Bovine spongiform encephalopathy (BSE)
Bovine spongiform encephalopathy (BSE) is a transmissible, neurodegenerative, fatal brain disease of cattle characterized by postmortem finding of sponginess of the brain and spinal cord. The disease was first reported in 1985 and is called mad cow disease.
Etiology: It is believed to be caused by unconventional agent which is neither bacteria nor virus but an infectious agent containing protein molecule called "Prion" or Pr P (prion protein) or a small sequence of nucleotide. The disease has similarity with other transmissible spongiform encephalopathy (TSE) like scrapie of sheep and goat, chronic wasting disease of mule deer, transmissible mink encephalopathy and feline spongyform encephalopathy and human diseases like Kuru and Creutzfeld- Jackobs disease. The infectious agents do not cause inflammatory changes or elicit immunological reaction but induce abnormal fibrillar structures.
The disease has a long incubation period of 4 to 5 years, but ultimately is fatal for cattle within weeks to months of its onset. The disease was first recognized and defined as a patho logical entity in the United Kingdom in November 198 6. Initial epidemiological investigations and examination of archived brains indicated that the first cases occurred around April 1985. Subsequently, the largest freeborn epidemic of a transmissible spongiform encephalopathy (TSE) occurred which has had severe economic effects and has caused concern for public health.
Pathogenesis: The casual agent, prion or Pr P, or a small nucleotide sequence bring about development of vacuoles in the brain, resulting in sponginess of brain and spinal cord and preventive passage of nerve impulses.
Clinical signs: The initial clinical signs of this fatal neurological disease are non- specific, typically involving behavioural changes. As the clinical phase progresses the disease is typified by alterations in mental state and of sensation and ataxia. Affected animals in early stages remain alert, have an anxious look and reduced milk yield. They are reluctant to move, and show altered gait like high stepping and uncoordinated movements. These animals become hypersensitive and apprehensive, and reveal aggressiveness and jumping movements. Later on pole scratching, nose licking and recumbency are noticed. The majority of affected animals reach the advanced stages within two to three months from the onset, when slaughter on welfare grounds becomes necessary.
On postmortem examination gross lesions are not observed except sponginess of brain and spinal cord. The pathognomonic histological changes include bilateral symmetric intracytoplasmic vacuolation of neurons and grey matter neuropil.
Diagnosis: It is diagnosed by clinical symptoms and can be confirmed on postmortem and histopathological examinations as mortality rates are almost 100%. The disease should be differentiated from hypomagnesemia, nervous form of ketosis, hypocalcemia, trypanosomiasia, chlorinated hydrocarbons poisoning, rabies, listeriosis, lead toxicity and brain abscess, tumors or cysts.
Treatment and control: There is no treatment or vaccine available against the disease. So the only way to check its occurrence is to avoid use of offal of infected animals as a source of animal protein for animals and human beings. There has been significant decline in the incidence of BSE in affected countries with ban implemented against use of animal protein as a feed source for cows. As there is no test available to detect the disease in live animals, the effective control measures could not be developed.