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{{Bovine spongiform encephalopathy}} | {{Bovine spongiform encephalopathy}} | ||
{{CMG}} | {{CMG}}; {{AE}} {{Adnan Ezici}} | ||
==Overview== | ==Overview== | ||
Bovine spongiform encephalopathy is a transmissible [[spongiform encephalopathy]] of cattle associated with abnormal prion proteins in the brain. Affected animals develop excitability and salivation followed by [[ataxia]]. This disorder has been associated with consumption of [[scrapie]] infected ruminant derived protein. This condition may be transmitted to humans, where it is referred to as variant or new variant CREUTZFELDT-JAKOB SYNDROME. | Bovine spongiform encephalopathy is a transmissible [[spongiform encephalopathy]] of cattle associated with abnormal prion proteins in the brain. Affected animals develop excitability and salivation followed by [[ataxia]]. This disorder has been associated with consumption of [[scrapie]] infected ruminant derived protein. This condition may be transmitted to humans, where it is referred to as variant or new variant CREUTZFELDT-JAKOB SYNDROME. Publius Flavius Vegetius Renatus records cases of a disease with similar characteristics in the 4th and 5th Century AD. The origin of the disease itself remains unknown. The current scientific view is that infectious proteins called [[prion]]s developed through spontaneous mutation, probably in the 1970s, and there is a possibility that the use of [[Organophosphate|organophosphorus pesticides]] increased the susceptibility of cattle to the disease. Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989. It is believed that the disease may be transmitted to human beings who eat infected carcasses. In humans, it is known as new variant [[Creutzfeldt-Jakob disease]] (vCJD or nvCJD), and by June 2007, it had killed 165 people in Britain, and six elsewhere with the number expected to rise because of the disease's long incubation period. Based on the biochemical signatures of the disease-associated [[prion protein]], Bovine spongiform encephalopahty (BSE) may be classified as either classic or atypical. Atypical BSE may further be classified into H- and L-types. Due to the accumulation of [[amyloid protein]] in the brain in cattles with L-type BSE, its also known as bovine amyloidotic spongiform encephalopathy (BASE). It is understood that Bovine spongiform encephalopathy (BSE) is caused by a misfolded [[prion]] [[protein]]. Misfolded prion proteins carry the disease between individuals and cause deterioration of the [[brain]]. BSE is a type of [[transmissible spongiform encephalopathy]] (TSE). Bovine spongiform encephalopathy (BSE) may be caused by different strains including the classic BSE strain (which is responsible for the outbreak in the United Kingdom) and two atypical strains (H and L strains). Bovine spongiform encephalopathy must be differentiated from other diseases that cause hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, [[tremors]], [[ataxia]], disrupted milk production, and weight loss in animals, such as scrapes, [[rabies]], encephalitic listeriosis, [[hypomagnesemia]], [[lead poisoning]], downer cow syndrome, nervous ketosis, polioencephalomalacia, ingestion of plant or fungal tremoragens, [[intracranial abscess]] or tumors, trauma to the spinal column, and other [[viral]] and [[bacterial]] neuroinfectious diseases. Following an [[epizootic]] of BSE in Britain, 165 people (up until 2007) acquired and died of a disease with similar neurological symptoms subsequently called [[Creutzfeldt-Jakob disease|vCJD]], or (new) variant Creutzfeldt-Jakob disease. It is estimated that 400,000 cattle infected with BSE entered the human food chain in the 1980s. Although the BSE epizootic was eventually brought under control by culling all suspect cattle populations, people are still being diagnosed with [[Creutzfeldt-Jakob disease|vCJD]] each year. It is notable that there are no cases reported in Australia and New Zealand where cattle are mainly fed outside on grass pasture and, mainly in Australia, non-grass feeding is done only as a final finishing process before the animals are processed for meat. The most potent risk factor in the development of bovine spongiform encephalopathy is the consumption of meat-and-bone meal (MBM) by cattle. There is insufficient evidence to recommend routine screening for bovine spongiform encephalopathy (BSE). The symptoms of bovine spongiform encephalopathy typically develop 2-8 years after exposure to [[prion]]s. [[Prognosis]] is generally poor, and death occurs approximately 3 months after the appearance of the first clinical signs. Bovine spongiform encephalopathy is primarily diagnosed based on the clinical presentation. However, [[postmortem]] examination should be performed for the definitive diagnosis. The postmortem investigation might be done with either [[western blot]], [[ELISA]], rapid test for BSE (ID-Lelystad), or [[histopathology]]. The confirmation of the diagnosis is possible either with the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Lelystad), or vacuolation of [[neurons]] and neuropil in the histopathologic examination of [[medulla oblongata]] specimen. The most common symptoms of bovine spongiform encephalopathy include hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, [[tremors]], [[ataxia]], disrupted milk production, and weight loss in animals. Common physical examination findings of bovine spongiform encephalopathy include [[ataxia]], [[tremor]], abnormal head carriage, [[hyperesthesia]], excessive licking, loss of weight, recumbency, and abnormal ear position. Laboratory findings consistent with the diagnosis of bovine spongiform encephalopathy include the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Leystad), the detection of Scrapie-Associated Fibrils in the brain tissue (by electron microscopy), and specific histopathologic findings such as vacuolation of [[neurons]] and neuropil. There are no ECG findings associated with bovine spongiform encephalopathy. There are no x-ray findings associated with bovine spongiform encephalopathy. There are no echocardiography/ultrasound findings associated with bovine spongiform encephalopathy. There are no CT scan findings associated with bovine spongiform encephalopathy. [[MRI|T2-weighted (T2W) MRI]] may be helpful in the diagnosis of bovine spongiform encephalopathy. Findings on T2W-MRI suggestive of bovine spongiform encephalopathy include T2W-MRI hyperintensity in the [[thalamus|thalamic nuclei]]. There are no other imaging findings associated with bovine spongiform encephalopathy. There are no other diagnostic studies associated with bovine spongiform encephalopathy. There is no treatment for bovine spongiform encephalopathy. There are no recommended therapeutic interventions for the management of bovine spongiform encephalopathy. [[Surgery|Surgical intervention]] is not recommended for the management of bovine spongiform encephalopathy. Effective measures for the primary prevention of bovine spongiform encephalopathy include control measures such as surveillance, banning specified risk materials, culling sick animals, and excluding all animals more than 30 months of age from the human food and animal feed supplies. There are no established measures for the secondary prevention of bovine spongiform encephalopathy. | ||
==Historical Perspective== | |||
Publius Flavius Vegetius Renatus records cases of a disease with similar characteristics in the 4th and 5th Century AD. The origin of the disease itself remains unknown. The current scientific view is that infectious proteins called [[prion]]s developed through spontaneous mutation, probably in the 1970s, and there is a possibility that the use of [[Organophosphate|organophosphorus pesticides]] increased the susceptibility of cattle to the disease. Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989. It is believed that the disease may be transmitted to human beings who eat infected carcasses. In humans, it is known as new variant [[Creutzfeldt-Jakob disease]] (vCJD or nvCJD), and by June 2007, it had killed 165 people in Britain, and six elsewhere with the number expected to rise because of the disease's long incubation period. | |||
==Classification== | |||
Based on the biochemical signatures of the disease-associated [[prion protein]], Bovine spongiform encephalopahty (BSE) may be classified as either classic or atypical. Atypical BSE may further be classified into H- and L-types. Due to the accumulation of [[amyloid protein]] in the brain in cattles with L-type BSE, its also known as bovine amyloidotic spongiform encephalopathy (BASE). | |||
==Pathophysiology== | |||
It is understood that Bovine spongiform encephalopathy (BSE) is caused by a misfolded [[prion]] [[protein]]. Misfolded prion proteins carry the disease between individuals and cause deterioration of the [[brain]]. BSE is a type of [[transmissible spongiform encephalopathy]] (TSE). | |||
==Causes== | |||
Bovine spongiform encephalopathy (BSE) may be caused by different strains including the classic BSE strain (which is responsible for the outbreak in the United Kingdom) and two atypical strains (H and L strains). | |||
==Differentiating Xyz from Other Diseases== | |||
Bovine spongiform encephalopathy must be differentiated from other diseases that cause hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, [[tremors]], [[ataxia]], disrupted milk production, and weight loss in animals, such as scrapes, [[rabies]], encephalitic listeriosis, [[hypomagnesemia]], [[lead poisoning]], downer cow syndrome, nervous ketosis, polioencephalomalacia, ingestion of plant or fungal tremoragens, [[intracranial abscess]] or tumors, trauma to the spinal column, and other [[viral]] and [[bacterial]] neuroinfectious diseases. | |||
==Epidemiology and Demographics== | |||
Following an [[epizootic]] of BSE in Britain, 165 people (up until 2007) acquired and died of a disease with similar neurological symptoms subsequently called [[Creutzfeldt-Jakob disease|vCJD]], or (new) variant Creutzfeldt-Jakob disease. It is estimated that 400,000 cattle infected with BSE entered the human food chain in the 1980s. Although the BSE epizootic was eventually brought under control by culling all suspect cattle populations, people are still being diagnosed with [[Creutzfeldt-Jakob disease|vCJD]] each year. It is notable that there are no cases reported in Australia and New Zealand where cattle are mainly fed outside on grass pasture and, mainly in Australia, non-grass feeding is done only as a final finishing process before the animals are processed for meat. | |||
==Risk Factors== | |||
The most potent risk factor in the development of bovine spongiform encephalopathy is the consumption of meat-and-bone meal (MBM) by cattle. | |||
==Screening== | |||
There is insufficient evidence to recommend routine screening for bovine spongiform encephalopathy (BSE). | |||
==Natural History, Complications, and Prognosis== | |||
The symptoms of bovine spongiform encephalopathy typically develop 2-8 years after exposure to [[prion]]s. [[Prognosis]] is generally poor, and death occurs approximately 3 months after the appearance of the first clinical signs. | |||
==Diagnosis== | |||
===Diagnostic Study of Choice=== | |||
Bovine spongiform encephalopathy is primarily diagnosed based on the clinical presentation. However, [[postmortem]] examination should be performed for the definitive diagnosis. The postmortem investigation might be done with either [[western blot]], [[ELISA]], rapid test for BSE (ID-Lelystad), or [[histopathology]]. The confirmation of the diagnosis is possible either with the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Lelystad), or vacuolation of [[neurons]] and neuropil in the histopathologic examination of [[medulla oblongata]] specimen. | |||
===History and Symptoms=== | |||
The most common symptoms of bovine spongiform encephalopathy include hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, [[tremors]], [[ataxia]], disrupted milk production, and weight loss in animals. | |||
===Physical Examination=== | |||
Common physical examination findings of bovine spongiform encephalopathy include [[ataxia]], [[tremor]], abnormal head carriage, [[hyperesthesia]], excessive licking, loss of weight, recumbency, and abnormal ear position. | |||
===Laboratory Findings=== | |||
Laboratory findings consistent with the diagnosis of bovine spongiform encephalopathy include the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Leystad), the detection of Scrapie-Associated Fibrils in the brain tissue (by electron microscopy), and specific histopathologic findings such as vacuolation of [[neurons]] and neuropil. | |||
===Electrocardiogram=== | |||
There are no ECG findings associated with bovine spongiform encephalopathy. | |||
===X-ray=== | |||
There are no x-ray findings associated with bovine spongiform encephalopathy. | |||
===Echocardiography and Ultrasound=== | |||
There are no echocardiography/ultrasound findings associated with bovine spongiform encephalopathy. | |||
===CT scan=== | |||
There are no CT scan findings associated with bovine spongiform encephalopathy. | |||
===MRI=== | |||
[[MRI|T2-weighted (T2W) MRI]] may be helpful in the diagnosis of bovine spongiform encephalopathy. Findings on T2W-MRI suggestive of bovine spongiform encephalopathy include T2W-MRI hyperintensity in the [[thalamus|thalamic nuclei]]. | |||
===Other Imaging Findings=== | |||
There are no other imaging findings associated with bovine spongiform encephalopathy. | |||
===Other Diagnostic Studies=== | |||
There are no other diagnostic studies associated with bovine spongiform encephalopathy. | |||
==Treatment== | |||
===Medical Therapy=== | |||
There is no treatment for bovine spongiform encephalopathy. | |||
=== Interventions === | |||
There are no recommended therapeutic interventions for the management of bovine spongiform encephalopathy. | |||
===Surgery=== | |||
[[Surgery|Surgical intervention]] is not recommended for the management of bovine spongiform encephalopathy. | |||
===Primary Prevention=== | |||
Effective measures for the primary prevention of bovine spongiform encephalopathy include control measures such as surveillance, banning specified risk materials, culling sick animals, and excluding all animals more than 30 months of age from the human food and animal feed supplies. | |||
===Secondary Prevention=== | |||
There are no established measures for the secondary prevention of bovine spongiform encephalopathy. | |||
==References== | ==References== | ||
Latest revision as of 15:00, 5 January 2022
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Bovine Spongiform Encephalopathy Microchapters |
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Differentiating Bovine Spongiform Encephalopathy from other Diseases |
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Bovine spongiform encephalopathy overview On the Web |
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Directions to Hospitals Treating Bovine spongiform encephalopathy |
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Risk calculators and risk factors for Bovine spongiform encephalopathy overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Adnan Ezici, M.D[2]
Overview
Bovine spongiform encephalopathy is a transmissible spongiform encephalopathy of cattle associated with abnormal prion proteins in the brain. Affected animals develop excitability and salivation followed by ataxia. This disorder has been associated with consumption of scrapie infected ruminant derived protein. This condition may be transmitted to humans, where it is referred to as variant or new variant CREUTZFELDT-JAKOB SYNDROME. Publius Flavius Vegetius Renatus records cases of a disease with similar characteristics in the 4th and 5th Century AD. The origin of the disease itself remains unknown. The current scientific view is that infectious proteins called prions developed through spontaneous mutation, probably in the 1970s, and there is a possibility that the use of organophosphorus pesticides increased the susceptibility of cattle to the disease. Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989. It is believed that the disease may be transmitted to human beings who eat infected carcasses. In humans, it is known as new variant Creutzfeldt-Jakob disease (vCJD or nvCJD), and by June 2007, it had killed 165 people in Britain, and six elsewhere with the number expected to rise because of the disease's long incubation period. Based on the biochemical signatures of the disease-associated prion protein, Bovine spongiform encephalopahty (BSE) may be classified as either classic or atypical. Atypical BSE may further be classified into H- and L-types. Due to the accumulation of amyloid protein in the brain in cattles with L-type BSE, its also known as bovine amyloidotic spongiform encephalopathy (BASE). It is understood that Bovine spongiform encephalopathy (BSE) is caused by a misfolded prion protein. Misfolded prion proteins carry the disease between individuals and cause deterioration of the brain. BSE is a type of transmissible spongiform encephalopathy (TSE). Bovine spongiform encephalopathy (BSE) may be caused by different strains including the classic BSE strain (which is responsible for the outbreak in the United Kingdom) and two atypical strains (H and L strains). Bovine spongiform encephalopathy must be differentiated from other diseases that cause hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, tremors, ataxia, disrupted milk production, and weight loss in animals, such as scrapes, rabies, encephalitic listeriosis, hypomagnesemia, lead poisoning, downer cow syndrome, nervous ketosis, polioencephalomalacia, ingestion of plant or fungal tremoragens, intracranial abscess or tumors, trauma to the spinal column, and other viral and bacterial neuroinfectious diseases. Following an epizootic of BSE in Britain, 165 people (up until 2007) acquired and died of a disease with similar neurological symptoms subsequently called vCJD, or (new) variant Creutzfeldt-Jakob disease. It is estimated that 400,000 cattle infected with BSE entered the human food chain in the 1980s. Although the BSE epizootic was eventually brought under control by culling all suspect cattle populations, people are still being diagnosed with vCJD each year. It is notable that there are no cases reported in Australia and New Zealand where cattle are mainly fed outside on grass pasture and, mainly in Australia, non-grass feeding is done only as a final finishing process before the animals are processed for meat. The most potent risk factor in the development of bovine spongiform encephalopathy is the consumption of meat-and-bone meal (MBM) by cattle. There is insufficient evidence to recommend routine screening for bovine spongiform encephalopathy (BSE). The symptoms of bovine spongiform encephalopathy typically develop 2-8 years after exposure to prions. Prognosis is generally poor, and death occurs approximately 3 months after the appearance of the first clinical signs. Bovine spongiform encephalopathy is primarily diagnosed based on the clinical presentation. However, postmortem examination should be performed for the definitive diagnosis. The postmortem investigation might be done with either western blot, ELISA, rapid test for BSE (ID-Lelystad), or histopathology. The confirmation of the diagnosis is possible either with the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Lelystad), or vacuolation of neurons and neuropil in the histopathologic examination of medulla oblongata specimen. The most common symptoms of bovine spongiform encephalopathy include hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, tremors, ataxia, disrupted milk production, and weight loss in animals. Common physical examination findings of bovine spongiform encephalopathy include ataxia, tremor, abnormal head carriage, hyperesthesia, excessive licking, loss of weight, recumbency, and abnormal ear position. Laboratory findings consistent with the diagnosis of bovine spongiform encephalopathy include the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Leystad), the detection of Scrapie-Associated Fibrils in the brain tissue (by electron microscopy), and specific histopathologic findings such as vacuolation of neurons and neuropil. There are no ECG findings associated with bovine spongiform encephalopathy. There are no x-ray findings associated with bovine spongiform encephalopathy. There are no echocardiography/ultrasound findings associated with bovine spongiform encephalopathy. There are no CT scan findings associated with bovine spongiform encephalopathy. T2-weighted (T2W) MRI may be helpful in the diagnosis of bovine spongiform encephalopathy. Findings on T2W-MRI suggestive of bovine spongiform encephalopathy include T2W-MRI hyperintensity in the thalamic nuclei. There are no other imaging findings associated with bovine spongiform encephalopathy. There are no other diagnostic studies associated with bovine spongiform encephalopathy. There is no treatment for bovine spongiform encephalopathy. There are no recommended therapeutic interventions for the management of bovine spongiform encephalopathy. Surgical intervention is not recommended for the management of bovine spongiform encephalopathy. Effective measures for the primary prevention of bovine spongiform encephalopathy include control measures such as surveillance, banning specified risk materials, culling sick animals, and excluding all animals more than 30 months of age from the human food and animal feed supplies. There are no established measures for the secondary prevention of bovine spongiform encephalopathy.
Historical Perspective
Publius Flavius Vegetius Renatus records cases of a disease with similar characteristics in the 4th and 5th Century AD. The origin of the disease itself remains unknown. The current scientific view is that infectious proteins called prions developed through spontaneous mutation, probably in the 1970s, and there is a possibility that the use of organophosphorus pesticides increased the susceptibility of cattle to the disease. Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989. It is believed that the disease may be transmitted to human beings who eat infected carcasses. In humans, it is known as new variant Creutzfeldt-Jakob disease (vCJD or nvCJD), and by June 2007, it had killed 165 people in Britain, and six elsewhere with the number expected to rise because of the disease's long incubation period.
Classification
Based on the biochemical signatures of the disease-associated prion protein, Bovine spongiform encephalopahty (BSE) may be classified as either classic or atypical. Atypical BSE may further be classified into H- and L-types. Due to the accumulation of amyloid protein in the brain in cattles with L-type BSE, its also known as bovine amyloidotic spongiform encephalopathy (BASE).
Pathophysiology
It is understood that Bovine spongiform encephalopathy (BSE) is caused by a misfolded prion protein. Misfolded prion proteins carry the disease between individuals and cause deterioration of the brain. BSE is a type of transmissible spongiform encephalopathy (TSE).
Causes
Bovine spongiform encephalopathy (BSE) may be caused by different strains including the classic BSE strain (which is responsible for the outbreak in the United Kingdom) and two atypical strains (H and L strains).
Differentiating Xyz from Other Diseases
Bovine spongiform encephalopathy must be differentiated from other diseases that cause hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, tremors, ataxia, disrupted milk production, and weight loss in animals, such as scrapes, rabies, encephalitic listeriosis, hypomagnesemia, lead poisoning, downer cow syndrome, nervous ketosis, polioencephalomalacia, ingestion of plant or fungal tremoragens, intracranial abscess or tumors, trauma to the spinal column, and other viral and bacterial neuroinfectious diseases.
Epidemiology and Demographics
Following an epizootic of BSE in Britain, 165 people (up until 2007) acquired and died of a disease with similar neurological symptoms subsequently called vCJD, or (new) variant Creutzfeldt-Jakob disease. It is estimated that 400,000 cattle infected with BSE entered the human food chain in the 1980s. Although the BSE epizootic was eventually brought under control by culling all suspect cattle populations, people are still being diagnosed with vCJD each year. It is notable that there are no cases reported in Australia and New Zealand where cattle are mainly fed outside on grass pasture and, mainly in Australia, non-grass feeding is done only as a final finishing process before the animals are processed for meat.
Risk Factors
The most potent risk factor in the development of bovine spongiform encephalopathy is the consumption of meat-and-bone meal (MBM) by cattle.
Screening
There is insufficient evidence to recommend routine screening for bovine spongiform encephalopathy (BSE).
Natural History, Complications, and Prognosis
The symptoms of bovine spongiform encephalopathy typically develop 2-8 years after exposure to prions. Prognosis is generally poor, and death occurs approximately 3 months after the appearance of the first clinical signs.
Diagnosis
Diagnostic Study of Choice
Bovine spongiform encephalopathy is primarily diagnosed based on the clinical presentation. However, postmortem examination should be performed for the definitive diagnosis. The postmortem investigation might be done with either western blot, ELISA, rapid test for BSE (ID-Lelystad), or histopathology. The confirmation of the diagnosis is possible either with the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Lelystad), or vacuolation of neurons and neuropil in the histopathologic examination of medulla oblongata specimen.
History and Symptoms
The most common symptoms of bovine spongiform encephalopathy include hyperesthesia, nervousness, reluctance to be milked, aggression, low head carriage, tremors, ataxia, disrupted milk production, and weight loss in animals.
Physical Examination
Common physical examination findings of bovine spongiform encephalopathy include ataxia, tremor, abnormal head carriage, hyperesthesia, excessive licking, loss of weight, recumbency, and abnormal ear position.
Laboratory Findings
Laboratory findings consistent with the diagnosis of bovine spongiform encephalopathy include the detection of PrPBSE in the brain tissue (either by western blot, ELISA, or ID-Leystad), the detection of Scrapie-Associated Fibrils in the brain tissue (by electron microscopy), and specific histopathologic findings such as vacuolation of neurons and neuropil.
Electrocardiogram
There are no ECG findings associated with bovine spongiform encephalopathy.
X-ray
There are no x-ray findings associated with bovine spongiform encephalopathy.
Echocardiography and Ultrasound
There are no echocardiography/ultrasound findings associated with bovine spongiform encephalopathy.
CT scan
There are no CT scan findings associated with bovine spongiform encephalopathy.
MRI
T2-weighted (T2W) MRI may be helpful in the diagnosis of bovine spongiform encephalopathy. Findings on T2W-MRI suggestive of bovine spongiform encephalopathy include T2W-MRI hyperintensity in the thalamic nuclei.
Other Imaging Findings
There are no other imaging findings associated with bovine spongiform encephalopathy.
Other Diagnostic Studies
There are no other diagnostic studies associated with bovine spongiform encephalopathy.
Treatment
Medical Therapy
There is no treatment for bovine spongiform encephalopathy.
Interventions
There are no recommended therapeutic interventions for the management of bovine spongiform encephalopathy.
Surgery
Surgical intervention is not recommended for the management of bovine spongiform encephalopathy.
Primary Prevention
Effective measures for the primary prevention of bovine spongiform encephalopathy include control measures such as surveillance, banning specified risk materials, culling sick animals, and excluding all animals more than 30 months of age from the human food and animal feed supplies.
Secondary Prevention
There are no established measures for the secondary prevention of bovine spongiform encephalopathy.