University of Southeastern Philippines

Iñigo St., Bo. Obrero, Davao City, 8000

MATHEMATICAL MODELING FOR SPREAD OF DISEASES

In partial fulfillment
of the course requirements for the subject
MATH 315 – Differential Equation

Submitted by:
TOMANGONG, CHRISTIAN DOMINIQUE M.
TULIBAO, RON JERALD S.
UYAMOT, MIKAELA SAI
VILLARIN, JNOVAH MICAH
BS Mathematics 3

Presented to:
RICKY F. RULETE, Ph. D.
Faculty, Mathematics and Statistics Department

December 2023
 INTRODUCTION

The development of mathematical models to approximate real-world problems has been

one of the most critical aspects of the theoretical development of each branch of science. These

mathematical models frequently include an equation in which a function and its derivatives play

essential roles. Such equations are called differential equations [7]. Differential equations can be

used to model almost everything that changes continuously. These equations, known for including

functions and their derivatives, offer a flexible way to illustrate and examine ongoing changes in

various scientific situations.

[3] Infectious diseases commonly spread through the direct transfer of bacteria, viruses, or

other germs from one person to another. In the study of epidemics, where the spread of diseases

and epidemics occurs as a dynamic process, using differential equations becomes especially

interesting. This can occur when a person with the bacteria or virus touches, kisses, or

coughs/sneezes on someone who isn't already infected. Sickness-causing germs can also spread

through indirect contact. For example, many germs can stay on things like tables, doorknobs, or

faucet handles. [2] An example of it are dengue fever, polio, measles, and etc. [2] Epidemics could

be about a disease or another health-related behavior like smoking, where the rates are noticeably

higher than what you'd expect in a community or region. This study explores how diseases spread

and understand the important role that mathematical modeling plays in unraveling the complexities

of epidemics.

[8] Mathematical model of infectious disease is central in epidemiology and might play an

essential role in predicting and estimating disease transmission, recovery, deaths, and other

significant parameters separately. Bernoulli created the first article addressing the mathematical

modeling of epidemics in 1760. He developed a mathematical model to examine and predict the
effects of variolation. To make predictions about a spread of disease, it is crucial that mathematical

models become tools utilized throughout science and medicine to provide insights, generate

hypotheses, and devise experiments to test them.

The connection between the spread of diseases and Ordinary Differential Equations

(ODEs) lies in the capability of ODEs to encompass the fundamental principles governing the

dynamics of epidemiology. Scientists can create models using Ordinary Differential Equations

(ODEs) by establishing variables for susceptible, infected, and recovered individuals, allowing

them to simulate the advancement of diseases within a population. Additionally, several models

have been developed to quickly and accurately predict how something spreads in a network. [5]

For instance, in epidemiology, compartmental models such as susceptible-infectious-recovered

(SIR) and susceptible-infectious-susceptible (SIS), are often applied to the mathematical modeling

of infectious diseases. The SIR model was first introduced by Kermack and McKendrick in 1927.

It was considered one of the early triumphs of mathematical epidemiology due to its formulation

that predicted the behavior of an epidemic. The SIR model is a model in which an individual's

infectivity is determined by the time the individual became infective. The SIR model is one of the

simplest and most powerful models for modeling infectious diseases and studying the mechanisms

by which diseases spread in order to evaluate strategies that can control the pandemic. [5] One can

solve the system of differential equations that describes the epidemic model using computational

methods (Butcher, 1996).

As we explore how Ordinary Differential Equations (ODEs) used to create models in

relation to epidemics, we want to understand the complexities of how epidemics spread through

populations. By doing this, we hope to show how important mathematical models are in helping

make decisions about public health, which can benefit people worldwide.
 OBJECTIVE

1. Create mathematical models to precisely explain and forecast the dynamics of disease spread

among populations by utilizing ordinary differential equations.

2. Compute and resolve these ordinary differential equations to represent the relationships among

susceptible, recovered, and infected persons and comprehend the transmission of diseases.

3. With the aid of these mathematical models, examine the effects of several parameters on the

transmission of diseases, including population size, contact rates, and intervention tactics.

4. By evaluating the efficacy of control measures like vaccination campaigns or social distancing

and providing direction for creating focused disease prevention and control strategies, use the

models to influence public health decision-making.

DISCUSSION

Mathematical modeling is crucial in comprehending the dynamics of epidemic spread and

formulating effective control measures. It offers valuable insights into transmission dynamics and

aids in identifying critical parameters for mitigating diseases within the population. Among the

prevalent ordinary differential equation (ODE) models, the susceptible-infectious-removed (SIR)

and susceptible-exposed-infectious-removed (SEIR) models are widely employed [1].

One (or more) infected person is introduced into a community of individuals susceptible to

the disease in question. Contact infection transfers the disease from the infected to the unaffected.

Each infected person goes through the course of his illness and is eventually eliminated from the

list of people who are sick, either through recovery or death. During the period of his illness, his

chances of recovery or death vary from day to day. The stage of the illness also determines the
chances that the affected may spread infection to the unaffected. As the disease spreads, the

number of unaffected community members decreases. Since the course of an epidemic is short

compared to an individual's life, the population may be considered constant, except in as far as it

is modified by deaths caused by the epidemic disease itself. Over time, the epidemic may come to

an end. One of the most important problems in epidemiology is whether this termination occurs

only when no susceptible individuals remain or whether the interaction of the various factors of

infectivity, recovery, and mortality can result in termination even when many susceptible

individuals remain in the unaffected population [4].

THEORY

The population 𝑁 is divided into three categories in the SIR model: susceptible, infected,

and recovered. We let the time (𝑡) be the independent variable as we look into the changes in the

three categories with respect to time. We then let the following variables:

𝑆 = 𝑆(𝑡) be the number of susceptible individuals,

𝐼 = 𝐼(𝑡) be the number of infected individuals, and

𝑅 = 𝑅(𝑡) be the number of recovered individuals.

with 𝑆(𝑡) + 𝐼(𝑡) + 𝑅(𝑡) = 𝑁.

Susceptible are all capable of being infected at time 𝑡, and are not immune to the disease.

Infected are the people who are symptomatic and asymptomatic sick people and are capable of

spreading the infection. The recovered are those who have recovered from the disease, are immune

and don't spread the infections anymore. We assume the following assumptions of this model: no

births or immigration, thus, the population is fixed; recovery provides total immunity, there is a
fixed infection rate per day, and there is a fixed recovery time. At time 𝑡 = 0, an initial condition,

we have the following:

𝑆(0) = 𝑆0

𝐼(0) = 𝑅0

𝑅(0) = 0

At the beginning of an epidemic, the number of recovered people is 0, there are a small number of

infected people, and a large number of susceptible. 𝑅0 is a parameter describing the average

number of new infections due to a sick individual. It’s commonly called the basic reproduction

number. It’s a fundamental concept in epidemiology. If 𝑅0 > 1 the epidemic ill persists otherwise

it will die out. If a disease has an 𝑅0 = 3 for example, so on average, a person who has this sickness

will pass it on to three other people.

The classical deterministic SIR model is formulated with a system of differential equations

that govern the behavior of 𝑆(𝑡), 𝐼(𝑡), and 𝑅(𝑡). For each of 𝑆(𝑡), 𝐼(𝑡), and 𝑅(𝑡), we have a rate

of change with respect to time 𝑡.

𝑑𝑆
- the rate of change of susceptible with respect to time;
𝑑𝑡

𝑑𝐼
- the rate of change of infected individuals with respect to time;
𝑑𝑡

𝑑𝑅
- the rate of change of recovered individuals with respect to time.
𝑑𝑡

The system of differential equations of the SIR model is as follows:

𝑑𝑆
= −𝛽𝑆𝐼
𝑑𝑡
 𝑑𝐼
= 𝛽𝑆𝐼 − 𝛾𝐼
𝑑𝑡

𝑑𝑅
= 𝛾𝐼
𝑑𝑡

where 𝛽, 𝛾 are constants.

𝑑𝑆
The formulation of the rate of change of susceptible 𝑑𝑡 : the 𝑆𝐼 represents the interaction of

the susceptibles with the infected, the constant 𝛽 represents the contacts per infected per day, and

the negative sign means that the population of susceptibles is getting smaller as time goes on, as
𝑑𝐼
they transition to being infected. The formulation of the rate of change of the infected : 𝛽𝑆𝐼
𝑑𝑡

represents the transition of susceptibles to being infected, −𝛾𝐼 represents the loss of infected

people as they transition to being recovered, and 𝛾 represents the recoveries per person per day.

𝑑𝑅
And the formulation of the rate of change of recovered : 𝛾𝐼 represents the gain of the recovered
𝑑𝑡

people as they transition from being infected to being recovered. The figure below shows the

course of a spread of disease that lasts 100 days in an area with 1,000 individuals. The bottom (x)

axis is time, and the left (y) axis is the population or the number of people.

Figure 1: The Graph of a Solved SIR Model

susceptible (blue) persons decreases as the number of infected (red) people increases at the

beginning of the epidemic. The number of recovered (green) people increases gradually. In this

model, after the pandemic is over, everyone has been infected and recovered. This is not always

the case; some susceptible individuals may remain uninfected.

EXAMPLE

For a particular virus - Hong Kong flu in New York City in the late 1960’s - hardly anyone

was immune at the beginning of the epidemic, so almost everyone was susceptible. We will assume

that there was a trace level of infection in the population, say, 10 people. Thus, our initial values

for the population variables are

𝑆(0) = 7,900,000

𝐼(0) = 10

𝑅(0) = 0

In terms of the scaled variables, these initial condition are

𝑆(0) = 1

𝑆(0) = 1.27 × 10−6

𝑅(0) = 0

(Note: the sum of our starting populations is not exactly 𝑵, nor is the sum of our fractions

exactly 1. The trace level of infection is so small that this won’t make any difference). Our

complete model is
 𝑑𝑠
= −𝛽 𝑆𝐼, 𝑆(0) = 1,
𝑑𝑡

𝑑𝑖
= 𝐵𝑆𝐼 − 𝛾𝐼, 𝐼(0) = 1.27 × 10−6 ,
𝑑𝑡

𝑑𝑟
= 𝛾𝐼, 𝑅(0) = 0.
𝑑𝑡

We don’t know values for the parameters 𝛽 and 𝛾 yet, but we can estimate them, and then

adjust them as necessary to fit the excess death data. We have already estimated the average period
𝟏
of infectiousness at three days, so that would suggest 𝛾 = 𝟑. If we guess that each infected would

1
make a possibly infecting contact every two days, then 𝛽 would be 2. We emphasize that this is

just a guess.

Figure 2: The Solution Curves for the Choices of 𝛽 and 𝛾

[1] Deng et al. (2022). Mathematical Models Supporting Control of COVID-19. China CDC

Weekly, 4(40), 895–901. https://doi.org/10.46234/ccdcw2022.186

[2] Epidemic, Endemic, Pandemic: What are the Differences? (2023, March 14). Columbia

University Mailman School of Public Health.

https://www.publichealth.columbia.edu/news/epidemic-endemic-pandemic-what-are-differences

[3] Infectious diseases - Symptoms & causes - Mayo Clinic. (2022, February 18). Mayo Clinic.

https://www.mayoclinic.org/diseases-conditions/infectious-diseases/symptoms-causes/syc-

20351173

[4] Kermack, W. O., & McKendrick, A. G. (1927). A contribution to the mathematical theory of

epidemics. Proceedings of the royal society of london. Series A, Containing papers of a

mathematical and physical character, 115(772), 700-721.

[5] Kosma, C. (2023, April 9). Neural Ordinary Differential Equations for Modeling Epidemic

Spreading. OpenReview. https://openreview.net/forum?id=yrkJGne0vN

[6] Smith, D. & Moore, L. (2004, December). The SIR Model for Spread of Disease - The

Differential Equation Model. Retrieved from https://maa.org/press/periodicals/loci/joma/the-sir-

model-for-spread-of-disease-the-differential-equation-

model?fbclid=IwAR34U7DN6jFifNYaAu8nbrp96AItiRufmDf7MdaeMmH0aIChn8lFZl87_V8

[7] Rainville, E.D., Bedient, P.E., and Bedient, R.E. (1996). Elementary Differential Equations,

8th Edition. Pearson

Equations with Jump diffusion for SIR Model. In 2021 7th international conference on

optimization and applications (ICOA) (pp. 1-4). IEEE.