Spotlight on Modeling: The Possum Plague

Similar documents
Systems of Differential Equations

Mathematical Epidemiology Lecture 1. Matylda Jabłońska-Sabuka

Applications in Biology

Section 8.1 Def. and Examp. Systems

Thursday. Threshold and Sensitivity Analysis

Figure The Threshold Theorem of epidemiology

Stability of SEIR Model of Infectious Diseases with Human Immunity

A Note on the Spread of Infectious Diseases. in a Large Susceptible Population

Mathematical Modeling and Analysis of Infectious Disease Dynamics

LAW OF LARGE NUMBERS FOR THE SIRS EPIDEMIC

Fixed Point Analysis of Kermack Mckendrick SIR Model

Models of Infectious Disease Formal Demography Stanford Summer Short Course James Holland Jones, Instructor. August 15, 2005

Project 1 Modeling of Epidemics

Differential Equations Handout A

(e) Use Newton s method to find the x coordinate that satisfies this equation, and your graph in part (b) to show that this is an inflection point.

Final Project Descriptions Introduction to Mathematical Biology Professor: Paul J. Atzberger. Project I: Predator-Prey Equations

Non-Linear Models Cont d: Infectious Diseases. Non-Linear Models Cont d: Infectious Diseases

M469, Fall 2010, Practice Problems for the Final

Dynamical models of HIV-AIDS e ect on population growth

Qualitative Analysis of a Discrete SIR Epidemic Model

Global Analysis of an Epidemic Model with Nonmonotone Incidence Rate

Epidemics in Networks Part 2 Compartmental Disease Models

ME 406 S-I-R Model of Epidemics Part 2 Vital Dynamics Included

Mathematical Analysis of Epidemiological Models: Introduction

A NEW SOLUTION OF SIR MODEL BY USING THE DIFFERENTIAL FRACTIONAL TRANSFORMATION METHOD

Australian Journal of Basic and Applied Sciences

1 The pendulum equation

Introduction to SEIR Models

Math 232, Final Test, 20 March 2007

Dynamics of Disease Spread. in a Predator-Prey System

Lab 5: Nonlinear Systems

The SIRS Model Approach to Host/Parasite Relationships

MA 138 Calculus 2 for the Life Sciences Spring 2016 Final Exam May 4, Exam Scores. Question Score Total

Introduction to Epidemic Modeling

SYMBIOTIC MODELS WITH AN SIR DISEASE

We have two possible solutions (intersections of null-clines. dt = bv + muv = g(u, v). du = au nuv = f (u, v),

Dynamics of a Population Model Controlling the Spread of Plague in Prairie Dogs

István Faragó, Róbert Horváth. Numerical Analysis of Evolution Equations, Innsbruck, Austria October, 2014.

Modeling the Spread of Epidemic Cholera: an Age-Structured Model

The death of an epidemic

Any live cell with less than 2 live neighbours dies. Any live cell with 2 or 3 live neighbours lives on to the next step.

ECS 289 / MAE 298, Lecture 7 April 22, Percolation and Epidemiology on Networks, Part 2 Searching on networks

Getting Started With The Predator - Prey Model: Nullclines

Predator - Prey Model Trajectories and the nonlinear conservation law

SIR model. (Susceptible-Infected-Resistant/Removed) Outlook. Introduction into SIR model. Janusz Szwabiński

The SIR Disease Model Trajectories and MatLab

Modeling with differential equations

Analysis of Numerical and Exact solutions of certain SIR and SIS Epidemic models

HETEROGENEOUS MIXING IN EPIDEMIC MODELS

GLOBAL DYNAMICS OF A MATHEMATICAL MODEL OF TUBERCULOSIS

SIR Epidemic Model with total Population size

The dynamics of disease transmission in a Prey Predator System with harvesting of prey

A NUMERICAL STUDY ON PREDATOR PREY MODEL

Exam 2. Principles of Ecology. March 25, Name

A New Mathematical Approach for. Rabies Endemy

Modeling the Immune System W9. Ordinary Differential Equations as Macroscopic Modeling Tool

Epidemics and information spreading

The Spreading of Epidemics in Complex Networks

Three Disguises of 1 x = e λx

(mathematical epidemiology)

APPM 2360 Lab 3: Zombies! Due April 27, 2017 by 11:59 pm

PARAMETER ESTIMATION IN EPIDEMIC MODELS: SIMPLIFIED FORMULAS

Ordinary Differential Equations

MATH 56A: STOCHASTIC PROCESSES CHAPTER 0

SMA 208: Ordinary differential equations I

STABILITY OF EIGENVALUES FOR PREDATOR- PREY RELATIONSHIPS

University of Leeds. Project in Statistics. Math5004M. Epidemic Modelling. Supervisor: Dr Andrew J Baczkowski. Student: Ross Breckon

CBA Practice Exam - Ecology

MODELING AND ANALYSIS OF THE SPREAD OF CARRIER DEPENDENT INFECTIOUS DISEASES WITH ENVIRONMENTAL EFFECTS

Ecology. Part 4. Populations Part 5. Communities Part 6. Biodiversity and Conservation

Modelling of the Hand-Foot-Mouth-Disease with the Carrier Population

Resilience and stability of harvested predator-prey systems to infectious diseases in the predator

STABILITY ANALYSIS OF A GENERAL SIR EPIDEMIC MODEL

Bifurcation Analysis of a SIRS Epidemic Model with a Generalized Nonmonotone and Saturated Incidence Rate

arxiv: v2 [q-bio.pe] 3 Oct 2018

MATHEMATICAL MODELS Vol. III - Mathematical Models in Epidemiology - M. G. Roberts, J. A. P. Heesterbeek

CS224W: Analysis of Networks Jure Leskovec, Stanford University

STUDENT VERSION DISEASE SPREAD

Kasetsart University Workshop. Mathematical modeling using calculus & differential equations concepts

Epidemic model for influenza A (H1N1)

Introduction to Stochastic SIR Model

Modelling the spread of bacterial infectious disease with environmental effect in a logistically growing human population

A comparison of delayed SIR and SEIR epidemic models

adaptivetau: efficient stochastic simulations in R

Applied Calculus. Review Problems for the Final Exam

The Fractional-order SIR and SIRS Epidemic Models with Variable Population Size

3.5 Competition Models: Principle of Competitive Exclusion

Math 310: Applied Differential Equations Homework 2 Prof. Ricciardi October 8, DUE: October 25, 2010

A Simple Ecological Model

Lesson 9: Predator-Prey and ode45

dy dt = a by y = a b

2D-Volterra-Lotka Modeling For 2 Species

Delay SIR Model with Nonlinear Incident Rate and Varying Total Population

MATH 415, WEEKS 7 & 8: Conservative and Hamiltonian Systems, Non-linear Pendulum

Math 341 Fall 2006 Final Exam December 12th, Name:

Physics: spring-mass system, planet motion, pendulum. Biology: ecology problem, neural conduction, epidemics

Student Background Readings for Bug Dynamics: The Logistic Map

Global Analysis of an SEIRS Model with Saturating Contact Rate 1

On the Spread of Epidemics in a Closed Heterogeneous Population

Behavior Stability in two SIR-Style. Models for HIV

Transcription:

70 Spotlight on Modeling: The Possum Plague Reference: Sections 2.6, 7.2 and 7.3. The ecological balance in New Zealand has been disturbed by the introduction of the Australian possum, a marsupial the size of a domestic cat with the proper name Trichosurus vulpecula. The animal was introduced in the 1830s for a planned fur trade. But there are no natural predators in the forests of New Zealand and the possum population rapidly increased. Today the estimated population is 70 million and only a few areas are possum-free. The animals have become a reservoir of a type of tuberculosis with about half of the possum population infected. This poses a threat of transfer of the disease to the livestock that form an important part of the New Zealand economy. An intense effort is underway to understand possum ecology and the disease. This effort includes the construction of mathematical models for the possum/disease dynamics. The simplest of these models is treated here. Our approach will be somewhat telegraphic, and we leave the detailed analysis to the reader. 13 Modeling the Population/Disease Dynamics Suppose that P is the population of possums and I is the subpopulation of infected possums, both measured in units of tens of millions. Note that P I and that the population of healthy possums is P I. A dynamical model for P(t) and I(t) is P = (a b)p αi I = βi(p I) (α + b)i where time t is measured in years, a and b are the respective natural birth and death rate coefficients measured in units of year 1, and α is the disease-induced death rate coefficient in year 1 units. The number β [measured in units of (10 7 year) 1 ] is the mass action coefficient that measures the effectiveness of interactions in transmitting the disease from the population I of the diseased to the population P I of healthy animals. Once a possum contracts tuberculosis, it never recovers, so there is no subpopulation of recovered. This model is only a crude approximation to reality and neglects such factors as patchiness (i.e., spatial variations in the population levels) and differences due to age (1) 13 This spotlight is adapted from the note Percy Possum Plunders by Graeme Wake, Professor of Applied Mathematics at the University of Aukland, New Zealand. The note appeared in the newsletter CODEE (Winter 1995). A detailed paper, Thresholds and Stability Analysis of Models for the Spatial Spread of a Fatal Disease, that includes other mathematical models of the possum population dynamics, was written by Wake and his colleagues K. Louie and M. G. Roberts and appeared in IMA Journal for Mathematics Applied to Medicine and Biology 10, (1993), pp. 207 226. Wake is a distinguished mathematician who enjoys applying mathematics to real problems like the possum plague discussed here. He uses mathematical techniques to help untangle the mysteries of why piles of wool being shipped overseas frequently begin to smolder in the holds of the ships, and why fish-and-chips shops in Australia suddenly catch fire. An excellent general reference on mathematical models for the spread of disease is an article by another distinguished applied mathematician, H. W. Hethcote, Qualitative Analysis of Communicable Disease Models, Math. Biosci. 28 (1976), pp. 335 356.

71 structure in the possum population. But the model is surprisingly effective in giving a macroscopic picture of the situation and in giving some indication of how much effort is going to be needed to change the long-term outcome. Nonconstant solutions of system (1) can t be expressed in terms of elementary functions, so we must rely on mathematical theory and computer simulation to understand solution behavior. Scaling the Variables, Population Equilibrium Levels System (1) has four parameters, a, b, α, and β. We can scale the populations P and I and time t to reduce the number of parameters before we do computer simulations: Scaling is discussed in the WEB SPOTLIGHT ON SCALING AND UNITS. P = hx, I = jy, t = ks (2) where h, j, and k are positive scaling constants which are to be determined. From system (1), the relations in (2), and the Chain Rule we have d P = d P dx ds dt dx ds dt = h dx = (a b)hx αjy k ds di dt = di dy ds dy ds dt = j dy (3) k ds = βjy(hx jy) (α + b) jy The scaling constants will be chosen to focus attention on the coefficients of the x-term in the first ODE of system (3) and the y-term in the second. If we set Also see Problem 6. h = j = α/β, k = 1/α, c = (a b)/α, r = (α + b)/α (4) then system (1) becomes a system in dimensionless variables and parameters: dx ds = cx y dy ds = y(x y) ry = (x y r)y (5) y y = x R x There is a reason for focusing on the parameters c and r. The most likely way to reduce the possum population is to reduce its birth rate or raise its natural death rate, that is, alter a or b in the formulas in (4), and so change c and r. Let s look at the region R, 0 y x; because the scaled number y of infected animals cannot exceed the entire scaled population x. By requiring that c + r 1, we can ensure that if 0 y 0 x 0, then the orbit starting at (x 0, y 0 ) stays in the region 0 y x as time increases (see Problem 8). The equilibrium points of system (5) are the intersection points of the nullclines cx y = 0 and (x y r)y = 0. The equilibrium points are the origin and a point whose coordinates are x = r/(1 c), y = cr/(1 c) The latter equilibrium point disappears if c = 1. If c = 0, then (x, 0) is an equilibrium point in the region R for each x 0.

72 dx/ds = x y, dx/ds = y, FIGURE 1 The unlikely case of possum extinction: c = 1, r = 2. FIGURE 2 Another unlikely situation: the infected population dies off if c = 0 and r = 2. Computer Simulations One goal of the computer simulation is to determine whether the population orbits x = x(s), y = y(s) of system (5) tend to an equilibrium point or become unbounded as s increases. We can accomplish this by a study of the orbits of the system for various values of c and r. EXAMPLE 1 From Extinction to Explosion Set r = 2 in system (5) and plot orbits in the region R for c = 1, 0, 1.5, and 0.25. Figures 1 4 show the results. In Figure 1, c = 1 and all orbits in R tend to the origin; that is, as s advances, the possums die out (and the disease, presumably, with them). Despite appearances, the orbits in Figure 2 (where c = 0) are not all asymptotic to a single equilibrium state (x, 0). Zooming on the region near (1, 0) will show that the seven orbits tend to seven different equilibrium points. Each equilibrium point models a disease-free possum population. Figure 3 (c = 1.5) shows a disastrous situation. Figure 4 (c = 0.25) shows the intriguing scenario where the possum population and its diseased subpopulation approach an equilibrium state. This may be interpreted in terms of the disease becoming endemic and the healthy and diseased populations at equilibrium. Figures 5 and 6 show an oscillating orbit, its approach to another endemic equilibrium (22/19, 11/190) and the corresponding component graphs in the case c = 0.05 and r = 1.1 (somewhat more realistic than the values c = 0.25, r = 2 of Figure 4). But the time between successive population maxima is so large that it would take years of observation before one could decide whether the data support the validity of a model like this.

73 dx/ds = 1.5x y, dx/ds = 0.25x y, FIGURE 3 The nightmare of explosive growth: c = 1.5, r = 2. FIGURE 4 Healthy and infected populations stabilize: c = 0.25, r = 2. dx/ds = 0.05x y, dy/ds = y(x y) 1.1y x(0) = 7, y(0) = 3.5 FIGURE 5 Approach to stable equilibrium where disease is endemic at low population levels: c = 0.05, r = 1.1. dx/ds = 0.05x y, dy/ds = y(x y) 1.1y x(0) = 7, y(0) = 3.5 FIGURE 6 Population bursts during approach to low population levels x = 22/19 1.16 and y = 11/190 0.06: c = 0.05, r = 1.1. s s Looking Ahead This possum model is a model in the making. It isn t yet known whether this or some other model will provide the breakthrough in understanding the dynamics of the situation and how the basic problem can be resolved. Any ideas? The possum/tuberculosis model is one of a large number of disease models proposed over the last seventy-five years to understand the dynamics of the spread of disease (see Problems 1 5).

74 PROBLEMS Modeling the Outbreak of an Epidemic: Kermack McKendrick SIR Model. We may model the evolution of an epidemic in a fixed population by dividing the population into three distinct classes: S = Susceptibles are those who have never had the illness and can catch it I = Infectives are those who are infected and are contagious R = Recovered are those who had the illness and have recovered Assume that the disease is mild (everyone eventually recovers), that the disease confers immunity on the recovered, and that the diseased are infective until they recover. 1. The SIR Model Argue that the evolution of the epidemic may be modeled by the nonlinear system of first-order ODEs, S = asi, I = asi bi, R = bi, where the parameter b represents the reciprocal of the period of infection and a represents the reciprocal of the level of exposure of a typical person. [Hint: Compare with models for predator-prey interaction in Section 7.3.] 2. Onset of Epidemic Show that an epidemic can only occur if the susceptible population is large enough. Specifically, find the threshold value for S above which more people are infected each day than recover. 3. German Measles Suppose that German measles lasts for four days. Suppose also that the typical susceptible person meets 0.3% of the infected population each day and that the disease is transmitted in 1 out of every 6 contacts with an infected person. Find the values of the parameters a and b in the SIR model. How small must the susceptible population be for this illness to fade away without becoming an epidemic? Verify by plotting the component graph for I(t) for your choice of I(0) and for values of S(0) that are 50% above and 50% below the threshold value found in problem 2. Plot over 0 t 30 and discuss what you see. 4. Dependence on S(0) Suppose that another illness has parameter values a = 0.001 and b = 0.08, and suppose that 100 infected individuals are introduced into a population. Investigate how the spread of the infection depends on the size of the population by plotting S-, I-, and R-component graphs for 0 t 50, I(0) = 100, R(0) = 0, and values of S(0) ranging from 0 to 2000 in increments of 500. How does the value of S(0) affect the speed with which the epidemic runs its course? 5. I as a function of S Using a = 0.001 and b = 0.08, find I as a function of S, I 0 and S 0. Plot I(t) against S(t) for various values of S 0 and I 0, 0 < S 0 < 1600, 0 < I 0 < 1250. Zooming near the origin, look at the long-term behavior. Interpret your graphs in terms of the model. [Hint: di/ds = 1 + b(as) 1.] The Possum Plague Model. 6. Scaling the Possum Plague Suppose that the possum populations P and I are measured in millions and that time is measured in years. Show that if the scale constants h and j, k of (2) and (4) are measured, respectively, in units of 10 7 and (years) 1, then x, y, and s are dimensionless variables. 7. Write the possum model in terms of the susceptibles, S = P I, and the infected, I. Then introduce scaled variables z = x y, y, and s (where x, y, and s are as in the text), write the z and y ODEs, find the equilibria, and plot orbits for z 0, y 0 with the values of c and r as given in Figures 1 5. Interpret your graphs (zoom if necessary). 8. Suppose that R is the region in the first quadrant bounded by the lines y = x and y = 0 (R includes its boundaries). Show that if c + r 1, then orbits of system (5) that originate in R stay in R as t increases. 9. Parameter Study Make a parameter study of the possum plague model, using parameters of your choice. Relate your conclusions to an assessment of the situation in New Zealand.