Abstract This paper discusses Creutzfeldt-Jakob disease (CJD), also known as spongiform transmissible encephalopathis or infectious amyloidoses, is a dementing disease that results from a prion. Specifically, it describes the definition, occurrence, onset, symptoms and fatal outcome of the disease.This paper asserts that by studying the disease as it manifests in various cases, doctors can become familiar with earlier symptoms and diagnosis, and prepare families in advance. With such preparation, families can obtain closure in advance of the inevitable outcome and reach the closure stage sooner.
From the Paper "The case study shows that the onset of more commonly psychiatric systems associated with mental illness precludes the early diagnosis of the disease. Instead, warning factors such as neurological symptoms should also be viewed as a warning sign of the disease. This can be particularly helpful in diagnosing familial cases. A known family history of the disease can be helpful in early diagnosis and also in making decisions regarding the care of the patient.
"According to the Memory and Aging Center (2008), many tools are available today that can be helpful in diagnosing the disease more accurately. The MRI for example can accurately detect the abnormalities displayed by the disease and rule out other possibilities such as mental illness. Because of the existing behavioral and movement manifestations of the disease, this tool often requires sedation or general anesthesia in severe cases, as patients are required to be still during the examination process. FLAIR and DWI images are also useful in showing abnormalities that are caused by the disease."
Abstract This paper discusses the devastating Creutzfeldt-Jakob disease (CJD). It describes the initial symptoms of CJD and it progression throughout the illness. The paper then analyzes the link between CJD and the prion protein in the brain. It also looks at diagnosis of the disease. The paper then goes on to research if the fact that CJD is limited to the central nervous system and olfactory-nerve tissue could indicate that some other factor besides the prion is involved. The paper presents the research design, its challenges and results.
Table of Contents:
Introduction
Research Question
Methods
Research Team
Funding
Results
Leadership Skills
Challenges
Summary
From the Paper "Very little is known about CJD in terms of what causes the mutation of the prion protein. Whereas sporadic CJD was always marked by low incidence since the 1920s, there is currently an alarming increase in the incidence of the disease in Switzerland. The reasons for this increase need to be studied immediately. After a decade of focus on the prion protein, studies are needed to determine underlying factors that may be affecting that protein to mutate. The mechanism by which the prion can avoid the immune system needs to be studied, along with the central question of how a protein can destroy neurons. The idea that a protein can destroy is a total paradox which needs to be resolved. Other questions concern how patients might be diagnosed without the need for invasive procedures."
Abstract This paper discusses Mad Cow Disease, otherwise known as Bovine Spongiform Encephalopathy or as Creutzfeldt-Jakob disease in humans. It discusses the history, background and pathophysiology of the disease. It then goes on to describe prevention and treatment options for the disease, concluding that there are no effective treatments available. The paper concludes by discussing nursing and collaborative care for patients with the disease.
Table of Contents:
Epidemiology
Pathophysiology
Prevention and Treatment
Differences in Classic CJD and Variant CJD Nursing and Collaborative Care
From the Paper "Variant CJD has a median age at death of 28 years. The duration of the illness is approximately 13-14 months. Some of the clinical signs and symptoms include: prominent psychiatric/behavioral symptoms, painful dyesthesiasis; and delayed neurologic signs. The "Pulvinar sign" on an MRI is present in greater than 75% of most of the Variant CJD. The presence of "florid plaques" on neuropathology is usually in large numbers and easily detected. The agent is readily detected in the lymphoid tissue. There is a marked accumulation of protease-resistance prion protein noted in the brain. This is why the Variant CJD is much more easily detected because it shows up on more tests."
A discussion of the discovery of mad cow disease, to the present, and the role the media/government has played in control, prevention, and the dissemination of information.
Abstract Examines the treatment of Mad-cow disease in the media, and by the government.
Discusses the following topics
Bovine Spongiform Encephalopathy and Scrapie
What Transmissible Spongiform Encephalopathies Do
Two Theories on the Action of Transmissible Spongiform Encephalopathies
British Government Admits Mad Cow Disease Exists (1987)
Testing Results by the British government MAFF
Culpability of the British Medical Society
The Spread of CJD Steps Taken by the British Government
From the Paper "Where the industry has gone wrong is in listening to the PR people. The mad-cow epidemic is not an information management issue?it is a disease that will not go away.? These words are from an interview with Dr. Pringle, a member of the Sperling Biomedical Foundation, and the founder of www.mad-cow.org. I believe that they highlight what has been fundamentally wrong about the treatment of mad-cow disease by the British government and the British media. Several grave errors have been made about the treatment of this issue, and they continue to have repercussions today, as we explore America's mad-cow incidents, and rising problems in Europe, Asia, and South America. At the time this paper was written, mad cow disease had been confirmed in domestic cattle in Belgium, France, Ireland, Liechtenstein, Luxembourg, the Netherlands, Portugal, Switzerland, Spain and Germany."
Abstract Mad Cow Disease is a brain disease of cattle, which was first identified in the United Kingdom in the mid-1980s. Although not as widespread as some other livestock diseases, such as hoof-and mouth-disease, the Mad Cow Disease has attracted a lot of publicity because of its apparent apparent ability to transmit to humans, the fact that there is no known cure for the disease and the horrifying nature of the brain decay it causes. This paper explains the cause of the disease, how it affects the organisms, how it is transmitted from one organism to another, and the ways in which it could be transmitted to humans. The paper also discusses the human equivalents of the disease.
Paper Outline:
Cause of the Disease
How the Disease Affects the Organism
How is the Disease Transmitted from one Organism to Another
The Ways in Which it Could be Transmitted from Cows to Humans
Human Equivalents of the Disease
Works Cited
From the Paper "This theory about the spread of disease is based on the observation that incidences of the disease have mostly been found in the UK where feeding of meat and bone meal to cattle was most common. Although other European countries also fed meat and bone meals to cattle as a protein supplement, the British laws about high temperature sterilization of the protein meal were relatively lax in order to keep meat prices competitive."
Abstract Ever since Mad Cow Disease sparked terror in international headlines, the public has been concerned about eating beef. Mad Cow Disease is not, however, the first or only prion-caused disease. Several others, including Creutzfeldt-Jakob Disease (CJD) and kuru in humans and a host of agricultural animal disorders join Mad Cow in both cause and effects, the major effect being horror. This paper argues that, while the presence on the planet of a disease that literally lays waste to human brain tissue is frightening, there are two probabilities that can be seen as reasons not to be terrified. Instead, people could be hopeful that research sparked by the publicity surrounding Mad Cow Disease will eventually bring answers to such sociologically and medically devastating diseases as Alzheimer's Disease, and other lesser known but just as deadly diseases such as Lou Gehrig's Disease. The paper shows that these two probabilities are first, that prion-caused diseases are much less prevalent than media hype would indicate and, second, that a cure or vaccination is relatively certain to be discovered in the near to medium term.
Paper Outline:
Introduction
Methods
Discussion
Conclusion
References
From the Paper "Questions have arisen regarding why these particles are not attacked by the body's defense mechanisms, and the answer, Mahy noted, is that they are so odd, they are simply not recognized and therefore cannot be neutralized. Prions contain no nucleic acid and are therefore extremely " extremely resistant to inactivation by chemical or physical interventions that would inactivate viruses" (Mahy 1998) because there is no vector through which to deliver the 'poison'. Even more so than viruses, then, it is reasonable to wonder whether prions are, in fact, alive. And if they are not alive, then how can they infect an organism? Do they replicate like bacteria and viruses, or what?"
Tags: Stanley, Prusiner, protein, sterilization, kuru
Abstract The paper discusses the efficiency of the German governmental agencies and beef industry in estimating the risk of mad cow disease negatively affecting German consumers of beef during the years 2001 to 2004. The paper further discusses how the German governmental agencies and industry managers performed risk management strategies and policies through the selection and implementation of appropriate measures after the outbreak of mad cow disease in Germany in 2000 and until 2004. In addition, the paper looks at how the risk communication was conducted in relation to the true possibility that humans can contract Creutzfeldt-Jacob Disease (CJD), a variant of BSE.
Outline:
Objective
Introduction
Perceived Risk Analysis
Rational Problem-Solving
Food Safety Regulation Reform
Research Risk and Assessment
Food Industry Supports Government
Summary and Conclusion
From the Paper "The work of Grannis, Green and Bruch (2004) entitled: "Animal Health: The Potential Role for Livestock Disease Insurance" state that "animal disease can cause significant production losses and a reduction in livestock receipts." Grannis, Green and Bruch state that an opportunity development exists in assisting the management of livestock disease risks and one example is Germany. "Evidence from Germany demonstrates that both alternative value and consequential loss policies for livestock producers can be developed and can work in parallel with government indemnity programs. In Germany, indemnity payments are made based on predetermined and published payment schedules. These schedules are capped by maximum values that do not represent the value of superior commercial animals. Policies are available to insure the difference between the value indemnified according to the published government schedule and the value of the animal under regular, nondisease market conditions".
