Coursework confirmation Yes A 1 ao +0 No om Marking comments General comments ‘The student was interested in how to model diseases using mathematics. She came to the conclusion that she wanted to study the SIR model. In having conversations with the student, the student planned on using real-life examples at the school when we had a hand foot mouth disease outbreak, however it did not make it into the exploration. The exploration simply describes the SIR model that one might find in a university textbook. ‘A Communication (4) The exploration includes an introduction. Rationale and aim are briefly described in the introduction. The aim is not fulfilled as the application of the SIR was not done. The ‘exploration is hard to read filled with technical language usually in quotations. 44 B Mathematical presentation (3) There are examples of equations, graphs, and tables. They are labelled clearly. However, variables are not defined when equations are first shown. 28 © Personal engagement (4) The student mentions why she wanted to study the SIR model. The student is attempting to study unfamiliar mathematics. v4 D Reflection (3) There is only some reflection in the conclusion where the student acknowledges the limitations of the exploration. There is no other evidence of reflection throughout the113 E Use of mathematics (6) There is mathematics used which is commensurate with the level of the course. However, the explanations need to be deeper to show good understanding. Also, no mathematics was applied in this exploration. 361 1. Introduction A-Intreduction includes codienale and aim. [was always a person who was fascinated by everyday observations and with biology being a subject that I really enjoy, I wanted to link my exploration withthe subject. The linked | medical field is of much interest to me too. Keeping these interests in mind, I set out to look 4® cersmnel ienreres for a topic which linked math and biology. I managed to find my topic while researching the spread of smallpox for biology class and the idea of being able to mathematically model ie explotis scansiing ox caiasropic arn apidersis war insiguing 0 mv Baya did iy veoerct,1 Ciflenend cs ‘was trying to understand the modelling process and how it is applied. This exploration’ aims to understand, evaluate and apply the SIR Model Bonet all sebleS “eFined > -8-—B A= Snoutt Diagram 1. A visual of how the SIR works, the number of susceptible individuals become infected in a certain time (t) is defined, in the equation (1.2), by BSI. The number of infected individuals recovering is defined by al , where“ «” the rate at which infected become recovered and multiplying with the number of J gives the number of recovered individuals. I, Background (general) and History: ‘The SIR Model-S-susceptible, infectious, R-recovered-was first used by Kermack and MeKendrick in 1927 (IDM). “In the pas, mathematicians, like Bernoulli, have used basic differential equations to model the spread of such diseases as smallpox.” (Watson 5). The method of inoculation was associated with the risk of death, hence, with the model and its results which showed that “inoculating all new-born inthe country was still more advantageous to society as whole than the individual risk of death associated with the inoculation itself (Watson 5) Thus, smallpox was eradicated due tothe compulsory vaccine, although it was discovered later, andthe varilation (Watson 5). ie eee = comment on Wed AS MOBS:‘The Basic Assumptions: m. 4, The population is closed hence, there are no deaths or births the population size remiains constant, iti justified by the use ofthe model over a very short period of time, 2. The infected become infections immediately after becoming infected, hence there is no latency period (Weiss 2). D-no teFlection 3. ‘The model works for infections and viruses that cause the individuals to build immunity against the disease and be immune to it, hence they are never susceptible, after recovering. 4. Social and economic factors such as age, sex and race do not affect the number people infected and the rate of transition ofthe disease. 5. The susceptible (S) group do not have any form of “inherited immunity” _ Law of Mass Action: The law of mass action when applied to Epidemiology states, “that the fate a which an net pases ina popultin is proportional jin tthe product fhe number of persons / who are infectious and the number of S who are susceptible to the infection” (Wilson and Worcester 24). It is defined by Edwin B. Wilson and Jane Worcester, in term of the equation (1), where C stands for rate of new infections, r the constant: peony sie c=g=r1s a Beda? According to M. E. J. Newman, “the number of new cases of the disease in a time interval is proportional to the product of numbers infected and susceptible hosts in the previous time interval” (2002). Moreover, the basis of the law is that the infectious (J) individuals uniformly De Why mix with the susceptible (S) inthe population. Although this assumption is unrealistic, with ¢ the “proper choice of a constant r the equation (1) yields a theoretical curve of new cases” uncealistic> (Wilson and Worcester 25). Hence, the rate at which the number of suspected individuals aretuming into infected is the same, however this also undermines the fact that not all interactions result in an infected person and the rate of infected becoming recovered while leaving the infected number of people and joining the recovered is also the same. This is the reason why in order to monitor change in the infected population, 4 the rate at which people become recovered, c's subtracted from the numberof poople becoming infected, $15 while to figure out the number of people in the recovered population is represented by the people leaving the infected population *~ al”. Allin all it shows that due to the law of mass action the number of people leaving one group and moving to the next group is the same. Advantages and Disadvantages of using the SIR model: This model has been very useful in determining whether the epidemic will occur or die down before occurring, According to Megan Watson, the models serves as an ethical and reasonable way to test out theories, due to the fact that “models don’t require manipulation of actual people, experiments that would ‘otherwise be considered ‘unfeasible or unethical” can be executed through simulations” (Watson 5) and (Meyers 880). Furthermore, these models can be used in a continuous-time Do whet does period or a discrete time period, and these models are also deterministic. Ais mean? @ The rate at which Infected individuals are removed from the ‘Infected’ section B The rate at which Susceptible move fo becoming infected and infectious = The rate of change inthe number of susceptible. dS/dtis called the derivative of 5 with respect to & in other words, the rate of change of S in respect 10 g the rate of change in the numberof infected. Change of 7 ‘with respect to ¢ § the rate of change of R in respect to ¢ 7 Time BS, ‘The numberof suscepiible individuals that could become infected. B—she voriables/ parameters hat cppeow here have a\ready been used:e ‘Susceptible T Tinfected R Recovered N Total Population '. The SIR Model ~ continuous and without vital dynamics Table 1, Parameter, Variables and Deri &— £48 (11) 4=L1s—al (12) Explanation: This set of differential equations represent the Susceptible (S), Infectious (I) and Recovered (R) population of the total population N. According to the model, the population is divided into these three groups and the number of people in each group after a certain time is given by the right hand side ofthe equation. Equation (1.1) : This equation shows the change in the number of susceptible individuals, but using the Parameter f to control the rate at which the infected come in contact with the susceptible, which is defined by -/ . The parameter “p is the average number of disease-spreading contacts made by each infected individual in unit time” (CalebSvobodny). Hence, when SI, the value would not be the just a product rather only a section ofits the product due to the “B' In this equation (1.1), — 4-15, the sign is negative because the difference in ‘S” is defined by the number of individuals becoming infected through equation (1.1) but since thes number of susceptible is decreasing, the sign is always negative. A simple way of considering “$7 is one infectious individual and how many susceptible individuals this individual can infect. So, as stated in the assumptions and section IV, the law of mass action allows us to assume that the change in the number of both infected and susceptible individuals are inversely proportional since when ‘~ al "leaves the infected it becomes as represented by equation (1.3), = al . Hence, if one infected person is able to infect the whole susceptible Population for example, inthe ratio is 1:10, then if there are 10 infected individuals, then the B- win ratio would be 10:100, Thus, in the equation we muliply Sand Butin the coment ofthe 2 ig the ‘equation it is clear that there is time involved and so, the beta (B) controls the transmission of SA™® 2 the infection from infected to susceptible. An example of beta would be, ws “joo + i raminin ite. pope come ncn is. _ > Since there are no deaths or births "al ppt ‘being considered in this model, it is called the ‘without vital dynamic SIR model’, so ‘equation (2) is applicable because the individuals only move from one group to another and is 4 closed population. Equation (2) can be obtained by adding ~ £18 (1.1) + $-18—al (1.2) + af (1.3), we see that the terms cancel out and we are left with zero showing that equation (2) is correct. Y = hy can we S@+1+RO=N Q) i w and a equations? Sy =8,-BLS, Q1) Na“ LABIS,-al(22) E- mort exieresion ho Ruy =al, 23) is necde aa Tez Vis «SHO rdecstanelir) B Rate of infection 0.29/day n Rae of removal Oisiay b Tnitially infected no. of T people x, Time increment _ 100 day_ Initially susceptible 1000 D- where ore fies volues Com — fromTable 2. Values for flu (Pandem-data) Explanation of equations (2.1), (2.2) and (2.3): these equations are very similar to 1.1, 1.2 and 1.3 except these are for certain time intervals and so it finds out the number of susceptible when one is added to the time S,,, a B- Student? ‘elation figure 1. When this data is graph over 100 days the graph looks like, This shows that although it has become an epidemic, everyone will recover. Another example would be of Measles: i w x Ta EE hie « 0.144 aos N 1000 ee pot: Ss 999, eSort aw! i T foc B ‘Table 3. Values for Measles (Pandem-data) Pepin Figure 2. showing the graph for the spread of measles over 100 days. V. An Endemic Model= w-pst-ys 4 =psI-al—y B-al-e r Rate death and bint, Assumption death and birth rat is the same W The total numberof individuals 7 Rate at which Infected individuals die- w The rate which susceptible individuals are bom, ® TRate at which recovered individuals die. Ww The number of births into the population, Table 4. The new parameters and variables emaore “there is constant inflow of new susceptible Nj (due to births), and outflows (as natural E yor” deaths) at rate (yS, xR and yN) in respective classes.” (Lawot 18). Nonetheless, the 6 population (N) stays the same because the rate of death and birth isthe same at any given time (0. Conelusion: It can be seen that the different versions of the SIR model allows researchers to focus on different aspects of the models, the ordinary differential equations (ODE) used in the model were unknown to me before this research started and so the limitation it posed was thatthe explanation might not have been dep and clear should ave ben Furthermore, the SIR model is although not very accurate because there are many underlying seo tte elon rah cei et vet sete wld exon epidemic or endemic. In our daily life just by looking atthe spread of a certain contagious disease we can see that the SIR model can be very useful from looking atthe spread of a _ghudert ackrodedges \nitakion of cxplereriendisease in a small community to a much wider range of applications. Which is what fascinated me the SIR model used mathematics to show a correlation between different information and data about the population.Work cited Bansal, S., B.T. Grenfell, and L.A. Meyers (2007) When individual behaviour matters ‘homogeneous and network models in epidemiology. Journal of the Royal Society Interface 4: 879-891. IDM. “SIR and SIRS Models.” SIR and SIRS Models - Generic Model Documentation, institutefordiseasemodeling github io/Documentation/general/model-sir html#sir-and- sirs-models Johnson, Teri. “Mathematical Modeling of Diseases: Susceptible-Infected-Recovered (SIR) Model .” ResearchCate , 2009, ‘www.researchgate.net/publication/242272678_Mathematical_Modeling_of Diseases S uusceptible-Infected-Recovered_SIR_Model Lawot, Niwas. “Mathematical Modeling Of Smallpox Withoptimal Intervention Policy.” STARS, 2006, stars. library uct edu/etd/902/, Newman, M. E, J. “Spread of Epidemic Disease on Networks.” Physical Review E, vol. 66, no. 1, 2002, doi:10.1103/physreve.66.016128. Pandem data. “Make Your Own Model .” Make Your Own SIR Model, ‘www pandemsim,com/data/index php/make-your-own-sir-model/ Weiss, Howard. “The SIR Model and the Foundations of Public Health.” Revista Electrinica De Divulgacié Matematica, vol. 2013, 2013, pp. 1-17., ‘mat uab.cat/matmav/PDFV2013/v2013n03 pdf. Wilson, Edwin B., and Jane Worcester. “The Law of Mass Action in Epidemiology.” Proceedings of the National Academy of Sciences of the United States of America, vol. 31, no, 1, 1945, pp. 24-34. JSTOR, www jstor.org/stablel87857.