Figures
Abstract
In this paper, a three dimensional discrete eco-epidemiological model with Holling type-III functional response is proposed. Boundedness of the solutions of the system is analyzed. Existence condition and stability of all fixed points are discussed for the proposed model. Furthermore, we obtained the transcritical bifurcation surfaces of the system by bifurcation theory. Based on the explicit criteria for the Neimark Sacker bifurcation and flip bifurcation, we obtained that the system undergoes these two types of bifurcations at the positive fixed point. Then we apply a hybrid control strategy that based on both parameter perturbation and a state feedback strategy to control the Neimark-Sacker bifurcation. Finally, some numerical simulations are carried out to support the analytical results.
Citation: Fei L, Lv H, Wang H (2024) Bifurcation and hybrid control of a discrete eco-epidemiological model with Holling type-III. PLoS ONE 19(7): e0304171. https://doi.org/10.1371/journal.pone.0304171
Editor: Fausto Cavalli, University of Milano–Bicocca: Universita degli Studi di Milano-Bicocca, ITALY
Received: December 18, 2023; Accepted: May 8, 2024; Published: July 18, 2024
Copyright: © 2024 Fei et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: All relevant data are within the manuscript and its Supporting information files.
Funding: Supported by Science and technology project of Jiangxi Provincial Education Department (Program No. GJJ211926), the Jiangxi Provincial Natural Science Foundation (Program No. 20212BAB201020,No.20232BAB201002.), the National Natural Science Foundation of China (Program No. 12161058,No.12361025.).
Competing interests: The authors have declared that no competing interests exist.
Introduction
Eco-epidemiology is considered to be a relatively new branch of mathematical biology that studies both ecological and epidemiological issues simultaneously. In 1986, Anderson and May [1] firstly considered disease factor in the predator-prey system. They coupled the epidemiological model developed by Kermack and Mckendrick [2] to a Lotka-Volterra predator-prey model [3, 4]. Chattopadhyay and Arino [5] coined the term ‘eco-epidemiology’ [6, 7], and proposed a predator-prey epidemiological model with disease spreading in prey, and one of its simplified models takes the form as follows
(1)
where S, I, Y represent the populations of susceptible prey species, infected prey species and predator species, respectively. In 2001, Chattopadhyay et al [8] studied the practical problem of Pelicans at risk in the Salton Sea based on this model.
The Salton Sea, the largest inland water body in California, USA, is a eutrophic salty lake. In the summer, the weather reaches 128 degrees Fahrenheit and the water evaporates very quickly [9]. This process increases the salinity of the Salton Sea and reduces oxygen levels, as saltwater is more difficult to combine with oxygen than freshwater. Four types of fishes are very common in Salton Sea, namely Tilapia, Corvina, Croaker, and Sargo. Among them, Tilapia is the most abundant because of its amazing reproductive rate [10]. The Salton Sea is the main habitat for many migratory birds such as pelicans, but thousands of water birds (most of which are pelicans) and fish have died. The real cause of this is not yet clear, but there is growing evidence pointing to toxic algal blooms. Algal blooms grow and die very quickly, and in doing so, it draws oxygen from seawater. A lack of oxygen in the tissues of infected fish can lead to outbreaks of botulism, and the later stages of the disease cause the infected fish to rise closer to the surface in search of oxygen. As reported by US Geological Survey National Wildlife Health Center, many white pelicans died from botulism type C between 1978 and 2003 [11]. In 1996, over 8500 white Pelicans died due to infection with type C botulism in the Salton Sea. Millions of dead or sick fish can transmit botulism to Pelicans and other migratory birds that feed on fish. As pelicans prey on vulnerable fish, the ingestion of botulinum has lead to the development of avian botulism [12]. In the past, many research has been done considering various aspects of interaction and interrelation of Tilapia fish, botulism type C, and Pelican birds. System (1) and its extensions have been investigated under different conditions and functional response. Such as the eco-epidemiological predator-prey model with diseases in the prey [13–17], with a disease in the predator [18–21], with disease in both populations [22–24], with delay [25, 26] and with Holling type functional response [27–30].
However, these studies mostly focus on continuous time system, and rarely involve discrete time system. It is also important to consider discrete-time models. Firstly, discretization of continuous time model is the basis of obtaining numerical approximate solution [31]. Secondly, due to the fact that statistical data of epidemics are collected in discrete time, it is more convenient and accurate to describe epidemics with a discrete-time model [32, 33]. Thirdly, many species, such as monocarpic plants, and semelparous animals have independent and non-overlapping generations, and their births occur during the regular breeding season. Their interactions are described using difference equations or discrete-time models [34]. Moreover, even a single-species discrete-time model can exhibit bifurcation, chaos, and more complex dynamic behaviors. Recently, discrete-time models have received more and more attention, see [35–40] and the references cited therein. Whereas, these studies mainly focus on two-dimensional discrete-time systems, with relatively few studies on the dynamics of three-dimensional discrete-time systems, and even fewer studies on the dynamics of three-dimensional discrete-time eco-epidemiological systems.
Lately, several works related to discrete-time eco-epidemiological models have appeared in the literature. In [41], the authors considered the discretization system of system (1) with ratio-dependent Michaelis-Menten functional response. Then, in [42], the authors considered a discrete system with saturated incidence rate based on paper [41], and obtained the stability, bifurcation and chaos of the system. In [43], the authors considered the discretization system of system (1) with Holling type-II functional response. But there has been limited study on three-dimensional discrete-time systems with Holling type-III functional response, due to its highly non-linear nature. This motivated us to consider a discrete-time eco-epidemiological model with Holling type-III functional response incorporating disease in prey to study the interaction between Tilapia and the Pelican. In this article, the existence and stability of fixed points, bifurcation analysis and a hybrid control strategy are discussed. Through this article, we make the following assumptions.
- (A1) The disease is spread among the prey population Tilapia only and the disease is not genetically inherited. The infected population does not recover or become immune. The prey is divided into two classes, susceptible x and infective y. The disease incidence rate adopts bilinear incidence rate βxy, and β is the transmission coefficient.
- (A2) In the absence of disease, the prey population Tilapia grows according to the logistic law with intrinsic growth rate r and carrying capacity K. Only susceptible prey is capable of reproducing, the infective preys cannot produce offsprings due to the disease or by predation before having the possibility of reproducing. However, as infected prey still consumes resources, it still contributes to carrying capacity. Thus, the growth rate for the prey is rx(1 − (x + y)/K).
- (A3) The predator population Pelican consumes only the infected Tilapia. This is conform to the fact that the infected individuals are less active and can be more easily captured [8].
- (A4) The predator consumes prey following Holling type-III functional response. In fact, if the predator actively seeks out large concentration of prey the Holling type-III function f(X) = aX2/(m + X2) is more appropriate, where a is the maximum predation rate and m is half saturation constant. Since the slope of this function goes to zero for small values of X(f’(0)=0), it may be suspected that the food chain will be destabilized if prey concentration becomes too small [44]. However, after a certain value of X, the predators increase their feeding rates until some saturation level is reached (f(X) → a when X → ∞). Holling type III functional response is mostly used when the number of predator encounters the prey population with a very lower amount due to unavailability of prey but when the prey becomes available then the response behaves like the Holling II type functional response (f(X) = aX/(m + X)) [45]. Although both Holling II and III functional responses are approaching an asymptote, the former is decelerating and the latter is sigmoid [46]. Holling [46] suggested that the type II responses are characteristic of predators, which have no learning ability or when give only one type of prey for which to search, whereas type III responses are characteristic of vertebrate predators where switching and learning are more common. We show the Holling type-II and III function in Fig 1.
Under the above assumptions, we formulate the following discrete-time eco-epidemiological model
(2)
where xn, yn, zn ≥ 0 represent the densities of susceptible prey population Tilapia, infected prey population Tilapia and their predator population Pelican at time n, respectively. Here parameters r, K, β, m, a, b, c, d are all nonnegative constants and their biological meanings are given Table 1.
The rest of this paper is organized as follows. In Section 2, The boundedness of solutions of system (2) is given. In Section 3, we study the existence and stability of the fixed points. In Section 4, the transcritical bifurcation of boundary fixed points and the flip and Neimark-Sacker bifurcation of positive fixed points are analyzed. In Section 5, we use a hybrid control strategy to control the Neimark-Sacker bifurcation and the flip bifurcation. Finally, numerical simulations and conclusions are given in Section 6.
Boundedness
For system (2) we always assume that all initial values are non-negative and all the parameters are positive. The boundedness of solutions of system (2) is given by the following lemma.
Lemma 1 Let μ = min(c, d), then all the solutions of system (2) will lie in the region
for all initial values x0, y0, z0 ≥ 0 as n → + ∞.
Proof 1 For system (2), we always assume that x0, y0, z0 ≥ 0. Because the environmental carrying capacity of the prey population is K, therefore xn ≤ K.
Let xn + yn + zn = Mn, adding all the equations of system (2), we get
(3)
where μ = min{c, d}.
If there exists l ∈ N such that Ml+1 > Ml, then we get
Hence, we have that Ml ≤ M*, where M* = (r + 1)K/μ. We claim that Mn ≤ M* for all n ≥ l. Otherwise, we assume that there exists a q ∈ N such that Mq > M*, where q ≥ l. Let
be the smallest integer such that
, then
. From inequality (3) we get
, which is a contradiction. Hence the claim is hold.
If Mn+1 ≤ Mn for all n ∈ N. Let , we claim that
. Otherwise, we assume that
. Taking limit of equation
we get
But
for large enough n ∈ N, which is a contradiction. Hence the claim is proved. Thus, all the solutions of system (2) will lie in the region B.
Existence of fixed points and stability
In this section, we give the sufficient and necessary conditions for the existence of fixed points for system (2), and analyze their properties.
Defined R0 = βK/c. Because β is the transmission coefficient, so βK represents the number of newly infected individuals when all the prey populations are susceptible at the beginning of the disease. For c is the death rate of infected prey because of natural death and disease induced mortality, so 1/c is the duration of infection of an infected prey. Therefore, R0 is the disease reproduction number in the prey.
Firstly, on the sufficient and necessary conditions for the existence of the nonnegative fixed points of system (2), we give the the following theorem.
Theorem 1 System (2) has only two fixed points E0(0, 0, 0) and E1(K, 0, 0) if and only if R0 ≤ 1, exactly three fixed points E0(0, 0, 0), E1(K, 0, 0) and if and only if(r, K, β, m, a, b, c, d) ∈ Λ1 ∪ Λ2, where
(5)
exactly four fixed points E0(0, 0, 0), E1(K, 0, 0),
, E3(x*, y*, z*) if and only if (r, K, β, m, a, b, c, d) ∈ Λ3, where
(6)
where Λi’s (i = 1, 2, 3) are defined in (4).
Proof 2 In Ω, the fixed points of system (2) satisfy
(7)
Clearly, (0, 0, 0) and (K, 0, 0) are always the solution of (7). Then we consider other possible solutions.
Since the second equation in (7) implies yn = 0 if xn = 0, the third equation in (7) implies zn = 0 if yn = 0. Therefore, for the boundary equilibrium point, we only need to consider the case of xn ≠ 0, yn ≠ 0, zn = 0. If xn ≠ 0, yn ≠ 0, zn = 0 and R0 ≤ 1, the second equation in (7) holds only if yn = 0. Thus, there are only two solutions (0, 0, 0) and (K, 0, 0) of (7) when R0 ≤ 1. If xn ≠ 0, yn ≠ 0, zn = 0 and R0 > 1, (7) has a solution , where
are given in (5).
When R0 > 1, because , from the third equation of (7) we can see that when ab ≤ d, the third equation of (7) holds only if zn = 0. When ab > d, if zn ≠ 0, from the third equation of (7), we can get
. From the first equation of (7), we can get
. If
, the second equation of (7) not holds. If
, the second equation of (7) holds only if zn = 0. If zn = 0, then xn = 0, yn = 0 or xn = K, yn = 0 or
,
. Thus, there are only three solutions (0, 0, 0), (K, 0, 0) and
of (7) when (r, K, β, m, a, b, c, d) ∈ Λ1 ∪ Λ2.
When ab > d and , if zn ≠ 0, from the third equation of (7), we can get
. From the first equation of (7), we get
From the second equation of (7), we get
so (7) has a unique positive solution (x*, y*, z*), where x*, y*, z* are given in (6). If zn = 0, then xn = 0, yn = 0 or xn = K, yn = 0 or
,
. Thus, there are exactly four fixed points E0(0, 0, 0), E1(K, 0, 0),
and E3(x*, y*, z*) if and only if (r, K, β, m, a, b, c, d) ∈ Λ4.
For a discrete dynamical system on R3, let the Jacobian matrix of this system at a fixed point (x, y, z) be J(x, y, z). We denote the three eigenvalues of J(x, y, z) by λi (i = 1, 2, 3). We recall some concepts for a discrete dynamical system on R3 [47]. If |λi| < 1 for all eigenvalues, then (x, y, z) is called a sink and is locally asymptotically stable; if |λi| > 1 for some eigenvalues and |λj| < 1 for the others, then (x, y, z) is called a saddle and is unstable; if |λi| > 1 for all eigenvalues, then (x, y, z) is called a source and is unstable; if |λi| = 1 for any eigenvalue, then (x, y, z) is called non-hyperbolic.
Theorem 2 (1) The fixed point E0 is always unstable.
(2) For the fixed point E1, we have the following conclusions.
(a) If R0 < 1 and 0 < r < 2, E1 is locally asymptotically stable.
(b) If R0 > 1 or r > 2, E1 is unstable.
(c) If R0 = 1 or r = 2, E1 is non-hyperbolic.
Proof 3 Because the Jacobian matrix of system (2) at E0 is given by
one of the eigenvalue of matrix J(E0) is λ1 = 1 + r > 1, so the fixed point E0 is always unstable.
The Jacobian matrix of system (2) at E1 is given by
If R0 < 1 and 0 < r < 2, we get |λ1| = |1 − r| < 1, |λ2| = |βK − c + 1| < 1, |λ3| = 1 − d < 1. In this case, E1 is locally asymptotically stable. If R0 > 1 or r > 2, we get |λ1| = |1 − r| > 1 or |λ2| = |βK − c + 1| > 1, |λ3| = 1 − d < 1. Therefore, E1 is unstable in this case. If R0 = 1 or r = 2, we get λ1| = |1 − r| = 1 or |λ2| = |βK − c + 1| = 1, |λ3| = 1 − d < 1. Thus, E1 is non-hyperbolic in this case.
Lemma 2 [48] Let F(λ) = λ2 + Bλ + C, where B and C are constants. Suppose F(1) > 0 and λ1, λ2 are two roots of F(λ) = 0. Then
- (1) |λ1| < 1 and |λ2| < 1 if and only if F(−1) > 0 and C < 1;
- (2) |λ1| < 1 and |λ2| > 1 if and only if F(−1) < 0;
- (3) |λ1| > 1 and |λ2| > 1 if and only if F(−1) > 0 and C > 1;
- (4) λ1 = −1 and |λ2| ≠ 1 if and only if F(−1) = 0 and B ≠ 0, 2;
- (5) λ1 and λ2 are a pair of conjugate complex roots and |λ1| = |λ2| = 1 if and only if |B| < 2 and C = 1.
Next, we consider the fixed point E2. The Jacobian matrix of system (2) at E2 is
The corresponding characteristic equation of J(E2) is
where
Let , for the fixed point E2, we have the following conclusions.
Theorem 3 (1) When ab ≤ d and R0 > 1 or ab > d and , we get
(a) E2 is locally asymptotically stable if and
;
(b) E2 is unstable if or
and
;
(c) E2 is non-hyperbolic if and
or
and
.
(2) When ab > d and , E2 is non-hyperbolic.
(3) When ab > d and , E2 is unstable.
Proof 4 Obviously, f(λ) has one eigenvalue w1. When ab ≤ d and R0 > 1, we have
when ab > d and
, we get
also have
Thus, we get 0 < w1 < 1, when ab ≤ d and R0 > 1 or ab > d and
. Since
, by the Lemma 2 we know that E2 is locally asymptotically stable if
and
. E2 is unstable if
or
and
. E2 is non-hyperbolic if
and
or
and
.
When ab > d and , we get w1 = 1. Thus, E2 is non-hyperbolic.
When ab > d and , we get w1 > 1. Therefore, E2 is unstable.
Lemma 3 (Jury-criterion [49]) For the equation λ3 + a2λ2 + a1λ + a0 = 0, all roots lie within the unit disk if and only if the following conditions
are satisfied, where a0, a1, a2 are real numbers.
In the follows, we use Lemma 3 to analyze the stability of the positive fixed point E3.
Theorem 4 When E3 exists, E3 is locally asymptotically stable if and only if the following inequations hold true
(8)
where
(9) Proof 5 The Jacobian matrix of system (2) at E3 is
The corresponding characteristic equation of J(E3) is
where bi (i = 0, 1, 2) are defined in (9). According to Lemma 3, we get that E3 is locally asymptotically stable if and only if condition (8) is satisfied.
Bifurcations analysis
In this section, we investigate possible bifurcation of system (2).
Transcritical bifurcation
In this subsection, we will give the transcritical bifurcation of system (2).
Theorem 5 In Ω, system (2) has two transcritical bifurcation surfaces
and
for E1 and E2, respectively. That is, transcritical bifurcation happens for E1 when the parameter crosses Ω1 into Λ1 ∪ Λ2 and E2 appears near E1; transcritical bifurcation happens for E2 when the parameter crosses Ω2 into Λ3 and E3 appears near E2.
Proof 6 From Theorem 2, we know that the eigenvalues for E1 are 1 − r, βK − c + 1 and 1 − d. In Ω1, we require r < 2 to ensure |1 − r| < 1. In this case, the unique non-hyperbolic case is exact βK − c + 1 = 1, which corresponds to transcritical bifurcation surface Ω1. For the critical case βK − c = 0, that is R0 = 1, system (2) has only two fixed points E0 and E1. It is not hard to check that
which means that the parameter goes into Λ1 ∪ Λ2 when R0 increases from 1. Thus, the third fixed point E2 appears by Theorem 1, i.e., transcritical bifurcation happens for E1. We observe that E2 is sufficiently close to E1 when 0 < R0 − 1 ≪ 1.
When E2 exists, from Theorem 3, we know that one of the eigenvalues for E1 is w1. If and
, i.e., 2rc/(βK) − 4 < r(βK − c) < rc/(βK), r < 4βK/c, the modulus of the other two eigenvalues with E2 is less than 1. In this case, the unique non-hyperbolic case is exact w1 = 1, which corresponds to transcritical bifurcation surface Ω2. When the parameter crosses Ω2 into Λ3, the forth fixed point E3 appears by Theorem 1, i.e., transcritical bifurcation happens for E2. We observe that E3 is sufficiently close to E2 when
.
Let G(λ) = λ3 + b2λ2 + b1λ + b0 is the characteristic polynomial of J(E3). From Theorem 1, we know that when E3 exists, we have ab − d > 0 and βx* − c > 0. Thus, we can judge that
This indicates that a fold bifurcation not happens for E3 of system (2). Thus, in the following, we will investigate the flip bifurcation and Neimark-Sacker bifurcation for E3 of system (2).
Flip bifurcation
In this subsection, we will discuss parametric conditions under which the unique positive fixed point of system (2) undergoes a flip bifurcations. For this purpose, an explicit criterion for flip bifurcation is implemented without finding the eigenvalues of the system. The criterion is formulated using a set of simple equalities or inequalities that consist of the coefficients of the characteristic equation derived from the Jacobian matrix. Next, let’s introduce this criterion first [50].
Consider an n-dimensional map xn+1 = fμ(xn), where xn+1, xn ∈ Rn and μ ∈ R is a parameter. Assume that f has a fixed point x0 and the characteristic polynomial of an n-dimensional map fμ at x0 takes the form
where σ0 = 1 and σi = σi(μ, v) (i = 1, 2, ⋯, n), μ is the bifurcation parameter, and v is the control parameter or the other to be determined. Consider the sequence of determinants
,
, where
i = 1, ⋯, n.
Lemma 4 [50] Assume that fμ has a fixed point x0. A flip bifurcation takes place at μ = μ0 if and only if the following conditions (H1) Eigenvalue assignment: ,
,
and
for j = n − 2, n − 4, ⋯, 1 (resp. 2), when n is odd (resp. even). (H2) Transversality condition:
are satisfied, where
stands for the derivative of σi(μ) with respect to μ at μ = μ0.
When n = 3, and we choose r as the perturbation parameter, in the following theorem, we give the parametric conditions for the flip bifurcation takes place at r = r0 for E3 of system (2).
Theorem 6 The fixed point E3(x*, y*, z*) of system (2) undergoes a flip bifurcation at r = r0 if the conditions
(10)
are satisfied, where bi (i = 0, 1, 2) are defined in (9),
is derivative of bi(r) with respect to r at r = r0, and r0 is a possible real root of equation 1 − b2(r) + b1(r) − b0(r) = 0.
Proof 7 For n = 3 and r0 is the perturbation parameter. According to the criterion introduced in Lemma 4, if the conditions (H1) and (H2) are satisfied, then a flip bifurcation occurs at r0 for system (2). That is
Then we get the conditions (10).
Neimark-Sacker bifurcation
In this subsection, we discuss parametric conditions under which the unique positive fixed point E3 of system (2) undergoes a Neimark-Sacker bifurcations. For this purpose, an explicit criterion for Neimark-Sacker bifurcation is implemented without finding the eigenvalues of the system. We state the explicit criterion as follow.
Lemma 5 [51] If the following conditions (C1) Eigenvalue assignment: ,
,
,
,
, for i = n − 3, n − 5, ⋯, 1 (or 2), when n is even(or odd, resp.), (C2) Transversality condition:
, (C3) Non-resonance condition cos(2π/l)≠φ or resonance condition cos(2π/l) = φ, where l = 3, 4, 5 ⋯ and
, are satisfied, then Neimark-Sacker bifurcation occurs at μ0 for map fμ.
When n = 3 and r is taken as the bifurcation parameter, we give the parametric conditions for the Neimark-Sacker bifurcation takes place at r = r0 for E3 of system (2) in the following.
Theorem 7 The fixed point E3(x*, y*, z*) of system (2) undergoes a Neimark-Sacker bifurcation at r = r0 if the conditions
(11)
are satisfied, where bi (i = 0, 1, 2) are defined in (9), and r0 is a possible real root of equation 1 − b1(r) + b0(r)(b2(r) − b0(r)) = 0.
Proof 8 For n = 3 and r is the perturbation parameter. According to the criterion introduced in Lemma 5, if the conditions (C1), (C2) and (C3) are satisfied, then Neimark-Sacker bifurcation occurs at r0 for system (2). That is
Then we get the conditions (11).
Bifurcation control
In order to prevent the serious damage or even extinction of the population caused by infectious diseases, a stable positive fixed point may be needed to maintain the sustainable development of the eco-epidemiological system. That is, it is better for the positive fixed point E3 to be an asymptotically stable of system (2) if it exists. Therefore, we would like to take certain control measures to avoid the happening of bifurcations. For this purpose, in this section we provide for system (2) a hybrid control, which is based on feedback control strategy and parameter perturbation (see [52, 53]).
Corresponding to the system (2), we construct a controlled system
(12)
where 0 < θ < 1, and θ is called a control parameter. Obviously, controlled system (12) is exactly (2) if θ = 1. System (12) has same fixed points as (2). The Jacobian matrix for (12) at E3(x*, y*, z*) is
The corresponding characteristic equation of Jcon is
(13)
where
(14)
Then by Lemma 3 we have the following theorem.
Theorem 8 When E3 exists, the unique positive fixed point E3 of system (12) is locally asymptotically stable if and only if
(15)
where ci (i = 0, 1, 2) are defined in (14).
Proof 9 Clearly, we only need to prove that the modulus of all eigenvalue is less than 1 for characteristic equation (13), which is equivalent to
by the conditions given in Lemma 3, then we get the conclusion in this theorem.
Numerical simulations and conclusions
In this section, we give the phase portraits, bifurcation diagrams, and Lyapunov exponents to illustrate our theoretical results numerically. We selected parameters based on the reference [8, 43] that studied the interaction between Pelican and Tilapia in the Salton Sea, and their biological meanings are stated in Table 1.
Firstly, we show that E3 is locally stable when condition (8) is satisfied. Taking (r, K, β, m, a, b, c, d) = (1.8, 40, 0.006, 10, 0.5, 0.7655, 0.0019, 0.01) ∈ Λ3, which satisfy condition (8). We give the phase portraits of system (2) starting from (38, 0.1, 1), (39, 0.2, 2), (40, 0.3, 3), separately, in Fig 2(i). We can see that the trajectories of system (2) approach the fixed point E3(39.4, 0.5, 9.3). In Fig 2(ii), we give the stable region (Green region) of system (2) at E3 for β, a, b ∈ (0, 1) and other parameters are same as Fig 2(i). The red region is the area Λ3 where E3 exists. These are consistent to our Theorem 4.
In Fig 3, we show the phase diagram of system (2) with different β values. Taking (r, K, β, m, a, b, c, d) = (1.8, 20, 0.015, 10, 0.5, 0.8, 0.3, 0.2) ∈ Ω1, we show the orbits starting from (15, 5, 1), (16, 4, 2), (17, 3, 3), separately, in Fig 3(i) and observe that system (2) has fixed point (0, 0, 0) and (K, 0, 0). (0, 0, 0) is always unstable, and (K, 0, 0) is locally asymptotically stable. When we change β from 0.015 to 0.016, we observe that another fixed point appears in Fig 3(ii). That is, transcritical bifurcation happens for E1 when the parameter crosses Ω1 into Λ1 ∪ Λ2. Taking (r, K, β, m, a, b, c, d) = (1.8, 20, 0.0185, 10, 0.5, 0.8, 0.3, 0.2) ∈ Ω2, we show the orbits starting from (15, 5, 1), (16, 4, 2), (17, 3, 3), separately, in Fig 3(iii) and observe that system (2) has three fixed points. When we change β from 0.0185 to 0.02, we observe that another fixed point appears in Fig 3(iv). That is, transcritical bifurcation happens for E2 when the parameter crosses Ω2 into Λ3. These are consistent to our Theorem 5.
In Fig 4, we show the twice transcritical bifurcations when changing β in [0.012, 0.03] and taking (r, K, m, a, b, c, d) = (1.8, 20, 10, 0.5, 0.8, 0.3, 0.2) with initial value (x0, y0, z0) = (16, 4, 1). In fact, bifurcation diagram shows the stable fixed point as β varies. In Fig 4, we iterate system (2) for 10000 times and observe the changes of the stable fixed point. In Fig 4(i), we observe that when β ≤ 0.015, the abscissa of the stable fixed point is 20, i.e. the value of K, which means that stable fixed point is E1 = (K, 0, 0) in this case. When β increases from 0.015, we can see that xn starts to decrease. This is because the abscissa of fixed point E2 is , therefore, the x decreases as β increases. This means that another stable fixed point E2 emerges and the first transcritical bifurcation happens at β = 0.015. After β = 0.0185, the slope of the curve changes. This means the stable fixed point E3 emerges and the second transcritical bifurcation happens at β = 0.0185. The corresponding bifurcation diagrams for (β, yn) and (β, zn) are given in Fig 4(ii) and 4(iii) separately.
In Fig 5, we show the flip bifurcation of system (2) by choosing r as the perturbation parameter. This diagram, which was obtained by changing r in [2.5, 3] and taking (K, β, m, a, b, c, d) = (20, 0.08, 10, 0.8, 0.7655, 0.0019, 0.1) with initial value (x0, y0, z0) = (17.76, 1.39, 15.17). When r = 2.66133, we get Pr(−1) = 1 − b2 + b1 − b0 = 0, the characteristic equation of J(E3) is
(16)
Eq (16) has a root λ1 = −1 and the other two roots are λ2 = 0.73340 and λ3 = −0.05275. So that we have |λ2,3| < 1. Further, we can verify that
Thus the conditions in Theorem 10 are satisfied. We get system (2) undergoes a flip bifurcation at E3. In Fig 5(i)–5(iii), we give the flip bifurcation diagrams for system (2) in the (r, xn)-plane, (r, yn)-plane and (r, zn)-plane. The Maximum Lyapunov exponents corresponding to Fig 5(i)–5(iii) are calculated and plotted in Fig 5(iv), which are consistent with the bifurcation diagram. For example, when r ∈ (2.5, 2.66133), the Maximum Lyapunov exponents are negative, which denote the system is stable. At r = 2.66133, the Maximum Lyapunov exponent is 0, which is corresponding to the flip bifurcation point. After that, we observe that some Lyapunov exponents are bigger than 0, some are smaller than 0, confirming the existence of the chaotic regions in the parametric space. In general the positive Lyapunov exponent is considered to be one of the characteristics implying the existence of chaos [54, 55].
In Fig 6, we show the Neimark-Sacker bifurcation of system (2) by choosing r as the perturbation parameter. By changing r in [1.7, 2.1], taking (K, β, m, a, b, c, d) = (40, 0.06, 10, 0.5, 0.7655, 0.0019, 0.01) with initial value (x0, y0, z0) = (38.788, 0.518, 92.1998). When r = 1.791065, we get , the characteristic equation of J(E3) is
which has a root λ1 = 0.97994 and a pair of conjugate complex roots λ2,3 = −0.96030 ± 0.27897i, and |λ2,3| = 1. Further, we get that
and
From cos(2π/l) = −0.96030, we can obtain that l = 2.1978. So the non-resonance condition is satisfied. In Fig 6(i) and 6(ii), we observe that when r ≤ 1.791065, E3(x*, y*, z*) is stable. In Fig 6(iii), we can see when r > 1.791065, E3(x*, y*, z*) becomes unstable, and an attractive closed invariant curve appears. In this case, we get system (2) undergoes a Neimark-Sacker bifurcation at E3. This is consistent with Theorem 11.
In Fig 7, we give the Neimark-Sacker bifurcation diagrams for system (2) in the (r, xn)-plane, (r, yn)-plane and (r, zn)-plane. The Maximum Lyapunov exponents corresponding to Fig 7(i)–7(iii) are calculated and plotted in Fig 7(iv), which are consistent with the bifurcation diagram. When r ∈ (1.7, 1.791065), the Maximum Lyapunov exponents are negative, which denote the system is stable. At r = 1.791065, the Maximum Lyapunov exponent is 0, which is corresponding to the Neimark-Sacker bifurcation point. After that, we observe that some Lyapunov exponents are positive and some are negative, confirming the existence of the chaotic regions in the parametric space.
In Fig 8, we show the hybrid control method is effective in controlling Neimark-Sacker bifurcation for system (2). We take (r, K, β, m, a, b, c, d,) = (1.791065, 40, 0.06, 10, 0.5, 0.7655, 0.0019, 0.01) with an initial value of (38.788, 0.518, 92.1998). From Fig 6, we know that in this case, system (2) undergoes a Neimark-Sacker bifurcation at E3. We give the corresponding time-series graph in Fig 8(i)–8(iii) for system (2). In this case, from the condition (15), we get
According to Theorem 8, we know that when condition (15) is satisfied, we can control E3 to be a stable fixed point. After a simple calculation, we obtained that E3 is stable when 0.0205565 < θ < 1. Thus, we take θ = 0.99999, and give the time-series graph in Fig 8(iv)–8(vi) for system (12). We observe that the Neimark-Sacker bifurcation of system (2) is controlled effectively. We give the stable region of system (12) for β, θ ∈ (0, 1) in Fig 9.
In this paper, we have constructed the mathematical model to describe an interaction between Tilapia as a prey, Pelicans as predator, and botulism type C as the cause of disease in Tilapia. We discuss the dynamical behaviors of the system (2), establish that the system solution is bounded and get that the system has at most four fixed point depending on values of the system parameters. We obtained a threshold value R0 = βK/c such that R0 ≤ 1 leads to the complete disappearance of infected prey from the ecosystem and the eradication of the disease from the prey population. If the death rate of infected prey c is high and transmission rate from uninfected prey to infected prey β is low, then the chance of disease eradication from the ecosystem will be high. This means that we can control the spread of the disease by killing botulism type C with drugs. The local asymptotic stability of different fixed points are discussed here. The fixed point E0(0, 0, 0) is always unstable, which implies that the system can never be collapsed for any values of the system parameters. The fixed point E1(K, 0, 0) and are locally asymptotically stable under some parametric restrictions. There exists a set of values of the system parameters for which the positive fixed point E3(x*, y*, z*) is locally asymptotically stable, i.e. both the populations can survive with positive density level. We notice that the stability of the fixed points is greatly influenced by the model parameters. We show that under certain parametric conditions system (2) undergoes transcritical bifurcations at boundary fixed points E1 and E2, using bifurcation theory. Further, by the explicit criteria for a flip bifurcation and a Neimark-Sacker bifurcation, we prove that the system undergoes both flip and Neimark-Sacker bifurcations at the fixed point E3 under some parametric conditions. From the ecological point of view, flip bifurcation is associated with the emergence of chaotic behavior, demonstrating the evolution of the prey and predator populations. An invariant curve bifurcates from the fixed point, meaning that predator and prey can coexist in a stable way and reproduce their densities. The dynamics on the invariant curve may be either periodic or quasi-periodic [40]. The Maximum Lyapunov exponents are numerically computed to confirm further the complexity of the dynamical behavior. Finally, we use the hybrid method to control the Neimark-Sacker bifurcation at fixed point E3. The result indicate that the nonlinear dynamics of such eco-epidemiology model not only depend on more bifurcation parameters but also are very sensitive to parameter perturbations, which are important for the control of biological species or infectious diseases. Finally, numerical simulations are carried out to confirm the validity of the theories and the effectiveness of the control method.
References
- 1. Anderson R M, May R M. The invasion, persistence and spread of infectious diseases within animal and plant communities. Philos Trans R Soc Lond. Ser B. 1986 May;(314), 533–570. pmid:2880354
- 2. Kermack W O, McKendrick A G. Contributions to the mathematical theory of epidemics–I. 1927. Proc Soc Lond Ser. 1991 Jan;(115), 700–721.
- 3.
Lotka A J. Elements of physical biology. Williams & Wilkins, Baltimore. 1925.
- 4.
Volterra V. Lecons sur la theorie mathematique de la lutte pour la vie Gauthier-Villars, Paris. Gauthier-Villars, Paris, 1931.
- 5. Chattopadhyay J, Arino O. A predator-prey model with disease in the prey. Nonlinear Anal.1999;(36), 747–766.
- 6. Alzahrani A K, Alshomrani A S, Pal N, et al. Study of an eco-epidemiological model with Z-type control. Chaos Soli Frac. 2018 Aug;(113), 197–208.
- 7. Saifuddin M, Biswas S, Samanta S, et al. Complex dynamics of an eco-epidemiological model with different competition coefficients and weak Allee in the predator. Chaos, Soli Frac. 2016 Oct;(91), 270–285.
- 8. Chattopadhyay J, Bairagi N. Pelicans at risk in Salton sea-an eco-epidemiological model. Ecol Mode. 2001 Jan;(136), 103–112.
- 9. Greenhalgh D, Khan Q J A, Al-Kharousi F A. Eco-epidemiological model with fatal disease in the prey. Nonl Anal: Real World Appl. 2020 Jun;(53), 103072.
- 10. Mondal S, Samanta G P. Pelican–Tilapia interaction in Salton sea: an eco-epidemiological model with strong Allee effect and additional food. Mode Earth Syst Envi. 2022;(8), 799–822.
- 11. Rocke T, Converse K, Meteyer C, et al. The impact of disease in the American white pelican in North America. Waterbirds. 2005 Dec;(28), 87–94.
- 12. Kundu K, Chattopadhyay J. A ratio-dependent eco-epidemiological model of the Salton Sea. Math meth appl sci. 2006 Sep;(29), 191–207.
- 13. Arora C, Kumar V. Dynamics of predator–prey system with migrating species and disease in prey population. Diff Equa Dyna Sys,. 2021 Jun;(29), 87–112.
- 14. Jang S R J, Wei H C. Deterministic predator-prey models with disease in the prey population, J Biol Syst. 2020;(28), 751–784.
- 15. Saha S, Maiti A, Samanta G P. A Michaelis-Menten predator-prey model with strong Allee effect and disease in prey incorporating prey refuge. Inter Bifu Chaos. 2018;(28), 1850073.
- 16. Saha S, Samanta G P. A prey-predator system with disease in prey and cooperative hunting strategy in predator, J. Physics A: Math Theo. 2020 Nov;(53), 485601.
- 17. Xiao Y N, Chen L S. Modeling and analysis of a predator-prey model with disease in the prey Math bios. 2001 May;(171), 59–82. pmid:11325384
- 18. Ejaz A, Nawaz Y, Arif M S, et al. Stability analysis of predator-prey system with consuming resource and disease in predator species. Comp Mode Engi Sci. 2022 Jan;(132), 489–506.
- 19. Mondal A, Pal A K, Samanta G P. On the dynamics of evolutionary Leslie-Gower predator-prey eco-epidemiological model with disease in predator. Ecol Gene Geno. 2019 Feb;(10), 100034.
- 20. Xu R, Zhang S. Modelling and analysis of a delayed predator-prey model with disease in the predator. Appl Math Comp. 2013 Nov;(224), 372–386.
- 21. Zhang S, Yuan S, Zhang T. Dynamic analysis of a stochastic eco-epidemiological model with disease in predators. Stud Appl Math. 2022 Feb;(149), 5–42.
- 22. Bera S P, Maiti A, Samanta G P. A prey-predator model with infection in both prey and predator. Filomat. 2015 Jan;(29), 1753–1767.
- 23. George R, Rezapour S, Alharthi M S, et al. On efficient numerical approaches for the study of the interactive dynamics of fractional eco-epidemiological models. Mathematics. 2023 Apr;(8), 13503–13524.
- 24. Kant S, Kumar V. Stability analysis of predator–prey system with migrating prey and disease infection in both species. Appl Math Mode. 2017 Feb;(42), 509–539.
- 25. Dutta P, Sahoo D, Mondal S, et al. Dynamical complexity of a delay-induced eco-epidemic model with Beddington–DeAngelis incidence rate. Math Comp Simu. 2022 Jul;(197), 45–90.
- 26. Thakur N K, Srivastava S C, Ojha A. A Comprehensive Study of Spatial Spread and multiple Time Delay in an Eco-Epidemiological Model With Infected Prey. Inte J Mode Simu Scie Comp. 2024.
- 27. Bai H F, Xu R. Global stability of a delayed eco-epidemiological model with Holling type-III functional response. Math Meth Appl Sci. 2014 Aug; (37), 2120–2134.
- 28.
Samanta G. Deterministic, Stochastic and Thermodynamic Modelling of Some Interacting Species[M]. Berlin: Springer, 2021.
- 29. Zhang J F, Li W T, Yan X P. Hopf bifurcation and stability of periodic solutions in a delayed eco-epidemiological system. Appl math comp. 2008 May;(198), 865–876.
- 30. Saha S, Samanta G. Modeling of insect-pathogen dynamics with biological control. Math Biol Bioi. 2020 Mar;(15), 268–294.
- 31. de Jesus L F, Silva C M, Vilarinho H. Dynamics of a discrete eco-epidemiological model with disease in the prey. J Diff Equa Appl. 2021 Jan;(27), 132–155.
- 32. Biswas M, Bairagi N. Discretization of an eco-epidemiological model and its dynamic consistency. J Diff Equa Appl. 2017 Mar;(23), 860–877.
- 33. Hu Z,Teng Z D,Jiang H. Stability analysis in a class of discrete SIRS epidemic models, Nonl Anal: Real World Appl. 2012 Oct;(13), 2017–2033.
- 34. Santra P K, Mahapatra G S, Phaijoo G R. Bifurcation and chaos of a discrete predator-prey model with Crowley-Martin functional response incorporating proportional prey refuge. Math Probl Eng. 2020 Jan; (2020), 1–18.
- 35. Banerjee R, Das P, Mukherjee D. Stability and permanence of a discrete-time two-prey one-predator system with Holling type-III functional response. Chaos Soli Frac. 2018 Dec;(117), 240–248.
- 36. Fei L, Chen X. Bifurcation and control of a predator-prey system with unfixed functional responses. Disc Cont Dyna Syst. 2022 Oct;(27), 5701–5721.
- 37. He Z, Li B O. Complex dynamic behavior of a discrete-time predator-prey system of Holling-III type. Adva Diff Equa. 2014 Jul; (2014), 1–13.
- 38. Islk S, Kangalgil F. Dynamical analysis and chaos control of a fractional-order Leslie-type predator-prey model with Caputo derivative. Inter Biom. 2024;(17).
- 39. Singh A, Sharma V S. Bifurcations and chaos control in a discrete-time prey–predator model with Holling type-II functional response and prey refuge. J Comp Appl Math. 2023 Jan;(418), 114666.
- 40. Uddin M J, Rana S M S, Isik S, et al. On the qualitative study of a discrete fractional order prey-predator model with the effects of harvesting on predator population. Chaos, Soli Frac. 2023 Otc;(175), 113932.
- 41. Hu Z, Teng Z, Jia C, et al. Complex dynamical behaviors in a discrete eco-epidemiological model with disease in prey. Adva Diff Equa. 2014 Oct; (2014), 1–19.
- 42. Hu Z, Teng Z, Zhang T, et al. Globally asymptotically stable analysis in a discrete time eco-epidemiological system. Chaos, Soli Frac. 2017 Jun; (2017), 20–31.
- 43. Din Q, Ishaque W. Bifurcation analysis and chaos control in discrete-time eco-epidemiological models of pelicans at risk in the Salton Sea. Inte J Dyna Cont. 2020 Jan;(8), 132–148.
- 44. Sahoo B, Poria S. Diseased prey predator model with general Holling type interactions. Appl Math comp. 2014 Jan;(226), 83–100. pmid:32287497
- 45. Majumdar P, Debnath S, Sarkar S, Ghosh U. The complex dynamical behavior of a prey-predator model with Holling type-III functional response and non-linear predator harvesting. Inte. J Mode. Simu. 2022 Apr; (42), 287–304.
- 46. Holling C S. The functional response of predators to prey density and its role in mimicry and population regulation. Memo Ento Soci Cana. 1965;(45), 3–60.
- 47.
Guckenheimer J, Holmes P. Nonlinear oscillations, dynamical systems, and bifurcations of vector fields. Springer Science & Business Media, New York, 1983.
- 48. Liu X, Xiao D. Complex dynamic behaviors of a discrete-time predator–prey system[J]. Chaos Soli Fract. 2007 Apr;(32), 80–94.
- 49. Li Q,Xiao Y N. Bifurcation analyses and hormetic effects of a discrete-time tumor model, Appl Math Comp. 2019 Dec;(363), 124618.
- 50. Wen G L, Chen S J, Jin Q T. A new criterion of period-doubling bifurcation in maps and its application to an inertial impact shaker. J Soun Vibr. 2008 Mar;(311), 212–223.
- 51. Wen G. Criterion to identify Hopf bifurcations in maps of arbitrary dimension. Phys Rev E. 2005 Aug;(72), 026201. pmid:16196678
- 52. Luo X S, Chen G, Wang B H, et al. Hybrid control of period-doubling bifurcation and chaos in discrete nonlinear dynamical systems. Chaos Soli Fract. 2003 Nov;(18), 775–783.
- 53. Yuan L G, Yang Q G. Bifurcation, invariant curve and hybrid control in a discrete-time predator–prey system. Appl Math Mode. 2015 Apr;(39), 2345–2362.
- 54. Alligood K T, Sauer T D, Yorke J A, et al. Chaos: an introduction to dynamical systems. SIAM Review. 1998, 40(3): 732–732.
- 55.
Ott E. Chaos in dynamical systems. 2nd edn. Cambridge University Press, Cambridge, 2002.