INTRODUCTION
Bovine spongiform encephalopathy or BSE is a prion disease discovered in local domesticated cattle that was known since it has gained the hub of interest in the areas of research on both the animal and human forms of the scrapie class of disorders [1].
BSE was determined at first in November 1986 in the research laboratories of the state veterinary service in the course of regular diagnostic neuropathological perusal of food animal ailments [2].
The very first clinical case happened in April 1985 but the presence of a fresh disorder was first established microscopically in November 1986. Epizootiological studies show that the cattle suddenly became successfully uncovered to a scrapie-like agent in ruminant-procured feed in the form of flesh and bone meal [3].
THE BSE EPIDEMIC
The first established instances of BSE were in Great Britain in 1986, succeeding remitment of the brain of two cows with atypical developing neurological indications from two veterinary inspection centers in southern England to the Pathology Department of the Central Veterinary Laboratory. It is probably the instances of BSE lead up to the recognition of these first confirmed cases but was not diagnosed. Later the verification of the first cases, expanding numbers of the cases was diagnosed in the coming year and there was identification that this might be an epidemic of a fresh disorder in the cattle. Epizootiology inspections were instituted to try to discover hints to the origin of the disease [4].
Table 1. The number of histologically confirmed cases of BSE in Great Britain each year from 1988-1992, and the percentage increase compared to the previous year (taken from reference no.5)
CAUSES OF THE BSE EPIDEMIC
A hypothesis made was that BSE was started from scrapie. Britain has a huge, topographically extensive population of the sheep with endemic scrapie. The certainty that sheep are the only substantially established organic reservoir of scrapie like agents in animals, provide hard assisting arguments. But flesh and bone meal extracted from both the ovine and bovine wastes has been utilized in cattle fodder for several decapods. This lifts the salient question of why a crucial epidemic of BSE initiated in 1980s and not sooner. Various components may have furnished to the beginning of BSE, including a gradual rise in the density of the UK sheep population between 1970s and 1980s. Nevertheless, a prior epidemiological finding was that susceptibility to sepsis must have started instantly, around the winter of 1981-1982, which suggested a modification in, perhaps, a single limiting factor. At present-day, there is no confirmation to put forward that BSE might become a naturally infectious disorder of cattle, in the same way that scrapie is of sheep [5].
TRANSMISSION OF BSE TO DIFFERENT SPECIES
The immensity of the prion species fence between cattle and humans remains unspecified. We can only assume that communication of the BSE agent happen, symptoms of contamination will not happen throughout the human life’s duration. The species fence has, however, been controlled during exploratory transmission of the BSE agent to sheep, 57 goats, 57 pigs, 58 mice, 37 mink59 and the baboon monkey60 (Table 2). The evolution of spongiform encephalopathy in 2 baboon monkeys, roughly four years after the intra analytical and intraabdominal objection with homogenates made out of 0-2 g of bovine brain tissue, established that primates are not immune to this infection. For now there are no goals to enlarge the BSE research schedule to incorporate either the oral challenge of the usual baboon or the question of other primates with the BSE agent. This is on the foundation that feasible incubation intervals might be very lengthy, and as the consequences of such research could not be hypothesized to the human population. However, it is feasible that bovine tissues which were unable to originate infection in rodents may in the end cause disorder in the primates and humans. It is consequently of keen scientific attentiveness to find out which of the primates are not immune to BSE, and under which situation. Just Before 1985, spongiform encencephalopathies were known to spread in only three animal species apart from human. These species were scrapie in sheep, chronic wasting disease of mule deer and elk, and communicable mink encephalopathy. Since then, spongiform encephalopathy has been identified in other captive animal species, including the domestic cat and the ostrich (Table 3). Epidemiological examinations have assumed that some of these cases may have been caused by the BSE agent. At last, the pattern of disease and histological change in the brains of mice, incorporated with brain homogenates from affected animals and BSE infected cattle, was same [6].
Table 2. Species susceptible to the BSE (taken from reference no. 6)
Table 3. Species associated to the BSE (taken from reference no.6)
CREUTZFELDT-JAKOB DISEASE
It’s a BSE disease spread to humans from cattle. It’s a type of neurodegenerative disease that is the ordinary type of human prion disease. There are 4 different types of CJD seen: sporadic (sCJD), genetic (gCJD), iatrogenic (iCJD) and variantCJD (vCJD). It was first reported in the twenties of the last century by two German research workers. It was communicated to chimpanzee by Gibbs, Gajdusek and several more in 1968. It is a distinctive disease as it’s both genetic and infective in nature [7].
CONCLUSION
It was inferred from the given reading that BSE is a form of prion disease in domestic cattle whose first clinical record was reported in April 1985 and a fresh case was reported in 1986, November. It has led to BSE epidemic in the Great Britain but Epizootiology inspections were instituted to try to discover hints to the origin of the disease. Further there were many assumptions for the BSE epidemic causes but at present-day, there is no confirmation to put forward that BSE might become a naturally infectious disorder of cattle, in the same way that scrapie is of sheep.
Earlier it was assumed that BSE was spread in only three animal species apart from human but later identified in other captive animal species, including the domestic cat and the ostrich. Then there is a BSE disorder spread to humans by cattle that is known as Creutzfeldt - Jakob disease.
REFERENCES
Wells, G.A.H.; Wilesmith, J. W. The Neuropathology and Epidemiology of Bovine Spongiform Encephalopathy. Brain Pathology 1955, 5(1), 91-103.
Wells, G. A.H.; Wilesmith, J. W.; McGill, Iain S. Bovine Spongiform Encephalopathy: A Neuropathological Perspective. Brain Pathology 1991, 1, 69-78.
Bradley, R.; Wilesmith, J. W. Epidemiology and control of bovine spongiform encephalopathy (BSE). British Medical Bulletin 1993, 49(4), 932-959.
Smith, P.G.; Bradley, R.Bovine spongiform encephalopathy (BSE) and its epidemiology. British Medical Bulletin 2003, 66(1), 185-198.
Kimberlin, R.H. Bovine Spongiform Encephalopathy: An Appraisal of the Current Epidemic in the United Kingdom. Intervirology 1993, 35(1-4), 208-218.
Patterson, W. J.; Dealler, S. Bovine spongiform encephalopathy and the public health. Journal of Public Health Medicine 1995, 17(3), 261-268.
Sikorska, B.; Knight, R.; Ironside, J.W.; Liberski, P.P. Creutzfeldt-Jacob Disease, Neurodegenerative Diseases 2012, 76-90
By Bhawani Chauhan
sabirtabhawani890@gmail.com
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