Choose your own epidemic

Spongiform Encephalopathy and Kuru in Montana
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Abstract
In the world health history, acellular infectious agents have been known to cause the most contagious infections that pose a great challenge in their dissemination and containment. Viruses, prions, and viroids utilize their host’s cellular composition to survive and spread pathogenic diseases. Although they fall under the same class of acellular infectious agents with viruses, prions differ in their cellular composition in that they lack nucleic acid; that is, they have no RNA or DNA. This essay assesses the epidemiology of prions which are known to cause neurodegenerative diseases in mammals. In particular, I will assess the bovine spongiform encephalopathy (BSE) disease in cattle and variant Creutzfeldt-Jacob disease (CJD). Also, the paper covers the spread of an outbreak of BCE in an animal ranch in the Washington state, Montana. Further, an analysis of the etiology of the diseases in the ranch follows as well as recommendations for the farm management on how to successfully contain the outbreak and treat the affected organisms.
Key Words: Bovine Spongiform Encephalopathy (BSE), Creutzfeldt-Jacob disease (CJD), prion, etiology, and epidemiology.
Introduction
In the history of biological scientific research, scientists have had a long debate with a consensus that it was impossible for infectious pathogens to spread diseases without using nucleic acids. However, biologist Stanley Prusiner, a Novel-Prize winner, pioneered the research to prove that infectious agents can spread infections without using either RNA or DNA (genes) (Simons et al.

, 2017). For instance, prions are small agents that utilize their proteinaceous property to spread infections. Unlike viruses, prions have no RNA or DNA in their cell structure but use protein to alter the protein structure of their hosts hence generate more infectious particles that infect their host (Simons et al., 2017). The variant prion protein, PrP, is the causative agent of spongiform encephalopathy in cattle and Kuru in humans. Recently, we conducted our USDA surveillance program in a sample of 40, 000 cows across various states in the US. The tests revealed that three cows from a cattle ranch in Montana contained the PrP prion that causes ‘cow madness’. As will be discussed below, the outbreak has affected at least five ranch workers who exhibited symptoms of CJD while three cows were suspected to be ill of BSE and one cow died of the same disease. In its right, BSE is a deadly disease that has far-reaching effects on both animal health and public health.
Analysis of the BSE and CJD Outbreak
Brief Epidemiology
Scientists have proved that BSE is caused by a structural variant of the normal cellular protein that is termed as PrP; a prion protein. The prion protein occurs in two forms; PrPc (normal form) and PrPSc (infectious form). In its advent into the body, the infectious prion protein, PrPSc attaches itself to the normal form, PrPc hence changing its structure to the harmful protein (Iulini et al., 2017). PrPsc is characterized by a conformed shape that is evident in the brain lesions of affected organisms. BSE can be spread among cattle through the use of cattle nervous tissue in the cattle feeds. BSE is transmitted to humans in the form of the variant Creutzfeldt-Jacob disease. Humans contract BSE through consumption of cattle products that have the bovine origin (Iulini et al., 2017). Also, BSE can be spread through blood transfusion. Further, Iulini and colleagues note that persons who cook or are in contact with meat or other cattle products face a risk of getting infected with BSE (Iulini et al., 2017).
Methodology of Surveillance
As an association mandated with the responsibility to see into the well-being of the public and agriculture in general, USDA conducts annual tests on animals nationwide on ‘cow madness’. In the last exercise, I was accompanied by a group of sixteen agricultural officers to a cattle ranch in Montana. At the farm we conducted interviews on the management to assess the kind of animal feeds that the cattle were taking as well as any medication that could elude cases of genetic mutation. Also, I extracted spinal fluids from the infected workers for further laboratory tests.
Diagnosis and Results
The physical examination of the suspected cattle revealed symptoms such as aggressiveness, general weakness, excessive weight loss, inability to standup, and a sense of difficulty in coordination. In practice, it is difficult to diagnose live animals of BSE since the surest means of identifying the disease is the existence of lesions in the brain tissue. However, in the Montana case, I conducted microscopy on the brain tissue from the dead cow which revealed the presence of lesions in the brain as well as a ‘spongy’ image of the brain (Manix et al., 2015).
In humans, to diagnose variant CJD requires a combination of both clinical procedures as well as neuropathological examination. In my case, I invited the affected workers to the state of the art USDA laboratory for a neurological examination (Manix et al., 2015). The patients exhibited symptoms such as muscle twitching and spams and abnormal reflexes. One of the patients had signs of dementia, visual-spatial perception, and coordination difficulties; an indicator that the infection was beyond the incubation period. To further confirm the CJD infection, I used an electroencephalogram which revealed an abnormal brain pattern in all the patients (Manix et al., 2015).
Etiology of the Outbreak
My analysis revealed that the BSE outbreak had affected the ranch and its local surrounding. After conducting genetic analysis of the tissues from the dead cow, I discovered traces of genetic mutation that was as a result of infection with the prion protein. Further, the management eluded that they unknowingly introduced nervous tissue into the cattle feeds hence resulting in transmitting the infection to other cattle. In our interviews at the ranch, we discovered that the workers fed on beef that was obtained from the ranch. Therefore they were infected with the variant CJD disease.
Conclusion and Recommendations
A BSE outbreak can result in big losses to farmers if not managed well. For instance, for the cattle ranch in Montana, the management revealed that the dead cow and the other three infected cows had claimed more than three-quarter of the anticipated quarterly profit. Aside from that, BSE infection in humans can result in loss of life and economic loses since the diagnosis and treatment of CJD can be very costly.
In my recommendation to the farm management, I will instruct that the infected cattle are separated from other cattle while they undergo treatment (Simons et al., 2017). Also, I will recommend that the farm management destroys all of their cattle feedstock and introduce a new line of feeds. In addition to that, the management should conduct weekly medical check-ups on the other cattle for the next six months. In that way, the outbreak will be handled to forestall future losses (Simons et al., 2017).
References
Iulini, B., Costas, E. V., Corona, C., Meloni, D., Favole, A., Mazza, M., … & Casalone, C. (2017). Classical and Atypical Bovine Spongiform Encephalopathy: Epidemiology, Pathogenesis and Diagnosis. In Prion-An Overview. Intec.
Manix, M., Kalakoti, P., Henry, M., Thakur, J., Menger, R., Guthikonda, B., & Nanda, A. (2015). Creutzfeldt-Jakob disease: updated diagnostic criteria, treatment algorithm, and the utility of brain biopsy. Neurosurgical focus, 39(5), E2.
Simmons, M., Ru, G., Casalone, C., Iulini, B., Cassar, C., & Seuberlich, T. (2017). Discontools: Identifying gaps in controlling bovine spongiform encephalopathy. Transboundary and emerging diseases.