The aftermath of the Mad cow disease scandal

Figure 1: Do you want your brain to look like this? Source: (Icahn School of Medicine 2023)

 

Brief introduction

On 20 March 1996, the UK government formally recognised that consuming contaminated cattle can result in humans contracting the disease. Bovine Spongiform Encephalitis (BSE) (also known as Mad Cow Disease) infected cattle, when consumed by humans, could result in becoming infected with the ailment. The problem started when cows were fed with cow waste products such as the brain, which could already be infected. As more and more cows ate such contaminated feed, and when these cows died, they would be rendered into more or such contaminated feed to be fed to more cows, perpetuating and worsening the spread of the disease (Kimberlin 1996). The severity of the crisis could be attributed to the poor management by the UK government, who insisted that British beef was safe despite research at the time indicating that their test results were unknown and inconclusive at the time (Zwanenberg and Millstone 2005). As a measure to counteract the worsening situation, the UK resorted to mass cattle culling as embargoes against British beef were enforced by the European Commission to stop exports on a global basis until “eradication” was achieved (Zwanenberg and Millstone 2005).

BSE effect on humans

Directly affected by the crisis were estimated to be about 7000 people who succumbed to the disease termed Variant Creutzfeldt–Jakob disease (Yam 2003), which is often fatal and incurable. The disease was propagated through rogue misfolded proteins termed Prions, which, when introduced to the body, could infect healthy brain tissue and alter the brain structure into a sponge-like consistency, with the prognosis often being fatal (CDC n.d.).

The rogue prion’s effect on the environment

Of greater concern are the dangers of what happens if we do not thoroughly destroy these infectious prions and release these rogue proteins into the environment. Prions can remain infectious even when buried in soil, as long as 16 years after initial burial (Saunders, Bartelt-Hunt and Bartz 2008). The risk these prions can bring to humans is their eventual return as it infects animals in the food chain until it reaches us. For example, animals grazing from contaminated soils, such as cattle, would become infected. Due to the long incubation period before these animals show symptoms, these animals pose a risk to human health if we were to consume this contaminated meat.

The thorough destruction of prions is one effective way to stop this perpetual cycle of disease. However, we must first stop polluting the environment by thoroughly and properly disposing of contaminated livestock. During the BSE outbreak, contaminated cattle were dumped into landfills to rot, allowing for the mass introduction of prions into the environment as these prions bond to the soil (Saunders, Bartelt-Hunt and Bartz 2008). The severity of prions and their long-lasting impacts on the environment is poorly studied (Saunders, Bartelt-Hunt and Bartz 2008), and this is problematic since the anthropogenic pollution of prions has the potential to be severe. While the disease is currently rare and limited mainly to England and France (Icahn School of Medicine 2023), it can become widespread if mishandled sufficiently, like in the case of the UK.

It is also in the livestock industry’s interest to stop these prions since the BSE outbreak has demonstrated the dangers of neglecting this more obscure source of pollution. After all, a ban on meat sales could be economically decimating for the industry. Perhaps, people should pay more attention to what they eat by knowing what actually goes into producing food.

 

Bibliography

CDC. n.d. Variant Creutzfeldt-Jakob Disease (vCJD). Accessed January 17, 2023. https://www.cdc.gov/prions/vcjd/diagnostic-criteria.html.

Icahn School of Medicine. 2023. Creutzfeldt-Jakob disease. https://www.mountsinai.org/health-library/diseases-conditions/creutzfeldt-jakob-disease.

Kimberlin, Richard H. 1996. “Speculations on the Origin of BSE and the Epidemiology of CJD.” In Bovine Spongiform Encephalopathy: The BSE Dilemma, by Clarence J. Gibbs, 155 – 175. Massachusetts: Springer. doi:10.1007/978-1-4612-2406-8.

Saunders, Samuel E., Shannon L. Bartelt-Hunt, and Jason C. Bartz. 2008. “Prions in the environment: occurrence, fate and mitigation.” Epub 2008 (Pubmed Central) 2 (4): 162 – 169. doi:https://doi.org/10.4161%2Fpri.2.4.7951.

Yam, Philip. 2003. “Chapter 9: Mad Cow’s Human Toll.” In The Pathological Protein, by Philip Yam, 137 – 152. New York: Copernicus Books. doi:https://doi-org.libproxy1.nus.edu.sg/10.1007/0-387-21755-X_9.

Zwanenberg, Patrick Van, and Erik Millstone. 2005. “The aftermath of 20 March 1996.” In BSE: risk, science and governance, by Patrick Van Zwanenberg and Erik Millstone, 199 – 208. Oxford University press. doi:https://doi.org/10.1093/acprof:oso/9780198525813.003.0008.