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The Relationship Between Bovine Spongiform Encephalopathy,
By Dr Deryck D. Pattron, Ph.D., Thu Dec 8th
The Relationship Between Bovine Spongiform Encephalopathy,
By Dr Deryck D. Pattron, Ph.D., Thu Dec 8th
Bovine Spongiform Encephalopathy (BSE) or Mad Cow Disease is achronic, progressive degenerative, neurological disease ofcattle that has been linked to a form of Creutzfeldt-Jakobdisease (CJD), a fatal degenerative brain disease in humans. BSEbelongs to a family of diseases known as the transmissiblespongiform encephalopathies (TSEs). TSE animal diseases found inthe United States include scrapie in sheep and goats, chronicwasting disease in deer and elk, transmissible spongiformencephalopathy in mink, feline spongiform encephalopathy incats, and in humans: kuru, both classic and variantCreutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinkersyndrome, and fatal familial insomnia. In November 1986, the first reported cases of BSE occurred inBritain. During the period 1989 to early 2001, more than 1million cases of BSE were identified. Other countries around theworld at this same time also reported similar cases of BSE.These countries included Denmark, France, Germany, Italy,Ireland, Belgium, The Netherlands, Spain, Portugal, Spain andSwitzerland, Canada, the Falkland Islands and Oman. Symptoms of BSE in cattle include loss of muscular coordination,inability to stand up, listlessness, decreased milk production,and loss of body weight. Affected animals also show signs ofbehavioral change, for example, nervousness, aggression and alack of interest in surroundings. The period from infection toonset of the disease, known as the incubation period, is fromtwo to eight or more years. Once symptoms develop, animalsprogressively deteriorate and die within several months. (Article continued below)
Where is the BSE agent found in cattle? Autopsies of diseasedcattle brains revealed anatomical and morphological changesconsistent with that of spongy like texture, similar to that ofSwiss cheese. Current scientific research confirms that BSEinfectivity occurs in the brain, trigeminal ganglia, tonsils,spinal cord, dorsal root ganglion, and distal ileum of the smallintestine of cattle experimentally infected with the BSE agent.Research also confirms that BSE infectivity is in the brain,spinal cord, and retina of the eyes of cattle infected with theagent under field conditions. Although bone marrow hasdemonstrated infectivity in experimentally infected cattle,these findings are not conclusive. What causes BSE? The general consensus among scientists andresearchers is that the causative agent believed to cause BSE isan abnormal form protein called prion. This abnormal protein isfound in brain, spinal cord, tonsils and small intestines ofcattle. The exact origin of the causative agent, prion, issomewhat controversial. Some researchers believe that prionscome from cattle bones, hide and other inedible tissue afterslaughter. While others believe that the origin of prions camefrom sheep. Yet other sources recently indicated that prions maybe of human origin. Irregardless of the origin of prions, cattleand other ruminants can become infected only after consumingcontaminated feed containing recycled animal tissues and prions.Prions are extremely resistant to heat, ionizing radiation,normal sterilization process and common disinfectants thatnormally inactivate viruses and bacteria. This may explain whyrendered recycled animal tissue may still be infective afterprocessing. Can BSE be transmitted from one cow to another cow or ruminant?BSE is not a contagious disease. There is no evidence that thedisease is transmitted through direct contact oranimal-to-animal spread. The primary means by which animalsbecome infected is through consumption of feed contaminated withthe infectious BSE agent or prions. Is BSE transferable
to humans? Since the initial report of thedisease, there has been much speculation that it might betransferable to humans through beef products. The appearance ofCJD in several dairy farmers in Britain in the early 1990sheightened the alarm. In March 1996 the British Ministry ofHealth announced the discovery of ten cases of a unique type ofCJD, called new variant CJD or vCJD. This type of CJD differsfrom the classical form in that victims are all under the age of42 (the classical form of the disease typically develops aroundage 65), the victims display unusual psychiatric problems,distinct brain tissue changes are identified during an autopsy,and the victims have no family history of the disease. TheBritish government found that the victims may have contractedthe disease through contact with BSE-infected cattle before theeradication of suspected animals had taken effect. What causes vCJD? Since 1996, a number of studies have confirmedthat BSE in cattle can be transmitted to humans and cause vCJD.Studies have linked the time and location of the BSE epidemic incattle to more than 94 human cases of vCJD found in Britain,France, and Ireland. In studies in which scientists injectedmonkeys and mice with brain tissue from BSE-infected cows orbrain tissue from vCJD-infected humans, the animals develop thesame type of brain degeneration. This degeneration isdistinguishable from the degeneration following injection withbrain tissue from cases of the classical form of CJD. TheBritish government in 1996 announced that BSE may be transmittedto humans. Creutzfeldt-Jakob Disease (CJD) form of human spongiformencephalopathy caused by an infection of the brain, probably bya particle called a prion. The disease causes fatal degradationof brain tissue and produces a dementia that affects men andwomen, often between the ages of 50 and 65. Some 90 percent ofcases progress to death within one year, sometimes within onemonth. Symptoms include loss of speech, difficult swallowing,rigid limbs, and contraction of the facial muscles, with deathoften resulting from a complication following these symptoms.The remaining 10 percent of cases develop dementia and mayslowly decline over several years. There is no record of anyonerecovering from the disease and there is no known treatment. Creutzfeldt-Jakob disease is found worldwide but is relativelyrare, affecting about 0.9 people per million in the UnitedStates. The mean age of death is 67 years. Deaths fromCreutzfeldt-Jakob disease are uncommon in people under age 50.In people age 70 to 74 years, the disease causes 5.7 deaths permillion people. Although the hypothesis of the cattle-to-human transmissionremains unproven, it is supported by the results of a number ofscientific studies, including two released in 1997. Laboratorymice injected with brain tissue from BSE-infected cows andanother group injected with brain tissue from vCJD-infectedhumans both developed the same symptoms of brain degenerationand the infection was ultimately fatal in both groups. Inaddition, researchers found the same prion strain in both groupsof mice. In one of the studies, researchers injected a thirdgroup of mice with tissue from humans who had died of classicalCJD; these mice developed no symptoms and survived the trial. Is there a BSE test for meat? At present there exists no testfor BSE. The only confirmatory test is done at post-mortem andinvolves microscopic examination of brain tissue usingimmunocytochemistry to confirm suspected cases of the disease. How long can BSE be in an animal before it shows signs of thedisease? The incubation period is from 30 months to eight years.Following the manifestation of clinical signs the animal'scondition deteriorates very rapidly from two weeks to sixmonths, resulting in death. What measures are necessary to prevent BSE? (i)Introducecompulsory destruction of suspect and disease animals; (ii)Stopfeeding of rendered animal tissue to cows and other ruminants;(iii)Ban imports of diseases cattle or other ruminant carcassesfrom countries known to have BSE; (iv)Ban imports of live cowsand other ruminants from countries known to have BSE; (v)Sickor disease animals should not enter the human food supply andslaughtered animals used for human food should have ante-mortemand post-mortem health certificates; (vi)Introduce mandatorytesting and surveillance to detect early cases of BSE; (vii)Although scientific evidence shows that cooking does not killthe BSE infective agent, all meat products should be thoroughlycooked for at least 70 ºC as a necessary precautionary measure;(viii)Develop and implement appropriate legislation to prevent,reduce and control the spread of BSE; (ix)Adopt restrictions ontechniques to mechanically remove meat from bones; (x)Meat fromtested animals should not be certified until test results arefinal; (xi)Specific risk material such as the skull, brain,trigeminal ganglia, eyes, vertebral column, spinal cord anddorsal root ganglion of cattle 30 months of age or older and thesmall intestines should be prohibited in the human food supply;(xii)Ban any stunning procedure that would dislocate portionsof brain tissues for example air-injection stunning and replacesuch procedure with more humane procedure(s).
About the author:Dr. Pattron is a Public Health Scientist, Ministry of Health,Trinidad. | Sign In |
