Difference between revisions of "Bovine spongiform encephalopathy"
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By Kevin Pan
By Kevin Pan
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Introduce the topic of your paper. What microorganisms are of interest? Habitat? Applications for medicine and/or environment?
Bovine Spongiform Encephalopathy
There has been a decline in cases of mad cow disease recently due to a ban on feeding cattle meat and bone meat. Besides feeding surveillance, important regulations are important for containing this disease. In England, a stringent control system was implemented that prevented any animals over 30 months to be sold as human food and animal feed5.
In the United States, prevention measures began in 1989 by banning import products from nations where BSE was found. In 1997, the FDA banned ruminant-based protein supplements that were being used as cattle feed6. A USDA inspector will inspect all cattle that are sent out for consumption and any cattle suspected of having BSE are sent for further testing. Due to these stringent restrictions, BSE is prevalent in less than one infected cattle per 1 million. Additionally, most of the vCJD deaths have not occurred in the United States.
The largest known epidemic of mad cow disease occurred in England. 177 people died after contracting variant Creutzfeldt-Jakob disease, whom are believed to have been caused by eating cattle infected with BSE. In 1992 and 1993, 36,680 and 34,370 cattle died due to this disease7. In 2006, a 10 year ban on British beef was finally removed to allow for importation of British beef. After 10 people had died of CJD in 1996, the British government finally acknowledged that people were getting sick off of a variant of BSE. Most cases of CDJ have occurred in the UK with nearly all of them happening between 1980-1996 (Campbell 2006).
There are three variations of this disease: variant, sporadic and familial. Variant is caused by the consumption of infected food. Sporadic CJD is what causes the majority of CJD and occurs at random—the trigger for this form is currently unknown. Familial CJD is when a genetic mutation causes the formation of the abnormal prions. This disease has an onset usually in the 45 to 75-year old age group, with peak onset between 60 and 65 years (Collinge 2001). This disease has a high mortality rate, with around 70% of those affected dying within 6 months. In about 1/3 of the cases, patients present symptoms of fatigue, depression, weight loss, headaches and insomnia.
Another disease that is similar to BSE is Kuru, which is a neurological disorder that is found in the Fore people of Papua New Guinea contracted. There was a peak mortality rate of 2%. After numerous studies, it is now understood that this disease was transferred among tribe members due to their funerary cannibalistic rituals. This disease was first noted in the mid 1950’s and was found long after cannibalistic rituals ended in that region. This disease is characterized by tremors, headaches, coordination problems and arm and leg pain. This disease primarily affected women and children because they were the primary participants in the funerary rituals, so many villages ended up becoming desolate of women (Mead et al 2009).
Treatment of prion diseases has thus far been very difficult due to the prions’ resilience towards common sterilization techniques. There have been compounds that inhibit the prion diseases when applied during the inoculation phase, but no treatments have been effective when administered before or during the onset of the disease (Korth et al 2001).
An issue that some medicines have is their ability to bass the blood-brain barrier, which restricts the ability for medicines to reach the central nervous system. There are studies that research which medicines can pass the barrier and inhibit the prions. One such method involves treating the abnormal prion (PrPSc) with tricyclicacridine and phenothiazine derivatives. Phenothiazine are compounds with a tricyclic scaffold and an aliphatic side chain that extends from the middle ring component (Korth et al 2001). Quinacrine, which has been used as an antimaralial drug for over 60 years, is the leading candidate for treatment of patients with variant CJD due to its high potency, but has also been shown to not produce any therapeutic effects. To successfully inhibit PrPSc formation, the ideal amount of carbon atoms in the aliphatic side chain is around 3 to 4. This medicine also suggests the importance of the aliphatic side chain in inhibiting abnormal prion formation. The actual mechanism by which quinacrine and chlorpromazine act on PrPSc is unknown. Other treatments include Congo red, which binds to the β-sheet structures and are believed to act nonspecifically on the PrPSc template by separating the infectious template (Korth et all 2001).
Other methods of treatment involve anti-prion antibodies that can cross the blood-brain barrier. In one study, the researchers were able to grow an anti-prion antibody that was capable of passing the blood-brain barrier in vitro; it also did not display any type of neurotoxic effects.
In a study done by Baxter et al (2005)., they were able to show the effectiveness of radio frequency gas plasma treatment against misfolded prion proteins. In this specific study, the used surgical equipment were treated with gas-plasma to remove residual contamination and they found no apparent damage to the instruments. They were able to reduce residual contamination to levels undetectable by SEM.
Recently, a Texas man died and autopsies revealed that he died of mad cow disease. This was only fourth reported vCJD case in the world since 2012. Researchers are trying to determine how he could have been infected with this disease. They found out that the man was a US citizen that was born outside of the United States and had been previously exposed to the BSE/vCJD agent in either Kuwait, Lebanon or Russia. The Canadian Food inspection Agency also recently confirmed another case of mad cow disease in a cow from Alberta. However, no part of the cow has entered the human food or animal feed systems.