Results in Control and Optimization 7 (2022) 100099

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Results in Control and Optimization

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

Qualitative analysis and control of predator switching on an

eco-epidemiological model with prey refuge and harvesting
A.K. Pal a , Anindita Bhattacharyya b ,∗, Ashok Mondal c
a Department of Mathematics, S. A. Jaipuria College Kolkata, India
b Department of Mathematics, Amity University, Kolkata, India
c
Department of Mathematics, Regent Education and Research Foundation, Kolkata, India

ARTICLE INFO ABSTRACT

Keywords: In this paper, an eco-epidemiological model has been studied where disease of prey population is
Eco-epidemiological model modelled by a Susceptible–Infected (SI) scheme. Prey switching strategy is adopted by predator
Refugia population when they are provided with two types of prey, susceptible and infected prey.
Harvesting
However switching may happen due to several reasons such as shortage of preferable prey or
Stability analysis
risk in hunting the plentiful prey. In this work, we have proposed a prey–predator system with
Hopf-bifurcation
a particular type of switching functional response where a predator feeds on susceptible and
infected prey but it switches from one type of prey to another when a particular prey population
becomes lower. Both the species are supposed to be commercially viable and undergo constant
non-selective harvesting. The stability aspects of the switching models around the infection-free
state from a local as well as a global perspective has been investigated. Our aim is to study the
role of harvesting and refuge of susceptible population on the dynamics of disease propagation
and/or annihilation of an epidemiological model under consideration of switching phenomena.
Numerical simulations are done to demonstrate our analytical results.

1. Introduction

The prey–predator relationship is basically the interaction between two species which as a result affects the population of each
species. In nature, during the time of interaction of multiple species different disease may occur and spread among the species.
Analytical research and practical observations have also fixed the wide spread presence of distinct micro parasite infectious diseases.
This observation has inspired various ecologists and biologists to study the influence of epidemiological parameters in the domain of
ecology. The branch of Mathematical biology that joins ecology and epidemic is known as eco-epidemiology. Recent past years many
researchers [1–10] got involved in studying the mathematical modelling of disease dominated eco-epidemiological populations.
Haque and Chattopadhyay [11] investigated the role of transmissible diseases in a prey–predatory system with infection in prey.
Mondal et al. [12] discussed a Leslie–Gower predator–prey model with disease developed in the predator population. Also Mondal
et al. [13] described a delayed pest–plant ecological model with infection in the pest population. In this work the interactions
between plant and susceptible pest and also between susceptible and infected pest were taken into consideration. Other developing
topic in ecology is harvesting. There are increasing data which verifies that harvesting has a significant impact on dynamic evolution
of a population species. The effect of constant rate harvesting has been studied by many authors [11–21]. Keeping all this situation
in view, we have formulated a mathematical model of one predator–one prey interaction where the prey disease is modelled by a
Susceptible–Infected (SI) epidemic scheme. It is also assumed that the predator consumes the susceptible prey in addition to the

∗ Correspondence to: Department of Mathematics, Amity University, Kolkata 700135, India.

E-mail address: ambhattacharyya@kol.amity.edu (A. Bhattacharyya).

https://doi.org/10.1016/j.rico.2022.100099
Received 21 December 2021; Received in revised form 18 January 2022; Accepted 11 February 2022
Available online 18 February 2022
2666-7207/© 2022 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license
(http://creativecommons.org/licenses/by-nc-nd/4.0/).
A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

infected prey according to the modified Holling type II response function and the effect of constant harvesting on susceptible prey
and predator is considered.
In prey–predator system one enriching concept is predator switching depending on its choice of predation. Predator has a natural
tendency always to feed himself on a natural habitat where the prey population is in abundant and once due to its high predation
this abundancy reduces and prey population becomes insufficient for predation. As a result the predator changes its preference to
some other habitat and this change of preference is known as predator switching. In case of eco-epidemiological model this kind
of switching can be considered due to the infection in the prey population. Infected prey population become always weaker due to
parasite infection and it becomes easy for predator to access and catch them. After a certain period of high predation, predator shift
their attention and switch to susceptible prey population. This characteristic of changing prey preference of predator leads to a well-
known phenomenon of predator switching and this switching phenomenon was studied by many authors [22–31]. Bhattacharyya
and Mukhopadhyay [32] investigated the effect of predator switching with and without prey group defence under non-homogeneous
mixing of the population and they also studied mathematical analysis of the bifurcating solutions of a prey–predator model with
switching predator [33,34]. Saha and Samanta [35] also studied a two prey one predator system with switching effect that affects
the Hopf bifurcation of the system with respect to different biological parameters.
Many researchers have considered the consequence of harvesting on several types of prey–predator model. Particularly, Brauer
and Soudack [36,37] established a predator–prey system with consideration of constant harvesting in prey population to study their
dynamical behaviour. They also noted that harvesting reduces the region of asymptotic stability in the predator–prey plane. Leard
et al. [38] considered a Michaelis–Menten-type ratio-dependent predator–prey model with non-constant harvesting in the prey.
Martin and Ruan [18] proposed predator–prey models with delay and constant-rate harvesting in the prey and observed that the
maximum sustainable yield (MSY) depends on the environmental carrying capacity. Yunfei et al. [39] proposed and investigated a
toxin-producing phytoplankton–zooplankton model with harvesting in which both the species are assumed to undergo commercial
misuse for food. They recognized stability conditions of equilibria as well as existence conditions of a Hopf bifurcation. They noted
that volatilization may result in the annihilation of the populations and consideration of an appropriate strategy of harvesting would
confirm the stainability which actually match with the reality. Zhang et al. [40] studied the problem of combined harvesting of the
prey–predator model with prey reserve. Lenzini and Rebaza [41] studied a ratio-dependent prey–predator model by considering
non-constant harvesting for the predator. Pal and Samanta [42,43] considered an eco-epidemiological model incorporating a prey
refuge and discussed the stability analysis of the dynamics of the system.
In the present study, we formulate a mathematical model of prey–predator interaction where the prey suffers from micro-parasite
infection. Harvesting strategy is adopted by susceptible prey and predator population and we have studies the effect of constant
harvesting on the system. The main interesting part of this paper is the consideration of predator switching phenomenon and due to
that how community stability of prey predator system changes. Although researchers have already considered the predator switching
phenomena in two prey one predator system but a very few researcher have considered linear switching in epidemic model. Our
model is one prey one predator model which is SI model as well and second order predator switching is in consideration also.
In eco-epidemiological community our model considers a second order predator switching which is not considered earlier by any
researcher in epidemic model and this consideration is more realistic from eco-epidemiological aspect also. Thus our model is more
general and realistic than the previous studies. The other queries of this paper are to investigate the biological parameters those help
community stability of prey–predator dynamics. The paper is structured as follows. In Section 2, we formulated a three-dimensional
epidemic predator–prey model incorporating refuge in susceptible population, harvesting in susceptible prey and predator and
predator switching phenomenon. Positivity and boundedness of the system is developed in subsection of Section 2. Extinction
scenario of the subpopulations is discussed in the subsection also. Equilibria and stability analysis are presented in Section 3. Also
the global stability of boundary equilibrium, Persistence and Hopf Bifurcation are discussed in subsections of Section 3. Numerical
simulation and outcomes are given in Section 4 followed by a brief discussion is given in Section 5.

2. The basic mathematical model

Before introducing the eco-epidemiological model, we shall first describe the assumptions we have taken into considerations:

1. According to a logistic law with carrying capacity 𝐾(𝐾 > 0) in the absence of disease the prey population density use to
grow.
2. Prey population is divided in two classes in the presence of viruses and those are: The susceptible prey and the infected prey
which are denoted by 𝑆(𝑇 ) and 𝐼(𝑇 ) respectively. Hence at time 𝑇 , the total prey population becomes 𝑁(𝑇 ) = 𝑆(𝑇 ) + 𝐼(𝑇 ).
3. As the disease is not inherited genetically so that the infected populations are unable to recover or become immune. It is
taken in our assumption that the disease transmission follows the simple law of mass action 𝜆𝑆(𝑇 )𝐼(𝑇 ) where 𝜆 denotes the
infection rate.
4. The predator population density 𝑌 (𝑇 ) is considered here as a specialist one as the growth rate of predator depends only on
the susceptible and infected prey populations.
5. The refuge effect in the population of prey is also paid due attention in the present investigation.
6. The harvesting effect for the infected prey and predator has been taken under consideration.

On the basis of the above assumptions a three species model is considered:

( 𝑆 + 𝜂𝐼 ) 𝐶 (1 − 𝑚)𝑆𝑌
𝑑𝑆 𝜆𝑆𝐼
= 𝑅𝑆 1 − − − 1 − 𝐻1 𝑆,
𝑑𝑇 𝐾 𝐴 + 𝑆 𝐵 + (1 − 𝑚)𝑆

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

𝑑𝐼 𝜆𝑆𝐼 𝐶 𝐼𝑌
= − 2 − 𝐷1 𝐼, (1)
𝑑𝑇 𝐴+𝑆 𝐵+𝐼
𝑑𝑌 𝑒1 𝐶1 (1 − 𝑚)𝑆𝑌 𝑒 𝐶 𝐼𝑌
= + 2 2 − 𝐷2 𝑌 − 𝐻2 𝑌
𝑑𝑇 𝐵 + (1 − 𝑚)𝑆 𝐵+𝐼
with initial conditions 𝑆(0) ≥ 0, 𝐼(0) ≥ 0, 𝑌 (0) ≥ 0 and 0 < 𝑚 < 1. All the model parameters are assumed to be positive constants
with following interpretation:
𝑅: intrinsic growth rate of susceptible prey population,
𝐾: carrying capacity of susceptible prey population,
𝜆: rate of infection,
𝜂: conversion rate of prey population from susceptible to infected,
𝐶1 and 𝐶2 : maximum predation rates of 𝑆 and 𝐼,
𝐴: half stabilization constant,
𝐵: half saturation constant,
𝑚: effect of refuge of susceptible population,
𝐷1 : death rate of infected prey,
𝐷2 : death rate of the predator,
𝐻1 : harvesting rate of the susceptible prey,
𝐻2 : harvesting rate of the predator,
𝑒1 and 𝑒2 : encounters rate of predator per prey with refuge and without refuge respectively.
𝑆
Now we make the model dimensionless by using 𝑠 = 𝐾 ; 𝑖 = 𝐾𝐼 ; 𝑦 = 𝐾
𝑌
; 𝑡 = 𝑅𝑇 .
Using this substitutions in our epidemiological model we get

( ) 𝜆 𝑠𝑖 𝑐 (1 − 𝑚)𝑠𝑦
𝑑𝑠
= 𝑠 1 − (𝑠 + 𝜂𝑖) − ℎ1 − 1 − 1 ,
𝑑𝑡 𝑎 + 𝑠 𝑏 + (1 − 𝑚)𝑠
𝑑𝑖 𝜆 𝑠𝑖 𝑐 𝑖𝑦
= 1 − 2 − 𝑑1 𝑖, (2)
𝑑𝑡 𝑎+𝑠 𝑏+𝑖
𝑑𝑦 𝑝 (1 − 𝑚)𝑠𝑦 𝑝 𝑖𝑦
= 1 + 2 − (𝑑2 + ℎ2 )𝑦
𝑑𝑡 𝑏 + (1 − 𝑚)𝑠 𝑏 + 𝑖
with initial condition 𝑠(0) ≥ 0, 𝑖(0) ≥ 0, 𝑦(0) ≥ 0 and 0 < 𝑚 < 1. The remaining dimensionless parameters are defined by
𝜆 𝐴 𝐵 𝐶 𝐶 𝐾 𝐻 𝐻 𝐷 𝐷
𝜆1 = , 𝑎 = , 𝑏 = , 𝑐1 = 1 , 𝑐2 = 2 , ℎ1 = 1 , ℎ2 = 2 , 𝑑1 = 1 , 𝑑2 = 2 , 𝑝1 = 𝑒1 𝑐1 and 𝑝2 = 𝑒2 𝑐2 .
𝑅 𝐾 𝐾 𝑅 𝑅 𝑅 𝑅 𝑅 𝑅
In the system (2) consumption rate of predator for infected (or susceptible) prey depends on that particular prey only. It is
observed from theoretical research as well as field observations that predators have a spontaneous instinct to consume immoderate
number of infected preys as the infected prey may become weaker due to the parasite infection and they stay in locations which
are easily reachable by the predator. Chattopadhyay and Bairagi [44] and Sarkar et al. [45] studied tilapia and pelican interaction
models for the Salton Sea. In both models, the authors assumed that due to infection, tilapia becomes weak and pelicans interact
only with infected tilapia. Later using the same viewpoint, Greenhalgh and Haque [46] described a ratio-dependent predator–prey
interaction model where susceptibles experienced no predation. This is unlikely to be realistic for most species. Chattopadhyay
et al. [47] modified the model by introducing interaction of pelicans with susceptible fish and assumed that feeding on infected fish
increases the death rate of the pelicans. Contemporary modelling literature on eco-epidemiology [33–35] has also confirmed that
predator species prefers to catch prey species which are abundant in the habitat i.e., the predator feeds preferentially on the most
numerous prey species in the environment. This tendency of preferential predation will result in substantial reduction in the infected
prey species which in turn would compel the predator to shift its attention towards susceptible prey temporarily. This predatorial
characteristic of changing the prey types leads to the well-known phenomenon of predator switching inclusion of which makes the
model more relatable with the natural ecological environment. This concept of switching of predation encourages us to modify our
basic model that incorporates switching of the predator among susceptible and infected prey population.
( ) 𝜆 𝑠𝑖 𝑐 (1 − 𝑚)𝑠𝑦
𝑑𝑠
= 𝑠 1 − (𝑠 + 𝜂𝑖) − ℎ1 − 1 − 1 ( )2 ,
𝑑𝑡 𝑎+𝑠 𝑖
1 + (1−𝑚)𝑠
𝑑𝑖 𝜆 𝑠𝑖 𝑐2 𝑖𝑦
= 1 − ( )2 − 𝑑1 𝑖, (3)
𝑑𝑡 𝑎+𝑠 (1−𝑚)𝑠
1+ 𝑖
𝑑𝑦 𝑝1 (1 − 𝑚)𝑠𝑦 𝑝2 𝑖𝑦
= ( )2 + ( )2 − (𝑑2 + ℎ2 )𝑦
𝑑𝑡 𝑖
1 + (1−𝑚)𝑠 1 + (1−𝑚)𝑠
𝑖

(1−𝑚)𝑠𝑦 𝑖𝑦
The functions ( )2 and ( )2 mathematically characterize the switching mechanism. From an ecological viewpoint these
𝑖 (1−𝑚)𝑠
1+ (1−𝑚)𝑠
1+ 𝑖

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.

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

2.1. Positivity and boundedness of the system

In this section, we shall discuss the positivity and boundedness of the variables of the system (3) and equilibrium analysis of the
corresponding system. The following theorem ensures the positivity and boundedness of the underlying system.

Theorem 2.1.1. All solutions of the system (3) that starts in ℜ3+ remain positive forever.

Proof. From the first subequation of the system (3) we obtain

[( ) 𝜆 𝑖(𝑡) 𝑐 (1 − 𝑚)𝑠(𝑡)𝑦(𝑡) ]
𝑑𝑠
= 𝑠(𝑡) 1 − (𝑠(𝑡) + 𝑖(𝑡)𝜂) − ℎ1 − 1 − 1 ( )2 .
𝑑𝑡 𝑎 + 𝑠(𝑡) 𝑖(𝑡)
1 + (1−𝑚)𝑠(𝑡)

Thus,
[ 𝑡 {( ) 𝜆 𝑖(𝜃) 𝑐 (1 − 𝑚)𝑦(𝜃) } ]
𝑠(𝑡) = 𝑠(0)𝑒𝑥𝑝 1 − (𝑠(𝜃) + 𝜂𝑖(𝜃)) − ℎ1 − 1 − 1( )2 𝑑𝜃 > 0
∫0 𝑎 + 𝑠(𝜃) 𝑖(𝜃)
1 + (1−𝑚)𝑠(𝜃)

for 𝑠(0) > 0.

Similarly,
[ 𝑡{ 𝜆1 𝑠(𝜃) 𝑐2 𝑦(𝜃) } ]
𝑖(𝑡) = 𝑖(0)𝑒𝑥𝑝 − ( )2 − 𝑑1 𝑑𝜃 > 0
∫0 𝑎 + 𝑠(𝜃) (1−𝑚)𝑠(𝜃)
1+ 𝑖(𝜃)

for 𝑖(0) > 0 and

[ 𝑡{ 𝑝1 (1 − 𝑚)𝑠(𝜃) 𝑝2 𝑖(𝜃) } ]
𝑦(𝑡) = 𝑦(0)𝑒𝑥𝑝 ( )2 + ( )2 − (𝑑2 + ℎ2 ) 𝑑𝜃 > 0
∫0 𝑖(𝜃)
1 + (1−𝑚)𝑠(𝜃) 1 + (1−𝑚)𝑠(𝜃)
𝑖(𝜃)

for 𝑦(0) > 0.

Theorem 2.1.2. The solution of the system (3) which starts in ℜ3+ is bounded.

Proof. Let 𝑊 (𝑡) = 𝑒1 𝑠(𝑡) + 𝑒2 𝑖(𝑡) + 𝑦(𝑡).

So for large time t:

𝑊 ′ (𝑡) = 𝑒1 𝑠′ (𝑡) + 𝑒2 𝑖′ (𝑡) + 𝑦′ (𝑡)

𝑒1 𝜆1 𝑠𝑖 𝑒2 𝜆1 𝑠𝑖
= 𝑒1 𝑠(1 − (𝑠 + 𝑖𝜂) − ℎ1 ) − + − 𝑒2 𝑑1 𝑖 − (𝑑2 + ℎ2 )𝑦
𝑎+𝑠 𝑎+𝑠
𝑒2 𝜆1 𝑠𝑖
≤ 𝑒1 𝑠 + − (𝑑2 + ℎ2 )𝑦
𝑎+𝑠
( 𝜆 𝑠 )
1
= 2𝑒1 𝑠 + 𝑒2 + 1 𝑖 − 𝑒1 𝑠 − 𝑒2 𝑖 − (𝑑2 + ℎ2 )𝑦
𝑎+𝑠
( 𝜆 )
1
≤ 2𝑒1 + 𝑒2 + 1 − 𝜅𝑊
𝑎+1
{ }
where 𝜅 =min 𝑒1 , 𝑒2 , (𝑑2 + ℎ2 ) .

( 𝜆 )
𝑑𝑊 1
+ 𝜅𝑊 ≤ 2𝑒1 + 𝑒2 +1
𝑑𝑡 𝑎+1
= 𝜇(𝑠𝑎𝑦)
𝜇
⟹ 𝑊 (𝑡) ≤ (1 − 𝑒−𝜅𝑡 ) + 𝑊 (𝑠(0), 𝑖(0), 𝑦(0))𝑒−𝜅𝑡
𝜅
As 𝑡 → ∞, 0 < 𝑊 (𝑡) ≤ 𝜇𝜅 ,
Therefore all the solutions of system (2) enter into the region:
{ 𝜇}
𝛺 = (𝑠, 𝑖, 𝑦) ∶ 0 < 𝑠(𝑡) ≤ 1, 0 < 𝑖(𝑡) ≤ 1, 0 < 𝑦(𝑡) ≤ 1; 0 < 𝑊 (𝑡) ≤ .
𝜅

2.2. Extinction scenarios

Following theorem provides the criterion for which predator population goes extinct from the system in long run.

Theorem 2.2.1. If 𝑝1 (1 − 𝑚)3 + 𝑝2 < 𝑑2 + ℎ2 then

lim 𝑦(𝑡) = 0
𝑡→∞

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

Proof. For large time 𝑡:

𝑑𝑦 { 𝑝 (1 − 𝑚)3 𝑠3 𝑝2 𝑖3 }
1
= 𝑦 + − 𝑑2 − ℎ2
𝑑𝑡 2 2
(1 − 𝑚) 𝑠 + 𝑖 2 2
𝑖 + (1 − 𝑚) 𝑠2 2
{ }
≤ 𝑦 𝑝1 (1 − 𝑚)3 𝑠3 + 𝑝2 𝑖3 − 𝑑2 − ℎ2
{ }
≤ 𝑦 𝑝1 (1 − 𝑚)3 + 𝑝2 − 𝑑2 − ℎ2
= −𝜇𝑦

where 𝜇 = 𝑑2 + ℎ2 − 𝑝1 (1 − 𝑚)3 − 𝑝2 .
Hence,

lim 𝑦(𝑡) = 0.
𝑡→∞

Remark: If the overall growth rate of predator fails to exceeds its sum of mortality rate and harvesting rate, then with time, the
predator population goes extinct from the system (3).

3. Equilibrium points and their stability

The proposed system (3) has the following equilibrium points:

(𝑖) Trivial equilibrium point 𝐸0 (0, 0, 0) which exists always.
(𝑖𝑖) Axial equilibrium point 𝐸1 (1 − ℎ1 , 0, 0) exists if ℎ1 < 1.
𝑑 +ℎ2 𝑝 (1−ℎ )(1−𝑚)−(𝑑 +ℎ )
(𝑖𝑖𝑖) Infection free equilibrium point is 𝐸2 (𝑠2 , 0, 𝑦2 ) where 𝑠2 = 𝑝 2(1−𝑚) and 𝑦2 = 1 𝑝1 𝑐 (1−𝑚)2 2 2 . This equilibrium exists if and
1 1 1
only if 𝑝1 (1 − ℎ1 )(1 − 𝑚) > 𝑑2 + ℎ2 .
∗
(𝑖𝑣) The interior equilibrium 𝐸3 = (𝑠3 , 𝑖3 , 𝑦3 ) where (𝑠3 , 𝑖3 , 𝑦3 ) is the positive solution of
( ) 𝜆 𝑖 𝑐1 (1 − 𝑚)𝑦
1 − (𝑠 + 𝜂𝑖) − ℎ1 − 1 − ( )2 = 0
𝑎+𝑠 𝑖
1 + (1−𝑚)𝑠
𝜆1 𝑠 𝑐2 𝑦
− ( )2 − 𝑑1 = 0 (4)
𝑎+𝑠 (1−𝑚)𝑠
1+ 𝑖
𝑝1 (1 − 𝑚)𝑠 𝑝2 𝑖
( )2 + ( )2 − (𝑑2 + ℎ2 ) = 0
𝑖
1 + (1−𝑚)𝑠 1 + (1−𝑚)𝑠
𝑖

3.1. Local stability analysis

Local stability conditions of the equilibrium points can be determined by the eigenvalues of the corresponding Jacobian matrices.
Now, the Jacobian matrix of system (3) is given by

⎛𝑎11 𝑎12 𝑎13 ⎞

𝐽 = ⎜𝑎21 𝑎22 𝑎23 ⎟
⎜ ⎟
⎝𝑎31 𝑎32 𝑎33 ⎠
where
{ }
𝑖2
𝑐1 (1 − 𝑚)𝑦 1 + 3 (1−𝑚)
𝑎𝜆1 𝑖 2 𝑠2
𝑎11 = 1 − 2𝑠 − ℎ1 − 𝜂𝑖 − − { }2
(𝑎 + 𝑠)2 𝑖2
1 + (1−𝑚) 2 𝑠2

𝜆1 𝑠 2𝑐1 𝑖𝑦
𝑎12 = −𝜂𝑠 − + { }2 ,
𝑎+𝑠 𝑖2
(1 − 𝑚)𝑠 1 + (1−𝑚) 2 𝑠2

𝑐1 (1 − 𝑚)𝑠
𝑎13 = −
𝑖2
1+ (1−𝑚)2 𝑠2 ( 2 𝑠2
)
𝜆1 𝑎𝑖 2𝑐2 𝑠𝑦 𝜆1 𝑠 𝑐2 𝑦 1 + 3(1−𝑚)𝑖2
𝑎21 = +( ) , 𝑎22 = − ( ) − 𝑑1
(𝑎 + 𝑠)2 1 + (1−𝑚)
2 𝑠2 𝑎+𝑠 2 𝑠2 2
𝑖2 1 + (1−𝑚)
𝑖2
{ }
3𝑖2
−𝑐2 𝑖3 𝑝1 (1 − 𝑚)𝑦 1 + (1−𝑚)2 𝑠2 2𝑝 (1 − 𝑚)2 𝑠𝑦
𝑎23 = , 𝑎31 = { }2 − { 2 } ,
𝑖2 + (1 − 𝑚)2 𝑠2 2 2 𝑠2 2
𝑖
1 + (1−𝑚) 2 𝑠2 𝑖 1 + (1−𝑚) 𝑖 2

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

𝑖
2𝑝1 𝑦 (1−𝑚)𝑠 3(1−𝑚)2 𝑠2
1+ 𝑖2
𝑎32 = − { } + 𝑝2 { }2 , 𝑎33 = 0
(1−𝑚)2 𝑠 2 2 (1−𝑚)2 𝑠2
1+ 𝑖2
1+ 𝑖2

⎛1 − ℎ1 0 0 ⎞
For 𝐸0 = (0, 0, 0): 𝐽 |𝐸0 = ⎜ 0 −𝑑1 0 ⎟
⎜ ⎟
⎝ 0 0 −𝑑2 − ℎ2 ⎠
So 𝜆1 = 1 − ℎ1 , 𝜆2 = −𝑑1 , 𝜆3 = −𝑑2 − ℎ2

Theorem 3.1.1. The trivial equilibrium 𝐸0 (0, 0, 0) is stable if and only if ℎ1 > 1 otherwise it will be a saddle point.
For 𝐸1 = (1 − ℎ1 , 0, 0):
( 𝜆1 )
⎛−(1 − ℎ1 ) (1 − ℎ1 ) −𝜂 − −𝑐1 (1 − 𝑚) ⎞
⎜ 𝑎 + 1 − ℎ1 ⎟
$𝐽𝐸1 = ⎜ 𝛼(1 − ℎ1 ) ⎟
⎜ 0 − 𝑑1 0 ⎟
⎜ 𝑎 + (1 − ℎ1 ) ⎟
⎝ 0 0 𝑝1 (1 − 𝑚)(1 − ℎ1 ) − 𝑑2 − ℎ2 ⎠
′ ′ ′
Here, 𝜆1 < 0, 𝜆2 < 0 always once 𝐸1 exists and 𝜆3 < 0 if 𝑝1 (1 − 𝑚)(1 − ℎ1 ) < 𝑑2 + ℎ2

Theorem 3.1.2. The equilibrium point 𝐸1 (1 − ℎ1 , 0, 0) is stable if and only if 𝑝1 (1 − 𝑚)(1 − ℎ1 ) < 𝑑2 + ℎ2 , otherwise it will be a saddle
point.
For 𝐸2 = (𝑠2 , 0, 𝑦2 ):

⎛𝑎(2) 𝑎(2) 𝑎(2) ⎞

⎜ 11 12 13
⎟
𝐽𝐸2 =⎜ 0 𝑎(2)
22
0 ⎟ , 𝑤ℎ𝑒𝑟𝑒
⎜ (2) ⎟
⎝𝑎31 0 0 ⎠
𝜆1 𝑠2
𝑎(2)
11
= 1 − 2𝑠2 − ℎ1 − 𝑐1 (1 − 𝑚)𝑦2 , 𝑎(2)
12
= −𝜂𝑠2 − 𝑎+𝑠2
, 𝑎(2)
13
= −𝑐1 (1 − 𝑚)𝑠2 ,
𝜆1 𝑠2
𝑎(2)
22
= 𝑎+𝑠2
− 𝑑1 , 𝑎(2)
31
= 𝑝1 (1 − 𝑚)𝑦

𝜆1 𝑠 2
So, one eigen value is 𝜆′1 = 𝑎22 = 𝑎+𝑠2
− 𝑑1 and other two eigen values are roots of the equation 𝜆2 − 𝑎11 𝜆 − 𝑎13 𝑎31 = 0. So, two
𝑑1 𝑎
eigen values have always negative real part as 𝑎11 < 0 and 𝑎13 𝑎31 < 0 always. But one eigen value 𝜆′1 is negative if 𝑠2 < 𝜆1 −𝑑1
.

Theorem 3.1.3. The equilibrium point 𝐸2 (𝑠2 , 0, 𝑦2 ) is stable if and only if (𝑑2 + ℎ2 )(𝜆1 − 𝑑1 ) < 𝑑1 𝑎𝑝1 (1 − 𝑚) and is a saddle point when
(𝑑2 + ℎ2 )(𝜆1 − 𝑑1 ) > 𝑑1 𝑎𝑝1 (1 − 𝑚)
⎛𝑎(∗) 𝑎(∗) 𝑎(∗) ⎞
⎜ 11 12 13 ⎟
Now for 𝐸 (𝑠 , 𝑖 , 𝑦 ): 𝐽 |𝐸 ∗ = ⎜𝑎(∗) 𝑎(∗) 𝑎(∗) ⎟ where
∗ ∗ ∗ ∗
21 22 23
⎜ (∗) (∗) ⎟
⎝𝑎31 𝑎32 0 ⎠

𝜆1 𝑠∗ 𝑖 ∗ 2𝑐 (1 − 𝑚)3 𝑠∗ 2 𝑖∗ 2 𝑦∗
𝑎(∗)
11
= −𝑠∗ + −(1 )2
(𝑎 + 𝑠∗ )2
(1 − 𝑚)𝑠∗ 2 + 𝑖∗ 2
𝜆1 𝑠∗ 2𝑐1 𝑖∗ 𝑦∗
𝑎(∗)
12
= −𝜂𝑠∗ − + { }2 ,
𝑎 + 𝑠∗ 𝑖∗2
(1 − 𝑚)𝑠∗ 1 +
(1−𝑚)2 𝑠∗2

𝑐1 (1 − 𝑚)𝑠∗
𝑎(∗)
13
=−
𝑖∗ 2
1+
(1−𝑚)2 𝑠∗2
𝜆1 𝑎𝑖 2𝑐2 𝑠∗ 𝑦∗ −2𝑐2 𝑠∗ 2 𝑖∗ 2 𝑦∗ (1 − 𝑚)2
𝑎(∗)
21
= +( (∗)
) , 𝑎22 = ( )2
(𝑎 + 𝑠∗ )2 1+ (1−𝑚)2 𝑠∗ 2
𝑖∗ 2 𝑖∗ 2 + (1 − 𝑚)2 𝑠∗ 2
{ ∗2
}
−𝑐2 𝑖∗ 3 𝑝1 (1 − 𝑚)𝑦∗ 1 + 3𝑖 2 ∗2 2𝑝 (1 − 𝑚)2 𝑠∗ 𝑦∗
(1−𝑚) 𝑠
𝑎(∗)
23
= , 𝑎(∗)
31
= { } − {2 } ,
𝑖∗ 2 + (1 − 𝑚)2 𝑠∗ 2 𝑖∗ 2
2 2 ∗2 2
1+ 2 ∗2
𝑖 1 + (1−𝑚)∗2 𝑠
(1−𝑚) 𝑠 𝑖
𝑖 3(1−𝑚)2 𝑠∗2
2𝑝1 𝑦∗ (1−𝑚)𝑠∗ 1+
𝑖∗ 2
𝑎(∗)
32
= −{ } + 𝑝2 { (∗)
}2 , 𝑎33 = 0
2
(1−𝑚)2 𝑠∗ 2 (1−𝑚)2 𝑠∗2
1+ ∗2
1+
𝑖 𝑖∗2

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

Characteristic equation for 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ) is

𝜆3 + 𝑃1 𝜆2 + 𝑃2 𝜆 + 𝑃3 = 0 (5)
where 𝑃1 = −(𝑎11 + 𝑎22 ), 𝑃2 = 𝑎11 𝑎22 − 𝑎12 𝑎21 − 𝑎13 𝑎31 − 𝑎23 𝑎32 and 𝑃3 = 𝑎32 (𝑎11 𝑎23 − 𝑎13 𝑎21 ) + 𝑎31 (𝑎13 𝑎22 − 𝑎12 𝑎23 ). Consider, ▵= 𝑃1 𝑃2 − 𝑃3 ,
and so by Routh–Hurwitz criterion all the roots of Eq. (5) have negative real parts if 𝑃1 > 0, 𝑃3 > 0 and ▵> 0. Hence we have the following
theorem:

Theorem 3.1.4. Interior equilibrium point 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ) is locally asymptotically stable (LAS) if 𝑃1 > 0, 𝑃3 > 0 along with 𝑃1 𝑃2 − 𝑃3 > 0.

3.2. Global behaviour

In this section we look at the disease free equilibrium point from the global perspective. We rewrite system (3) as
𝑑𝑠
= 𝑠𝑓1 (𝑠, 𝑖, 𝑦)
𝑑𝑡
𝑑𝑖
= 𝑖𝑓2 (𝑠, 𝑖, 𝑦) (6)
𝑑𝑡
𝑑𝑦
= 𝑦𝑓3 (𝑠, 𝑖, 𝑦)
𝑑𝑡
where
( ) 𝜆 𝑖 𝑐1 (1 − 𝑚)𝑦
𝑓1 (𝑠, 𝑖, 𝑦) = 1 − (𝑠 + 𝜂𝑖) − ℎ1 − 1 − ( )2 ,
𝑎+𝑠 𝑖
1 + (1−𝑚)𝑠
𝜆1 𝑠 𝑐2 𝑦
𝑓2 ∗ (𝑠, 𝑖, 𝑦) = − ( )2 − 𝑑1 ,
𝑎+𝑠 (1−𝑚)𝑠
1+ 𝑖
𝑝1 (1 − 𝑚)𝑠 𝑝2 𝑖
𝑓3 (𝑠, 𝑖, 𝑦) = ( )2 + ( )2 − (𝑑2 + ℎ2 )
𝑖
1 + (1−𝑚)𝑠 1 + (1−𝑚)𝑠
𝑖

The system has only one disease free equilibrium 𝐸2 = (𝑠 [ 2 , 0, 𝑦2 ). Let us define ]
𝐹1 (𝑥) = 𝑓2 (𝑥, 0, 𝑦2 ); 𝐹2 (𝑦) = −𝑓1 (𝑠2 , 𝑦, 𝑦2 ) and 𝐹3 (𝑧) = − 𝑓2 (𝑠2 , 0, 𝑧) − 𝑓1 (𝑠2 , 0, 𝑧) .
𝜕𝑓 𝜕𝑓1 𝜕𝑓2 𝜕𝑓1
As 𝜕𝑠2 > 0, 𝜕𝑖
< 0, 𝜕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) 1 𝐹 (𝑦) 𝑦 𝐹 (𝑧)

2 3
𝑉 = 𝑑𝑥 + 𝑑𝑦 + 𝑑𝑧 (7)
∫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 and also 𝑉 (𝑠2 , 0, 𝑦2 ) = 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 (𝑠2 , 𝑖, 𝑦2 ) + 𝐹2 (𝑖) 𝑓2 (𝑠, 𝑖, 𝑦) − 𝑓2 (𝑠, 0, 𝑦2 ) +
[ ]
𝐹3 (𝑦) 𝑓3 (𝑠, 𝑖, 𝑦) − 𝑓3 (𝑠2 , 0, 𝑦) + 𝐹1 (𝑠)𝑓1 (𝑠2 , 𝑖, 𝑦2 ) + 𝐹2 (𝑖)𝑓2 (𝑠, 0, 𝑦2 ) + 𝐹3 (𝑦)𝑓3 (𝑠2 , 0, 𝑦2 )
[ 𝜕𝑓 𝜕𝑓 ]
= 𝐹1 (𝑠) (𝑠 − 𝑠2 ) 1 (𝑠, ̃ 𝑖, 𝑦) + (𝑦 − 𝑦2 ) 1 (𝑠, 𝑖̃, 𝑦)
𝜕𝑠 𝜕𝑦
[ 𝜕𝑓 𝜕𝑓 ]
+ 𝐹2 (𝑖) 𝑖 2 (𝑠, 𝑖̃, 𝑦) + (𝑦 − 𝑦2 ) 2 (𝑠, 𝑖, 𝑦) ̃ +
𝜕𝑖 𝜕𝑦
[ 𝜕𝑓3 𝜕𝑓3 ]
𝐹3 (𝑦) (𝑠 − 𝑠2 ) (𝑠,
̃ 𝑖, 𝑦) + 𝑖 (𝑠, 𝑖̃, 𝑦)
𝜕𝑠 𝜕𝑖
𝜕𝑓 𝜕𝑓 𝜕𝑓 𝜕𝑓
Now from the definition 𝑓𝑖 s, 𝜕𝑦1 < 0, 𝜕𝑦2 < 0, 𝜕𝑠3 > 0, 𝜕𝑖3 > 0. Again, 𝐹3 (𝑦) < 0 will hold provided that 𝑅 large and 𝑓2 (𝑠2 , 0, 𝑦2 ) > 0.
This condition implies that 𝐹1 (𝑠) > 0. Moreover, 𝐹2 (𝑖) ≥ 0 is always true.
𝜕𝑓 𝜕𝑓
Therefore, 𝑑𝑉
𝑑𝑡
≤ 0 when 𝜕𝑠1 < 0, 𝜕𝑖2 < 0, where 𝑠1 < 𝑠̃ < 𝑠, 0 < 𝑖̃ < 𝑖, 𝑦1 < 𝑦̃ < 𝑦.
𝜕𝑓1 𝜆1 𝑖 2𝑐1 (1−𝑚)3 𝑦𝑖2
Now, 𝜕𝑠
= −1 − (𝑎+𝑠) 2 − 𝑖2 +(1−𝑚)2 𝑠2 which is always < 0 and
𝜕𝑓2 2𝑐 (1−𝑚)2 𝑠2 𝑖𝑦
𝜕𝑖
= − 𝑖22+(1−𝑚)2 𝑠2 which is also < 0 always. Therefore, by LaSalle’s Theorem [48], 𝐸2 will be a global attractor for the system.

3.3. Persistence

In the context of ecology, persistence means the long term survival of all species which exist initially.

7
A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

Theorem 3.3.1. The system (3) is persistent if the following conditions hold good:
{ 𝑑 𝑎 𝑑 + ℎ2 }
1
(𝑖) 1 − ℎ1 > 𝑚𝑎𝑥 , 2
𝜆1 − 𝑑1 𝑝1 (1 − 𝑚)
{ 𝑑 𝑎 𝑑 + ℎ2 }
1
(𝑖𝑖) 𝑚𝑎𝑥 , 2 < 𝑠2 < 1 − 𝑐1 (1 − 𝑚)𝑦2
𝜆1 − 𝑑1 𝑝1 (1 − 𝑚)

Proof. Let us consider the average Lyapunov function in the form 𝑉 (𝑠, 𝑖, 𝑦) = 𝑠𝛾1 𝑖𝛾2 𝑦𝛾3 where each 𝛾𝑖 (𝑖 = 1, 2, 3) is assumed to be
positive. In the interior of ℜ3+ , we have
[( ) 𝑐 (1 − 𝑚)𝑦 ]
𝑉̇ 𝜆 𝑖
= 𝜓(𝑥, 𝑦, 𝑧) = 𝛾1 1 − (𝑠 + 𝜂𝑖) − ℎ1 − 1 − 1 +
𝑉 𝑎 + 𝑠 𝑏 + (1 − 𝑚)𝑠
[ 𝜆 𝑠 𝑐 𝑦 ] [ 𝑝 (1 − 𝑚)𝑠 𝑝 𝑖 ]
1
𝛾2 − 2 − 𝑑1 + 𝛾3 1 + 2 − (𝑑2 + ℎ2 ) (8)
𝑎+𝑠 𝑏+𝑖 𝑏 + (1 − 𝑚)𝑠 𝑏 + 𝑖
The permanence of the system can be proved by showing that 𝜓(𝑥, 𝑦, 𝑧) > 0, for all the equilibrium of the system. The values of
𝜓(𝑥, 𝑦, 𝑧) > 0 at the boundary equilibria 𝐸0 , 𝐸1 , 𝐸2 are the following:

𝐸0 ∶ 𝜓(0, 0, 0) = 𝛾1 − 𝛾2 𝑑1 − 𝛾3 (𝑑2 + ℎ2 )
[ ] [ ]
𝜆1 (1−ℎ1 )
𝐸1 ∶ 𝜓(1 − ℎ1 , 0, 0) = 𝛾1 ℎ1 + 𝛾2 𝑎+1−ℎ − 𝑑1 + 𝛾3 𝑝1 (1 − 𝑚)(1 − ℎ1 ) − (𝑑2 + ℎ2 ) Now the condition 𝜓(0, 0, 0) > 0 is trivially satisfied
1
for some 𝛾𝑖 > 0(𝑖 = 1, 2, 3). Also, if the inequalities (i) & (ii) hold 𝜓 is positive at 𝐸1 , 𝐸2 for some 𝛾𝑖 > 0(𝑖 = 1, 2, 3). Therefore system
(2)is persistence if the conditions (i) & (ii) are fulfilled. Hence proved.

3.4. Hopf bifurcation at 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ )

The characteristic equation of the system (3) at 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ) is given by

𝜆3 + 𝑄1 (𝑚)𝜆2 + 𝑄2 (𝑚)𝜆 + 𝑄3 (𝑚) = 0, (9)

where
( )
𝑄1 (𝑚) = − 𝑎11 + 𝑎22 ,
( )
𝑄2 (𝑚) = 𝑎11 𝑎22 − 𝑎12 𝑎21 − 𝑎13 𝑎31 − 𝑎23 𝑎32 , (10)
{ }
𝑄3 (𝑚) = 𝑎32 (𝑎11 𝑎23 − 𝑎13 𝑎21 ) + 𝑎31 (𝑎13 𝑎22 − 𝑎12 𝑎23 ) . (11)

In order to observe the existence of instability of system (3), let us consider 𝑚 as bifurcation parameter. For this purpose let us first
state the following theorem:

Theorem 3.4.1 (Hopf Bifurcation Theorem [49]). If 𝑄𝑖 (𝑚), 𝑖 = 1, 2, 3 are smooth functions of 𝑚 in an open interval about 𝑚∗ ∈ ℜ such
that the characteristic Eq. (9) has
𝑑𝜉
(i) a pair of complex eigenvalues 𝜆 = 𝛼(𝑚) ± 𝑖𝛽(𝑚) (with 𝛼(𝑚), 𝛽(𝑚) ∈ R) so that they become purely imaginary at 𝑚 = 𝑚∗ and |
𝑑𝑚 𝑚=𝑚
∗ ≠0

(ii) the other eigen value is negative at 𝑚 = 𝑚∗

Then a Hopf bifurcation occurs around 𝐸4 at 𝑚 = 𝑚∗ (i.e., a stability change of 𝐸 ∗ accompanied by the creation of a limit cycle at 𝑚 = 𝑚∗ ).

Theorem 3.4.2. The system (3) possesses a Hopf bifurcation around 𝐸 ∗ when 𝑚 passes through 𝑚∗ provided 𝐴1 (𝑚∗ ) > 0, 𝐴3 (𝑚∗ ) > 0 and
𝐴1 (𝑚∗ )𝐴2 (𝑚∗ ) = 𝐴3 (𝑚∗ ).

Proof. For 𝑚 = 𝑚∗ , the characteristic equation of the system (9) at 𝐸 ∗ becomes

(𝜆2 + 𝐴2 )(𝜆 + 𝐴1 ) = 0
√ √
providing roots 𝜆1 = 𝑖 𝐴2 , 𝜆2 = −𝑖 𝐴2 and 𝜆1 = −𝐴1 . Thus there exists a pair of purely imaginary eigenvalues and a strictly
negative real eigenvalue. Also 𝐴𝑖 (𝑖 = 1, 2, 3) are smooth functions of ℎ1 . So, for ℎ1 in a neighbourhood of ℎ∗1 , the roots have the form
𝜆1 (𝑚) = 𝑢1 (𝑚) + 𝑖𝑢2 (𝑚), 𝜆2 (𝑚) = 𝑢1 (𝑚) − 𝑖𝑢2 (𝑚), 𝜆3 = −𝑢3 (𝑚)(𝜆3 (𝑚) = −𝐴1 (𝑚)) where 𝑢𝑖 (𝑚), 𝑖 = 1, 2, 3 are real.
𝑑
Next we shall verify the transversality conditions: 𝑑𝑚 (𝑅𝑒(𝜆𝑖 (𝑚)))|𝑚=𝑚∗ ≠ 0, 𝑖 = 1, 2.
Substituting 𝜆 = 𝑢1 (𝑚) + 𝑖𝑢2 (𝑚) into the characteristic Eq. (9) we get

(𝑢1 + 𝑖𝑢2 )3 + 𝐴1 (𝑢1 + 𝑖𝑢2 )2 + 𝐴2 (𝑢1 + 𝑖𝑢2 ) + 𝐴3 = 0 (12)

Now, taking derivative of (12) with respect to 𝑚, we get,

3(𝑢1 + 𝑖𝑢2 )2 (𝑢̇1 + 𝑖𝑢̇2 ) + 2𝐴1 (𝑢1 + 𝑖𝑢2 )(𝑢̇1 + 𝑖𝑢̇2 ) + 𝐴̇ 1 (𝑢1 + 𝑖𝑢2 )2 + 𝐴2 (𝑢̇1 + 𝑖𝑢̇2 )+
𝐴̇ 2 (𝑢1 + 𝑖𝑢2 ) + 𝐴̇ 3 = 0 (13)

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

Fig. 1. Stable behaviour and phase portrait of the equilibrium point 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ).

Comparing real and imaginary parts from both sides of (13):

𝑃1 𝑢̇1 − 𝑃2 𝑢̇2 + 𝑃3 = 0 (14)

𝑃2 𝑢̇1 + 𝑃2 𝑢̇2 + 𝑃4 = 0 (15)

where

𝑃1 = 3(𝑢21 − 𝑢22 ) + 2𝐴1 𝑢1 + 𝐴2 , 𝑃2 = 6𝑢1 𝑢2 + 2𝐴1 𝑢2 ,

𝑃3 = 𝐴̇ 1 (𝑢21 − 𝑢22 ) + 𝐴̇ 2 𝑢1 + 𝐴̇ 3 , 𝑃4 = 2𝐴̇ 1 𝑢1 𝑢2 + 𝐴̇ 2 𝑢2 (16)

From (15) and (15), we get

𝑃2 𝑃4 + 𝑃1 𝑃3
𝑢̇1 = − (17)
𝑃12 + 𝑃22

Now, 𝑃3 = 𝐴̇ 1 (𝑢21 − 𝑢22 ) + 𝐴̇ 2 𝑢1 + 𝐴̇ 3 = 𝐴̇ 1 (𝑢21 − 𝑢22 ) + 𝐴̇ 2 𝑢1 + 𝐴̇ 1 𝐴2 + 𝐴̇ 2 𝐴1 , at 𝑚 = 𝑚∗ :

√
Case I: 𝑢1 = 0, 𝑢2 = 𝐴 √2 √
𝑃1 = −2𝐴2 , 𝑃2 = 2𝐴1 𝐴2 , 𝑃3 ≠ 𝐴̇ 2 𝐴1 , 𝑃4 = 𝐴̇ 2 𝐴2
Therefore, 𝑃2 𝑃4 + 𝑃1 𝑃3 ≠ 2𝐴1 𝐴2 𝐴̇ 2 − 2𝐴1 𝐴2 𝐴̇ 2 = 0 √
So, 𝑃2 𝑃4 + 𝑃1 𝑃3 ≠ 0 at ℎ1 = ℎ∗1 , when 𝑢1 = 0, 𝑢2 = 𝐴2 .
√
Case II : 𝑢1 = 0, 𝑢2 = − √ 𝐴2 √
𝑃1 = −2𝐴2 , 𝑃2 = −2𝐴1 𝐴2 , 𝑃3 ≠ 𝐴̇ 2 𝐴1 , 𝑃4 = −𝐴̇ 2 𝐴2
Therefore, 𝑃2 𝑃4 + 𝑃1 𝑃3 ≠ 2𝐴1 𝐴2 𝐴̇ 2 − 2𝐴1 𝐴2 𝐴̇ 2 = 0 √
So, 𝑃2 𝑃4 + 𝑃1 𝑃3 ≠ 0 at 𝑚 = 𝑚∗ , when 𝑢1 = 0, 𝑢2 = − 𝐴2 .
𝑑 𝑃 𝑃 +𝑃 𝑃 |
Therefore, 𝑑𝑚 (𝑅𝑒(𝜆𝑖 (𝑚)))|𝑚=𝑚∗ = − 2 42 12 3 | ≠ 0 and 𝑢3 (𝑚∗ ) = −𝐴1 (𝑚∗ ) < 0
𝑃1 +𝑃2 |𝑚=𝑚∗
Hence by Theorem 3.4.1, the result follows.
Remarks: Similarly, ℎ2 and 𝜆1 can be taken as bifurcating parameters.

4. Numerical simulation

Analytical studies can never be completed without numerical verification of the results. In this section we present computer
simulation of some solutions of the system. Beside verification of our analytical findings, these numerical solutions are very important
from the practical point of view. To explain the results numerically we choose the parameter of the system as 𝜂 = 0.1, 𝛼 = 1.1, 𝑎 =
0.8, 𝑐1 = 0.6, 𝑚 = 0.8, 𝑏 = 0.5, ℎ1 = 0.8, 𝑐2 = 0.9, 𝑑1 = 0.01, 𝑒1 = 0.8, 𝑒2 = 2.4, 𝑑2 = 0.01, ℎ2 = 0.09. This choice of parameters satisfy
the condition of Theorem 3.1.4 and consequently 𝑥∗ = 0.03082, 𝑦∗ = 0.04572, 𝑧∗ = 0.1046. Hence 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ) exists and is locally
asymptotically stable (see Fig. 1).

4.1. Influence of harvesting

In this eco-epidemiological study, the impact of harvesting rate of susceptible prey and predator play a major role in describing
the dynamics of the system. Here ℎ1 and ℎ2 are the main parameters controlling the system behaviour. We varied the parameters ℎ1
and ℎ2 respectively and observed different types of behaviour of system (2). To see the effect of harvesting rate on the dynamical

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

Fig. 2. Effect of harvesting rate of susceptible prey (ℎ1 ) on subpopulation dynamics.

Fig. 3. Effect of harvesting rate of predator (ℎ2 ) on subpopulation dynamics.

Table 1
Effect of harvesting of susceptible prey population (ℎ1 ) on sub-populations.
Sl No. ℎ1 𝑠 𝑖 𝑦
1 0.2 0.4611 0.07081 1.963
2 0.4 0.3286 0.06483 1.276
3 0.6 0.1888 0.0555 0.6745
4 0.8 0.0308 0.04583 0.1043
5 1.0 0.000 0.000 0.000

Table 2
Effect of harvesting of predator population (ℎ2 ) on sub-populations.
Sl No. ℎ2 𝑠 𝑖 𝑦
1 0.02 0.08655 0.01867 0.4877
2 0.04 0.08001 0.02667 0.3350
3 0.06 0.06583 0.03393 0.2403
4 0.08 0.0448 0.04151 0.1547
5 0.10 0.01267 0.05055 0.03871

population, we perform at Fig. 2 by using various values of ℎ1 . This figure shows that by increasing harvesting rate on susceptible
prey subpopulation, the size of all subpopulation decreases at long time and convergence of solution occurs in slower rate (see
Table 1). Similar behaviour of the subpopulation is observed for various values of the predator harvesting rate ℎ2 . Fig. 3 shows
that by increasing harvesting rate on predator subpopulation, the size of subpopulation of susceptible prey and predator decreases
at long time and convergence of solution occurs in slower rate. But in case of subpopulation of infected prey increases at long
time as predator harvesting increases and convergence of solution occurs in slower rate. As switching of predator from infected
prey population to susceptible prey population is considered in this ecological model, therefore the increment of harvesting rate of
predator may increase the infected prey population with longer time interval (see Table 2).

4.2. Influence of susceptible prey refuge (𝑚)

In this subsection, we shall observe the influence of susceptible prey refuge on each population when the interior equilibrium
point exists and stable. In this eco-epidemiological model the refuge of susceptible prey population also plays an important role for
the dynamics of the system. Fig. 4 performs the effect of refuge on different sub-population dynamics. It is identified that due to
switching of predator from infected prey population to susceptible prey, as prey refuge increases the predator population height

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

Table 3
Effect of refugia of susceptible prey population (𝑚) on sub-populations.
Sl No. 𝑚 𝑠(𝑡) 𝑖(𝑡) 𝑦(𝑡)
1 0.80 0.05486 0.03905 0.095292
2 0.84 0.05693 0.0399 0.09901
3 0.88 0.05901 0.04086 0.1024
4 0.92 0.06123 0.04106 0.1059

Fig. 4. Effect of refuge of susceptible prey (𝑚) on subpopulation dynamics.

Fig. 5. Effect of refuge 𝑚 on phase portrait.

Fig. 6. Stable behaviour and phase portrait of the equilibrium point 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ).

increases and it converges faster with larger time. As switching is from infected to susceptible prey population, the effect of refuge
on infected prey is not remarkably feasible (see Fig. 5 and Table 3).
Fig. 6 shows stable behaviour and corresponding phase portrait about the coexistent point (0.03082, 0.04572, 0.1046) for the value
of refuge (𝑚 = 0.9) keeping other parameters as before to validate Theorem 3.1.4. Fig. 7 shows that if refuge is reduced (𝑚 = 0.4)
then the system becomes unstable.

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

Fig. 7. Stable behaviour and phase portrait of the equilibrium point 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ).

Fig. 8. Bifurcation diagram for parameter 𝑚 along 𝑥 -axis.

Then it follows from Theorem 3.4.1 that the system undergoes a Hopf bifurcation taking 𝑚 as a bifurcation parameter. If we
choose 𝑚 = 𝑚∗ = 0.7733 it is easy to see that system (2) undergoes a Hopf bifurcation of periodic solution occurs at 𝑚 = 𝑚∗ = 0.7733.
When 𝑚 = 0.4; the positive equilibrium point is unstable (see Fig. 7), and when 𝑚 = 0.9; the positive equilibrium point is stable (see
Fig. 6). To demonstrate this dynamical behaviours of system (2) with respect to 𝑚, bifurcation diagram is plotted in Fig. 8.

4.3. Influence of predation rate on susceptible prey population (𝑐1 )

In this subsection, the influence of predation rate on susceptible prey population over the subpopulation has been observed
when the coexistence point exists and stable. Fig. 9 shows stable behaviour and corresponding phase portrait for low predation rate
(𝑐1 = 0.7) on susceptible prey population keeping other parameters as before to validate Theorem 3.1.4.
A stability study around the coexistence state, however, revealed that unstable behaviour around this coexistence state may
occur when there is more predation on susceptible prey (𝑐1 = 2.3) and it is numerically simulated in Fig. 10.
It is observed from Figs. 9 and 10 that if the predation on susceptible prey population is low then the stable behaviour is
observed around the coexistence state and as the predation increases the stable behaviour becomes unstable. Hence it follows from
Theorem 3.4.1 that the system undergoes a Hopf bifurcation taking 𝑐1 as a bifurcation parameter. If we choose 𝑐1 = 𝑐1∗ = 0.8136
it is easy to see that system (2) undergoes a Hopf bifurcation of periodic solution occurs at 𝑐1 = 𝑐1∗ = 0.8136. To demonstrate this
dynamical behaviours of system (2) with respect to 𝑐1 , we have plotted the bifurcation diagram in Fig. 11.

5. Discussions

Switching is a well-known predatorial characteristics which is basically a consumption planning of predator and it is frequency-
dependent, i.e., the predator chooses to consume that prey which presents in the system with sufficient amount. When the predator
has a choice between two or more prey species then only prey switching can be applied in the system. In this manuscript we have

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

Fig. 9. Numerical simulation of the switching model around 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ) with low predation rates showing stable behaviour.

Fig. 10. Numerical simulation of the switching model around 𝐸 ∗ (𝑠∗ , 𝑖∗ , 𝑦∗ ) with high predation rates showing unstable behaviour.

Fig. 11. Bifurcation diagram for parameter 𝑚 along 𝑥 -axis.

established modelling study to observe how this prey switching behaviour controls the growth of the predator population and also
the effect of other controlling parameters like harvesting, refuge etc. on the system.
Here, two prey-one predator system has been considered where the predator population chooses the prey population for
consumption according to their abundance. Susceptible prey population here grow with logistic law and the growth of the infected
prey population depends on the infection rate on the susceptible prey. The predator is considered here as a specialist one as the

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A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

growth rate of predator depends only on the susceptible and infected prey populations and initially predator consumes infected prey
population as they are weak and easy to catch. But as the susceptible prey population becomes abundant in the system, predators
switch from infected to susceptible prey population. The proposed model is biologically well-behaved as the system variables is
positive and bounded for all time. The extinction criterion shows that if the overall growth rate of predator fails to exceed the
mortality and harvesting rate, then with time, the predator will go for extinction from the system. Though the model admits four
steady states, we have concerted on two steady states which has eco-epidemiological importance—infection free boundary state and
the interior state of coexistence.
Stability analysis shows that planar equilibrium point and also coexistence equilibrium points are asymptotically stable under
some parametric restriction. Since stability around infection-free equilibrium implies extinction of infected prey, this study indicates
that controlled harvesting of predator population is able to control prey infection. The infected prey free equilibrium changes from
unstable to stable through saddle–node bifurcation when mortality of infected prey crosses the bifurcation threshold. Global study
on this boundary equilibrium is performed using LaSalle’s theorem and it is observed that this infected prey free equilibrium will
be a global attractor. Further, the consumption rate of predator for susceptible prey species (𝑐1 ) also plays an important role. It
is observed in the numerical simulation that, 𝑐1 has a stabilizing as well as destabilizing effect; an increasing value of 𝑐1 can turn
a stable system into an oscillating system through Hopf bifurcation. Moreover, stable behaviour is also observed in the system in
certain range of refuge of susceptible prey (𝑚) but decrement of this parameter can lead to a system with oscillation. Hence the
system can exhibit Hopf bifurcation by regulating the refuge of the susceptible prey population. It is also observed that due to the
consideration of switching of prey in the system the refuge of susceptible population could not affect much the subpopulation of
infected prey in long run of time. Constant harvesting rates of prey and predator have also effects on the subpopulation growth with
long time. Lastly, we can conclude that our model with prey switching behaviour, prey refuge and harvesting of prey and predator
gives rise to rich dynamics which is very much relevant in our eco-epidemiological system.
Here, we have not assumed the effect of time delay which is biologically more realistic and relevant. Therefore, this assumption
can be modified in future work.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared
to influence the work reported in this paper.

Acknowledgments

The authors are grateful to the reviewers for their valuable suggestions, which have improved the scientific content andpresen-
tation of the work.

References

[1] Hadeler KP, Freedman HI. Predator–prey populations with parasite infection. J Math Biol 1989;27:609–31.
[2] Venturino E. Epidemics in predator–prey models: Diseases in the prey. IMA J Math Appl Med Biol 2002;19(3):185–205.
[3] Arino O, D. Axelrod, M. Kimmel, M. Langlais, editors. Mathematical Population Dynamics: Analysis of Heterogeneity, Vol. 1, Theory of Epidemics. Winnipeg,
Canada: Wuerz Publishing; 1995, p. 381–93.
[4] Xiao Y, Chen L. Modeling and analysis of a predator–prey model with disease in the prey. Math Biosci 2001;171:59–82.
[5] Hethcote HW, Wang W, Han L, Ma Z. A predator–prey model with infected prey. Theor Popul Biol 2004;66:259–68.
[6] Hall SR, Duffy MA, Caceres CE. Selective predation and productivity jointly drive complex behavior in host-parasite systems. Amer Nat 2005;165(1):70–81.
[7] Mukhopadhyay B, Bhattacharyya R. Dynamics of a delayed epidemiological model with nonlinear incidence: The role of infected incidence fraction. J Biol
Syst 2005;13(4):341–61.
[8] Fenton A, Rands SA. The impact of parasite manipulation and predator foraging behavior on predator–prey communities. Ecology 2006;87(11):2832–41.
[9] Bairagi N, Roy PK, Chattopadhyay J. Role of infection on the stability of a predator–prey system with several functional responses—A comparative study.
J Theoret Biol 2007;248:10–25.
[10] Mena-Lorca J, Hethcote HW. Dynamic models of infectious diseases as regulators of population sizes. J Math Biol 1992;30:693–716.
[11] Haque M, Chattopadhyay J. Role of transmissible disease in an infected prey-dependent predator–prey system. Math Comput Model Dyn Syst
2007;13:163–78.
[12] Ashok Mondal, Pal AK, Samanta GP. On the dynamics of evolutionary Leslie–Gower predator–prey eco-epidemiological model with disease in predator.
Ecol Genetics Geonomics 2019;(10). http://dx.doi.org/10.1016/j.egg.2018.11.002.
[13] Ashok Mondal, Pal AK, Samanta GP. Analysis of a delayed eco-epidemiological pest plant model with infected pest. Biophys Rev Lett 2019;14(3):141–70.
http://dx.doi.org/10.1142/S1793048019500061.
[14] Chaudhuri KS. A bio-economic model of harvesting a multispecies fishery. Ecol Model 1986;32:267–79.
[15] Chaudhuri KS, Saha Roy S. On the combined harvesting of a prey–predator system. J Biol Syst 1996;4(3):373–89.
[16] Goh BS, Leitmann G, Vincent TL. Optimal control of a prey–predator system. Math Biosci 1974;19:263–86.
[17] Ianelli J, Lamberson RH. History and future of models in fisheries science. Nat Resour Model 2003;16(4):1–5.
[18] Martin A, Ruan S. Predator–prey models with delay and prey harvesting. J Math Biol 2001;43:247–67.
[19] Mesterton-Gibbons M. On the optimal policy for combined harvesting of predator and prey. Nat Resour Model 1988;3:63–89.
[20] Mesterton-Gibbons M. A technique for finding optimal two-species harvesting policies. Nat Resour Model 1996;92:235–44.
[21] Xiao D, Jennings LS. Bifurcations of a ratio-dependent predator–prey system with constant rate harvesting. SIAM J Appl Math 2005;65(3):737–53.
[22] Holling CS. Principles of insect predation. Ann Rev Entomol 1961;6:163–82.
[23] Ma RM. In Some Mathematical Problems in Biology, Vol. 4. Providence, R.1: Am. Math. Sot; 1974.
[24] Murdoch WW, Oaten A. Functional response and stability in predator–prey systems A. Ecol Res 1975;9(7).
[25] Roughgarden J, Feldman M. Species packing and predation pressure Ecology 1975;56:489.

14
A.K. Pal, A. Bhattacharyya and A. Mondal Results in Control and Optimization 7 (2022) 100099

[26] Steele JH. Structure of Marine Ecosystems. Harvard University Press; 1974.
[27] Tansky M. Switching effect in prey-predator system. J Theoret Biol 1978;70(3):263–71.
[28] Mukhopadhyay B, Bhattacharyya R. Role of predator switching in an eco-epidemiological model with disease in the prey. Ecol. Model 2009;220:931–9.
[29] May RM. Some Mathematical Problems in Biology, Vol. 4. Providence, RI: American Mathematical Society; 1974.
[30] Murdoch WW. Switching in general predators: Experiments on predator specificity and stability of prey populations. Ecol Mong 1969;39(1969):355–64.
[31] Khan QAJ, Balakrishnan E, Wake GC. Analysis of a predator–prey system with predator switching. Bull Math Biol 2004;66:109–23.
[32] Bhattacharyya R, Mukhopadhyay B. Spatial dynamics of nonlinear prey–predator models with prey migration and predator switching. Ecol Complex
2006;3:160–9.
[33] Mukhopadhyay B, Bhattacharyya R. Bifurcation analysis of an ecological food-chain model with switching predator. Appl Math Comput 2008;201:260–71.
[34] Bhattacharyya R, Mukhopadhyay B. On an eco-epidemiological model with prey harvesting and predator switching: Local and global perspectives. Nonlinear
Anal RWA 2010;11:3824–33.
[35] Saha Sangeeta, Samanta Guruprasad. Modelling of a two prey and one predator system with switching effect. Comput Math Biophys 2021;9:90–113.
[36] Brauer F, Soudack AC. Stability regions and transition phenomena for harvested predator–prey systems. J Math Biol 1979;7:319–37.
[37] Brauer F, Soudack AC. Stability regions in predator–prey systems with constant rate prey harvesting. J Math Biol 1979;8(1979):55–71.
[38] Leard B, Lewis C, Rebaza J. Dynamics of ratio-dependent predator–prey models with non-constant harvesting. Disc Cont Dyn Syst S 2008;1(2):303–15.
[39] Yunfei L, Yongzhena P, Shujing G, Changguo L. Harvesting of a phytoplankton–zooplankton model. Nonlinear Anal. Real World Appl 2010;11:3608–19.
[40] Zhang R, Sun J, Yang H. Analysis of a prey–predator fishery model with prey reserve. Appl Math Sci 2007;1:2481–92.
[41] Lenzini P, Rebaza J. Non-constant predator harvesting on ratio-dependent predator–prey models. Appl Math Sci 2010;4(16):791–803.
[42] Pal AK, Samanta GP. Stability analysis of an eco-epidemiological model incorporating a prey refuge. Nonlinear Anal Model Control 2010;15(4):473–91.
[43] Pal AK, Samanta GP. A ratio-dependent eco-epidemiological model incorporating a prey refuge. Univ J Appl Math 2013;1(2):86–100. http://dx.doi.org/
10.13189/ujam.2013.010208.
[44] Chattopadhyay J, Bairagi N. Pelicans at risk in Salton Sea an eco-epidemiological model. Ecol Model 2001;136:103–12. http://dx.doi.org/10.1016/S0304-
3800(00)00350-1.
[45] Sarkar R, Chattopadhyay J, Bairagi N. Effects of environmental fluctuation on an eco-epidemiological model of the Salton Sea. Environmetrics
2001;12(3):289–300.
[46] Greenhalgh D, Haque MA. Predator–prey model with disease in the prey species only. Math Methods Appl Sci 2007;30:911–29. http://dx.doi.org/10.1002/
mma.815.
[47] Chattopadhyay J, Bairagi N. Pelicans at risk in Salton sea—An eco-epidemiological study. Ecol. Model 2001;136:103–12.
[48] Hale JK. Ordinary Differential Equations,. New York: Wiley-Interscience,; 1969.
[49] Murray JG. Mathematical Biology. Berlin: Springer-Verleg; 1989.

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