Bovine spongiform encephalopathy (BSE), widely referred to as "mad cow disease," is a chronic degenerative disease affecting the central nervous system of cattle. The disease was first diagnosed in 1986 in Great Britain.
BSE has had a substantial impact on the livestock industry in the United Kingdom. The disease also has been confirmed in domestic cattle in Belgium, France, Ireland, Liechtenstein, Luxembourg, the Netherlands, Portugal, and Switzerland. The U.S. Department of Agriculture's (USDA) Animal and Plant Health Inspection Service (APHIS) is enforcing import restrictions and is conducting surveillance for BSE to ensure that this serious disease does not become established in the United States.
Clinical Signs
Cattle affected by BSE experience progressive degeneration of the nervous system. Affected animals may display changes in temperament, such as nervousness or aggression, abnormal posture, incoordination and difficulty in rising, decreased milk production, or loss of body weight despite continued appetite. Affected cattle die. The causative agent of the disease is not completely characterized, and there is neither any treatment nor a vaccine to prevent the disease.
The incubation period (the time from when an animal becomes infected until it first shows disease signs) is from 2 to 8 years. Following the onset of clinical signs, the animal's condition deteriorates until it either dies or is destroyed. This process usually takes from 2 weeks to 6 months. Most cases in Great Britain have occurred in dairy cows between 3 and 6 years of age.
Currently, there is no test to detect the disease in a live animal; veterinary pathologists confirm BSE by postmortem microscopic examination of brain tissue or by the detection of the abnormal form of the prion protein. BSE is so named because of the spongy appearance of the brain tissue of infected cattle when sections are examined under a microscope.
History
From November 1986 (when BSE was first identified as a separate disease entity) until July 2, 1999, 175,065 head of cattle in more than 34,800 herds were diagnosed with BSE in Great Britain. The epidemic peaked in January 1993 at almost 1,000 new cases reported per week. Agricultural officials in Great Britain have taken a series of actions to eradicate BSE, including making BSE a notifiable disease, prohibiting the inclusion of mammalian meat-and-bone meal in feed for all food-producing animals, prohibiting the inclusion of animals more than 30 months of age in the animal and human food chains, and destroying all animals showing signs of BSE and other animals at high risk of developing the disease.
As a result of these actions, the rate of newly reported cases of BSE is decreasing. Currently, approximately 60 new cases are found in Great Britain per week.
Epidemiology
There are different scientific hypotheses concerning the origins of BSE. Epidemiologic data suggest that BSE in Great Britain may have been caused by feeding cattle rendered protein produced from the carcasses of scrapie-infected sheep. Scrapie has a long incubation period up to 60 months and has been endemic in Great Britain for centuries. An alternate theory is that BSE had existed in undetectable levels in the British cattle population prior to 1986. The practice of using products such as meat-and-bone meal as a source of protein in cattle rations has been common for several decades. Changes in rendering operations in the early 1980's may have played a part in the appearance of the disease and the large number of cases that developed.
There is no evidence that BSE spreads horizontally, i.e., by contact between unrelated adult cattle or from cattle to other species. Limited research suggests that maternal or vertical transmission may occur at a very low level. This low level most likely would not perpetuate the epidemic under British farming conditions. Research continues in this area.
BSE is classified as a transmissible spongiform encephalopathy (TSE). The agent responsible for BSE and other TSE's is smaller than the smallest known virus and has not been completely characterized. There are three main theories on the nature of the agent: (1) the agent is a virus with unusual characteristics, (2) the agent is a prion an exclusively host-coded protein that is modified to a partially protease-resistant form after infection, and (3) the agent is a virino a small, noncoding regulatory nucleic acid coated with a host-derived protective protein. The BSE agent is extremely resistant to heat and to normal sterilization processes. It also does not evoke any detectable immune response or inflammatory reaction in host animals.
In cattle naturally infected with BSE, the BSE agent has been found only in brain tissue, in the spinal cord, and in the retina. Additional studies have identified BSE infectivity in the distal ileum, bone marrow, dorsal root ganglion, and trigeminal ganglion of calves that had been fed brain material from BSE-infected animals.
The presence of the BSE agent in tissues is determined by inoculating animals, usually mice, with material believed to be infected with BSE. Mouse inoculation studies take a long time (up to 700 days) to detect the agent, and failure to identify it in tissues may indicate either true absence of the agent or simply the limited sensitivity of current diagnostic methods.
Related Diseases
The TSE family of diseases includes scrapie, which affects sheep and goats; transmissible mink encephalopathy; feline spongiform encephalopathy; chronic wasting disease of deer and elk; and kuru, both classical and variant Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomnia, five rare diseases in humans. TSE's have also been reported in Europe in captive wild ruminants, cats, and monkeys. The occurrence of TSE's in captive wild animals is believed to have resulted from BSE-contaminated feed.
On March 20, 1996, the United Kingdom's Spongiform Encephalopathy Advisory Committee (SEAC) announced the identification of 10 cases of vCJD. These 10 cases differed from other routinely diagnosed cases of classical CJD in that they shared an early age at onset of symptoms, an unusual clinical course with psychiatric problems, an overall prolonged duration of illness, and, under microscopic examination, different lesions in brain tissues.
SEAC concluded that, although there was no direct scientific evidence of a link between BSE and vCJD, based on current data and in the absence of any credible alternative, the most likely explanation at that time was that the cases were linked to exposure to BSE before the introduction of a specified bovine offal (SBO) ban at slaughter in 1989. The SBO ban excluded from human consumption brain, spinal cord, and other organs with potential BSE infectivity. As of July 1999, 45 probable cases of vCJD had been identified.
It is important to clarify the difference between classical CJD and vCJD. Classical CJD occurs each year at a rate of 1 to 2 cases per 1 million people throughout the world, including in the United States and other countries where BSE has never occurred and among vegetarians and meat eaters alike. Classical CJD occurs sporadically and is not linked to BSE. According to the U.S. Department of Health and Human Services' Centers for Disease Control and Prevention (CDC), no cases of vCJD have been found in the United States.
Research published in October 1997 found evidence to further link vCJD to BSE. Investigators in the United Kingdom found that BSE and vCJD are of the same strain. In addition, classical CJD and known scrapie strains were not similar to vCJD or BSE.
USDA Actions in Response to BSE
The United States has one of the most aggressive BSE surveillance programs in the world. BSE has not been diagnosed in the United States, and USDA has worked proactively to keep it that way. In cooperation with USDA's Food Safety and Inspection Service (FSIS), APHIS has taken stringent measures in prevention, education, surveillance, and response.
To prevent BSE from entering the country, since 1989 APHIS has prohibited the importation of live ruminants from countries where BSE is known to exist in native cattle. Other products derived from ruminants, such as fetal bovine serum, bonemeal, meat-and-bone meal, bloodmeal, offal, fats, and glands, are also prohibited from entry, except under special conditions or under USDA permit for scientific or research purposes.
On December 12, 1997, APHIS stopped the importation of all live ruminants and most ruminant products, including meat-and-bone meal, offals, glands, etc., from Europe until APHIS scientists can assess the disease risk and evaluate surveillance activities in individual countries. In addition to the countries already known to have BSE, these new restrictions apply to Albania, Austria, Bosnia-Herzegovina, Bulgaria, Croatia, Czech Republic, Denmark, Federal Republic of Yugoslavia, Finland, Germany, Greece, Hungary, Italy, the former Yugoslavian republic of Macedonia, Norway, Poland, Romania, Slovak Republic, Slovenia, Spain, and Sweden.
APHIS educates veterinary practitioners, veterinary laboratory diagnosticians, industry, and producers on the clinical signs and pathology of BSE.
APHIS leads an ongoing, comprehensive, interagency surveillance program for signs of BSE in the United States. APHIS veterinary pathologists and field investigators have received training from their British counterparts in diagnosing BSE. FSIS antemortem inspection procedures include identifying animals with central nervous system conditions. Animals identified with such conditions are prohibited from slaughter and referred to APHIS for review. APHIS' surveillance program is based on laboratories' histopathologically examining brains from high-risk cattle, i.e., adult cattle that exhibit clinical signs of a neurological disorder. In addition, using a technique called immunohistochemistry, scientists test brain tissues for the presence of the protease-resistant prion protein. Samples are submitted from nonambulatory cattle and from neurologically ill cattle and rabies-negative cattle identified on the farm, at slaughter, or at veterinary diagnostic laboratories and teaching hospitals. As of August 20, 1999, more than 8,400 brains from the United States and Puerto Rico have been examined with no evidence of BSE or other TSE detected.
APHIS also monitors the remaining cattle imported from Great Britain, Belgium, and other European countries (before the bans on imports from those countries went into effect). As of August 25, 1999, of the 496 cattle imported from Great Britain and Ireland between 1981 and 1989, 10 animals are still alive. The animals are quarantined and observed regularly. To date, no evidence of BSE has been detected. APHIS continues to attempt to purchase the 10 live animals for diagnostic research purposes. The 2 Belgian cattle imported in 1996 and 34 European cattle imported in 1996-97 that are still alive are currently under quarantine, and APHIS is attempting to buy these animals as well.
APHIS has also drafted an emergency response plan to be used in the event that BSE is introduced into the United States. In addition, APHIS' TSE Working Group monitors and assesses all ongoing events and research findings regarding TSE's. APHIS continually revises and adjusts prevention and diagnostic measures as it receives new information and knowledge.
As an additional preventative measure, APHIS supports the Food and Drug Administration's (FDA) regulation (effective August 4, 1997) prohibiting the use of most mammalian protein (with certain exceptions) in the manufacture of animal feeds given to ruminants. In addition, the final regulation also requires process and control systems to ensure that ruminant feed does not contain the prohibited mammalian tissues.
Getting the Word Out
As part of its increased surveillance activities, APHIS is continuing an education effort to inform U.S. cattle producers and veterinarians about this disease. Numerous briefings have been held for industry groups. In addition to press releases and factsheets, a videotape on BSE and an information packet were distributed to all APHIS field offices, State veterinarians, extension veterinarians, colleges of veterinary medicine, and industry groups.
For information about importing animals or animal products, contact
USDA, APHIS, Veterinary Services
National Center for Import/Export
Animals Program
Telephone: (301) 734-8170
Products Program
Telephone: (301) 734-7885
For public health information, contact CDC at (404) 639-3091. For food safety information, contact FSIS at (202) 205-0293 or call the USDA's Meat and Poultry Hotline at (800) 535-4555. For more information about the ruminant feed ban, call FDA's Consumer Hotline at (800) 532-4440.
Current information on animal diseases and suspected outbreaks is also available on the Internet. Point your Web browser to http://www.aphis.usda.gov to reach the APHIS home page.
source: http://www.aphis.usda.gov/oa/pubs/fsbse.html 14jan01
Bovine Spongiform Encephalopathy (BSE)
Bovine spongiform encephalopathy (BSE), widely known as "mad cow disease," is a chronic, degenerative disease affecting the central nervous system of cattle. Worldwide there have been more than 178,000 cases since the disease was first diagnosed in 1986 in Great Britain. BSE has had a substantial impact on the livestock industry in the United Kingdom. The disease has also been confirmed in native-born cattle in Belgium, Denmark, France, Germany, Ireland, Luxembourg, Liechtenstein, the Netherlands, Northern Ireland, Portugal, Spain and Switzerland. However, over 95% of all BSE cases have occurred in the United Kingdom. BSE is not known to exist in the United States.
BSE belongs to the family of diseases known as the transmissible spongiform encephalopathies (TSE's). These diseases are caused by a transmissible agent which is yet to be fully characterized. They share the following common characteristics:
a. a prolonged incubation period of months or
years;
b. a progressive debilitating neurological illness which is always fatal;
c. when examined by electron microscopy, detergent treated extracts of brain
tissue from animals or humans affected by these diseases reveal the presence of
scrapie associated fibrils (SAF);
d. pathological changes appear to be confined to the CNS and include vacuolation,
and astrocytosis;
e. the transmissible agent elicits no detectable specific immune response in the
host which has inhibited the development of a live animal diagnostic test.
TSE's are caused by similar uncharacterized agents that produce spongiform changes in the brain. TSE's include scrapie (which affects sheep and goats), transmissible mink encephalopathy, feline spongiform encephalopathy, chronic wasting disease of deer and elk, and in humans, kuru, CJD, Gerstmann- Straussler syndrome, fatal familial insomnia, and vCJD.
Affected animals may display changes in temperament, such as nervousness or aggression; abnormal posture; incoordination and difficulty in rising; decreased milk production; or loss of body condition despite continued appetite. There is no treatment, and affected cattle die.
The incubation period ranges from 2 to 8 years. Following the onset of clinical signs, the animal's condition deteriorates until it dies or is destroyed. This usually takes from 2 weeks to 6 months. Most cases in Great Britain have occurred in dairy cows between 3 and 6 years of age.
The causative agent of BSE as well as other TSE's is yet to be fully characterized. Three main theories on the nature of the agent have been proposed:
An unconventional virus.
A prion or abnormal partially-proteinase K-resistant protein, devoid of nucleic acid, capable of causing a cell to produce more abnormal protein.
A virino or "incomplete" virus composed of naked nucleic acid protected by host proteins.
The BSE agent (1) is smaller than most viral particles and is highly resistant to heat, ultraviolet light, ionizing radiation, and common disinfectants that normally inactivate viruses or bacteria; (2) causes no detectable immune or inflammatory response in the host; and (3) has not been observed microscopically.
There is no test to detect the disease in a live animal. Microscopic examination of brain tissue at necropsy is the primary laboratory method used to confirm a diagnosis of BSE. There are also several techniques used to detect the partially-proteinase resistant form of the prion (PrPres) protein. These techniques are immunohistochemistry and immunoblotting.
No cases of BSE have been confirmed in the U.S.A. despite 10 years of active surveillance.
These TSE's HAVE been found in the United States: Scrapie in sheep and goats, transmissible mink encephalopathy, and chronic wasting disease of deer and elk.
Epidemiologic data suggest that BSE in Great Britain is a common-source epidemic involving animal feed containing contaminated meat and bone meal as a protein source. The causative agent is suspected to be from either scrapie- affected sheep or cattle with a previously unidentified TSE. Changes in rendering practices in the early 1980's may have potentiated the agent's survival in meat and bone meal.
For more information about BSE in the United Kingdom, please visit the Ministry of Agriculture, Fisheries and Food, UK web site.
In native cattle: Ireland, Northern Ireland, France, Germany, Portugal, Spain, Switzerland, Netherlands, Belgium, Denmark, Luxembourg, Liechtenstein. While there is a decline in the number of cases of BSE in the United Kingdom, confirmed cases of BSE have risen in other European countries.
In cattle exported from Great Britain to Oman, the Falkland Islands, Germany, Denmark, Canada, Italy, and the Azores.
For more information, please see Office International des Epizooties.
There have been NO cases of BSE in native cattle in North America. The one case of BSE in a single cow in Canada imported from Great Britain has been dealt with by destroying the affected cow and all its herdmates, as well as other cattle determined to be a risk by animal health officials in Canada.
There is no evidence that BSE spreads horizontally, i.e., by contact between unrelated adult cattle of from cattle to other species. Some evidence suggests that maternal transmission may occur at an extremely low level. Results of British research show that there is approximately a 9-percent increase in the occurrence of BSE in offspring of BSE-affected dams as compared to calves born to dams where BSE was not detected. The study did not ascertain if this was the result of genetic factors or true transmission. The research did however point out that at this level if maternal transmission does occur it alone will not sustain the epidemic (Wilesmith et al. 1997).
CJD is a slow degenerative human disease of the central nervous system with obvious dysfunction, progressive dementia, and vacuolar degeneration of the brain. CJD occurs sporadically worldwide at a rate of 1 case per 1 million people per year. More rare are the related TSE conditions of Gerstmann- Straussler syndrome, kuru, and fatal familial insomnia.
The incidence of classical CJD in the United States (about 1 case per 1 million population per year) is similar to the incidence found in the rest of the world, which includes Australia and New Zealand--countries that have NOT reported either scrapie or BSE. CJD, which was first diagnosed in the 1920's, occurs with roughly the same frequency in Britain as in other countries at the present time.
For more information on CJD in the United States, please visit the Centers for Disease Control and Prevention's National Center for Infectious Diseases website.
On March 20, 1996, the UK's Spongiform
Encephalopathy Advisory Committee (SEAC) announced the identification of 10
cases of a new variant form of CJD (vCJD). All of the patients developed onset
of illness in 1994 or 1995. The following features describe how these 10 cases
differed from the sporadic form of CJD:
The affected individuals were much younger than the classical CJD patient. Typically, CJD patients are over 63 years old. The average patient age for the onset of variant CJD is 28 (range of 14 to 52) years.
The course of the disease in the vCJD averaged 13 months. Classical CJD cases average a 6 month duration.
In the variant cases, electroencephalographic (EEG) electrical activity in the brain was not typical of sporadic CJD.
Although brain pathology was recognizable as CJD, the pattern was different from sporadic CJD, with large aggregates of prion protein plaques.
Epidemiological and case studies have not revealed a common risk factor among
the cases of vCJD. According to the SEAC, all victims were reported to have
eaten beef or beef products in the last 10 years, but none had knowingly eaten
brain material. One of the affected individuals had been a vegetarian since
1991.
The SEAC concluded that although there was no direct scientific evidence of a link between BSE and vCJD, based on current data and in the absence of any credible alternative, the most likely explanation at that time was that the cases were linked to exposure to BSE before the introduction of control measures, in particular, the specified bovine offal (SBO) ban in 1989.
Research reported in later 1996 and 1997 has found evidence to further support a causal association between vCJD and BSE. Two significant studies published in the October 2, 1997 edition of Nature lead the SEAC to conclude that BSE agent is highly likely to be the cause of vCJD. Dr. Moira Bruce and colleagues at the Institute for Animal Health in Edinburgh, Scotland inoculated 3 panels of inbred mice and one panel of crossbred mice with BSE, vCJD and sporadic CJD. Interim results indicate that mice inoculated with BSE showed the same pattern of incubation time, clinical signs and brain lesions as mice inoculated with tissues from patients with vCJD. This provides evidence that BSE and vCJD have the same signature or are the same "strain". In addition, sporadic CJD and known scrapie strains were not similar to vCJD or BSE.
Results from another study published by Dr. John Collinge and colleagues of Imperial College School of Medicine, London, UK strongly support Bruce's results. Collinge's paper reports findings of BSE transmission to transgenic mice expressing only human PrP.
Another paper by Collinge et. al. in the October 24, 1996 edition of Nature also provides data to support the assocoation between vCJD and BSE.
More recently, studies using transgenic animals
expressing the bovine PrP have supported the view that BSE infected cattle are
responsible for vCJD. These mice not only propagated the BSE infectious agent in
the absence of a species barrier, but also were highly susceptible to vCJD and
natural sheep scrapie. Furthermore, the transgenic mice inoculated with either
vCJD or BSE had indistinguishable disease characteristics.
The vast majority of vCJD cases have been detected
in the United Kingdom although there have been two patients in France and one in
Ireland. The UK CJD Surveillance
Unit provides a monthly update. No cases of vCJD have been detected in the
U.S.
The Centers
for Disease Control have published an advisory for international travelers.
The reason it is thought that the vCJD cases in Britain were NOT caused by scrapie is because scrapie has existed in the sheep population in the United Kingdom for 250 years and has never been shown to be a human health risk.
For more information, please visit the United Kingdom's Department of Health website.
What is the USDA policy in regard to BSE, and
what actions has USDA taken?
The USDA policy has been to be proactive and preventative. APHIS has taken
measures in surveillance, prevention, education, and response. Import
restrictions have been in place since 1989, and active surveillance efforts
began in 1990. The USDA continually monitors and assesses all ongoing events and
research findings regarding spongiform encephalopathies, as new information and
knowledge may lead to revised conclusions and prevention measures. APHIS has
also created a Transmissible Spongiform Encephalopathy (TSE) Working Group to
analyze risks of BSE to the United States, disseminate accurate information
about the TSE's, and act as a reference source for responding to questions about
TSE's.
Is APHIS working with other agencies and groups
to coordinate efforts?
Yes. APHIS has actively shared information and met with State and Federal
agencies, including the Centers for Disease Control and Prevention(CDC), the
Food and Drug Administration (FDA), the Food Safety and Inspection Service
(FSIS), the National Institues of Health (NIH), and stakeholders to assure we
are taking the proper actions in response to changing knowledge and information
concerning BSE.
Is BSE a notifiable disease in the United
States?
Yes. Under Title 9 Code of Federal Regulations, Parts 71 and 161, BSE is a
reportable disease by accredited veterinarians.
What types of BSE
surveillance are we doing?
USDA-APHIS, in cooperation with USDA-FSIS and State diagnostic laboratories, has
a comprehensive surveillance program.
APHIS educates veterinary practitioners, veterinary laboratory diagnosticians, industry and producers on the clinical signs and pathology of BSE.
APHIS monitors the remaining cattle imported from the United Kingdom.
Since 1990, more than 60 veterinary diagnostic laboratories across the United States and USDA's National Veterinary Services Laboratories continue to examine hundreds of cattle brains each year submitted from adult cattle displaying neurologic signs either at slaughter or on the farm. FSIS performs antemortem slaughter inspection at all federally-inspected slaughter establishments, and inspectors are alert for central nervous system (CNS) disorders. Any CNS suspect animals are condemned and tested. Public health laboratories also submit to APHIS any samples that have tested negative for rabies.
The network of private veterinary practitioners that refers unusual cases to veterinary schools or State diagnostic laboratories around the United States provides an extensive informal but important surveillance system.
USDA has trained more than 250 State and Federal field veterinarians located throughout the United States in the recognition and diagnosis of foreign animal diseases, including BSE.
The Veterinary Medical Data Base maintained by Purdue University compiles diagnoses submitted by 27 U.S. veterinary schools, including many neurologic cases.
The Veterinary Diagnostic Laboratory Reporting System (VDLRS) maintains a data base on selected disease conditions submitted by 29 State and university veterinary diagnostic laboratories throughout the U.S., including the results of histologic examinations for BSE. VDLRS is a cooperative effort of the American Association of Veterinary Laboratory Diagnosticians , the United States Animal Health Association, USDA-APHIS-Veterinary Services' Centers for Epidemiology and Animal Health, and the 29 laboratories mentioned above.
Veterinary pathologists at zoos in the United States routinely conduct postmortem examinations on the brains of zoo animals exhibiting neurologic signs since BSE-like encephalopathies have been diagnosed in seven species of exotic Bovidae at zoos in England.
Has the United States imported cattle from the
United Kingdom?
Yes. Between 1981 and 1989, 496 cattle were imported from the United Kingdom and
the Republic of Ireland. These U.K. imports have been traced, and there are only
4 cattle still alive in the United States (as of February 1999). All of these
animals have been under quarantine since April 1996. APHIS is currently
attempting to purchase these cattle for diagnostic research purposes. In July
1989, the importation of live ruminants from the United Kingdom was banned.
In addition, 2 head of cattle imported from Belgium in 1996 are now under quarantine. APHIS, in cooperation with the States and industry, continues to purchase these animals for diagnostic purposes. No evidence of BSE has been found in any of these imported animals.
Can we account for all of the U.K.-imported
cattle?
All but 32 animals have been traced. All cattle of unknown status would be
greater than 10 years of age and would have a reduced likelihood of developing
BSE at this late date.
Does the United States still permit the feeding
of ruminant protein to ruminants?
On August 4, 1997, the Food
and Drug Administration (FDA) established regulations that prohibit the
feeding of most mammalian proteins to ruminants.
What proactive initiatives are underway to
educate farmers, veterinarians, extension agents, etc.?
An important part of the USDA's active surveillance program is the training of
veterinary practitioners in the clinical signs, diagnosis and sample submission
for BSE. Videotapes of cattle showing clinical signs of BSE have been
distributed to veterinarians in Federal and State governments, veterinary
diagnostic laboratories, and pathology departments of veterinary colleges.
Microscope slides showing typical BSE lesions have been distributed to the above
diagnostic laboratories, and Federal Foreign Animal Disease (FAD) diagnosticians
have trained in Great Britain in BSE recognition. BSE factsheets, risk
assessments, and reviews have also been sent to State and Federal veterinarians,
private practitioners, other industries, and to producers. In addition, APHIS
personnel have given numerous presentations to various animal health groups.
Finally, over 250 Federal and State veterinarians throughout the U.S. have been
trained in the recognition of FAD's including BSE.
What measures has USDA-APHIS taken to prevent
the introduction of BSE?
To prevent BSE from entering the United States, APHIS has restricted the
importation of live ruminants and certain ruminant products from countries where
BSE is known to exist.
On July 21, 1989, APHIS banned the importation of all ruminants and restricted the importation of certain cattle products from the United Kingdom.
On December 6, 1991, APHIS restricted the importation of ruminant meat and edible products and banned most byproducts of ruminant origin from countries known to have BSE (56 Federal Register [FR] 63868 and 63869). Prior to this, the products were restricted by not issuing permits.
Certain products cannot be imported into the United States, except under special permit for scientific, educational or research purposes, or under special conditions to be used in cosmetics. These products include serum, glands, collagen, etc.
Importation requests for ruminant material are considered individually, and authorization is granted only to those materials that would not allow exposure to ruminants in the United States.
As of December 12, 1997, APHIS has prohibited the importation of live ruminants and most ruminant products from all of Europe until a thorough assessment of the risks can be made. The new restrictions apply to Albania, Austria, Bosnia-Herzegovina, Bulgaria, Croatia, Czech Republic, Denmark, Federal Republic of Yugoslavia, Finland, Germany, Greece, Hungary, Italy, the former Yugoslavian republic of Macedonia, Norway, Poland, Romania, Slovak Republic, Slovenia, Spain, and Sweden. These actions are in addition to those already in place regarding countries that had reported BSE in native cattle.
This action was taken in 1997 because the Netherlands, Belgium, and Luxembourg have reported their first cases of BSE in native-born cattle. There is evidence that European countries may have had high BSE risk factors for several years and less-than-adequate surveillance. Additionally, Belgium reported that the cow diagnosed with BSE was processed into the animal food chain. This science-based decision was made to protect human and animal health, to ensure the security of U.S. export markets, and to shield the safety and the integrity of our food supply.
An interim rule was published and the comment period closed on March 9, 1998. The comments are currently being evaluated. Criteria to assess the risk factors were developed in accordance with the standards adopted by the Office of International Epizootics (OIE). APHIS has received information from a number of the European countries to assist in the risk analysis.
Have we allowed the importation of cattle semen
and embryos from BSE-affected countries?
Yes.
No BSE infectivity has been detected in embryos, semen, or reproductive tissues of BSE-affected cows and bulls. Embryo transfer experiments are underway in cattle and all interim results are negative, thus far. However, due to the inconclusive findings of the maternal transmission BSE study and two studies which found sheep scrapie to be transmitted via embryo transfer, the importation of embryos from BSE affected and high-risk countries has been suspended.
Importation protocols exceed the recommendation of the Office of International Epizootics (OIE). All bulls producing semen for export to the United States are required to meet all 5 of the following conditions:
The semen donor has not been on premises where BSE has occurred within 5 years of the date of embryo or semen collection;
The semen donor is not affected with BSE;
No progeny of the semen donor is affected with BSE;
The parents of the semen donor are not affected with BSE; and
The semen donor has not been fed ruminant-derived protein.
These importations were suspended during the first week of April 1996, in response to the reported possible association of vCJD cases in the United Kingdom and exposure to the BSE agent. We have since resumed the importation of bovine semen as there is no scientific evidence to support that semen harbors the BSE agent.
What actions are taken at USDA-inspected
slaughter establishments to ensure that cattle with BSE would not enter the
human food supply?
All cattle presented for slaughter in the United States are inspected before
slaughter by FSIS for signs of CNS impairment. Any animals exhibiting neurologic
signs during this inspection are condemned, and the meat is not permitted for
use as human food. The brains from these animals are submitted to USDA's
National Veterinary Services Laboratories for analysis.
Does USDA have a response plan in the event a
case of BSE or TSE is diagnosed in U.S. cattle?
In 1990, APHIS developed a plan to respond to a confirmation of BSE in the U.S.
In August 1996, a joint APHIS-FSIS working group updated this BSE response plan.
The purpose of the plan is to provide a step-by-step plan of action in the event
that a case of BSE is detected in the United States. The plan outlines those
events that should take place, including identification of a suspect animal,
confirmation, the epidemiologic investigation, animal and herd disposition
activities, and communication of information.
BSE
Response Plan Summary [PDF]
Contacts for More Information About BSE
For animal health issues, contact APHIS' Dr. Linda Detwiler at (609) 259-5825.
All general inquiries about APHIS' role regarding BSE or animal health should be referred to Legislative and Public Affairs at (301) 734-7799.
For questions related to food safety, meat and meat products, or meat inspection, contact:
Food Safety and Inspection Service
(202) 720-9113
For questions related to human health, Creutzfeldt-Jakob disease, contact:
Centers for Disease Control and Prevention
(404) 639-7292
For questions related to science, research, contact:
National Institutes of Health
(301) 496-5751
For questions related to food, feed, drugs, cosmetics, or biological products, contact:
Food and Drug Administration
(301) 443-1130
page source: http://www.aphis.usda.gov/oa/bse/ 16jan01
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