INFORMATION ON THE BSE
What is BSE?
What Causes BSE?
How Does BSE Spread?
Symptoms
Diagnosis
Treatment
Control
BSE is a progressive, fatal,
nervous disease of adult domestic cattle, which closely resembles Scrapie of sheep and goats; it was first
diagnosed in Britain in 1986.
The causal agent for BSE has not
been identified, but similarities between BSE
and Scrapie suggest that it belongs to a
group of incompletely characterized micro-organisms called “unconventional
viruses” or “prions”.
These agents, in addition to
Scrapie, cause transmissible mink encephalopathy, chronic wasting disease of
mule deer, and kuru and Creutzfeldt-Jakob disease of man.
Infectivity of such agents is
detected only by biological analysis in experimental host species, notably mice
and hamsters. Transmissibility of BSE has been established in mice and cattle.
There is no evidence that the transmissible spongiform encephalopathies of man
are acquired from animals.
Initial studies in Britain showed
an extended common source epidemic, consisting solely of index cases with no
evidence of transmission between cattle. The incidence of affected herds
increased with herd size. Nevertheless, national- and within-herd incidence was
generally low. The peak incidence was in 4-year-old cattle. There was no sex or
breed predisposition.
Available evidence supports a
food-borne exposure to a Scrapie-like agent by contamination of concentrate
rations.
The pathogenetic mechanisms (the
way in which the disease is caused) are as yet unknown, but data indicate an
oral route of infection and a minimum incubation period of 22
months.
Symptoms:
The clinical signs
are principally neurological, insidious in onset (spreading in a stealthy
manner), progress variably over weeks to months, and end in death.
Clinical onset is independent of
season or stage of lactation; signs include apprehensive behaviour that may
progress to aggression and frenzy, hyperesthesia (abnormally heightened
sensitivity) with kicking during milking, gait ataxia (loss of coordination),
and reduced milk yield or live weight loss. Incoordination, hypermetria
(irregularity of pacing), falling, and generalized paresis (restricted
capability for movement) are concurrent with behavioural changes, and later
become the dominant signs. Tremors and muscle fasciculations (twitches) also
occur. Intense pruritus (itchiness), as seen in Scrapie, is not a feature, but
some affected cattle do rub and scratch.
Welfare considerations,
unmanageable behaviour, recumbency (inability to get up), or emaciation
necessitate slaughter.
Significant necropsy findings are confined to
histological changes in the Central Nervous System. These comprise bilateral,
usually symmetrical, vacuolation of grey matter neuropil (spongiosis) and
neurons, similar to the lesions seen in Scrapie.
Diagnosis:
Initial clinical signs may be
subtle or resemble those of hypomagnesemia or nervous ketosis. Metabolic disorders can be ruled out on
serum biochemistry and failure to respond to therapy. Clinical evaluation must be based on
repeated examinations at intervals sufficient to detect progress of the signs.
Subsequent histological examination (examination of cells and tissue on a
microscopic level) of the brain is essential to confirm the diagnosis. Behavioural changes of BSE could be
confused with those of the furious form of rabies, but the usually protracted
clinical course of BSE contrasts with that of rabies. Differential diagnoses also include
encephalic listeriosis, lead poisoning and downer cow syndrome.
Treatment:
Treatment is
ineffective.
Interim statutory control measures
have been initiated in Britain, which assume that exposure of cattle to
Scrapie-contaminated tissue in meat and bone meal is the source of the
problem. These control measures
comprise notification of suspected clinical cases to regulatory authorities,
compulsory slaughter, histopathology of the brain, destruction of the carcass,
and payment of compensation.