Canadian Beef
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More fuel for the fire. Just heard on a news update another animal tested positive in Alberta. The animal is reported to be under 7 years old & after feed changes were put in effect. It sounds like it may have been feed older feed. Waiting for a more complete report on the news.
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Sorry, I am not the veterinarian in the family, that would be my brother, who specializes in large animal medicine. But this is what I heard from him (I will call and confirm). I know that it does occur spontaneously in sheep and goats, and diseases, previously unknown, as such may develop in other species. With todays news release, about a animal born after the feed ban, this may be more then just a theory...
Here, from some research, is excepts from the Veterinarian Merck manual.
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100200.htm&hide=1
Bovine Spongiform Encephalopathy: Introduction
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Bovine spongiform encephalopathy (BSE) is a progressive, fatal, neurologic disease of adult domestic cattle that resembles scrapie of sheep and goats ( Scrapie: Introduction); it was first diagnosed in Britain in 1986.
BSE has been transmitted experimentally to mice, pigs, sheep, goats, and marmosets. During the epidemic of BSE in Great Britain, small numbers of cases of spongiform encephalopathy occurred in six species of captive bred ungulates (nyala, gemsbok, eland, arabian oryx, kudu, and scimitar oryx) and in three species of felids (puma, cheetah, and ocelot) either kept in or originating from British zoologic collections. A low incidence has occurred in domestic cats in the British Isles, with one isolated case in Norway. The ungulates were infected from the same food-borne source as cattle (see below), and all species of felids were most likely infected by eating infected bovine tissues.
Only the UK has experienced a significant epidemic which, at its peak at the end of 1992, represented an annual incidence of ~1% of adult cattle. Lower incidences have occurred in indigenous cattle in Ireland, France, Switzerland, the Netherlands, and Portugal, and a few cases have occurred in Canada, Germany, Denmark, Italy, the Falkland Islands, and the Sultanate of Oman in animals exported from Great Britain.
There is no evidence that the transmissible spongiform encephalopathies of man are acquired from animals.
Etiology: The causal agent belongs to a group of incompletely characterized infectious agents called unconventional viruses or prions. These agents, in addition to scrapie, cause transmissible mink encephalopathy, chronic wasting disease of mule deer, and kuru and Creutzfeldt-Jakob disease of man.
Transmission, Epidemiology, and Pathogenesis: BSE occurred as a result of a food-borne exposure to a scrapie-like agent via contaminated meat and bone meal included in cattle rations. There is no evidence from epidemiologic studies in Britain that transmission occurs naturally between cattle such that infection will be maintained in the cattle population.
There is no sex and breed disposition, with no genotypic variation in susceptibility as occurs in sheep to the scrapie agent. The modal age at onset is 5 yr, with a range from 2 yr to the extent of the commercial lifespan of cattle. The within-herd incidence in affected herds is generally low, with an annual average of 2% of cattle developing clinical disease.
The complete pathogenesis is unknown, but data indicate that after oral exposure, the agent replicates in the lymphoreticular system followed by migration, via peripheral nerves, to the CNS.
Clinical Findings: Initial clinical signs are subtle and mainly behavioral in nature. The spectrum increases and progresses over weeks to months, with most animals reaching a terminal state by 3 mo. Repeated clinical examinations at intervals are recommended. Observations over a prolonged time can detect a reduced time spent ruminating and an increased frequency of nose licking, sneezing or snorting, nose wrinkling, head rubbing and tossing, and tooth grindingâ â€all indicative of a disturbance of the trigeminal nerve sensory area. Restrained animals exhibit exaggerated responses to the menace reflex, the corneal reflex, and sensation of nasal mucosae; frenzy, head shyness, and kicking also occur. Unrestrained animals in familiar environments demonstrate an increased startle response to unexpected visual, auditory, or tactile stimuli. If undisturbed, animals with advanced disease appear to have general hypokinesis, with long periods spent standing or idling with a low head carriage and a fixed, staring facial expression. Locomotory signs of gait ataxia, hypermetria, falling, and generalized paresis eventually become dominant. Weight loss and decreased milk production are common. Tremors and muscle fasciculations occur, but intense pruritus of the trunk, as seen in sheep scrapie, is rare. Euthanasia is advisable as soon as there is some certainty of the clinical diagnosis because animals become unmanageable and, when recumbent, their welfare is at risk.
Lesions: Specifically, lesions are confined to histologic changes in the CNS and comprise bilateral, usually symmetrical, vacuolation of gray matter neuropil (spongiosis) and neurons, similar to the lesions seen in scrapie. Gross pathologic changes associated with falling and recumbency may be present.
Diagnosis: Repeated clinical examinations do not provide a definitive diagnosis. Histologic examination of the hindbrain is essential for confirmation. Autolyzed brain tissue should be examined, after detergent extraction, by electron microscopy for scrapie-associated fibrils.
The furious form of rabies ( Rabies: Introduction) has clinical similarities, but the clinical course of BSE is more protracted. Other differential diagnoses include encephalic listeriosis ( Listeriosis: Introduction , Listeriosis: Introduction , Listeriosis), hypomagnesemia ( Hypomagnesemic Tetany In Cattle And Sheep: Introduction ), lead poisoning ( Lead Poisoning: Introduction), downer cow syndrome ( Problematic Bovine Sternal Recumbency: Introduction), space-occupying lesions in the CNS, and trauma to the spinal column. The protracted clinical course of the disease is helpful in differentiation, but in a small proportion of cases, the clinical duration is short (days or weeks), and the extent that animals have been observed needs to be considered.
Treatment and Control: Treatment is ineffective. Control has been effected in Britain by the statutory prohibition in 1988 of the use of ruminant-derived protein in ruminant rations. This has been adopted in a number of other countries. If such a program is applied effectively, the evidence is that it will control the disease in cattle.
Edit:Spoke to my Brother. Science has proven only the feed transmission of the disease in animals, and food as well as contaminated surgical instruments in Humans(Surgical instrument contamination is being studied in animals). There are numerous theoties as to the development of the disease even in sheep and goats. The theory of which I discussed above will not be scientifically proven until feed related issues are solved.
Here, from some research, is excepts from the Veterinarian Merck manual.
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100200.htm&hide=1
Bovine Spongiform Encephalopathy: Introduction
--------------------------------------------------------------------------------
Bovine spongiform encephalopathy (BSE) is a progressive, fatal, neurologic disease of adult domestic cattle that resembles scrapie of sheep and goats ( Scrapie: Introduction); it was first diagnosed in Britain in 1986.
BSE has been transmitted experimentally to mice, pigs, sheep, goats, and marmosets. During the epidemic of BSE in Great Britain, small numbers of cases of spongiform encephalopathy occurred in six species of captive bred ungulates (nyala, gemsbok, eland, arabian oryx, kudu, and scimitar oryx) and in three species of felids (puma, cheetah, and ocelot) either kept in or originating from British zoologic collections. A low incidence has occurred in domestic cats in the British Isles, with one isolated case in Norway. The ungulates were infected from the same food-borne source as cattle (see below), and all species of felids were most likely infected by eating infected bovine tissues.
Only the UK has experienced a significant epidemic which, at its peak at the end of 1992, represented an annual incidence of ~1% of adult cattle. Lower incidences have occurred in indigenous cattle in Ireland, France, Switzerland, the Netherlands, and Portugal, and a few cases have occurred in Canada, Germany, Denmark, Italy, the Falkland Islands, and the Sultanate of Oman in animals exported from Great Britain.
There is no evidence that the transmissible spongiform encephalopathies of man are acquired from animals.
Etiology: The causal agent belongs to a group of incompletely characterized infectious agents called unconventional viruses or prions. These agents, in addition to scrapie, cause transmissible mink encephalopathy, chronic wasting disease of mule deer, and kuru and Creutzfeldt-Jakob disease of man.
Transmission, Epidemiology, and Pathogenesis: BSE occurred as a result of a food-borne exposure to a scrapie-like agent via contaminated meat and bone meal included in cattle rations. There is no evidence from epidemiologic studies in Britain that transmission occurs naturally between cattle such that infection will be maintained in the cattle population.
There is no sex and breed disposition, with no genotypic variation in susceptibility as occurs in sheep to the scrapie agent. The modal age at onset is 5 yr, with a range from 2 yr to the extent of the commercial lifespan of cattle. The within-herd incidence in affected herds is generally low, with an annual average of 2% of cattle developing clinical disease.
The complete pathogenesis is unknown, but data indicate that after oral exposure, the agent replicates in the lymphoreticular system followed by migration, via peripheral nerves, to the CNS.
Clinical Findings: Initial clinical signs are subtle and mainly behavioral in nature. The spectrum increases and progresses over weeks to months, with most animals reaching a terminal state by 3 mo. Repeated clinical examinations at intervals are recommended. Observations over a prolonged time can detect a reduced time spent ruminating and an increased frequency of nose licking, sneezing or snorting, nose wrinkling, head rubbing and tossing, and tooth grindingâ â€all indicative of a disturbance of the trigeminal nerve sensory area. Restrained animals exhibit exaggerated responses to the menace reflex, the corneal reflex, and sensation of nasal mucosae; frenzy, head shyness, and kicking also occur. Unrestrained animals in familiar environments demonstrate an increased startle response to unexpected visual, auditory, or tactile stimuli. If undisturbed, animals with advanced disease appear to have general hypokinesis, with long periods spent standing or idling with a low head carriage and a fixed, staring facial expression. Locomotory signs of gait ataxia, hypermetria, falling, and generalized paresis eventually become dominant. Weight loss and decreased milk production are common. Tremors and muscle fasciculations occur, but intense pruritus of the trunk, as seen in sheep scrapie, is rare. Euthanasia is advisable as soon as there is some certainty of the clinical diagnosis because animals become unmanageable and, when recumbent, their welfare is at risk.
Lesions: Specifically, lesions are confined to histologic changes in the CNS and comprise bilateral, usually symmetrical, vacuolation of gray matter neuropil (spongiosis) and neurons, similar to the lesions seen in scrapie. Gross pathologic changes associated with falling and recumbency may be present.
Diagnosis: Repeated clinical examinations do not provide a definitive diagnosis. Histologic examination of the hindbrain is essential for confirmation. Autolyzed brain tissue should be examined, after detergent extraction, by electron microscopy for scrapie-associated fibrils.
The furious form of rabies ( Rabies: Introduction) has clinical similarities, but the clinical course of BSE is more protracted. Other differential diagnoses include encephalic listeriosis ( Listeriosis: Introduction , Listeriosis: Introduction , Listeriosis), hypomagnesemia ( Hypomagnesemic Tetany In Cattle And Sheep: Introduction ), lead poisoning ( Lead Poisoning: Introduction), downer cow syndrome ( Problematic Bovine Sternal Recumbency: Introduction), space-occupying lesions in the CNS, and trauma to the spinal column. The protracted clinical course of the disease is helpful in differentiation, but in a small proportion of cases, the clinical duration is short (days or weeks), and the extent that animals have been observed needs to be considered.
Treatment and Control: Treatment is ineffective. Control has been effected in Britain by the statutory prohibition in 1988 of the use of ruminant-derived protein in ruminant rations. This has been adopted in a number of other countries. If such a program is applied effectively, the evidence is that it will control the disease in cattle.
Edit:Spoke to my Brother. Science has proven only the feed transmission of the disease in animals, and food as well as contaminated surgical instruments in Humans(Surgical instrument contamination is being studied in animals). There are numerous theoties as to the development of the disease even in sheep and goats. The theory of which I discussed above will not be scientifically proven until feed related issues are solved.
