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Mad cow disease,
technically called bovine spongiform encephalopathy (BSE) is a
non inflammatory degeneration of brain of cattle, which is invariably
fatal.
Transmission:
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:
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Mad cow disease is one of the slow diseases; incubation period
for BSE is 3 to 6 years, and longer.
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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.
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The main symptom to be observed is a disorder in general
behavior
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There is a high degree of anxiety and often increased
aggressiveness.
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The animal avoids stepping over minor constructional
obstructions and refuses to go through gates and doors.
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Grinding of teeth is noticeable
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Ataxia of the fore and hindlimbs, falls, paresis and the
inability to get up
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General hypsersensitivity to tactile and acoustic stimulation,
especially in the area of head and neck, shoulder and
hindquarters
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The muzzle is noticeably licked more frequently and the movement
of the ear is more marked
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The affected cattle do not have a raised temperature
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50% of all the cases have a bradycardia due to vagotonia
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Due to a reduction in appetite, the cattle lose weight and the
production of milk decreases.
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The condition of the animals deteriorates between 2 weeks and 6
months after the onset of the clinical symptoms.
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Nearly 70% could be observed in milk cows and 30% in beef
cattle. The clinical picture by itself is a diagnosis on
suspicion.
Diagnosis:
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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