USDA (United States Department of Agriculture) declared on the 23rd December last that they had found a presumptive case of BSE (Bovine Spongiform Encephalopathy) in an adult Holstein cow in Washington. Members of BSE surveillance team sent the sample from the suspected case for diagnosis to the National Veterinary Services Laboratory, Ames, Iowa. The BSE diagnosis was made on December 22 and 23 by histopathology andimmuno-histochemical testing.

For further and cross confirmation, the sample was sent to Britain. They have also confirmed the case as BSE. The reaction to the events were instant both at home and abroad. Japan and some other countries have already imposed a ban on import of US meat, the share index of McDonalds has fallen and economists are forecasting a loss of about 27,000 million USD from down cut of meat export. The media hype has brought panic into global arena as 'world leader' is going to be affected by the case.

Turning to history: BSE popularly known, as `Mad Cow' is not a very old disease. It was first identified in Britain in November 1986 as a separate disease entity. Since, then about one million cattle have been affected by the malady. The epidemic peaked in January 1993 approximately 1,000 new cases were reported per week. Though BSE is not a very old disease but diseases with similar clinical manifestation, pathological lesions and nature are known from centuries. The group of disease generally termed as TSE (Transmissible Spongiform Encephalopathy) includes scrapie, which affects sheep and goats; transmissible minkencephalopathy; feline spongiform encephalopathy; chronic wasting disease of deer and elk; and in humans, kuru, both classic and variant Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomnia.

BSE was known to concerned scientific community since 1986 but the problem created panic across the world when on March 20, 1996, the United Kingdom's Spongiform Encephalopathy Advisory Committee (SEAC) announced the identification of 10 cases of variant Creutzfeldt-Jakob disease ( VCJD). These 10 cases had a characteristic clinical and pathological phenotype which differed from other routinely diagnosed cases of classic CJD. SEAC concluded that the cases were linked to exposure to BSE before the introduction of a specified bovine offal (SBO) ban at slaughter in 1989. The SBO ban excluded brain, spinal cord, and other organs with potential BSE infectivity from human consumption. Since then 153 cases of VCJD was diagnosed and 143 cases were from Great Britain.

Root of the evil: BSE in Great Britain may have been caused by feeding cattle rendered protein produced from the carcasses of scrapie-infected sheep or cattle with a previously unidentified TSE. The practice of using products such as meat-and-bone meal as a source of protein in cattle rations has been common for several decades. During 1970-80s feeding cattle meat-meal prepared at low temperature called Carvers Green Field became very popular in Britain. Changes in such rendering operations during that time may have played a part in the appearance of the disease. Whatever may be the route, prion of scrapy succeeded in overcoming species barrier and became a new disease entity in cattle.

The agent responsible for BSE and other TSEs is smaller than the smallest known virus and has not been completely characterised. There are three main theories on the nature of the agent: (1) the agent is a virus with unusual characteristics, (2) the agent is a prion -- and (3) the agent is a virino -- a small, noncoding regulatory nucleic acid coated with a host-derived protective protein. Among the hypothesis mentioned the second one has been able to draw the attention of scientific community as well as the media. Dr. Stanley Prusiner was awarded noble prize for the prion theory. Prion is defined as small proteinaceous infectious particles which resist inactivation by procedures that modify nucleic acids. The discovery that proteins alone can transmit an infectious disease has come as a considerable surprise to the scientific community. Evidence suggests that a prion is a modified form of a normal cellular protein known as PrPc (for cellular). This protein is found predominantly on the surface of neurones. The modified form of PrPc which may cause disease i.e. the prion is known as PrPsc or PrPbse (for scrapie/ BSE) which is relatively resistant to proteases and accumulates in cytoplasmic vesicles of diseased individuals.

It has been proposed that PrPsc when introduced into a normal cell causes the conversion of PrPc into PrPsc. The exact nature of the process is unknown but it could involve a chemical or conformational modification. The ultimate result is conversion of brain material to a spongy state.

Clinical symptoms of BSE: Cattle affected by BSE experience progressive degeneration of the nervous system. Affected animals may display changes in temperament, such as nervousness or aggression, abnormal posture, incoordination and difficulty in rising, decreased milk production, or loss of body weight despite continued appetite and affected cow dies finally. There is neither any treatment nor a vaccine to prevent the disease.

The incubation period (the time from when an animal becomes infected until it first shows disease signs) is from 2 to 8 years. Following the onset of clinical signs, the animal's condition deteriorates until it either dies or is destroyed. This process usually takes from 2 weeks to 6 months. Most cases in Great Britain have occurred in dairy cows between 3 and 6 years of age.

Human form of mad cow: The human form of VCJD differs from classical CJD. It predominantly affects younger people and average age of people has atypical clinical features, with prominent psychiatric sign at the time of clinical presentation and delayed onset of neurologic abnormalities, a duration of illness of at least 6 months, and a diffusely abnormal non-diagnostic electroencephalogram.

Bridging the gap: The question of probable transmission of BSE from cow to human was in the mind of every skeptic but the public bodies always denied the probability. At the onset of the crisis, the Agriculture Minister of Britain talked to newsmen while having British beef with her daughter to build confidence among people about safety of British meat. However, scientists now have strong evidences that supports the link between two diseases. The absence of confirmed cases of variant CJD in other geographic areas free of BSE supports a causal association.

In addition, the interval between the most likely period for the initial extended exposure of the population to potentially BSE-contaminated food (1984-1986) and onset of initial variant CJD cases (1994-1996) is consistent with known incubation periods for CJD.

An experimental study reported in June 1996 showed that three cynomologus macaque monkeys inoculated with brain tissue obtained from cattle with BSE had clinical and neuropathological features strikingly similar to those of variant CJD (Nature,1996).

A study published in 1996 indicated that a Western blot analysis of infecting prions obtained from 10 variant CJD patients and BSE-infected animals had similar molecular characteristics that were distinct from prions obtained from patients with other types.

Steps taken to control BSE and CJD: In Great Britain, the disease was first detected, the human form was first identified and the cattle industry suffered most. The experience of Great Britain is of immense importance. To control the disease they took many initiatives and the number of cases are declining. UK introduced Over Thirty Months (OTM) cattle slaughter rule. The rule bans the sale of meat for human consumption from most cattle aged over thirty months at slaughter. It was introduced by the government to protect public health from the risk of BSE and to safeguard consumer confidence in beef. The rule is applied strictly to all British cattle and for imported beef. A total of nearly 4.6 million cattle in the UK have been excluded from the food chain, mostly under the Over Thirty Month Slaughter Scheme (OTMS). They have also restricted the use of certain specified bovine offals (SBO) including brain and spinal cord for human consumption.

Under The Bovine Spongiform Encephalopathy Order 1988, sale, supply and use of Meat and Bone Meal (MBM) for feeding ruminants was banned and a scheme was taken to recall all the MBM for ruminant use.

Status of Bangladesh and needed steps: We are fortunate that our cattle farmers do not use MBM for their animals. The sheep population is very low and no case of scrapie was recorded. Moreover, Bangladesh does usually import cattle or meat from countries having BSE, but no BSE case was identified both among local and imported cattle. However, we must admit that we have some weakness also that may be proved sufficient to put us in great trouble. The country does not have any quarantine law and obviously no quarantine system is in practice. There is no veterinary control over import of MBM. Moreover, The Animal Disease Act is very old and has become almost obsolete under present context. The level of awareness regarding food safety is very low and system of abattoir control is almost non-existent. Although city corporations and municipalities run some ante mortem and post-mortem inspection programme but they are strained by many factors. These areas need immediate attention not only for preventing entry of BSE but also for safeguarding human and animal health.

A.K. Azad works with the Livestock Research Institute, Mohakhali, Dhaka.