Bovine Spongiform Encephalopathy is a progressive, fatal, and neurologic disease of adult cattle that resembles sheep and goats’ scrapie. The disease was first recognized in 1986 in Britain. BSE has been transmitted experimentally in the laboratory to mice, pigs, goats, sheep, and marmosets. During the epidemic of BSE in Britain, a small number of spongiform Encephalopathy occurred in six species of captive breed ungulates like gemsbok, eland, nyala, Kudu, Arabian Oryx, and Scimitar Oryx. The ungulates were infected by the food-borne source as cattle and field species were infected by consuming infected bovine tissues. There is a common infection in house cats of the British Isles.
Importance of Bovine Spongiform Encephalopathy
The United Kingdom experienced a significant endemic of BSE in 1992, and the incidence rate was in adult cattle was 1%. The lower incidence occurred in indigenous cattle in France, Ireland, Portugal, Netherland, and Switzerland. Few cases have occurred in Germany, Canada, Italy, Denmark, the Falkland Islands, and Oman in animals exported from Great Britain.
Causes of BSE
The causal agent of bovine spongiform Encephalopathy belongs to a group of incompletely characterized infectious agents called unconventional viruses or prions. Prions are the viral protein that may remain in the brain tissues and the bone marrow of affected animals. In addition to scrapie, these agents cause transmissible mink encephalopathy, chronic wasting disease in mule, deer, kuru, and mad cow disease or Crutzfeldt-Jackob disease of the human.
Transmission, Epidemiology, and Pathogenesis of BSE
Bovine spongiform Encephalopathy resulted from food-borne exposure to a scrapie-like agent via contaminated meat and bone meal included in cattle rations. There is no evidence from epidemiologic studies in Britain that transmission occurs naturally between cattle such that infection will be maintained in the cattle population.
There is no sex or breed disposition, with no genotypic variation in susceptibility in sheep due to the scrapie agent. The modal age at onset is five years, ranging from 2 years to the extent of the commercial lifespan of cattle. The within-herd incidence of the affected herd is generally low, with an annual average of 2% of cattle developing clinical cases.
The complete pathogenesis of Bovine Spongiform Encephalopathy is unknown. Still, data indicate that the agent replicates in the lymphoreticular system after oral exposure, followed by migration via peripheral nerves to the Central Nervous System (CNS).
Clinical Signs of BSE in Cattle
The initial clinical signs are subtle and mainly behavioral. The spectrum increases and progressive over weeks to months, with most animals reaching a terminal state by three months. Repeated clinical examinations at intervals are recommended. The trigeminal nerve disturbance signs are:
- Reduced time spent in rumination.
- Increase the frequency of nose licking.
- Sneezing or snorting, nose wrinkling.
- Head rubbing and tossing.
- Tooth grinding.
The restrained animal exhibits exaggerated response to menace reflex, the corneal reflex, and sensation of nasal mucosae, frenzy, head shyness, and kicking.
Unrestrained animals in familiar conditions demonstrate an increased startle response to unexpected visual, auditory, or tactile stimuli.
- General hypokinesis in an advanced stage.
- The animal stays in a standing position for a long time.
- Head remains in fixed and staring facial expression.
- Weight loss.
- Decreased milk production.
- Tremor and muscle fasciculation.
- Intense pruritis of the trunk.
Pathological Lesions of Bovine Spongiform Encephalopathy
Specific lesions are confined to histologic changes in the CNS and comprise bilateral, usually symmetrical, vacuolation of gray matter neuropil (spongiosis) and neurons. Similar lesions are seen in scrapie. Gross pathological changes associated with falling and recumbency may be present.
Diagnosis of BSE
The diagnosis of Bovine Spongiform ENcephalopathy can be made by following methods:
- Clinical examination of the animals that do not give a confirmatory diagnosis.
- Histologic examination of the affected animal’s hindbrain is essential for confirmation.
- You can find prions by PCR.
- Autolyzed affected brain tissues should be examined after detergent extraction by electron microscopy for scrapie and associated fibrils.
The furious form of Bovine rabies has clinical similarities, but the clinical course of BSE is more protracted. Other differential diagnoses include:
- Encephalopathic Listeriosis.
- Lead Poisoning.
- Downers Cow Syndrome.
- Space-occupying lesions of CNS.
- Trauma to the spinal column.
A protracted clinical course of the disease is helpful in differentiation. Still, in a small proportion of the case, the clinical duration is short, and the extent that animals have been observed needs to be considered.
Treatment and Control of Bovine Spongiform Encephalopathy
The treatment for BSE is ineffective. The control has been effective in Britain by the statutory prohibition in 1988 of ruminant-derived protein in ruminant rations. This has been adopted in several other countries. If such a program is applied effectively, the evidence is that it will control the disease in cattle.
Concluding Remarks on BSE in Cattle
BSE is a prion-based disease of the central nervous system of cattle. The disease has a severe public health significance. The prion from affected cattle is transmitted to the human body by consuming meat and meat products. The protein of BSE does not destroy by heat or refrigeration. The BSE has a significant effect on the beef industry. Many countries do not allow import beef from BSE affected countries.