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Mad Cow Disease

Mad cow disease, technically called bovine spongiform encephalopathy (BSE) is a non inflammatory degeneration of brain of cattle, which is invariably fatal.

At present, there is no scientific evidence to suggest that BSE is transmitted by contact between cattle, not from mother to offspring. There is overwhelming evidence that the feeding of the meat and bone meal plays a central role for the spread of BSE within the cattle.

Clinical Signs:

  • Mad cow disease is one of the slow diseases; incubation period for BSE is 3 to 6 years, and longer.

  • As the pathological prions destroy the brain, clinical symptoms develop in the form of sensitive and motoric abnormalities due to the degenerative changes in the central nervous system.

  • The main symptom to be observed is a disorder in general behavior

  • There is a high degree of anxiety and often increased aggressiveness.

  • The animal avoids stepping over minor constructional obstructions and refuses to go through gates and doors.

  • Grinding of teeth is noticeable

  • Ataxia of the fore and hindlimbs, falls, paresis and the inability to get up

  • General hypsersensitivity to tactile and acoustic stimulation, especially in the area of head and neck, shoulder and hindquarters

  • The muzzle is noticeably licked more frequently and the movement of the ear is more marked

  • The affected cattle do not have a raised temperature

  • 50% of all the cases have a bradycardia due to vagotonia

  • Due to a reduction in appetite, the cattle lose weight and the production of milk decreases.

  • The condition of the animals deteriorates between 2 weeks and 6 months after the onset of the clinical symptoms.

  • Nearly 70% could be observed in milk cows and 30% in beef cattle. The clinical picture by itself is a diagnosis on suspicion.

Field diagnosis of BSE is generally based on clinical signs and confirmed by characteristic pathological changes found in the brain of affected animals. Currently, there is no readily available method for diagnosis of mad cow disease in live animals. The diagnosis can only be made reliably on postmortem using histological examination of specific brain regions, showing the presence of vacuoles in the nerve cells.

Apart from that, immuno-histochemical, electron microscopic and immunological methods can be used for verification. In the case of BSE, the spongy changes are always bilaterally symmetrical and occur in typical areas, such as the medulla oblongata, hindbrain, midbrain, and diencephalons.

Differential Diagnosis:
For differential diagnosis, the following diseases can be taken into account: rabies, Borna's disease, listeriosis, botulism, cerebrocortical necrosis, vitamin B deficiency, lead poisoning, neural form of ketosis, pasture tetany, cerebral abscess.

Treatment and Control:
Use of bone meal and meat meal should be banned. Acridine and phenothiazine derivatives can inhibit the formation of abnormal prion structures and may delay development of BSE and scrapie, but they are not cures. No currently known compound completely prevents or reverses the effects, but it may eventually be possible to use effective combinations of drugs. Prion diseases are accompanied by disturbances in the antioxidant defence systems.

Attempts are being made to develop a vaccine to prevent infection or slow the development of transmissible spongiform encephalopathies including BSE.

The current scientific view is that BSE agent cannot be transmitted in milk. Therefore, there is no risk of human infection through consumption of milk or dairy products such as cheese, butter, yogurt, etc. These products are quite safe for human consumption.


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