculosis in cows’ milk at pasteurization temperatures. Appl Environ Microbiol 1996 Feb;62(2):631-636.
  115. Kochanek KD, Hudson BL. . Advance Report of Final Mortality Statistics, 1992. Monthly Vital Statistics Report. Centers for Disease Control and Prevention. 1995;43(6) supplement: page 23.
  116. Leukemia Society of America. Facts About Leukemia, Lymphoma, Multiple Myeloma, and Hodgkin’s Disease. New York, NY; 1995 p. 4.
  117. USDA:APHIS (Animal and Plant Health Inspection Service). DxMonitor: Animal Health Report. Winter 1995. Fort Collins, Colorado. P. 6-7. (Note: Florida in the 3rd quarter of 1995 had 31 of 42 cattle tested positive for a rate of approx. 74%).
  118. USDA:APHIS (Animal and Plant Health Inspection Service). DxMonitor: Animal Health Report. Winter 1995. Fort Collins, Colorado. P. 6-7.
  119. Johnson R, Kaneene JB. Bovine Leukemia Virus. Part III. Zoonotic Potential, Molecular Epidemiology, and an Animal Model. Compendium on Continuing Education for the Practicing Veterinarian 1991;13(10):1631-1637.
  120. Baumgartener L, Olson C, Onuma M. Effect of pasteurization and heat treatment on bovine leukemia virus. J Am Vet Med Assoc 1976 Dec 1;169(11):1189-1191.
  121. McClure HM, Keeling ME, et al. Erythroleukemia in two infant chimpanzees fed milk from cows naturally infected with the bovine C-type virus. Cancer Res 1974 Oct;34(10):2745-2757.
  122. Baumgartener LE. Bovine Leukemia Virus Transmission Studies. Diss Abstr Int (Sci) 1982;42(11):4319-B.
  123. Ferrer JF, Kenyon SJ, Gupta P. Milk of dairy cows frequently contains a leukemogenic virus. Science 1981 Aug 28;213(4511):1014-1016.
  124. Rubino MJ, Donham KJ. Inactivation of bovine leukemia virus-infected lymphocytes in milk. Am J Vet Res 1984 Aug;45(8):1553-1556.
  125. Baumgartener LE. Bovine Leukemia Virus Transmission Studies. Diss Abstr Int (Sci) 1982;42(11):4319-B.
  126. Donham KJ, Berg JW, Sawin RS. Epidemiologic relationships of the bovine population and human leukemia in Iowa. Am J Epidemiol 1980 Jul;112(1):80-92.
  127. Johnson R, Kaneene JB. 1991. Bovine Leukemia Virus. Part III. Zoonotic Potential, Molecular Epidemiology, and an Animal Model. Compendium on Continuing Education for the Practicing Veterinarian 13(10): 1631-1637.
  128. Ingersoll B. AIDS Cousin Infects Cattle; No Danger Seen. The Wall Street Journal. 1991. Friday, May 31.
  129. Van Der Maaten MJ, Whetstone CA. Studies of Cattle Naturally and Experimentally Infected with Bovine Lentivirus. Immunobiology of Viral Infections. Proc. 3rd Congress Europ. Soc. Vet. Virol. 1995. P. 353-357.
  130. Van Der Maaten MJ. Update of Bovine Leukosis Virus and Bovine Immunodeficiency Virus. TNAVC 1993 Proceedings. Pages 614-615.
  131. Archambault D, Nadin-Davis S, et al. The Bovine Immunodefeciency Virus: 1990-1992 Update. Vet Res 1993;24(2):179-187.
  132. Blair, A Dosemeci M, Heineman EF. Cancer and other causes of death among male and female farmers from twenty-three states. Am J Ind Med 1993 May;23(5):729-742.
  133. Johnson ES. Mortality among non white men in the meat industry. J Occup Med 1989 Mar 31(3):270-272.
  134. Donham KJ, Merchant JA, et al. Preventing respiratory disease in swine confinement workers: intervention through applied epidemiology, education, and consultation. Am J Ind Med 1990;18(3):241-261.
  135. Zuskin E, Mustajbegovic J, et. al, Respiratory function in poultry workers and pharmacologic characterization of poultry dust extract. Environ Res 1995 Jul; 70(1): 11-19.
  136. Pedersen B, Iversen M, et al. Pig farmers have signs of bronchial inflammation and increased numbers of lymphocytes and neutrophils in BAL fluid. Eur Respir J 1996 Mar;9(3):524-530.
  137. Johnson ES, Dalmas D, et al. Cancer mortality among workers in abattoirs and meat packing plants: an update. Am J Ind Med 1995 Mar;27(3):389-403.
  138. Outbreak of trichinellosis associated with eating cougar jerky-Idaho, 1995. MMWR Morb Mortal Wkly Rep 1996 Mar 15;45(10):205-206.
  139. White EG. Counsels on Diet and Foods. Hagerstown, MD: Review and Herald Publishing Association, 1976 p. 357. (italics supplied)
  140. White EG. Counsels on Diet and Foods. Hagerstown, MD: Review and Herald Publishing Association, 1976 p. 349.
  141. White EG. Counsels on Diet and Foods. Hagerstown, MD: Review and Herald Publishing Association, 1976 p. 414
  142. White EG. Counsels on Diet and Foods. Hagerstown, MD: Review and Herald Publishing Association, 1976 p. 460.
  143. Genisis 1:29. The Holy Bible. Authorized King James version.





Go to Alternative Living Index Page








 
Health Topics    

Home   |   About Us   |   Contact Us   |   Help

Terms and Conditions under which this service is provided to you. Read our Privacy Policy.
Copyright © 2001 - 2004 eCureMe, Inc All right reserved.