Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833

Contents lists available at ScienceDirect

Nonlinear Analysis: Real World Applications

journal homepage: www.elsevier.com/locate/nonrwa

On an eco-epidemiological model with prey harvesting and predator

switching: Local and global perspectives
R. Bhattacharyya a , B. Mukhopadhyay b,∗
a
Department of Science, The Calcutta Technical School, 110, S.N. Banerjee Road, Kolkata-700 013, India
b
Department of Science, Central Calcutta Polytechnic, 21, Convent Road, Kolkata-700 014, India

article info abstract

Article history: In this paper, we study an eco-epidemiological model where prey disease is modeled
Received 11 September 2009 by a Susceptible-Infected (SI) scheme. Saturation incidence kinetics is used to model the
Accepted 17 February 2010 contact process. The predator population adapt switching technique among susceptible
and infected prey. The prey species is supposed to be commercially viable and undergo
Keywords: constant non-selective harvesting. We study the stability aspects of the basic and the
Susceptible prey
switching models around the infection-free state and the infected steady state from a local
Infected prey
Saturation incidence
as well as a global perspective. Our aim is to study the role of harvesting and switching
Predator switching on the dynamics of disease propagation and/or eradication. A comparison of the local and
Harvesting global dynamical behavior in terms of important system parameters is obtained. Numerical
Global stability simulations are done to illustrate the analytical results.
© 2010 Elsevier Ltd. All rights reserved.

1. Introduction

Theoretical research and field observations have established the prevalence of various infectious diseases amongst the
majority of ecosystem populations. This has necessitated the study of the impact of epidemiological parameters in the
ecological domain. Eco-epidemiology is the branch of bio-mathematics that merges the above two otherwise independent
fields to understand the dynamics of disease propagation on the prey–predator population. Modeling studies on such eco-
epidemiological problems have grown enormously in the recent past [1–12]. These studies have emphasized the role of
disease in regulating various ecological aspects of the populations concerned.
Modeling studies on disease dominated ecological populations have addressed issues like disease related mortality,
reduction in reproduction, change in population sizes and disease induced oscillation of population states [13,8] Anderson
and May [1] formulated a prey–predator model with prey infection and observed destabilization due to infection. Hadeler
and Freedman [2] studied an SI modification of the Rosenzweig prey–predator model and obtained a threshold above which
an infected equilibrium or an (infected) periodic solution exists. Venturino analyzed prey–predator models with disease in
the prey [3] and the predator [7]. The role of prey infection on the stability aspects of a prey–predator model with different
functional responses was studied by Bairagi et al. [12]. Haque and Chattopadhyay [14] investigated the role of transmissible
diseases in a prey-dependent prey–predator system with prey infection. Han et al. [15] analyzed four eco-epidemiological
models for SIS and SIR diseases with standard and mass action incidents. The existence of strange attractors in an eco-
epidemiological model with standard incidence was demonstrated by Hilker and Malchow [16].
Contemporary modeling literature on eco-epidemiology has already established that predators have a natural tendency
to consume a disproportionate number of infected prey [17]. In most cases, parasite infection causes a change in the

∗ Corresponding author.
E-mail address: banibrat001@yahoo.co.in (B. Mukhopadhyay).

1468-1218/$ – see front matter © 2010 Elsevier Ltd. All rights reserved.
doi:10.1016/j.nonrwa.2010.02.012
 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833 3825

behavioral pattern of the prey that make them more vulnerable to predation. Due to infection, the prey species tends to
live in locations that are easily accessible to the predator. There are many examples of infected fish or aquatic snails living
close to the water surface and snails living on the top of vegetation. Moreover, the infected prey may become weaker, so
they are easily caught by the predator [18]. Peterson and Page [19] observed that wolf attacks on moose in Isle Royale
in Lake Superior are more successful when the moose are infected with lungworm. Predators like lions or wolves have a
natural tendency to select prey that are weakened by a disease [20,21]. Lafferty and Morris [22] observed experimentally
that predation rates of piscivorous birds on infected fish is much higher than that on susceptible fish.
The above-mentioned tendency of preferential predation would cause a substantial reduction in the number of infected
prey which in turn would compel the predator to shift its attention towards susceptible prey temporarily [23]. This
predatorial characteristic of changing the prey type exemplifies the well-known phenomenon of predator switching. A
number of modeling studies have been performed that involve this switching phenomenon [24–29]. Malchow et al. [30]
investigated an excitable plankton ecosystem model with virus infection that includes predator switching using a Holling
type-III functional response. Bhattacharyya and Mukhopadhyay [29] analyzed the effect of predator switching with and
without prey group defence under non-homogeneous mixing of the population. They also performed a mathematical
analysis of the bifurcating solutions of a prey–predator model with switching predator [31].
Commercial exploitation of ecological resources to meet the growing needs of society has been a topic of much concern
for ecologists, bio-economists and natural resource managers. The study of population dynamics with harvesting is a topic of
mathematical bio-economics and is mainly concerned with optimal management of renewable resources [32,33]. Harvesting
is commonly practised in fisheries, forestry and in wildlife management. It has a significant effect on the dynamical evolution
of the harvested species; it can have a stabilizing effect, a destabilizing effect and even an oscillation inducing effect [34–36].
The effect of constant rate harvesting has been investigated by many authors [37–46]. These investigations revealed very
rich and interesting dynamics such as stability of equilibria, existence of Hopf bifurcation, limit cycles, homoclinic loops,
Bogdanov–Takens bifurcation and even catastrophe. Population exploitation in the presence of parasites can have an even
more significant impact on the population dynamics. Parasites can reduce the abundance as well as yield by increasing
the mortality, reducing the fecundity and creating a decline in marketability of the harvested stock [47,48]. Moreover,
parasites can be eliminated locally from a population by reducing the hosts’ density [49]. Bairagi et al. [50] studied an eco-
epidemiological model with harvesting on the susceptible and infected prey. They have analyzed the role of harvesting in
regulating the cyclic behavior of the system, and in eliminating prey infection, together with its overall impact on the system
dynamics.
In the present research, we formulate a mathematical model of prey–predator interaction where the prey suffers micro-
parasite infection. It is conjectured that due to the ecologically well-established phenomenon of preferential predation on
infected prey, a substantial reduction in their number could occur which, in turn, would compel the predator to switch to
susceptible prey. It is also assumed that the prey species has a commercial value and both the susceptible and infected prey
undergo harvesting at a constant rate. We first study the stability behavior of the basic model (without switching) in order
to obtain parameter thresholds that can cause (i) eradication of prey infection and (ii) disease persistence. Then we study the
model with predator switching from the same perspective in an attempt to compare the role of harvesting in the presence
and absence of the switching behavior of the predator.

2. Model formulation

The basic model consists of two population subclasses—(i) prey population with density N (t ) and (ii) predators having
population concentration Y (t ). We make the following assumptions.
• The prey population grows logistically with intrinsic growth rate r and environmental carrying capacity k.
• Due to micro-parasite infection, the prey population is assumed to be divided into two subclasses, namely the susceptible
prey (S (t )) and the infected prey (I (t )); that is, at any instant of time t, N (t ) = S (t ) + I (t ).
• Only the susceptible prey is capable of reproducing. A logistic law is used to model the birth process with the assumption
that births should always be positive. The infected prey is removed by death at a rate d1 or by predation before the
possibility of reproducing. However, the infected population I contributes with S to population growth towards carrying
capacity.
• It is also assumed that the disease is spread only among the prey population and the disease is not genetically inherited.
The infected population does not recover or become immune.
• Susceptible prey become infected when they come in contact with infected prey, and this contact process is assumed
to follow the saturation incidence kinetics, with β measuring the force of infection and α the inhibition effect. This
incidence rate is more realistic than the bilinear one, as it includes the behavioral change and crowding effect of the
infected individuals and also prevents unboundedness of contact rate.
• The predators suffer loss due to natural death at a constant rate d2 . They consume susceptible and infected prey following
a Holling type-II functional response with predation coefficients p1 and p2 and half-saturation constant m. Consumed prey
is converted into predator with efficiency q.
• It is assumed that both the susceptible and the infected prey undergo commercial exploitation with h1 and h2 as the
exploitation rates, respectively. All the above-mentioned parameters are assumed to be positive.
3826 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833

With these assumptions, the prey–predator–parasite interaction with prey exploitation can be represented by the
following set of three coupled ordinary differential equations:
β SI
 
dS S+I p1 SY
= rS 1 − − − − h1 S
dt k 1 + αI m+S
dI β SI p2 IY
= − d1 I − − h2 I (2.1)
dt 1 + αI m+I
dY p1 SY p2 IY
= −d2 Y + q +q .
dt m+S m+I
System (2.1) will be studied with the initial conditions
S (0) = S0 > 0; I (0) = I0 > 0; Y (0) = Y0 > 0. (2.2)
We also assume that p1 , p2 > 0 and 0 < q ≤ 1. In the next proposition, we demonstrate that the linear combination of
susceptible prey, infected prey and predator population is less than a finite quantity.

Proposition 2.1. All the solutions of (2.1) are uniformly bounded.

Proof. We define W (t ) = S (t ) + I (t ) + Y (t ), where W : R+ → R+ is well defined and differentiable on some maximal
interval. Now,
 
dW S
≤ Sr 1 − − h1 S − (d1 + h2 )I − d2 Y
dt k
≤ Sr − h1 S − (d1 + h2 )I − d2 Y
≤ Mr − dW
where M = max{S (0), k}, d = min{h1 , (d1 + h2 ), d2 }. Multiplying both sides by edt , we get 0 ≤ W ≤ Mr
d
+ W (S0 , I0 , Y0 )e−dt .
Thus, for t → ∞, 0 ≤ W < Mr
d
. So all solutions of (2.1) starting in R3+ will remain within the region
 
Mr
Γ = (S , I , Y ) ∈ R+ : W ≤ 3
+ε (2.3)
d
for any ε > 0 and t → ∞. 

3. Stability study

System (2.1) possesses the following equilibria.

1. The trivial equilibrium ET =n(0, 0, 0).  o
2. The axial equilibrium EA = k 1 − r1 , 0, 0 .
h

3. The boundary equilibrium EB = (S1 , 0, Y1 ), where

md2
S1 = (3.1)
qp1 − d2
   
mq md2
Y1 = r 1− − h1 .
qp1 − d2 k(qp1 − d2 )
4. The equilibrium point of coexistence E ∗ = (S ∗ , I ∗ , Y ∗ ), where (S ∗ , I ∗ , Y ∗ ) is the positive solution (if one exists) of the
coupled system
βy
 
x+y p1 z
r 1− − − − h1 = 0
k 1 + αy m+x
βx p2 z
− d1 − − h2 = 0 (3.2)
1 + αy m+y
 
p1 x p2 y
−d 2 + q + = 0.
m+x m+y

The axial equilibrium point exists if r > h1 . Stability analysis around EA shows that it will be locally asymptotically stable
when
 
h1
β

h1
 qp1 k 1 − r
d1 + h2 > 1− ; d2 >  .
k r m+k 1−
h1
r

So the axial state will be stable for large loss rates of infected prey and the predator.
 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833 3827

The disease-free boundary equilibrium and the equilibrium point of coexistence are of significant epidemiological
importance. Accordingly, we will study in detail the stability aspects around these two states.
The disease-free point EB exists if
 
qp1 k md2
d2 < ; h1 < r 1 − . (3.3)
m+k k(qp1 − d2 )
p2
The roots of the characteristic equation of the community matrix corresponding to EB are [β S1 − d1 − m 1
Y − h2 ] and the
roots of the equation
qp21 Y1 mS1
 
rS1 p1 Y1 S1
λ −
2
− λ+ = 0. (3.4)
k (m + S1 )2 (m + S1 )3
h i
Now the roots of (3.4) will have negative real parts if
rS1
k
− p1 S1 Y1
(m+S12 )2
< 0, which implies that
  
md2 1 mqp1
h1 < r 1 − − . (3.5)
k(qp1 − d2 ) k qp1 − d2
h i
On the other hand, the existence of EB implies that h1 < r 1 − k(qp −2 d ) ; hence, (3.5) will hold automatically.
md
1 2

Again, β S1 − d1 − − h2 < 0 when β S1 − h2 < 0, which in turn implies that

p2 Y1
m

β md2
h2 > . (3.6)
qp1 − d2
Thus, the disease-free state EB will be locally asymptotically stable when
 
md2
h1 < r 1 − ≡ hmax (3.7)
k(qp1 − d2 )
1

β md2
h2 > 2 .
≡ hcrit
qp1 − d2
Since EB is the equilibrium point where the infected population concentration is zero, asymptotic stability around this steady
state would imply extinction of the infected species as t → ∞. Thus, the harvesting rates on the susceptible as well as the
infected prey species have a major role in eliminating prey infection.
Next we study the coexistent steady state E ∗ . The corresponding characteristic equation is
λ3 + Aλ2 + Bλ + C = 0 (3.8)
where
A = −(a11 + a22 ); B = (a11 a22 − a23 a32 − a12 a21 − a13 a31 )
C = (a11 a23 a32 − a12 a23 a31 − a13 a21 a32 + a13 a31 a22 )
rS ∗ p1 S ∗ Y ∗ rS ∗ β p1 S ∗
a11 = − + ; a12 = − − ; a13 = −
k (m + S ) ∗ 2 k (1 + α I )∗ 2 m + S∗
βI ∗
βα S I
∗ ∗ ∗ ∗
p2 I Y p2 I ∗
a21 = ; a22 = − + ; a23 = −
1 + αI ∗ (1 + α I )
∗ 2 (m + I )
∗ 2 m + I∗
qp1 mY ∗ qp2 mY ∗
a31 = ; a32 = . (3.9)
(m + S ∗ )2 (m + I ∗ )2
The system will be locally asymptotically stable around E ∗ if (i) A > 0; (ii) C > 0; and (iii) AB − C > 0; and it will be unstable
otherwise. Now, A > 0 implies that a11 + a22 < 0. So, for a11 + a22 > 0, instability may occur. From the expressions of
a11 and a22 it follows that positivity of (a11 + a22 ) is possible for large p1 and p2 . Thus heavy predation on susceptible and
infected prey may cause instability around E ∗ . Secondly, A > 0 together with C < 0 may cause instability around E ∗ . In
terms of system parameters,
rS ∗ I ∗ Y ∗ qmp2 β qp1 mI ∗ Y ∗
 
p2 p1
C = − +
k(m + I ∗ ) (m + I ∗ )2 (m + S ∗ )2 (1 + α I ∗ )2 (m + S ∗ )3 (m + I ∗ )2
h i
× −p2 (m + S ∗ ){(I ∗ − S ∗ ) + (m − α S ∗ I ∗ )} + α p1 S ∗ 2 (m + I ∗ )2 , (3.10)
and, consequently, C < 0 is equivalent to the following conditions:
(m + S ∗ )(m − α I ∗ S ∗ )
2
m + S∗

p1
I ∗ > S∗; < < . (3.11)
m+ I∗ p2 α S ∗ 2 (m + I ∗ )2
It is easy to see that the second inequality in (3.11) will hold automatically when I ∗ > S ∗ provided that p1 > p2 . Thus more
predation on susceptible prey has a destabilizing effect on the steady state of coexistence.
3828 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833

3.1. Global behavior

In this section we look at the disease-free equilibrium point from the global perspective. For this, we rewrite system (2.1)
as
dS
= Sf1 (S , I , Y )
dt
dI
= If2 (S , I , Y ) (3.12)
dt
dY
= Yf3 (S , I , Y ).
dt
The system has only one disease-free equilibrium, EB = (S1 , 0, Y1 ). Let us define
F1 (x) = f2 (x, 0, Y1 ); F2 (y) = −f1 (S1 , y, Y1 )
F3 (z ) = −[f2 (S1 , 0, z ) + f1 (S1 , 0, z )]. (3.13)
∂ f2 ∂ f1 ∂ f2 ∂ f1
As ∂S
> 0, < 0, ∂I ∂Y
< 0 and ∂Y
< 0 the functions F1 , F2 , F3 are strictly increasing in x, y, z, respectively. We next
consider the function
S
F1 (x) I
F2 (y) Y
F3 (z )
Z Z Z
V = dx + dy + dz . (3.14)
S1 x 0 y Y1 z
From the construction of V , it is seen that V is positive definite in the region
Ω = {(S , I , Y ) : S ≥ S1 ; I ≥ 0; Y ≥ Y1 };
also, V (S1 , 0, Y1 ) = 0. Now,
dV
= F1 (S )f1 (S , I , Y ) + F2 (I )f2 (S , I , Y ) + F3 (Y )f3 (S , I , Y )
dt
= F1 (S )[f1 (S , I , Y ) − f1 (S1 , I , Y1 )] + F2 (I )[f2 (S , I , Y ) − f2 (S , 0, Y1 )] + F3 (Y )[f3 (S , I , Y ) − f3 (S1 , 0, Y )]
+ F1 (S )f1 (S1 , I , Y1 ) + F2 (I )f2 (S , 0, Y1 ) + F3 (Y )f3 (S1 , 0, Y )
∂ f1 ∂ f1 e ∂ f2 e ∂ f2
   
= F1 (S ) (S − S1 ) (e S , I , Y ) + (Y − Y1 ) (S , I , Y ) + F2 (I ) I (S , I , Y ) + (Y − Y1 ) (S , I , e Y)
∂S ∂Y ∂I ∂Y
∂ f3 ∂ f3 e
 
+ F3 (Y ) (S − S1 ) (e S, I, Y ) + I (S , I , Y ) . (3.15)
∂S ∂I
∂f ∂f ∂f ∂f
Now, from the definition of fi s, ∂ Y1 < 0, ∂ Y2 < 0, ∂ S3 > 0, ∂ I3 > 0. Again, F3 (Y ) < 0 will hold provided that r is large and
f2 (S1 , 0, Y1 ) > 0. The above condition also implies that F1 (S ) > 0. Moreover, F2 (I ) ≥ 0 is always true.
Therefore, dVdt
≤ 0 when ∂∂fS1 < 0, ∂∂fI2 < 0, where S1 < e
S < S, 0 < e
I < I, Y1 < e Y < Y.
h i
∂f
Now, ∂ S1 = − kr + (m1+S1)2
p Y
< 0 when p1 is small. Also,
∂ f2 βS p2 Y
=− +
∂I (1 + α I )2 (m + I )2
∂f
and ∂ I2 < 0 for small p2 .
Therefore, dV
dt
≤ 0 when p1 and p2 are small, and in that case, by LaSalle’s Theorem [51], EB will be a global attractor for
the system.

4. The model with switching predator

In this section, we investigate a modification of the basic model that incorporates switching of the predator among
susceptible and infected prey.
β SI
 
dS S+I p1 SY
= rS 1 − − − − h1 S
dt k 1 + αI 1 + ( SI )2
dI β SI p2 IY
= − d1 I − − h2 I (4.1)
dt 1 + αI 1 + ( SI )2
dY p1 SY p2 IY
= −d2 Y + q +q .
dt 1 + ( SI )2 1 + ( SI )2
 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833 3829
h i h i
p1 SY p2 IY
The functions 1+(I /S )2
and 1+(S /I )2
mathematically characterize the switching mechanism. From an ecological viewpoint
these functions signify that the predation rate on a species decreases when the population density of that species becomes
rare compared to that of the other species.
System (4.1) possesses the following steady states.
1. The axial steady state EAS = (k, 0, 0).
2. The boundary state EBS = (S2 , 0, Y2 ) with

r (1 − ) − h1
d2
d2 kqp1
S2 = ; Y2 = . (4.2)
qp1 p1
3. The interior equilibrium ES∗ = (S3 , I3 , Y3 ), where (S3 , I3 , Y3 ) are the positive solutions of
βy
 
x+y p1 z
r 1− − − − h1 = 0
k 1 + αy 1 + (y/x)2
βx p2 z
− d1 − − h2 = 0 (4.3)
1 + αy 1 + (x/y)2
 
p1 x p2 y
−d 2 + q + = 0.
1 + (y/x)2 1 + (x/y)2

In a previous work [23], we have studied the behavior of a similar type of model around the origin (0, 0, 0). Here, we will
analyze the system around the two epidemiologically important equilibria EBS and ES∗ . We first consider the disease-free state
EBS . This equilibrium point will exist when h1 < r (1 − ). Local analysis around EBS reveals that the equilibrium point will
d2
kqp1
be a saddle when
β d2
 
h2 < − d1 (4.4)
qp1
and will be locally asymptotically stable if
β d2
 
h2 > − d1 . (4.5)
qp1
Thus, the infection-free equilibrium will exist and will be locally asymptotically stable when the harvesting on susceptible
prey is low and that on the infected prey is high. Hence, for the switching model, the local stability properties around the
infection-free state are controlled by the harvesting rates.
Next we consider the interior state ES∗ . The characteristic equation corresponding to the Jacobian matrix of ES∗ is

λ3 + P λ2 + Q λ + R = 0 (4.6)
where
P = −(b11 + b22 ); Q = (b11 b22 − b23 b32 − b12 b21 − b13 b31 )
R = (b11 b23 b32 − b12 b23 b31 − b13 b21 b32 + b13 b31 b22 )
rS3 2p1 S3 Y3 I3 rS3 β S3 2p1 I3 Y3
b11 = − − 2 ; b12 = − − +
k (I3 + S32 )2 k (1 + α I3 )2 I2
S3 (1 + 32 )2
S3

p1 S33 β I3 2p2 S3 Y3
b13 = − ; b21 = +
S32 + I32 1 + α I3 I3 {1 + ( I 3 )2 }
S
3

βα S3 I3 2p2 S3 Y3
b22 = − − (4.7)
(1 + α I3 ) 2
I3 {1 + ( I 3 )2 }2
S
3

I32
qp1 Y3 (1 − )
p2 I3 S32
b23 = − ; b31 =
1 + ( I 3 )2 {1 + ( SI33 )2 }2
S
3
2
 
qp2 Y3 S3
b32 = 1− .
{1 + ( ) }S3 2 2
I3
I32

Local asymptotic stability around ES∗ requires that (i) P > 0; (ii) R > 0; and (iii) PQ − R > 0. From (4.7), it follows that P > 0
is always true. If p1 and q are small, then R may be positive. But, even when R > 0, simple algebra reveals that (PQ − R) may
be negative for small p1 and p2 , and in that case the interior equilibrium point may become unstable.
3830 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833

Simulation of the basic model around the disease free equilibrium

40

Susceptible prey
30
20
10
0
0 50 100 150 200 250 300
4
Infected prey
2

–2
0 50 100 150 200 250 300
80
Predator

60
40
20
0
0 50 100 150 200 250 300
Time (t)

Fig. 1. Numerical simulation of the non-switching model around EB = (2, 0, 64.13) with harvesting rates satisfying (3.7). The parameter values are
r = 11.2; k = 30; β = 1.2; α = 2.5; p1 = 0.54; m = 0.5; h1 = 2.2; d1 = 0.4; p2 = 0.6; h2 = 3.5; d2 = 0.08; q = 0.25. The figure exhibits stable
coexistence of uninfected prey and predator and extinction of infected prey.

Finally, we study the global behavior of the disease-free equilibrium EBS of the switching model. We rewrite system (4.1)
in the form
dS
= Sg1 (S , I , Y )
dt
dI
= Ig2 (S , I , Y ) (4.8)
dt
dY
= Yg3 (S , I , Y ).
dt
The system has only one disease-free equilibrium EBS . Let us define
G1 (x) = g2 (x, 0, Y3 ); G2 (y) = −g1 (S3 , y, Y3 )
G3 (z ) = − [g2 (S3 , 0, z ) + g1 (S3 , 0, z )] . (4.9)
∂ g2 ∂ g1 ∂ g2 ∂ g1
Now, ∂S
> 0 and < 0 for small p1 , whereas
∂I
and are both negative. Consequently, G1 (x) and G3 (z ) are strictly
∂y ∂y
positive, whereas G2 (y) is strictly positive for small p1 . Also,
∂ g1 ∂ g2 ∂ g3
< 0; < 0; = 0. (4.10)
∂S ∂I ∂Y
We now define
S
G1 (x) I
G2 (y) Y
G3 (z )
Z Z Z
V = dx + dy + dz . (4.11)
S3 x 0 y Y3 z
Proceeding as in the previous section, and using LaSalle’s Theorem, it follows that EBS will be a global attractor if p1 is small.
Thus, for lower predation on the susceptible prey, the switching model will exhibit stable behavior around the uninfected
steady state.

5. Concluding remarks and numerical results

In this paper, we have studied a mathematical prey–predator model at the interface of ecology, epidemiology and bio-
economics. Switching is a well-established predatorial characteristic in the ecological domain; micro-parasite infection
among an ecological population is a very common epidemiological feature; and excessive species exploitation is a topic
of serious present-day concern. We have combined these three aspects in our modeling study. The main objective of the
work is to investigate how the dual phenomena of prey exploitation and predator switching influence the disease dynamics
of the prey population.
 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833 3831

Existence of global attractor around the disease free state

70

60

50

Predator
40

30

20

10

30 25
20 20
15
10 10
0 5
Infected prey Susceptible prey

Fig. 2. Phase plot of the non-switching model around EB = (2, 0, 64.13) with small p1 = 0.14, p2 = 0.12.

Time evolution for the basic model around E*

30
Susceptible prey

20
10
0
–10
0 50 100 150 200 250 300
20
Infected prey

10

–10
0 50 100 150 200 250 300
150
Predator

100

50

0
0 50 100 150 200 250 300
Time (t)

Fig. 3. Numerical simulation of the non-switching model around E ∗ with larger predation on susceptible prey. The parameter values are r = 11.2; k = 30;
β = 1.2; α = 0.5; p1 = 0.64; m = 0.5; h1 = 0.2; d1 = 0.4; p2 = 0.3; h2 = 0.3; d2 = 0.12; q = 0.25. The figure exhibits unstable characteristics.

Though the model admits four steady states, we have concentrated on the following steady states of eco-epidemiological
importance.
(i) The infection-free boundary state and (ii) the interior state of coexistence for both the basic (non-switching) and the
switching model. A local stability study of the basic model in the vicinity of the disease-free steady state revealed the
existence of some threshold harvesting rates, namely, hmax 2 , such that for h1 < h1
and hcrit and h2 > hcrit
max
1 2 the system
exhibits local asymptotic stability around the boundary state. Since stability around this state implies extinction of the
infected prey, our analysis indicates that controlled harvesting on the susceptible as well as the infected prey is able to
control prey infection. A stability study around the coexistent state, however, revealed that unstable behavior around this
equilibrium point may occur when there is more predation on susceptible prey. Next we have performed a global study on
the boundary state using Lasalle’s theorem. Our study demonstrated that this equilibrium point will be a global attractor
when predation on the prey species (both susceptible and infected) is small. Thus, unlike the local scenario, the predation
rates are the dominant parameters that control global eradication of the disease.
Our analysis of the switching model showed that when harvesting of susceptible prey is low and that of infected ones is
high, the boundary point will exhibit stable behavior. Thus intensive harvesting of the infected population could eradicate
3832 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833

Time evolution for the switching model around the disease free point

Susceptible prey
3

0
0 50 100 150 200 250 300
0.2
Infected prey
0.15
0.1
0.05
0
0 50 100 150 200 250 300
30
Predator

28
26
24
22
0 50 100 150 200 250 300
Time (t)

Fig. 4. Numerical simulation of the switching model around EBS with intensive harvesting of infected prey. h1 = 0.1; h2 = 0.8 showing stable coexistence.

Time evolution for the switching model around ES*

4
Susceptible prey

3
2
1
0
0 50 100 150 200 250 300 350 400 450 500
6
Infected prey

0
0 50 100 150 200 250 300 350 400 450 500
40

35
Predator

30

25
0 50 100 150 200 250 300 350 400 450 500
Time (t)

Fig. 5. Numerical simulation of the switching model around ES∗ with low predation rates showing unstable behavior.

prey disease for the switching model. However, a global study of the switching model again showed that low predation on
the susceptible prey could ensure global stability around the boundary state. Thus, though harvesting is capable of eradicating
prey infection in the local perspective, it is the predation rate that plays the key role in controlling prey disease in the global
context. Interestingly, the stability/instability criteria of the coexistent steady states of both models are also controlled by
the predation rates.
We have also performed a numerical study of the basic model and the switching model to visualize various analytical
results obtained so far. Parameter values (shown in the captions) are taken mainly from [23]. With these values, we have
first evaluated the disease-free equilibrium of the basic model as EB = (2, 0, 64.13). Fig. 1 shows the time graph of the
populations of the basic model when the harvesting rates satisfy (3.7); the figure indicates stable time evolution with
extinction of diseased prey. In Fig. 2, we depict the phase diagram around the disease-free state when predation on both
the susceptible and the infected prey is small, exhibiting a global attractor. We obtain the interior equilibrium point of the
 R. Bhattacharyya, B. Mukhopadhyay / Nonlinear Analysis: Real World Applications 11 (2010) 3824–3833 3833

basic model as E ∗ = (26.21, 0.45, 39.48). In Fig. 3, we simulate the model around the coexistent interior state with more
predation on susceptible prey, exhibiting unstable characteristics. Next, we study the switching model. The corresponding
disease-free state is calculated as EBS = (0.128, 0, 26.772). In Fig. 4, we depict stable time evolution around this state for
intensive harvesting on infected prey, satisfying (4.5). Finally, we have deduced the interior point of the switching model
ES∗ = (26.21, 0.45, 39.48). Fig. 5 shows the unstable population evolution around this state for low predation rates.

Acknowledgement

The authors are grateful to the reviewers for their valuable suggestions, which have improved the scientific content and
presentation of the work. The authors also acknowledge financial support from the Department of Science and Technology,
Ministry of Human Resource Development, Government of India (Grant No. SR/S4/MS:296/05).

References

[1] R.M. Anderson, R.M. May, The invasion, persistence and spread of infectious diseases within animal and plant communities, Philos. Trans. R. Soc. Lond.
B 314 (1986) 533–570.
[2] K.P. Hadeler, H.I. Freedman, Predator–prey populations with parasite infection, J. Math. Biol. 27 (1989) 609–631.
[3] E. Venturino, Epidemics in predator–prey models: Diseases in the prey, in: O. Arino, D. Axelrod, M. Kimmel, M. Langlais (Eds.), Mathematical Population
Dynamics: Analysis of Heterogeneity, Vol. 1, Theory of Epidemics, Wuerz Publishing, Winnipeg, Canada, 1995, pp. 381–393.
[4] J. Chattopadhyay, O. Arino, A predator–prey model with disease in the prey, Nonlinear Anal. 36 (1999) 747–766.
[5] J. Chattopadhyay, N. Bairagi, Pelicans at risk in Salton sea—An eco-epidemiological study, Ecol. Model. 136 (2001) 103–112.
[6] Y. Xiao, L. Chen, Modeling and analysis of a predator–prey model with disease in the prey, Math. Biosci. 171 (2001) 59–82.
[7] E. Venturino, Epidemics in predator–prey models: Disease in the predator, IMA J. Math. Appl. Med. Biol. 19 (2002) 185–205.
[8] H.W. Hethcote, W. Wang, L. Han, Z. Ma, A predator–prey model with infected prey, Theor. Popul. Biol. 66 (2004) 259–268.
[9] S.R. Hall, M.A. Duffy, C.E. Caceres, Selective predation and productivity jointly drive complex behavior in host-parasite systems, Amer. Nat. 165 (1)
(2005) 70–81.
[10] B. Mukhopadhyay, R. Bhattacharyya, Dynamics of a delayed epidemiological model with nonlinear incidence: The role of infected incidence fraction,
J. Biol. Syst. 13 (4) (2005) 341–361.
[11] A. Fenton, S.A. Rands, The impact of parasite manipulation and predator foraging behavior on predator–prey communities, Ecology 87 (11) (2006)
2832–2841.
[12] N. Bairagi, P.K. Roy, J. Chattopadhyay, Role of infection on the stability of a predator–prey system with several functional responses—A comparative
study, J. Theoret. Biol. 248 (2007) 10–25.
[13] J. Mena-Lorca, H.W. Hethcote, Dynamic models of infectious diseases as regulators of population sizes, J. Math. Biol. 30 (1992) 693–716.
[14] M. Haque, J. Chattopadhyay, Role of transmissible disease in an infected prey-dependent predator–prey system, Math. Comput. Model. Dyn. Syst. 13
(2007) 163–178.
[15] L. Han, Z. Ma, H.W. Hethcote, Four predator prey models with infectious diseases, Math. Comput. Modelling 34 (2001) 849–858.
[16] F.M. Hilker, H. Malchow, Strange periodic attractors in a prey–predator system with infected prey, Math. Popul. Stud. 13 (2006) 119–134.
[17] S.A. Temple, Do predators always capture substandard individuals disproportionately from prey population? Ecology 68 (1987) 669–674.
[18] J. Moore, Parasites and the Behaviour of Animals, Oxford University Press, 2002.
[19] R.O. Peterson, R.E. Page, The rise and fall of Isle Royale wolves, 1975–1986, J. Mamm. 69 (I) (1988) 89–99.
[20] L.D. Mech, The Wolf, Natural History Press, New York, 1970.
[21] G.B. Schaller, The Serengeti Lion: A Study of Predator Prey Relations, University of Chicago Press, Chicago, 1972.
[22] K.D. Lafferty, A.K. Morris, Altered behavior of parasitized killfish increases susceptibility to predation by bird final hosts, Ecology 77 (1996) 1390–1397.
[23] B. Mukhopadhyay, R. Bhattacharyya, Role of predator switching in an eco-epidemiological model with disease in the prey, Ecol. Model. 220 (2009)
931–939.
[24] C.S. Holling, Principles of insect predation, Ann. Rev. Entomol. 6 (1961) 163–182.
[25] R.M. May, Some Mathematical Problems in Biology, Vol. 4, American Mathematical Society, Providence, RI, 1974.
[26] W.W. Murdoch, Switching in general predators: Experiments on predator specificity and stability of prey populations, Ecol. Mong. 39 (1969) 355–364.
[27] M. Tansky, Switching effects in prey–predator system, J. Theoret. Biol. 70 (1978) 263–271.
[28] Q.A.J. Khan, E. Balakrishnan, G.C. Wake, Analysis of a predator–prey system with predator switching, Bull. Math. Biol. 66 (2004) 109–123.
[29] R. Bhattacharyya, B. Mukhopadhyay, Spatial dynamics of nonlinear prey–predator models with prey migration and predator switching, Ecol. Complex.
3 (2006) 160–169.
[30] H. Malchow, F.M. Hilker, R.R. Sarkar, K. Brauer, Spatiotemporal patterns in an excitable plankton system with lysogenic viral infections, Math. Comput.
Modelling 42 (2005) 1035–1048.
[31] B. Mukhopadhyay, R. Bhattacharyya, Bifurcation analysis of an ecological food-chain model with switching predator, Appl. Math. Comput. 201 (2008)
260–271.
[32] C.W. Clark, Bioeconomic Modelling and Fisheries Management, Wiley, 1985.
[33] C.W. Clark, The Optimal Management of Renewable Resources: Mathematical Bioeconomics, 2nd, edition, Wiley Interscience, 1990.
[34] J.P. Cohn, Saving the Salton Sea, Biosciences 50 (4) (2000) 295–301.
[35] M.I.S. Costa, Harvesting induced fluctuations: Insights from a thresholds management policy, Math. Biosci. 205 (2007) 77–82.
[36] N. Jonzen, E. Ranta, P. Lundberg, V. Kaitala, H. Linden, Harvesting induced fluctuations? Wildlife Biol. 9 (2003) 59–65.
[37] F. Brauer, A.C. Soudack, Stability regions and transition phenomena for harvested predator–prey systems, J. Math. Biol. 7 (1979) 319–337.
[38] F. Brauer, A.C. Soudack, Stability regions in predator–prey systems with constant rate prey harvesting, J. Math. Biol. 8 (1979) 55–71.
[39] K.S. Chaudhuri, A bio-economic model of harvesting a multispecies fishery, Ecol. Model. 32 (1986) 267–279.
[40] K.S. Chaudhuri, S. Saha Roy, On the combined harvesting of a prey–predator system, J. Biol. Syst. 4 (3) (1996) 373–389.
[41] B.S. Goh, G. Leitmann, T.L. Vincent, Optimal control of a prey–predator system, Math. Biosci. 19 (1974) 263–286.
[42] J. Ianelli, R.H. Lamberson, History and future of models in fisheries science, Nat. Resour. Model. 16 (4) (2003) 1–5.
[43] A. Martin, S. Ruan, Predator–prey models with delay and prey harvesting, J. Math. Biol. 43 (2001) 247–267.
[44] M. Mesterton-Gibbons, On the optimal policy for combined harvesting of predator and prey, Nat. Resour. Model. 3 (1988) 63–89.
[45] M. Mesterton-Gibbons, A technique for finding optimal two-species harvesting policies, Nat. Resour. Model. 92 (1996) 235–244.
[46] D. Xiao, L.S. Jennings, Bifurcations of a ratio-dependent predator–prey system with constant rate harvesting, SIAM J. Appl. Math. 65 (3) (2005) 737–753.
[47] A.P. Dobson, R.M. May, The effects of parasites on fish populations—Theoretical aspects, Int. J. Parasitol. 17 (1987) 363–370.
[48] H. McCallum, L. Gerber, A. Jani, Does infectious diseases influence the efficacy of marine protected areas? A theoretical framework, J. Appl. Ecol. 42
(2005) 688–698.
[49] C.S. Culver, A.M. Kuris, The apparent eradication of a locally established introduced marine pest, Biol. Invasion 2 (2000) 245–253.
[50] N. Bairagi, S. Chaudhuri, J. Chattopadhyay, Harvesting as a disease control measure in an eco-epidemiological system—A theoretical study, Math.
Biosci. 217 (2009) 134–144.
[51] J.K. Hale, Ordinary Differential Equations, Wiley-Interscience, New York, 1969.