A FURTHER INVESTIGATION ON THE PROPAGATION OF INFECTION IN A SQUARE LATTICE.

by

KRISTOFER NAEL B. MAYORDOMO

An Undergraduate Thesis submitted to the Physics Division Institute of Mathematical Sciences and Physics College of Arts and Sciences University of the Philippines Los Ba nos

In Partial Fulllment of the Requirements for the Degree of Bachelor of Science in Applied Physics

November 2013

CERTIFICATION This is to certify that this undergraduate thesis entitled, A Further Investigation on the Propagation of Infection in a Square Lattice. and submitted by Kristofer Nael B. Mayordomo to fulll part of the requirements for the degree of Bachelor of Science in Applied Physics was successfully defended and approved on 20 November 2013.

CHRYSLINE MARGUS N. PINOL, Ph.D.

Thesis Adviser

F. BALISTA, M.S.. JUNIUS ANDRE

Thesis Committee Chair The Institute of Mathematical Sciences and Physics (IMSP) endorses acceptance of this undergraduate thesis as partial fulllment of the requirements for the degree of Bachelor of Science in Applied Physics.

LOU SERAFIN M. LOZADA, M.S

VIRGILIO P. SISON, Ph.D.

Head Physics Division, IMSP

Director IMSP

This undergraduate thesis is hereby ocially accepted as partial fulllment of the requirements for the degree of Bachelor of Science in Applied Physics.

ZITA VJ. ALBACEA, Ph.D.

Dean College of Arts and Sciences

ABSTRACT

MAYORDOMO, KRISTOFER NAEL B. University of the Philippines Los Ba nos, November 2013. A Further Investigation on the Propagation of Infection in a Square Lattice.. Adviser: Chrysline Margus N. Pi nol, Ph.D. We aim to investigate further the dynamics of an Ising-based susceptible-infected model proposed by Crisostomo and Pi nol in 2012; specically, the eect of varying the location and number of infectives to the spread of infection in a closed population having homogeneous interaction. Results show that the rate of propagation of infection is independent of the location of the rst infective. Increasing the initial number of contagions generally hastens the spread of the disease. However, there exists a critical number after which we observe a change in the trend. Instead of speeding up, a further increase in the number of initial infectives slows down the propagation of infection. PACS: 75.10.HK[Classical spin models], 87.10.HK [Lattice models], b7.10. Rt [Monte carlo simulation], 0.5.a[Computational methods in statistical physics and nonlinear dynamics]

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Table of Contents
Abstract List of Figures 1 Introduction 1.1 Signicance of the study . . . . . 1.2 Objectives of the study . . . . . . 1.3 Scope and limitation of the study 1.4 Time and place of study . . . . . ii iv 1 3 5 5 5 6 6 7 8 8 9 11 11 12

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2 Review of literature 2.1 The deterministic model . . . . . . . . . . . 2.2 Stochastic models . . . . . . . . . . . . . . . 2.3 Some real-world applications . . . . . . . . . 2.3.1 Viral infections . . . . . . . . . . . . 2.3.2 Disease propagation and intervention 2.3.3 Ecological systems . . . . . . . . . . 2.3.4 Spread of information . . . . . . . . . 2.4 The Ising-based approach . . . . . . . . . .

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3 Methodology 16 3.1 Initialization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 3.2 Ising-model approach . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 3.3 Simulation specics . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 4 Results and Discussion 20 4.1 Single Infective . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 4.2 Multiple infectives . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 4.3 The eect of clustering . . . . . . . . . . . . . . . . . . . . . . . . . . 24 5 Summary and conclusion 30

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List of Figures
1.1 1.2 2.1 2.2 2.3 2.4 2.5 3.1 3.2 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8 4.9 4.10 4.11 4.12 4.13 4.14 4.15 The SIR model. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The SI model. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The compartmental representation of the SIR model. . . . . . The scale-free network. . . . . . . . . . . . . . . . . . . . . . SEIRZ framework. . . . . . . . . . . . . . . . . . . . . . . . . Procedure for the Ising-based malware epidemiological model. Procedure for the Ising-based SI model. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 3 7 10 12 13 14 17 18 21 21 21 22 23 23 24 24 25 25 26 26 27 27 28

Von Neumann (or nearest neighbor) interaction . . . . . . . . . . . . Flowchart of the procedure. . . . . . . . . . . . . . . . . . . . . . . . Infection Infection Infection Infection Infection Infection Infection Infection Infection Infection Infection Infection Infection Infection Infection curves associated with Case 1. . . . . . . . . . . . curves associated with Case 2. . . . . . . . . . . . rate as a function of temperature. . . . . . . . curves using randomly distributed I0 at N = 100. curves using randomly distributed I0 at N = 150. curves using randomly distributed I0 at N = 200. rate associated with Scenario 1 at N = 100. . . . rate associated with Scenario 1 at N = 150. . . . rate associated with Scenario 1 at N = 200. . . . curves using clustered I0 at N = 100. . . . . . . . curves using clustered I0 at N = 150. . . . . . . . curves using clustered I0 at N = 200. . . . . . . . rate asociated with Scenario 2 at N = 100. . . . . rate asociated with Scenario 2 at N = 150. . . . . rate asociated with Scenario 2 at N = 200. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Chapter 1 Introduction
Epidemiology pertains to the study of diseases in a population - its patterns, causes and eects [1]. The eld emerged as a result of peoples desire to nd a way to predict the occurrence and rate of spread of infection within a population, and if possible, prevent it from reaching a critical level. The conventional approach to studying a certain phenomenon usually involves experiments implemented in a smaller scale. This, however, when applied to diseases is often times impractical and unethical. Scientists, therefore, resort to mathematical models when studying the dynamics of the spread of infection within a population. The simplest epidemic model was rst introduced by William Oglivy Kermack and Anderson Gray McKendrick in 1927 [2]. More popularly known as SIR, the model describes the health of a population using three basic classes: (1) susceptible, the class vulnerable to the disease; (2) infected/infective, when the individual acquires the infection, and; (3) recovered or removed class, when the individual is either cured from the infection or dies. Transition between these states is presented in Figure 1.1. The rate of change from one state to another is constant and given by and for the infection and recovery, respectively. This may be represented using the following dierential equations:

dS = SI, dt dI = SI I, and dt dR = I. dt 1

(1.1) (1.2) (1.3)

Figure 1.1: The SIR model. The population is assumed to be a closed community. There are no births, migrations or deaths. The total population is xed to a constant number N (t) = S (t) + I (t) + R(t). The SIR model applies to many cases of infection. The most common example is a viral infection popularly known as smallpox [1]. A person acquires the disease. Symptoms manidfest over time, after which the person recovers. From this very simple model has emerged many dierent variants. It works with the assumption that a person, although already infected, remains vulnerable to the disease. Common examples are rubella and measles. Rigorous medical treatment does not make a child immune to these diseases [1]. The case of inuenza, on the other hand, may be simulated using the SIRS (Susceptible-Infective-RecoveredSusceptible) model. When a person recovers from inuenza, it does not assure that reinfection will not occur. Thus, he may again acquire the infection after recovery [4]. Due to its robustness1 , the SIR has been extended to model related systems. One good example would be the study conducted by Bettencourt, et, al. [5]. They used epidemiological models, including the SIR, to describe the diusion of ideas
1 in computational physics, robustness of a model is referred to as the stability and versatility of the model to describe a specic phenomena.

to a network of people. Investigations of these models characteristics have more important implications that transecend epidemiology alone.

1.1

Signicance of the study

In this study, we analyze the characteristics of the SI model introduced in [3]. Here, the health of the population is described using only two states: susceptible and infected (Fig.1.2). Mathematically,

Figure 1.2: The SI model.

dS = SI , and dt dI = SI. dt

(1.4) (1.5)

where S (t) is the susceptible state, while I (t) is the infective state. Following the model proposed by Kermack-McKendrick in 1927 [2], we assume a closed community. That is, at any given time, N (t) = S (t) + I (t) = constant. The above dierential equations are easily solvable:

S (t) =

N , and 1 + e (ttc ) N I (t) = . 1 + e (ttc )

(1.6) (1.7)

where tc is the time when half of the population is infected and is the rate of infection. Despite its simplicity, the SI model is not very popular to epidemiologists. Quick internet search gives us papers focusing on more complicated cases. This is inevitable due to the fact that most diseases are best simulated by higher order models such as the SIR and the SIS. However, there are also actual scenarios that can be best described using the simple, one-way SI model. An instant example would be diseases that do not yet have a cure, [7]. Every individual is susceptible to the HIV virus (AIDS). Once infected, the person stays in this condition for the remainder of his life, or until a cure is found in his lifetime. In fact, this became the central topic of the dissertation by Cruz [6]. The SI model also ts in describing an information network characterized by two states: received or unreceived. Nodes in received states are transmitters capable of spreading information to the unreceived nodes (information sinks) [7]. In a related study, the SI model is used to simulate the rate of collapse of areas covered by trees in wind-disturbed forests [8]. As illustrated, susceptible-infected systems are more than just epidemiological models. They can also be used to describe similar related phenomena. In the case of diseases, the SI model can provide more information when an infection is dangerous, or when it reaches an optimum level. In the case of communication networks, knowing the best way to spread information can help device better transmission strategies. Identifying the areas that are highly dense can help us predict where similar species will grow next. There are more related cases that can be characterized by the SI model, which gives us a leverage in understanding these systems better by simulation. Evidently, our study holds its mandate to gain a better understanding not just about the spread of epidemics, but also the world.

1.2

Objectives of the study

In this work, we investigate further the dynamics of disease spread in the Isingbased Susceptible-Infected (SI) model proposed by Crisostomo and Pi nol [3]. Specifically, we look at the eect of varying the position and number of initial infective/s to the spread of infection in a population.

1.3

Scope and limitation of the study

The Ising-based (SI) model assumes a xed population in an m m square lattice. There are no births, migration or deaths. Latent and incubation2 between the states are also disregarded, therefore, infection is instantaneous. Total number of individuals is constant and is equivalent to the size of the lattice, N = m2 .

1.4

Time and place of study

This study was conducted from June 2012 to October 2013 at the Computational Physics Laboratory, Institute of Mathematical Sciences and Physics, University of the Philippines Los Ba nos under the supervision of Dr. Chrysline Margus N. Pi nol, thesis adviser.

latent and incubation periods are dened in epidemiological modelling as stages in the exposure state [11].

Chapter 2 Review of literature

There are several approaches in which we can study the spread of an epidemic through modelling, depending on the factor that we need to consider: it can be by chance of infectivity (deterministic and stochastic), time of the disease spread (discrete or continuous), spatial distribution, or population structure (homogeneous or heterogeneous) [9] [10]. We rst take into account the basic approaches, the stochastic and the deterministic approach.

2.1

The deterministic model

The deterministic model is the earliest model proposed by Kermack and McKendrick in 1927 [1]. Characteristic parameters of the population are xed. It is then divided into classes or compartments that designate their condition (Figure 2.1). Since the transfer rate is xed for each class, this can be described through dierential equations:

dS = SI, dt dI = SI I, and dt dR = I. dt It also follows that, for a xed population

(2.1) (2.2) (2.3)

Figure 2.1: The compartmental representation of the SIR model.

S (t) + I (t) + R(t) = N, and dS dI dR + + = 0 dt dt dt

(2.4) (2.5)

This is the basic framework for most epidemiological models. However, the estimates obtained using the deterministic approach are only suitable for large populations[12].

2.2

Stochastic models

Stochastic or probabilistic models are useful when we want to take into account the probability of change and variability of a parameter in the population [11]. There are multiple approaches that can possibly be used in stochastic modelling, one of which is the Markov probabilistic model. Here, the transfer of states are given by

S+I 2I, and I R.

(2.6) (2.7)

It can be seen that the combination of a susceptible and an infective results to two infectives, and the infective will become recovered in the future. Rates of change 7

between the states are given by and , respectively. To be able to derive the dynamics of the population, we apply the Markovian process given by

t p(S, I ; t) =

(S + 1)(I 1)p(S + 1, I 1; t) N + (I + 1)p(S, I + 1; t) ( SI + pI )p(S, I ; t). N

(2.8)

In Trapmans dissertation [13], he cited another basic model used in the stochastic approach, the Reed-Frost model. The method assumes that the population is xed. The probability to become infected depends on the number of case of infection at a certain time t. In [14], this is denoted by Ct . Ct+1 = St (1 q Ct ) (2.9)

where St is the number of susceptibles, and (1 q Ct ) is the probability that an individual will make contact with an infective at least once. Furthermore, this expression is used to dene the probability of Ct+1 cases occuring at time (t + 1) given by P (Ct+1 ) = St ! (1 q Ct )Ct+1 (q Ct )St+1 . Ct+1 !St+1 ! (2.10)

Since stochastic modelling doesnt assume constant values, it provides a better way of simulating real-world phenomenon, as it takes into consideration that the individual characteristic might change. However, since the method relies on probability, it becomes too complicated for analysis and arriving at an explicit solution may become dicult.

2.3
2.3.1

Some real-world applications

Viral infections

Epidemiological modelling is commonly implemented to determine the behavior of a particular disease, usually on commonly occuring diseases. Inuenza is a popular option when studying epidemics. The uctuating seasonality of its occurrence became the topic of study implemented by Dusho, et, al. 8

[4]. They have reported that the uctuations might have been caused by inconsistency in its transmission rate. Moreover, the unpredictable behavior of contacts can lead to dierences in the rate of infection. To be able to simulate this phenomenon, the authors implemented a deterministic and a stochastic SIRS model. The solutions obtained from both methods were presented graphically to compare which approach yielded a more ecient result. Models in epidemiology are best utilized in studying incurable diseases, one of which HIV is an example [6]. The interest of this study started from the fact that even though control measures of these kinds of diseases are always accessible, the pathogen seem to evolve into new strains that are capable of being invasive. Ordinary and delay dierential equations were utilized to dene various cases of becoming infected, which is done through a rigorous mathematical approach. The scope of the study is divided into four major parts: structured epidemic model with two-ages; structured two-aged model with intraspecic competition; epidemic models with time-delay; and two-sex epidemic model incorporationg socio-economic and cultural factors. In 2003, we can recall that the SARS epidemic from China that caused a worldwide alarm. The desire to prevent and control this disease led to numerous studies, one of which is conducted by Wang, et, al. [15]. Their work revolved on studying the spatial component of disease spread. This is accomplished using available data from reported cases of SARS in Beijing implemented in an SEIR (Susceptible-ExposedInfected-Removed) model. Afterwards, the geographical pattern of infection was identied using a nearest neighbor heirarchal clustering technique.

2.3.2

Disease propagation and intervention

The rate of infection varies according to the change in its characteristic parameters. One of the factors can be the type of network used to model the epidemic [16]. In epidemiology, network with more realistic structure tend to yield relatable real-world data. An example of a reliable network is the scale-free network. The reliability of this network became the motivation of the paper by [7], where they used a scale-free network to construct an SI epidemic model with identical infectivity. In this model, the probability of one individual - represented by nodes 9

Figure 2.2: The scale-free network. to infect one another is given by x (t) = 1 1(1 )(x,t1) , (2.11)

where is the spreading rate, x is the susceptible individual, and (x, t 1) is the number of contacts between x and the infectives at time t 1. The nodes have identical infectivity A, and the rst infective is selected randomly. Furthermore, they also determined faster spreading strategies and the eect of targetized immunization. Another factor that can aect the behavior of disease spread is the homogenity or heterogenity of the disease spread. This is explicitly discussed in the work done by [17], where they explained how the models that rely on dierential equations account for homogenity in mixing, and therefore fails to become a realistic model in the long run. This is observed through a lattice-gas cellular automata model (LGCA). In this model, a lattice composed of hexagonal cells is used. The center of the cells in the lattice are connected altogether, which becomes the connection of each node. In each cell, there can be a number of individuals that can randomly be susceptible (S), infected (I) or recovered (R), which interact freely. The propagation is governed by a time evolution probability given by E given by

10

E = P oRoC

(2.12)

where P is the propagation step, R is the randomization step and C is the contact step. Moreover, they used mean-eld approximation to determine the dynamics of disease spread in the LGCA model.

2.3.3

Ecological systems

Epidemiological models can also extend to non-disease related topics, especially to elds where population models are used. In ecology, criticality is described as sudden change in the characteristic of a system undergoing change [8]. It has three types: classical, or the normal type where sudden change occur at the system when it is undergoing change; self-organized criticalities that are self-inicted or without varying initial parameters, and; robust criticality that contains both of the characteristics of the rst and the second. Here, lattice models were used to explore events that causes criticality, such as predator-prey and disturbance-recovery relations. The transition of these states are similar to the dynamics of a susceptible-infective system. Furthermore, the interaction between the relations listed are modelled using a stochastic spatial model.

2.3.4

Spread of information

Information in wired networks are dissipated through dierent protocols. These protocols are most of the time deterministic, which implies lower reliability. To solve this, [18] presented a stochastic model based on the structure used in epidemiology. The protocol was described as gossip driven, as it works by the nodes of the network communicating with the others and relaying information from its memory. The model created assumes a xed number of nodes in its network. Each node attempts to send the packet of data stored in its memory to the nodes connected to it. Since it is a stochastic model, the transfer rate is determined by probability, governed by the route length of one node to another. Bettencourt, et al. [5] infered that the population dynamics of diusion of ideas is relatable to the standard models in epidemiology. However, the knowledge

11

of this fact has not been utilized as much. This became the framework of his study, where he used the data on the physicists that adapted the use Feynman diagrams in USA, Japan and USSR. The basic framework is in Figure 2.3, where S is the susceptible state, E is the exposed state, I is the infective state, R is the recovered state, and Z is an additional skeptic state. From here, he derived SIR, SIZ and SIRZ models.

Figure 2.3: SEIRZ framework.

2.4

The Ising-based approach

Antonio, et al. [19] used the Ising model in malware epidemiology. In their paper, they explained that the transmission of computer virus can be dependent on whether the recepient in the network is oine or online. This is relatable to the spin-up and spin-down conguration in the Ising model. The network is modelled using an N N lattice, with the online nodes having a value of +1 and 1 for oine. The energy equation is computed using Ei,j = si,j Ji,j snearestneighbors . (2.13)

In which the oine nodes change into online. Also, these nodes are associated with

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a probability of becoming infected, given by Pinf = number of online infective nodes number of online nodes (2.14)

to be able to organize the steps of the procedure, we look into the owchart in Figure 2.4:

Figure 2.4: Procedure for the Ising-based malware epidemiological model. The Ising-framework is used in determining the network status of a node (online or oine). The change is determined by the enery equation described in Equation 2.13, and the probability given by
E

p = e kB T

(2.15)

where E is the change in energy, kb is the Boltzmann constant, and T dened as the network trac. The results explained that a more congested network, or a network where there are more online users, are more susceptible to infectibility rather than a lightly congested network. The Ising-model was also used in epidemiology. In [3], this model was used to model the behavior of a susceptible-infective system. Similar to [19], the dual state

13

characteristic of the SI model is related to the spin-up( = 1) and spin-down( = 1). The model is limited to a square lattice with periodic boundary conditions. To be able to determine the change of a susceptible to infected, the Hamiltonian energy of the system per time step is compared, given by H is calculated as H = J
i,j x,y

ij xy .

(2.16)

where J is the interaction parameter. If the recent energy is less than or equal to the previous, the change is accepted. If otherwise, the change will be dictated by the probability given by p = eH/T (2.17)

The adaptation of the Ising-model approach is presented graphically in Fig. 2.5

Figure 2.5: Procedure for the Ising-based SI model. In the study, the authors graphed of the resulting infection-time relation and observed that it follows the logistic behavior. This similar trend can be observed 14

in existing standard models for the SI. Furthermore, the eect of varying the initial parameters were also observed. Firstly, it was seen that increasing the interaction parameter, J , causes a decrease in the rate of infection. This is related to the inverse contact rate, or the frequency of interaction of one individual to the rest of the population. Next, it was also observed that varying the parameter, T , causes a directly proportional change to the rate of infection. That is, an increase in this parameter also causes an increase to the rate of infection. However, at extremely high values, the eect diminishes and ceases to cause change. This, on the other hand, is related to the scaled temperature of the population.

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Chapter 3 Methodology
A population of N individuals is modelled using an m m lattice. Each lattice site corresponds to one invididual. The population is divided into susceptibles, S and infected/infectives, I . A susceptible individual is represented by a value of 1; for an infected individual, = 1. Here, we assume a closed community. That is, there are no births, deaths or migrations. The population size is held constant, N (t) = m2 = S (t) + I (t).

3.1

Initialization

We begin the simulation with a population of susceptibles, xy = 1 (3.1)

for all xs and y s, where x and y denote individual positions in the lattice (row and column numbers, respectively). The rst infective is then planted by changing the of a randomly chosen site from 1 to +1.

3.2

Ising-model approach

To simulate the spread of infection or the transition from S I , we adopt the process outlined in [3]. During a particular iteration, a random susceptible is chosen. This susceptible will be infected (S I , 1 +1) if such change will result to a Hamiltonian H that is less than or equal to the Hamiltonian H of the previous conguration (prior to the infection), 16

 or, for the case when H > H , according to the Monte Carlo probability

p = eH/T .

(3.2)

In the Ising model, T represents the scaled temperature and the Hamiltonian, H is the energy of the system given by H=J
i,j x,y x,y

ij xy ,

(3.3)

where J is the interaction parameter and surrounding ij (see also Fig. 3.1).

ij xy considers only the interaction

within the Von Neumann neighborhood (x, y ) {(i, j + 1), (i, j 1), (i + 1, j ), (i 1, j )}

Figure 3.1: Von Neumann (or nearest neighbor) interaction To avoid duplicity, we consider only the neighbors at the top and to the left of each site. Equation 3.3 reduces to H=J
i,j

ij i1,j + i,j 1 .

(3.4)

We also present a graphical summary of the procedures in Figure 3.2.

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Figure 3.2: Flowchart of the procedure.

3.3

Simulation specics

In this study, we use the following parameters sets: Lattice size, 100 100, 150 150, 200 200; Interaction parameter, J = 1.0, and; Temperature range, 0.5 T 8.0. Furthermore, we consider two cases. First, we begin our simulation with a single infective. Second, we investigate the eect of introducing multiple infectives. For the case of single infective, we have two scenarios: rst, the initial infective is planted at the middle; and second, the initial infective at the edge of the lattice. We analyze the behavior of these congurations as a function of time, and compare their infection rates. Circular boundary conditions will not be applied on the lattice. For the case of multiple infectives, we start the simulation by assigning an arbitrary number of infectives, x. We let 18

I0 = I (t = 0) =

x . m2

(3.5)

Furthermore, we also consider two scenarios: infectives are clustered at the center; and infectives are randomly placed throughout the population. Lattices we have used are periodically bounded. We analyze the rate of infection for dierent values of I0 . To estimate the value for , we t the values of I and t I (t) = where: I (t) is the number of infectives at time t; Imax is the maximum number of infectives1 ; is the rate of infection, and; tc is the critical time , or the time when 50% of the population is infected. Imax 1 + e (ttc ) (3.6)

In a closed community, the maximum number of infectives is Imax = N = m m.

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Chapter 4 Results and Discussion

4.1 Single Infective

We investigate the eect of varying the position of the rst contagion on the rate of spread of infection. We also removed circular boundary conditions to invoke the eect of a real-world closed population. First, we begin the simulation by planting the rst infective in the middle of the lattice. Figure 4.1 show plots the fraction of infected individuals against time, for dierent values of the parameter T . Infection curves are logistic. Furthermore, an increase in the value of parameter T causes a relative rise in the rate of spread of infection. The maximum value for the fraction of infectives (y-axis) is reached faster at lower T s. For the second case, infection starts from an infective that is placed at the edge of the lattice. Associated plots are presented in Figure 4.2. We recover the same S-curves as in the rst case. To estimate the infection rate , we use a logistic t, I (t) = 1 1+ e (ttc ) . (4.1)

Again, tc is to the point of inection. This corresponds to the time when 50% of the total population are already infected by the disease. Calculated values are presented in Figure 4.3, for both cases. Each represents the average of 10 independent trials. Notice that the points overlap. The location of the rst contagion, therefore, has no signicant eect on the rate of propagation of infection.

20

Figure 4.1: Infection curves associated with Case 1.

Figure 4.2: Infection curves associated with Case 2.

Figure 4.3: Infection rate as a function of temperature.

4.2
We let

Multiple infectives

This time, we begin our simulations with an arbitrary number of infectives, x.

I0 = I (t = 0) = Fixing T at 2.0, we consider two scenarios.

x x = 2. N m

(4.2)

Scenario 1 I0 is distributed randomly throughout the lattice. 21

Scenario 2 I0 is clustered at the center of the lattice. Furthermore, we simulated the eect in three lattice sizes: 100 100, 150 150, 200 200. We investigate the eect of spreading I0 randomly across the lattice (population). Figure 4.4, 4.5 and 4.6 shows infection curves with shape more similar to the Figures ?? and 4.2, as well as the ones obtained by Crisostomo and Pi nol [3]. As expected, Imax is reached faster when there are more infectives to begin with. As the lattice size is increased, the S-shape of the curves are becoming less prevalent. This might have been caused by the fact that larger lattices require more iterations to be completely aected by the virus. Figure 4.7 , 4.8 and 4.9 contains corresponding values. Calculated infection rates increase with I0 . However, we observe a decline in beginning at 0.5 I0 0.6. The fall may be attributed to an increased likelihood clustering at larger values of I0 .

Figure 4.4: Infection curves using randomly distributed I0 at N = 100. Figure 4.10, 4.11 and 4.12 displays I versus t curves obtained using Scenario 2. This is for dierent values of I0 . Compared to previous results (for the case of a single infective), the S here is more pronounced. However, full infection is not obtained at bigger lattice sizes. Normally, we would expect the infection to spread faster when there are more contagions at the beginning of the simulation. The contrary can be 22

Figure 4.5: Infection curves using randomly distributed I0 at N = 150.

Figure 4.6: Infection curves using randomly distributed I0 at N = 200. observed in Figure 4.13, 4.14 and 4.15 . Calculated values decrease with increasing I0 .

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Figure 4.7: Infection rate associated with Scenario 1 at N = 100.

Figure 4.8: Infection rate associated with Scenario 1 at N = 150.

4.3

The eect of clustering

The discussion on the implications of structural patterns are commonly tackled in spatial models in epidemiology [20]. The implications of clustering, specically, are discussed in some studies.

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Figure 4.9: Infection rate associated with Scenario 1 at N = 200.

Figure 4.10: Infection curves using clustered I0 at N = 100. In [21], they presented the eect of local neighborhood structure in epidemic processes. The interest came from the limitation of the models that are derived from the stochastic and deterministic approaches, as there is no spatially explicit discussion on its eects. To explore this, the authors constructed a cellular automata

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Figure 4.11: Infection curves using clustered I0 at N = 150.

Figure 4.12: Infection curves using clustered I0 at N = 200. model and implemented two types of neighborhood: Moore1 and activity-space, or a constantly interacting neighborhood. Also, they have considered two cases of initial infection: a centralized group and a uniformly distributed one. In the results, they
Let x, y be the selected cell. The Moore neighborhood is {(x, y + 1), (x, y 1), (x 1, y ), (x + 1, y ), (x 1, y 1), (x + 1, y 1), (x 1, y + 1), (x + 1, y + 1)}.
1

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Figure 4.13: Infection rate asociated with Scenario 2 at N = 100.

Figure 4.14: Infection rate asociated with Scenario 2 at N = 150. have reported that for both cases - Moore and activity-space - the propagation of disease in a centralized group tends to cause a lower rate of infection. Clustering also have signicant implications in creating vaccination strategies. Earlier, we have presented the study by [17] regarding the lattice-based model using LGCA. The results of that study included the outcome of two kinds of vaccination

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Figure 4.15: Infection rate asociated with Scenario 2 at N = 200. strategies: the barrier type, where the vaccination shield a centralized group; and the uniformly distributed type, where the vaccination were distributed in the population. It was reported that the uniform vaccination caused an increase in the number of the recovered. However, the rate of infection also increased in the same mode of vaccination. There are also implications of clustering in real-world epidemic scenarios. In Australia, the recurrence of foot-and-mouth disease (FMD) on livestock led to the study by [22]. They created a spatio-temporal SIR cellular automata model to simulate the dynamics of the epidemic and its behavior over time and space in two areas in Queensland, Australia. They used available data on recorded livestock and feral pigs on both the regions of interest. It was discussed that besides the time of initial infection, the density of the infectious animals can aect the cause of an outbreak. Earlier, the study on the spatial dynamics of SARS in urban areas in China was presented [15], where they modelled the outcome of the epidemic using data from reported cases and clustering techniques. They have reported that even the disease will continue to spread over time, it will remain in clusters. Moreover, if preventive measures are continued, such as control of mobility and withholding the infectives in

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a region, it will cause a signicant decrease in the propagation of the disease. The clustering phenomenon is relatable to control measures done to prevent the spread of an epidemic. A more popular name for this method is quarantine. Sattenspiel and Herring [23] discussed that quarantines are measures that have been implemented during occurrences of an outbreak. In the paper, they simulated the potential eectivity of quarantine using data from the 1918-1919 u epidemic that occurred in Northern Canada through a compartmental model. The results presented show that eectivity of quarantine depends on the mobility of an individual. That is, when there is low mobility in the population, quarantines work as rst preventive measure. However, if the mobility is high, quarantines are less likely recommended.

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Chapter 5 Summary and conclusion

We have investigated two cases of single infectivity: rst, in the middle of the lattice, then, on any random point at the edge of the lattice. Observing the behavior of the rate of infection as a function of temperature, we have seen that the graphs were similar. Hence, varying the initial infectives location does not aect the spread of infection, despite having the circular boundary conditions removed. We have also explored the eect of varying the initial number in the population in two cases: randomly and grouped in the center. For the randomly distrbuted initial infection, we have observed that the spreading of disease is faster when there infected individuals are randomly placed in the population. However, beginning at 50% - 60%, the rate of infection slows down. For the clustered case, we have seen that the spread of infection becomes slower, thus, providing a possibility of controlling the infection. In the actual world, this can be related to the localization of infectious individuals as a control measure to avoid an epidemic outbreak.

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