Bovine spongiform encephalopathy ( BSE ), commonly known as mad cow disease , is a contagious spongiform encephalopathy and a fatal neurodegenerative disease in cows that may be passed to humans who already eats infected meat. BSE causes spongiform sponge and brain degeneration. BSE has a long incubation period of 2.5 to 5 years, usually affecting an adult cow from four to five years of age. BSE is caused by a protein that fails to fold-prion. In the UK, more than 180,000 cows are infected and 4.4 million people are slaughtered during the eradication program. According to statistical estimates made in 2006, 44,800 French livestock were infected by BSE between 1987 and 1997.
This disease may be most often transmitted to humans by eating foods contaminated with the brain, spinal cord, or infected carcinoma duct. However, infectious agents, although mostly concentrated in neural tissue, can be found in almost all tissues throughout the body, including blood. When transmitted to humans, it is known as the new Variant Creutzfeldt-Jakob disease (vCJD or nvCJD), and in June 2014 it has killed 177 people in Britain, and 52 elsewhere, especially in Western Europe. Between 460,000 and 482,000 animals infected with BSE have entered the human food chain prior to control on high-risk innards introduced in 1989.
The British and Irish investigations into BSE conclude epizootic-induced cows, usually herbivorous, are fed on the rest of the livestock in the form of meat and bone meal (MBM), a protein supplement in concentrated feed. Because dairy cows are generally fed concentrated feed after weaning, they usually develop this disease more often than beef cattle.
The cause of BSE may be from MBM contamination from sheep with scrapie processed at the same slaughterhouse. This epidemic may be accelerated by recycling infected bovine tissue prior to BSE recognition. The origin of the disease itself is still unknown. The infectious agent is typical for the high temperatures in which it remains feasible - over 600 Ã, Â ° C (1,112Ã, Â ° F). Contributing factor is the provision of infected protein supplements in very young calves.
Video Bovine spongiform encephalopathy
Classification
BSE is an infectious disease that primarily affects the central nervous system; it is a form of infectious spongiform encephalopathy, such as Creutzfeldt-Jakob disease and kuru in humans and scrapie in sheep, and chronic wasting disease in cervids.
Maps Bovine spongiform encephalopathy
Signs and symptoms
Symptoms are not seen immediately in cattle due to the very long incubation period of the disease. Some animals have been observed to have abnormal walking styles, behavioral changes, tremors and hyper responses to certain stimuli. Hindlimb ataxia affects animal gait and occurs when muscle control is lost. This results in poor balance and coordination. Behavioral changes may include aggression, anxiety related to a particular situation, anxiety, frenzy or an overall change in temperament. Some of the rare but previously observed symptoms also include persistent pacing, rubbing or licking. In addition, nonspecific symptoms have also been observed which include weight loss, decreased milk production, lameness, ear infections and grinding of teeth due to pain. Some animals may exhibit a combination of these symptoms, while others can only be observed showing one of the many reported. Once clinical symptoms appear, they usually get worse over the coming weeks and months, leading eventually to reactions, coma, and death.
Cause
The infectious agent in BSE is a specific type of protein misfold called a prion.
Prions can be transmitted to humans by eating food contaminated with them.
Prions are not destroyed even if beef or ingredients containing them are cooked or heated. Prion proteins carry disease between individuals and cause brain damage. Spongiform encephalopathy that can be transmitted (TSE) such as BSE can appear in animals carrying alleles that cause normal protein molecules previously to change from a helical alpha arrangement to a pleated beta sheet, which is a disease-causing form for a particular protein. Transmission can occur when healthy animals come into contact with contaminated tissue from others with the disease. In the brain, these proteins cause native cellular prion proteins to transform into an infectious state, which then continues to damage further prion proteins in exponential cascades. It produces protein aggregates, which then form a solid plaque fiber that leads to microscopic appearance of "holes" in the brain, degeneration of physical and mental abilities, and ultimately death.
Different hypotheses exist for the origin of prion proteins in cows. Two main hypotheses indicate that he may have jumped species from scrapie disease to sheep, or that he evolved from the spontaneous form of "mad cow disease" that has been seen occasionally in cattle for centuries. In the 5th century BC, Hippocrates described a similar illness in cattle and sheep, which he believed also occurred in humans. Publius Flavius ​​Vegetius Renatus noted cases of diseases with similar characteristics in the fourth and fifth centuries. The UK Government's inquiry takes the view that the cause is not scrapie, as originally postulated, but some events in the 1970s were impossible to identify.
Another theory suggests that the agent is a virus, virino, spiroplasm species, or Acinetobacter species.
Pathogenesis
The pathogenesis of BSE is not well understood or documented as other diseases of this nature. Although BSE is a disease that produces neurological defects, its pathogenesis occurs in areas outside the nervous system. There is a strong deposition PrP Sc originally located in the Peyer Ileal patch of the small intestine. The lymphatic system has been identified in the pathogenesis of chips. It has not, however, been determined to be an essential part of BSE pathogenesis. The Paleer Ileal Patch is the only organ of this system that has been found to play a major role in pathogenesis. The infectivity of the Paleer Ileal patch has been observed as early as 4 months after inoculation. The accumulation of PrP Sc was found to occur in real body macrophages of the Ileal Peyer patch. Macrophages of tangible bodies involved in permission PrP Sc are considered to play a role in the accumulation of PrP Sc in the Peyer patch. Accumulation of PrP Sc is also found in follicular dendritic cells; However, it was a lower rate. Six months after inoculation, there is no infectivity in any tissue, only on the ileum. This leads researchers to believe that disease agents replicate here. In a naturally confirmed case, there have been no reports of infectivity in the Ileal Peyer patch. Generally, in clinical trials, high doses of disease are given. In natural cases, it is hypothesized that low-dose agents are present, and therefore, infectivity can not be observed.
Diagnosis
The diagnosis of BSE continues to be a practical matter. It has an incubation period from month to year, where no symptoms are known, although pathways convert normal brain prion protein (PrP) into PrP Sc forms associated with disease and disease-related initiation has begun. Currently, there is hardly any known way to detect PrP Sc reliably except by checking the post-mortem brain tissue using neuropathology and immunohistochemistry methods. The accumulation of PrP Sc abnormally folded PrP forms is a characteristic of the disease, but is present at very low levels in easily accessible body fluids such as blood or urine. Researchers have tried to develop methods for measuring PrP Sc , but there is no method to use in materials such as blood that has been fully accepted.
Traditional methods of diagnosis depend on histopathologic examination of the cerebral medulla, and other tissues, post mortem . Immunohistochemistry can be used to show the accumulation of prion proteins.
In 2010, a team from New York described the detection of PrP Sc even when initially present only on one part in a hundred billion (10 -11 ) in brain tissue. This method combines amplification with a new technology called surround optical fiber immunoassay and some specific antibodies against PrP Sc . After strengthening and then concentrating PrP Sc , the sample was labeled with fluorescent dye using antibodies for specificity and finally loaded into a microcapillary tube. This tube is placed in a specially constructed device so that it is entirely surrounded by optical fibers to capture all the light emitted after the excited dye using a laser. This technique allows the detection of PrP Sc after fewer conversion cycles than others have achieved, substantially reducing the possibility of artifacts, as well as speeding testing. The researchers also tested their method on blood samples from apparently healthy sheep that later developed into scrapie. Animal brain is analyzed after any symptoms become apparent. The researchers could, therefore, compare the results of brain tissue and blood taken after the animal exhibits symptoms of the disease, with blood previously obtained in animal life, and from uninfected animals. The results show very clearly that PrP Sc can be detected in animal blood long before symptoms appear. After further development and testing, this method can be very useful in surveillance as a blood or urinal screening test for BSE.
Prevention
The ban on feeding meat and bone meal for livestock has resulted in a strong reduction in cases in countries where the disease has been present. In disease-free countries, control depends on import control, feeding regulations, and monitoring measures.
In British and US slaughterhouses, the brain, spinal cord, trigeminal ganglia, intestines, eyes, and tonsils of cattle are classified as specific risk ingredients, and must be disposed of appropriately.
Improved BSE-related feed bans apply in both the United States and Canada to help improve BSE prevention and removal.
Treatment
By 2018, there is no cure for BSE. Some symptoms such as twitches can be managed but otherwise treatment is palliative care.
Epidemiology
The tests used to detect BSE vary widely, as do regulations in different jurisdictions for when, and which cattle, should be tested. For example in the EU, livestock tested older (30 months or more), while many cows were slaughtered younger than that. At the end of the scale, Japan tested all the cattle at the time of the massacre. The test is also difficult, because the modified prion protein has very low levels in the blood or urine, and no other signals are found. The newer tests are faster, more sensitive, and less expensive, so the future figures may be more comprehensive. Even so, today the only reliable test is tissue examination during necropsy.
As for vCJD in humans, autopsy tests are not always done, so the numbers are, too, likely too low, but possibly by a lower fraction. In the United Kingdom, anyone with possible vCJD symptoms should be reported to the Creutzfeldt-Jakob Disease Control Unit. In the United States, the CDC refused to impose a national requirement that doctors and hospitals report cases of illness. Instead, agencies rely on other methods, including death certificates and urge doctors to send suspicious cases to the National Disease Pathology Surveillance Center (NPDPSC) at Case Western Reserve University in Cleveland, funded by the CDC.
To control the potential transmission of vCJD in the United States, the American Red Cross has established strict restrictions on the individual's eligibility to donate blood. Individuals who have spent cumulative time of 3 months or more in the UK between 1980 and 1996, or a cumulative time of 5 years or more from 1980 to be present in every combination of countries in Europe, are prohibited from donating blood.
Cases
North America
The first case was reported in North America in December 1993 from Alberta, Canada. Another Canadian case was reported in May 2003. The first known US incident occurred in December of the same year, although it was later confirmed as a Canadian imported Canadian cow to announce two additional BSE cases from Alberta in early 2005. In June 2005, John R Clifford, veterinary chief for veterinary inspection services of the US Department of Agriculture, confirmed the BSE case in Texas.
Practice in the United States related to BSE
Cheap and abundant soy foods in the United States as well as cottonseed food (1.5 million tonnes produced in the US each year, none suitable for humans or other simple abdominal animals), even cheaper than soybean meal. Historically, meat and bone meal, blood meal, and meat cuts almost always have higher prices as feed additives than oil seeds in the US, so there are not many incentives available to use animal products to feed ruminant animals. As a result, the use of animal byproducts is never common, as in Europe. However, US regulations only prohibit partial use of animal by-products in feed. In 1997, regulations prohibited the supply of mammalian by-products to ruminants such as cattle and goats. However, ruminant by-products can still be legally given to pets or other livestock, including pigs and poultry. In addition, it is legal for ruminants to be fed by the products of some of these animals. Therefore, some authors state that under certain circumstances, it is still possible for BSE events to increase in US cattle. Proposals to end the use of cow's blood, rest of the restaurant, and poultry waste (dirt, feathers, bedding material)
In February 2001, the US Government Accountability Office reported that the FDA, which is responsible for organizing the feed, did not adequately impose restrictions. Compliance with the rules proved very bad before the discovery of a cow in Washington infected with BSE in 2003, but industry representatives reported that compliance is now total. Even so, critics call the partial ban insufficient. Indeed, the US Creekstone Farms meat producer was forcibly prevented from performing BSE testing by the USDA, which under the 1913 law does not clearly have the authority to limit the sale of BSE test kits, allegedly to protect other manufacturers from being forced to perform the same tests to keep competitive.
USDA has issued a recall of beef supply involving the introduction of downer cattle to the food supply. The Hallmark/Westland Meat Packing Company was found to have used electric shocks to drive the calf cows into the slaughter system in 2007. Perhaps due to pressure from large agribusinesses, the United States has drastically reduced the number of cows examined for BSE.
Effects on the US beef industry
Japan is the main importer of US beef, purchasing 240,000 tonnes worth $ 1.4 billion in 2003. After the discovery of the first case of BSE in the US on December 23, 2003, Japan halted US beef imports. In December 2005, Japan again allowed US beef imports, but restored its ban in January 2006 after breach of the Japan-Japan beef import agreement: vertebral columns, which should have been removed before shipment, were included in the delivery of veal.
Tokyo generated US pressure to resume imports, ignoring consumer concerns about the safety of US beef, the Japanese consumer group said. Michiko Kamiyama from Food Safety Citizen Watch and Yoko Tomiyama from the Union of Japan Consumers said of this: "The government has prioritized the political schedule between the two countries, not on food security or human health."
Sixty-five countries impose full or partial restrictions on imports of US beef products due to concerns that US testing does not have sufficient accuracy. As a result, US beef exports declined from 1,300,000 metric tons in 2003, (before the first mad cow was detected in the US) to 322,000 metric tons in 2004. This has risen since then to 771,000 metric tons in 2007 and to 1,300 Metric tons in 2017.
On December 31, 2006, Hematech, Inc., a Sioux Falls-based biotech company, South Dakota, announced that it has used genetic engineering and cloning technology to produce livestock that lacks the genes needed for prion production - thus theoretically making them immune to BSE.
In April 2012, some South Korean retailers stopped importing beef from the United States after the BSE case was reported. Indonesia also stopped importing beef from the US after dairy cows with mad cow disease found in California.
Japanese
With 36 confirmed cases, Japan experienced one of a large number of BSE cases outside Europe. It is the only country outside of Europe and America to report non-import cases. The food safety reform given the BSE case resulted in the formation of the government's Food Safety Commission in 2003.
Europe
Cow is a natural herbivore, eating grass. In modern industrial agriculture, a variety of commercial feed is used, which may contain ingredients including antibiotics, hormones, pesticides, fertilizers, and protein supplements. The use of meat and bone meal, produced from soil and cooked food scraps from the slaughter process, and from the carcass of sick and injured animals such as cattle or sheep, as a protein supplement in livestock feed is widespread in Europe before around 1987. Worldwide, soybean meal is a major vegetable protein supplement fed to livestock. However, soy does not grow well in Europe, so cattle ranchers across Europe are turning to cheaper fodder as an alternative. The UK investigation rejected suggestions that changes to processing might have increased infectious agents in animal feed, saying, "changes in the process can not be entirely responsible for the emergence of BSE, and changes in regulation are not a factor at all." (The prions cause BSE is not destroyed by heat treatment.)
The first confirmed example where an animal fell ill with the disease occurred in 1986 in England, and subsequent laboratory tests indicated the presence of BSE; in November 1987, the UK Ministry of Agriculture accepted him to have a new disease in his hands. Furthermore, 177 people (as of June 2014) contracted and died of a disease with similar neurologic symptoms that came to be called (new) variants of Creutzfeldt-Jakob disease (vCJD). This is a separate disease of the classic 'Creutzfeldt-Jakob' disease, which is unrelated to BSE and has been known since the early 1900s. Three cases of vCJD occurred in people who had lived in or visited the UK - each in the Republic of Ireland, Canada, and the United States. Also, there are concerns about those who work with (and therefore inhaling) beef and bone meal, such as horticulture, who use it as fertilizer. The latest statistics on all types of CJD are published by the National Creutzfeldt-Jakob Disease Control Unit in Edinburgh, Scotland.
For many vCJD patients, direct evidence exists that they have consumed contaminated beef, and this is assumed to be the mechanism by which all affected people contract it. The incidence of the disease also seems to correlate with slaughtering practices that lead to a mixture of tissue nervous system with minced meat (minced) and other beef. An estimated 400,000 BSE-infected cows entered the human food chain in the 1980s. Although epizootic BSE is ultimately controlled by the culling of all suspected cow populations, people are still diagnosed with vCJD each year (although the current number of new cases decreases to less than five per year). This is associated with a long incubation period for prion disease, which is usually measured in years or decades. As a result, the full extent of human vCJD outbreaks remains unknown.
The scientific consensus is that the infectious BSE raw materials are not destroyed through cooking procedures, which means that even contaminated beef food prepared "done well" can remain contagious. In fact, the infectious agent still lives above 600 ° C (1,112 ° F).
Alan Colchester, a professor of neurology at the University of Kent, and Nancy Colchester, writes in the September 3, 2005 medical journal The Lancet proposes the theory that is the earliest origin of BSE in the United Kingdom is the import of Subcontinent Indian bone food containing human remains infected with CJD. The Indian government vigorously responded to the research, calling it "misleading, extremely naughty, fictitious, unreasonable," further adding that India maintains constant control and lacks any BSE or vCJD cases. The authors answer in the January 22, 2006 edition of The Lancet that their theory can not be proved only in the same sense as all other BSE origin theories and that theory requires further investigation.
During the investigation into the epistemic BSE, investigations are also conducted into the activities of the Department of Health Drug Administration (MCA). On May 7, 1999, David Osborne Hagger, a retired civil servant who worked in the Department of Health's Drug Division between 1984 and 1994, produced a written statement for the BSE Investigation in which he provided a report on his professional experience of BSE.
In February 1989, the MCA was asked to "identify relevant manufacturers and obtain information about bovine materials contained in children's vaccines, stock of this vaccine and how long it will take to switch to other products." In July, "the use of bovine insulin in small groups especially elderly patients was noted and recognized that alternative products for this group were not considered satisfactory." In September, the BSE Working Party of the Committee on Safety of Medicines (CSM) recommended that "no licensing action is needed nowadays in terms of products produced from bovine or cow-brained materials prepared in nutritional media and sourced from outside the United Kingdom. , The Strait Islands and the Republic of Ireland provided that the country of origin is known to be free of BSE, has a competent veterinary advisor and is known for practicing good farms. "
In 1990, the British Diabetic Association became concerned about the safety of bovine insulin. CSM assured them that "no insulin comes from cattle in the UK or Ireland and that the situation in other countries is being monitored."
In 1991, the European Commission "[stated] concerns about the possibility of transmitting BSE/scrapie agents to humans through the use of certain cosmetic treatments."
In 1992, sources in France reported to the MCA "that the BSE has now been reported in France and there are some licensed surgical sutures derived from French bovine material." Concerns also arise at the CSM meeting "regarding the possible risk of transmission of BSE agents in gelatin products." Over the years, the French government and the agricultural industry downplayed the epidemic rate, claiming only 923 confirmed cases. In 2004 the character was challenged in an article in The Review of Veterinary Research that put the figure at 300,000. The scientists behind this study then criticized the surveillance system, which indicated that they believed there was an official concealment. Epidemiologist Jean-Louis Thillier has finally concluded that between 1996 and 2006, over 300,000 BSE cases have infected national herd and that nine French people have died unnecessarily from the epidemic due to failure to report cases, a finding received by a judge ordering to report.
For this failure, France is strongly criticized internationally. Thillier himself questioned why there was never a ban on French beef or basic precautions to stop the food chain from becoming contaminated, suggesting "Perhaps because the French government forgot its role in ensuring the safety of food products, and this neglect cost the lives of nine people." Sydney Morning Herald added , "while French politicians blouse blame Britain for the emergence of the disease - and try to quarantine the country by banning imports of British beef - they fail to take steps to prevent a hidden epidemic at home."
In 2016 France confirmed further cases of BSE.
A number of other countries have isolated confirmed BSE outbreaks, including Spain, Portugal, Belgium and Germany. However, in all cases, including the UK and France, it is estimated that the number of cases is far less than the amount reported, so the true incidence could be much higher.
Prohibition against British beef
The BSE crisis caused the EU to ban the export of British beef with an effect from March 1996; The ban lasted for 10 years before it was finally appointed on May 1, 2006 despite attempts in May 1996 by British Prime Minister John Major to get a ban revoked. The ban resulted in a trade controversy between Britain and other EU countries, dubbed the "cattle war" by the media. Fixed limits for beef that contain "vertebral material" and for beef sold in bone. France continued to impose a ban on British beef illegally shortly after the European Court had ordered him to lift the blockade, despite never paying any penalties for doing so.
Russia is continuing to lift the ban after November 2012 after 16 years; the announcement was made during a visit by British veteran chief Nigel Gibbens.
It was successfully negotiated that the beef from Wales was allowed to be exported to the Dutch market, which was once an important market for Northern Irish beef. Of the two approved export companies in the UK in 1999, one in Scotland - a company where live beef is supplied from Northern Ireland. Because of the very low BSE incidence in Northern Ireland - only six BSE cases in 1999 - partly due to early adoption of herd markings and advanced computerized systems in the region, calls were made to remove the EU ban on exports with due regard for Northern Ireland beef.
Source of the article : Wikipedia
0 Comments