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The Epidemiology of Swine Flu Pandemic - Essay Example

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This essay "The Epidemiology of Swine Flu Pandemic" focuses on the virus that is seen as a worldwide emerging pandemic. The virus is caused by a diverse range of transmuting viruses that emerge every year. The flu mainly experiences small changes and it tends to spread every season. …
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The Swine Flu Pandemic Xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx Name Xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx Course Xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx Lecturer Xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx 20th April, 2012. Introduction With the recent outbreak of H1N1, the virus is seen as a worldwide emerging pandemic. The virus is caused by a diverse range of transmuting viruses which emerge every year. The flu mainly experience small changes and it tend to spread in each and every season (HMS 2009). The genetic changes which occurs in the virus makes certain that human beings must deal with a slightly new virus from time to time. Explanation of the outbreak, transmission and control of swine flu using the Triangle of epidemiology The health practitioners apply the epidemiology triangle model to assist individuals in gaining concepts related to communicable diseases, the triangle clearly describes the interplay between the agent, host as well as the environment by offering control and prevention, this is done by disordering the balance that exist in the triangle (Dorrance2009, pp.34). The outbreak, transmission and the control of swine flu can be explained by the use of an epidemiological triangle model (Shanta et al. 2009, pp. 283). The figure below clearly shows the explanation of swine flu when evaluated using the triangle of epidemiology. Source: http://www.cdc.gov/flu/weekly/ussurvdata​.htm. The agent The epidemic H1N1 termed as an influenza A virus categorized in the Orthomyxoviridae family group. The virus is spherical in shape, the enclosed particles are comprised of about eight single stress sections which are of the negative sense ribonucleic acid (RNA) and they are essentially enveloped in the nucleocapsid (VIT 2009). The H1N1 virus is enveloped in a lipid envelope with projecting exterior proteins comprised of both hem agglutinins and neuraminidase (Ryan 2008, pp. 56). The predominant surface protein is termed as the vital and most crucial component in resolving the epideological dynamics and it acts as both the hemagglutinin as well as the attachment protein deciding on the capability of the virus in bidding to as well as infecting cells of diverse species. This is achieved by appending to the sialic acid so as to infect cells from diverse species. (Peiris, Poon & Guan 2009) The NA antigen is another peripheral protein which is comprise of about twenty to twenty five percent of the entire surface protein. It is an enzyme which is referred to as neuraminidase since it slashes sialic acid from multifaceted carbohydrates (Abramson 2010, pp. 45). During infection it facilitates the release of the recentlycreated virus from surface receptors as well as from digests mucous discharge, thus offering a better opportunity for the virus to have access to the facade of susceptible cells and distributionthroughout the respiratory swathe.There exist other structuresthat are charged with the task virulence this structures include polymerase complex which consists of PB1, PB1-F2, PB2and PA, and PB1-F2 (Zamarin, Ortigoza & Palese 2006). Host The InfluenzaA viruses originates from a diverse range of creatures with the most common one been the aquatic birds. The other creatures from which the virus comes from is the human beings, horses, pigs and birds. Functional HA molecule and the expression of the sialic acid are vital aspects which ought to be present for an influenza virus to go into the host cell that are HA receptors. Human being species and the avian species vary slightly in sialyl-transfer as appearance in mucosal tissues as well as in the respiratory tissues (Sonoguchi et al 1985). It has been found that the swine tissues in most case depict two forms of the sialic acid this making it possible for the cells to co-infectedby both avian and human viruses this in one way increases the probability of genetic assortment in pigs (Khalik 2009). Most H1N1 viruses are derived from pigs and this leads to reassortment actions in swine and this may offer the virus additional virulence and also facilitate the virus in that it can be able to infect human beings. Environment Environment that one is in is another factor that really makes individuals susceptible to influenzaA virus. The virus is extremely resilient in the environment that one is in. it has been noted that low temperature as well as low humidity levels in the environment support of vaporizer transmission, this depicts the recurring nature of influenza A virus during temperate climates (Ferguson, Galvani and Bush, R.M. 2003).During tropical climates the virus is linked to rainfall this is so because individuals have to stay indoors this increasing their contact thus leading to high occurrence of the infections (Shaman, Goldstein and Lipsitch 2011). In essence the best suited environment for the virus is a selected population with no immunity, this makes certain that the pandemic spreads quickly. In temperate nations, influenza epidemics are experienced during winter (CDC 2010). Inhalation of respiratory drops that are infected with the virus is one of the major ways through which human beings get infected. Infected surfaces are also said to transmit the diseases but a large number of the infections are reported from areas where there is close contact such as schools (Shimada 2009). Control and prevention Various strategies applied so as control and prevent H1N1 viruses. One of the major ways of preventing and controlling is by the use of non-pharmaceutical measures. The non pharmaceutical approaches are mostly used in preventing human to human infections and the approaches that can be used are behavioural changes, social distancing and isolation (RelmanChoffnes 2010, pp 126). An example of such an approach is the closure of schools or gatherings, wearing of masks, strict observation of coughing etiquette and covering the nose when sneezing and cleaning of hand with detergents upon sneezing as well as reducing the level of contact with individuals who are infected (WHO 2010). Pharmaceutical approaches are also used in controlling and preventing the virus. One of such approach is immunization it offers the best prevention against influenza. Another pharmaceuticalapproachto the virus is bythe use of antiviral drugs and resistance (Cowlinget al. 2010). Anothercontrol is by the continuance of research related to this virus. International collaboration, research as well as surveillance will help reduce the virus this is because over time the research in this area is limited (Terence2009, pp. 56). Research will ensure that the molecular makers that are used as an indication of the virus transmission are determined. Causal factor and its difference with Risk factor Causal factors are the conditions that if present in a person’s body they will definitely lead to that person becoming infected with the disease in question (Terence 2009, pp.89). In epidemiology for any factor to be considered a causal factor it has to pass a causation test referred to as the “Hill’s Criteria” (Bradford 1965). The test compares the relationship between the factors claimed to be precursors of a disease and for is to be recognized as the cause it has to satisfy the criteria explained in the text below (Myers, Olsen and Gray 2007). 1. Sequential Relationship For a factor to be thought-off as a cause it must be traced to have been present whenever that disease is detected in an individual’s body (Van Kerkhove et al. 2011). It is the fundamental criterion for establishing causation. 2. Strength The correlation between the causal factor and its effect (disease) must be significantly large, for that factor to attain recognition as a causal factor. 3. Exposure-rate Relationship If the increase in amount of time one comes in contact with a causal factor or its amount leads to higher occurrence of the effect disease, there might be a causal connection, but absence of such a relationship does not make a factor is non-causal 4. Consistency If the same causal connection is reflected in studies conducted in varying conditions using different routines. An establishment of an express causation connection between a factor and a disease must be done after results of many trials to examine this implication are reconciled. it took numerous studies of the connection between tobacco smoking and cancer prior to concluded that consuming tobacco elevates the risk of cancer, but is does not the cause it. 5. Plausibility This connection must not be in contrast with existing facts on causation, the relationship must be rational, but this does not always mean that findings differing with what is known are wrong, they may even false a change in accepted “beliefs and principles”. 6. Factoring in other Explanations A causal connection must have looked at other hypothesis that had been ruled as not being the vectors of the disease in question. 7. Experiment Effects of a causal factor can be prevented in an environmental setting. 8. Specificity In this criterion a particular causal factor should be the source of a specific disease outcome. Swine Flu is caused by a virus named H1N1; an individual can acquire the virus by ingestion or breathing in of particles containing it (Van Kerkhove et al. 2011). Direct contact with particles of the virus in the mouth or the nose leads to one developing the disease later. This can be differentiated with Risk factors that only elevate the possibility of making contact with the H1N1 virus. Conclusion Influenza viruses seem to be an area of concern in modern day society. Through its review of the H1N1 virus using the epidemiological triangle model individuals be aware of the outbreak, transmission modes as well as measures to be put in place so as to curb the spread of the virus. References Abramson, J. S. 2010, Inside the 2009 Influenza Pandemic, World Scientific, New York Bradford, H. A 1965, “The Environment and Disease: Association or Causation?,” Proceedings of the Royal Society of Medicine, Volume 58, pp. 295-300 Centre for Disease Control (CDC) 2010, United States Surveillance Data, 2nd April 2010, http://www.cdc.gov/flu/weekly/ussurvdata​.htm. Cowling, B.J., Ng ,S., Ma, E.S., Cheng, C.K., Way, W., et al. 2010, Protective efficacy of seasonal influenza vaccination against seasonal and pandemic influenza virus infection during 2009 in Hong Kong ,Clinical Infectious Diseases, volume 51, pp. 1370–1379. Dorrance, J. M 2009,Global Time Bomb: Surviving the H1N1 Swine Flu Pandemic and Other Global Health Threats, Madrona Books, New York 140 pages. Ferguson, N.M., Galvani, A.P., Bush, R.M. 2003, Ecological and immunological determinants of influenza evolution, Nature, volume 422, pp. 428–433. Harvard Medical School (HMS) 2009, H1N1 and its descendents, 2nd April 2012, http://www.health.harvard.edu/press_releases/h1n1-flu-more-widespread-than-lethal. Khalik, S. 2009, H1N1 infections have crossed ‘tipping point’. The Straits Times, p. 1. , 2nd April 2012, http://www.straitstimes.com/Breaking%2BNews/Singapore/Story/STIStory_394119.html Myers, K.P., Olsen, C.W., Gray, G.C. 2007, Cases of swine influenza in humans: a review of the literature. Clinical Infectious Diseases, volume 44, pp. 1084-1088 Peiris, J., Poon, L & Guan, Y 2009, “Emergence of a Novel Swine origin influenza A virus (S-OIV) H1N1 virus in humans,” J. Clin. Virol., Vol.45, No.3, pp. 169-73 Relman, D. A., and Choffnes, E.R. 2010, The Domestic and International Impacts of the 2009-H1N1 Influenza A Pandemic: Global Challenges, Global Solutions: Workshop Summary, National Academies Press. Ryan, J.R. 2008, Pandemic influenza: emergency planning and community preparedness CRC Press, New York. Shaman, J., Goldstein, E., Lipsitch, M. 2011, Absolute humidity and pandemic versus epidemic influenza, American Journal of Epidemiology, volume 173, pp. 127–135. Shanta, M., Zimmer, M.D., and Donald, S. Burke, M.D. 2009, Historical Perspective — Emergence of Influenza A (H1N1) Viruses, New England Journal of Medicine, volume 361, pp. 279-285. Shimada, T 2009, “Epidemiology of influenza A (H1N1) virus infection in Japan, May-June 2009,” Eurosurveillance, Volume14, No.24 Sonoguchi, T., Naito, H., Hara, M., Takeuchi, Y., Fukumi, H. 1985, Cross-subtype protection in humans during sequential, overlapping, and/or concurrent epidemics caused by H3N2 and H1N1 influenza viruses.Journal of Infect Diseases, volume 151, pp. 81–88. Terence, S. 2009, Swine Flu / H1N1 - The Facts (Export Edition), Jessica Kingsley, New York. Van Kerkhove , M.D., Vandemaele K.A.H., Shinde, V., Jaramillo-Gutierrez, G., Koukounari, A., et al. 2011, Risk Factors for Severe Outcomes following 2009 Influenza A (H1N1) Infection: A Global Pooled Analysis 2nd April 2012, http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.1001053. Virus Investigation Team (VIT) 2009, Novel Swine-Origin Influenza A (H1N1): Emergence of a novel swine-origin influenza A (H1N1) virus in humans. New England Journal of Medicine, volume 360, pp. 2605-2615 World Health Organization (WHO) 2010, Pandemic influenza preparedness and response: WHO guidance document, World Health Organization. Zamarin, D., Ortigoza, B & Palese, P 2006, “Influenza A virus PB1-F2 Protein Contributes to Viral Pathogenesis in Mice,” J. Virol. Volume 80, pp. 7976-7983. Read More
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