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Research article

Dynamic behavior on a multi-time scale eco-epidemic model with stochastic disturbances

  • Received: 30 December 2024 Revised: 20 February 2025 Accepted: 04 March 2025 Published: 21 March 2025
  • In this paper, a multi-time scale stochastic eco-epidemic model where the prey population was infected with disease was proposed. The stochastic factors in the ecological environment and the fact that the growth and loss rates of predators were much smaller than those of prey were considered. First, the dynamical behavior of the deterministic model was analyzed, including the existence and the stability of the equilibrium points and the bifurcation phenomena. Second, the existence and uniqueness of global positive solutions and the ergodic property of stochastic model were discussed. Meanwhile, the solution trajectory which was perturbed was also analyzed by using random center-manifold and random averaging method. Finally, the stochastic P-bifurcation is shown by applying singular boundary theory and invariant measure theory. Numerical simulation also verified the correctness of the theoretical analysis.

    Citation: Yanjiao Li, Yue Zhang. Dynamic behavior on a multi-time scale eco-epidemic model with stochastic disturbances[J]. Electronic Research Archive, 2025, 33(3): 1667-1692. doi: 10.3934/era.2025078

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  • In this paper, a multi-time scale stochastic eco-epidemic model where the prey population was infected with disease was proposed. The stochastic factors in the ecological environment and the fact that the growth and loss rates of predators were much smaller than those of prey were considered. First, the dynamical behavior of the deterministic model was analyzed, including the existence and the stability of the equilibrium points and the bifurcation phenomena. Second, the existence and uniqueness of global positive solutions and the ergodic property of stochastic model were discussed. Meanwhile, the solution trajectory which was perturbed was also analyzed by using random center-manifold and random averaging method. Finally, the stochastic P-bifurcation is shown by applying singular boundary theory and invariant measure theory. Numerical simulation also verified the correctness of the theoretical analysis.



    The interaction between prey and predator has become one of the main relationships in ecology due to its universality and importance. Meanwhile, disease is one of the most common influencing factors on prey-predator systems in the natural environment. The study of disease dynamics in an ecological system is an important issue from both mathematical and ecological point of view, as spread of infectious diseases becomes an important factor to regulate animal population sizes. Many researchers have proposed and studied different predator–prey models in the presence of disease. Gupta and Dubey discussed bifurcation and chaos in a delayed eco-epidemic model [1]; dynamic behavior of an eco-epidemic model with two delays was analyzed by Jana et al.[2]; Debasis Mukherjee discussed the Hopf oscillation phenomenon of an eco-epidemic model [3].

    Meanwhile, as is well-known, the fluctuation in environmental changes is an important component of an ecosystem in natural ecological environments. Due to the stochastic perturbation in the real world, the dynamic behavior described by deterministic models cannot accurately predict the true future behavior of the system. Thus, considering the stochastic models with noise is reasonable. Related work could be found in Mukherjee [4]; Khare et al. [5]; and Zhang and Wu [6,7]. These indicate that many scholars have begun to pay attention to the impact of stochastic factors on ecological populations and have made many academic achievements.

    On the other hand, another practical issue in the ecological environment is that the growth rate of prey is generally much faster than that of predator in most systems. Therefore, in most applications, the dynamics of different variables in simple differential equation systems are scaled hierarchically. Based on the stochastic system, many authors have considered system research and management at different timescales. Wang and Roberts discussed the dynamics of a slow-fast stochastic system by using random slow manifold reduction [8]. Stochastic P-bifurcation and the asymptotic behaviors of a stochastic model of Alzheimer's disease, which has two timescales, were analyzed by Zhang and Wang [9].

    Random slow manifolds are geometrical invariant structures of multi-scale stochastic dynamical systems. It has been shown that the deterministic slow manifold has dramatic effect on the overall dynamical behavior. In [10], the authors discover that the bifurcation structure of the deterministic slow manifold creates a reaction channel for non-equilibrium transitions, leading to vastly increased transition rates. The random slow manifold also has a profound impact on the stochastic bifurcation for the stochastic dynamical system. It is beneficial to take advantage of random slow manifolds in order to examine dynamical behaviors of multi-scale stochastic systems, either through the slow manifolds themselves or by the reduced systems on these slow manifolds [11]. For multidimensional stochastic slow-fast systems, the reduction on random slow manifolds brings great convenience to the analysis of dynamic behavior.

    Based on the above discussion, this paper is to discuss a stochastic mathematical model which has two timescales with disease infection in the prey population. As far as we know, the study of the epidemic model considering stochastic noise and multi-time scale is not extensive, especially the further study of the stochastic system. In our work, the further reduction analysis of multi-time scale stochastic system using random slow manifold can analyze its dynamic behavior, such as stochastic bifurcations, while maintaining accuracy. This makes the analysis of the system closer to reality, more biologically significant and more comprehensive. The P-bifurcation analysis after dimension reduction also provides a more specific and further discussion on the dynamic behavior on the dynamical behavior of the ecosystem affected by stochastic noise.

    The rest of paper is divided as follows: In Section 2, a stochastic eco-epidemiological system with multi-time scale is presented. The stability and bifurcation of the equilibrium points of the model without noise are discussed in Section 3. In Section 4, the existence, boundedness, and ergodic property of solutions are analyzed on the stochastic model. In addition, the singular perturbation problem with random center-manifold method and the stochastic P-bifurcation are considered in Section 5. Finally, in Section 6, we end the paper with some concluding remarks.

    Zhang et al. [12] proposed a prey-diseased predator model with stochastic disturbances:

    {˙S(t)=rS(t)(1S(t)K)βS(t)I(t)+σ1S(t)dB1(t),˙I(t)=βS(t)I(t)d1I(t)cI(t)P(t)+σ2I(t)dB2(t),˙P(t)=P(t)(kcI(t)d2)+σ3P(t)dB3(t),

    where S(t),I(t), and P(t) represent the number of the susceptible prey, infective prey, and predator at time t, respectively. r denotes the increase rate, K is the environmental capacity, β denotes the disease transmission coefficient, and d1 represents the disease related mortality rate of I(t). k is the conversion efficiency of predator, while d2, c represent the natural mortality rate and the attack rate on infected prey of P(t), respectively. Bi(t)>0 (i=1,2,3) represents the standard Brownian motion with an intensity of i, and σi>0 (i=1,2,3) represents the intensities of environmental white noise. Bi(t)>0 (i=1,2,3) are independent of each other.

    In this paper, the different timescales are applied to the model due to multiple timescales revealing that the rate of reproduction and death of prey is often much faster than that of predators in actual situations. We take into account the timescale ε, which is selected as the ratio of the product of the predator's predation rate and predation conversion rate to the intrinsic growth rate of prey. Rescale the variables as

    ε=kcr,q=βr,h=d2kc,α=d1r,δ=ar

    and assume

    ˜t=rt,˜P=cPr,

    still using t to represent ˜t and P to represent ˜P.

    Moreover, considering that the susceptible prey and the infected prey are often subjected to the same interference as the same biological population in the same environment, the following dimensionless system can be obtained:

    {˙S=S(1SK)qSI+σ1SdB1(t),˙I=qSIIPαIδI2+σ1IdB1(t),˙P=εP(Ih)+σ2εPdB2(t), (2.1)

    where ε describes the timescale separation and 0<ε1. a represents the interspecific competition coefficient of I(t). Bi(t)>0 (i=1,2) represents the standard Brownian motion with an intensity of i while B1(t) and B2(t) are independent of each other. σi>0 (i=1,2) represents the intensities of environmental white noise. This model is applicable to infectious diseases that spread only in the prey population and have a high mortality rate while having no effect on predators, for example, mouse hepatitis virus and rabbit hemorrhagic disease virus.

    When σ1=σ2=0, the corresponding deterministic model of system (2.1) is

    {˙S=S(1SK)qSI,˙I=qSIIPαIδI2,˙P=εP(Ih). (3.1)

    In this section, the dynamics of the deterministic situation is mainly focused.

    By calculating, there are four equilibrium points for system (3.1): E1(0,0,0), E2(K,0,0), E3(K(δ+qα)q2K+δ,qKαq2K+δ,0), and E4(S,I,P), where S=K(1qh), I=h, P=qK(1qh)αδh.

    It is easy to see that the Jacobian matrix of (3.1) is given as

    J=(12SKqIqS0qIqSPα2δII0εPε(Ih)).

    For E1(0,0,0), the corresponding Jacobian matrix is

    J(E1)=(1000α000εh).

    Obviously, the eigenvalues of J(E1) are λ1=1>0, λ2=α<0, λ3=εh<0. Therefore, E1 is a saddle and always unstable.

    Theorem 3.1. For E2,

    (a) if q<αK, E2 is a stable node.

    (b) if q>αK, E2 is a saddle.

    (c) if q=qTC=αK, the system (3.1) undergoes a transcritical bifurcation.

    Proof. For E2(K,0,0),

    J(E2)=(1qK00qKα000hε),

    the eigenvalues of J(E2) are λ1=1<0, λ2=hε<0, λ3=qKα. If q<αK, λ3<0, E2 is stable. If q>αK, λ3>0, E2 is a saddle.

    If q=qTC=αK, λ3=0. Let V and W be two eigenvectors corresponding to the eigenvalue λ3 for the matrices J(E2) and J(E2)T, respectively. After calculation, we have

    V=(V1V2V3)=(α10),W=(W1W2W3)=(010).

    Moreover,

    F(S,I,P)=(S(1SK)qSIqSIIPαIδI2εP(Ih)),Fq(E2;qTC)=(SISI0)E2,qTC=(000),
    DFq(E2;qTC)V=(IS0IS0000)(α10)=(KK0),
    D2F(E2;qTC)(V,V)=(02(δ+α2K)0).

    Clearly, V and W satisfy

    WTFq(E2;qTC)=0,WT(DFq(E2;qTC)V)=K0,WT(D2F(E2;qTC)(V,V))=2(δ+α2K)0.

    By the Sotomayor theorem [13], when q=qTC, the transcritical bifurcation occurs at E2, and the two equilibrium points E2 and E3 coincide. The proof of Theorem 3.1 is finished.

    Theorem 3.2. For E3,

    (a) if h>qKαq2K+δ, E3 is a stable node.

    (b) if h<qKαq2K+δ, E3 is a saddle.

    (c) if h=hTC=qKαq2K+δ, the system (3.1) undergoes a transcritical bifurcation.

    To ensure the existence of E3, qK>α must be satisfied, and h is chosen to be the bifurcation parameter for ease of calculation. Then, the situation is similar to E2. By calculating, the following results are obtained:

    WTFh(E3;hTC)=0,WT(DFh(E3;hTC)V)=ε(q2K+δ)0,WT(D2F(E3;hTC)(V,V))=2ε(q2K+δ)0.

    By the Sotomayor theorem [13], when h=hTC, the transcritical bifurcation occurs at E3, and the two equilibrium points E3 and E4 coincide.

    For E4, its existence conditions are q>αK, h<1q, h<qKαq2K+δ. The corresponding Jacobian matrix is

    J(E4)=(qh1qK(1qh)0qhδhh0ε(qK(1qh)αδh)0),

    and the characteristic equation is

    λ3+a1λ2+a2λ+a3=0,

    where

    a1=1qh+δh,a2=h(δδqh+q2Kq3hK+ε(qKq2Khαδh)),a3=εh(1qh)(qKq2Khαδh),a1a2a3=h(δh+1qh)(δ(1qh)+q2K(1qh))+δhε(Kq2h+qKδhα).

    Due to the existence conditions, it is easy to know a1,a2,a3>0 and a1a2a3>0. According to the Routh-Hurwitz criterion, E4 is asymptotically stable.

    Considering the nonnegative nature of the ecological population, it is necessary to prove the existence of unique positive global solution for any positive initial condition of the system (2.1).

    Theorem 4.1. For any initial value (S(0),I(0),P(0))R3+, system (2.1) admits a unique global positive solution (S(t),I(t),P(t)) for all t0, and the solution remains in R3+ with probability one, namely,

    P{(S(t),I(t),P(t))R3+,for all t0}=1.

    Proof. Due to the coefficients of the system (2.1) satisfying the local Lipschitz condition, it always has solution (S(t),I(t),P(t))R3+ at t[0,τe) for any initial value (S(0),I(0),P(0))R3+, where τe is the moment of explosion. To prove that it is almost a global solution, it's simply needed to show that τe=. Let k0>0 be sufficiently large such that each component of (S(0),I(0),P(0)) lies within the interval [1k0,k0]. For any integer k>k0, the stopping time is defined:

    τk=inf{t(0,τe):min{(S(t),I(t),P(t))}1k or max{(S(t),I(t),P(t))}k},

    where inf=, and generally represents the empty set.

    Obviously, τk monotonically increases as k increases. Set τ=limkτk, then ττe is valid almost surely. It is known that if τ= holds almost surely, then τe= will hold almost surely and there is (S(t),I(t),P(t))R3+ for any t0. The following proof will use the method of proof by contradiction. If the statement is not true, there exist a pair of constants T>0 and ε1(0,1) such that P{τkT}ε1 for any integer kk0.

    Define a C2 function V:R3+R+

    V(S(t),I(t),P(t))=S(t)1lnS(t)+I(t)1lnI(t)+P(t)1lnP(t),

    from inequality u1lnu0(u>0), it can be inferred that V(S(t),I(t),P(t))0. Applying the generalized Itˆo formula to V, we have

    LV(S,I,P)=(11S)(S(1SK)qSI)+(11I)(qSIIPαIδI2)+(11P)(εP(Ih))+σ21+εσ222S+SK+α+δI+εh+εIP+P+σ21+εσ222K+1+α+δK+εh+P(εK+1)+σ21+εσ222. (4.1)

    By using inequality xaalnxa0 for any positive constant a, and combining formula (4.1) with positive constant ξ=2εK+1>0, we get

    L(eξtV(S,I,P))=eξt(ξV(S,I,P)+LV(S,I,P))eξt((ξ(S1lnS+I1lnI+P1lnP)+K+1+α+δK+εh+(εK+1)P+σ21+εσ222)=eξt((ξ(SlnS)ξ(IlnI)εK(PξεKlnP)+3ξ+K+1+α+δK+εh+σ21+εσ222)eξt((2ξξ(1lnξεK)+3ξ+K+1+α+δK+εh+σ21+εσ222)¯Keξt, (4.2)

    where ¯K=ξ|lnξεK|+K+1+α+δK+εh+σ21+εσ222>0, and further obtain

    d(eξtV(S,I,P))¯Keξt+σ1(S1)dB1(t)+σ1(I1)dB1(t)+σ2ε(P1)dB2(t). (4.3)

    Set

    ˜V(S(t),I(t),P(t))=¯Kξ+V(S(t),I(t),P(t))

    and obtain that

    d˜V(S(t),I(t),P(t))ξ˜V(S(t),I(t),P(t))dt+σ1(S1)dB1(t)+σ1(I1)dB1(t)+σ2ε(P1)dB2(t). (4.4)

    For any kk0 and t[0,T], integrating the two sides of the inequality (4.4) from 0 to τkT=min{τk,T}, we obtain

    ˜V(S(τkT),I(τkT),P(τkT))˜V(S(0),I(0),P(0))+τkT0ξ˜V(S(t),I(t),P(t))dt+σ1τkT0(S1)dB1(t)+σ1τkT0(I1)dB1(t)+σ2ετkT0(P1)dB2(t)=˜V(S(0),I(0),P(0))+τkT0ξ˜V(S(t),I(t),P(t))dt+M1(τkT)+M2(τkT)+M3(τkT), (4.5)

    where

    M1(τkT)=σ1τkT0(S1)dB1(t),M2(τkT)=σ1τkT0(I1)dB1(t),M3(τkT)=σ2ετkT0(P1)dB2(t)

    are three local martingales. Then, take expectation of the inequality (4.5) due to the fact that the solution of the system (2.1) is Ft adaptive, and we have

    E˜V(S(τkT),I(τkT),P(τkT))˜V(S(0),I(0),P(0))+ξτkT0E˜V(S(τkT),I(τkT),P(τkT))dt. (4.6)

    Based on the Gronwall inequality, it yields that

    E˜V(S(τkT),I(τkT),P(τkT))˜V(S(0),I(0),P(0))eξT. (4.7)

    Therefore, for any kk0, we define Ωk={ωΩk:τk=τk(ω)T}, then we have P(Ωk)ε1. Note that for each ωΩk, there is at least one in S(τk,ω), I(τk,ω), P(τk,ω) that equals k or 1k. Consequently, we have

    ˜V(S(τkT),I(τkT),P(τkT))min{k1lnk,1k1+lnk}.

    It can be concluded from formula (4.7):

    ˜V(S(0),I(0),P(0))eξTE(1Ωk(ω)˜V(S(τk,ω),I(τk,ω),P(τk,ω)))ε1 min{k1lnk,1k1+lnk},

    where 1Ωk(ω) is the indicator function of Ωk. It's clear to have the expression =˜V(S(0),I(0),P(0))eξT< as k tends to infinity, which shows contradiction. Accordingly, there exists a unique positive solution for stochastic system (2.1), and the proof is complete.

    Theorem 4.2. For any initial value (S(0),I(0),P(0))R3+, the solutions U(t)=(S(t),I(t),P(t)) of model (2.1) are stochastically ultimately bounded.

    Proof. To prove the validity of the property, it is to prove that for any 0<ε1<1, there is a positive constant ˜δ=˜δ(ε1) such that the solution U(t)=(S(t),I(t),P(t)) satisfies

    limtsupP{|U(t)|>˜δ}<ε1

    for any initial value (S(0),I(0),P(0))R3+.

    We define a function V:

    V(S,I,P)=Sθ+Iθ+Pθ,

    where (S,I,P)R3+ and θ>1.

    Applying the generalized Itˆo formula to V:

    L(etV(S,I,P))=etLV(S,I,P)+etV(S,I,P)=et(θSθ1(S(1SK)qSI)+θIθ1(qSIIPαIδI2)+θPθ1(εP(Ih))+θ(θ1)2(σ21Sθ+σ21Iθ+σ22εPθ)+Sθ+Iθ+Pθ)θet(Kθ(1+1θ)+Kθ(1θ+Kqα)+εPθ(Kh+1θ)(θ1)σ21Kθ+(θ1)2σ22εPθ)˜Ket, (4.8)

    let Kh+1θ=(θ1)2σ22; further, there is

    L(etV(S,I,P))θet(Kθ(1+1θ)+Kθ(1θ+Kqα)+(θ1)σ21Kθ)˜Ket, (4.9)

    where ˜K is a constant.

    Integrating the two sides of the inequality (4.8) from 0 to τkt and taking expectation, we have

    E(eτktV(S(τkt),I(τkt),P(τkt)))V(S(0),I(0),P(0))+˜KEτkt0esds.

    This shows that

    EV(S(t),I(t),P(t))etV(S(0),I(0),P(0))+˜K.

    Meanwhile, it could obtain that

    |U(t)|θ=(S2(t)+I2(t)+P2(t))θ23θ2 max{Sθ(t),Iθ(t),Pθ(t)}3θ2(Sθ(t)+Iθ(t)+Pθ(t)).

    Thus, we could have

    E|U(t)|θ3θ2(etV(S(0),I(0),P(0))+˜K),

    which implies that

    limtsup E|U(t)|θ3θ2˜K<.

    Obviously, a positive constant π1 could be found such that

    limtsup E|U(t)|<π1.

    Applying Markov's inequality and taking δ=π1ε1, for any 0<ε1<1, we have

    P{|U(t)>δ}E|U(t)|δ.

    Hence, the following inequality holds:

    limtsupP{|U(t)>δ}π1δ=ε1,

    and the proof is complete.

    When considering eco-epidemic models, when the disease will persist is always of interest. In this section, based on the theory of Has'minskki [14], an ergodic stationary distribution which reveals that the disease will persist is proved. Here is some theory about the stationary distribution.

    Lemma 4.1. ([14]) The Markov process X(t) has a unique ergodic stationary distribution μ() if there exists a bounded domain DEl with regular boundary Γ and

    A1: there is a positive number M such that li,j=1aij(x)ξiξjM|ξ|2, xD, ξRl.

    A2: there exists a nonnegative C2-function V such that LV is negative for any ElD. Then,

    Pχ{limT1TT0f(X(t))dt=Elf(x)μ(dx)}=1

    for all xEl, where f() is a function integrable with respect to the measure μ.

    Theorem 4.3. Assume that Rs0=1α+σ21+εh+ε2σ22>1, then system (2.1) has a unique stationary distribution μ() and it has the ergodic property.

    Proof. In view of Theorem 4.1, it has been known that for any initial value (S(0),I(0),P(0))R3+, there exists a unique global solution (S(t),I(t),P(t))R3+. In what follows, for the simplification, we denote S(t),I(t), and P(t) as S,I,P, respectively.

    The diffusion matrix of system (2.1) is given by

    A=(σ21S2000σ21I2000εσ22P2).

    Choose M=min(S,I,P)DkR3+{σ21S2,σ21I2,εσ22P2}, and we have

    3i,j=1aij(S,I,P)ξiξj=σ21S2ξ21+σ21I2ξ22+εσ22P2ξ23M|ξ|2,(S,I,P)Dk, ξ=(ξ1,ξ2,ξ3)R3,

    where Dk=(1k,k)×(1k,k)×(1k,k), then the condition A1 in Lemma 4.1 holds.

    Next, we focus on the condition A2, and define

    V1(S,I,P)=lnSlnIlnP+q+δα(S+I)+Pεh,V2(S,I,P)=lnP,V3(S,I,P)=1m+2(S+I+Pε)m+2,

    where m is a sufficiently small constant satisfying 0<m<min{ασ211,hσ22ε1}.

    By calculating, we have

    LV1=1+SK+qIqS+P+α+δIε(Ih)+σ21+ε2σ22+q+δα(SS2KIPαIδI2)+P(Ih1)(α+σ21+εh+ε2σ22)(1α+σ21+εh+ε2σ221)+α+(q+δ)KαKS+PIh=λ+α+(q+δ)KαKS+PIh, (4.10)

    where

    λ=(α+σ21+εh+ε2σ22)(1α+σ21+εh+ε2σ221)>0.

    Similarly, it can be obtained that

    LV2=ε(Ih)+ε2σ22, (4.11)
    LV3=(S+I+Pε)m+1(SS2KαIδI2Ph)+σ212S2(m+1)(S+I+Pε)m+σ212I2(m+1)(S+I+Pε)m+σ222εP2(m+1)(S+I+Pε)mS(S+I+Pε)m+11KSm+3αIm+2δIm+3hεm+1Pm+2+m+12(σ21Sm+2+σ21Im+2+σ22εmPm+2)B12KSm+3α2Im+2h2εm+1Pm+2, (4.12)

    where

    B=sup(S,I,P)R3+{S(S+I+Pε)m+1+m+12(σ21Sm+2+σ21Im+2+σ22εmPm+2)12KSm+3α2Im+2h2εm+1Pm+2}<.

    Define a Lyapunov function ¯V:R3+R as

    ¯V(S,I,P)=M0V1(S,I,P)+V2(S,I,P)+V3(S,I,P), (4.13)

    where M0 is a positive constant satisfying

    M0λ+C12,C1=sup(S,I,P)R3+{B12KSm+3α2Im+2h2εm+1Pm+2+εh+ε2σ22+M0PIh}. (4.14)

    It is easy to check that

    lim infk,(S,I,P)R3+Dk¯V(S,I,P)=+.

    Furthermore, ¯V(S,I,P) is a continuous function. Hence, ¯V(S,I,P) has a minimum point (S0,I0,P0) in the interior of R3+. Then, a nonnegative C2-function ˆV(S,I,P):R3+R+ is constructed as follows:

    ˆV(S,I,P)=¯V(S,I,P)¯V(S0,I0,P0). (4.15)

    From (4.10) to (4.15), it can be calculated that

    LˆVM0λ+M0(α+(q+δ)KαKS+PIh)+εh+ε2σ22+B12KSm+3α2Im+2h2εm+1Pm+2. (4.16)

    Now, we select a bounded closed set Dε1 as

    Dε1={(S,I,P)R3+:ε1S1ε1,ε1I1ε1,ε1P1ε1},

    where ε1>0 is a sufficiently small constant satisfying the following conditions in the set R3+Dε1:

    M0λ+C1+M0α+(q+δ)KαKε11, (4.17)
    M0ε1(1h)1+1m+1+C21, (4.18)
    M0ε1(1h)1+1m+1+C31, (4.19)
    12K(1ε1)m+3+C41, (4.20)
    α2(1ε1)m+2+C51, (4.21)
    h2εm+1(1ε1)m+2+C61, (4.22)

    where

    C2=sup(S,I,P)R3+{M0α+(q+δ)KαKS+εh+ε2σ22+B12KSm+3α2Im+2},C3=sup(S,I,P)R3+{M0α+(q+δ)KαKS+εh+ε2σ22+B12KSm+3h2εm+1Pm+2},C4=sup(S,I,P)R3+{M0(α+(q+δ)KαKS+PIh)+εh+ε2σ22+Bα2Im+2h2εm+1Pm+2},C5=sup(S,I,P)R3+{M0(α+(q+δ)KαKS+PIh)+εh+ε2σ22+B12KSm+3h2εm+1Pm+2},C6=sup(S,I,P)R3+{M0(α+(q+δ)KαKS+PIh)+εh+ε2σ22+B12KSm+3α2Im+2}.

    We can get that (4.17) holds from (4.14). For the sake of convenience, R3+Dε1 is divided into the following six domains:

    D1={(S,I,P)R3+:0<S<ε1},  D2={(S,I,P)R3+:0<I<ε1},D3={(S,I,P)R3+:0<P<ε1},  D4={(S,I,P)R3+:S>1ε1},D5={(S,I,P)R3+:I>1ε1},        D6={(S,I,P)R3+:P>1ε1}.

    Obviously, DCε1=D1D6. In order to verify LˆV(S,I,P)1 for any (S,I,P) in DCε1, we will clarify it on the above six domains.

    Case 1. For (S,I,P)D1, it follows from (4.16) and (4.17) that

    LˆVM0λ+M0(α+(q+δ)KαKS+PIh)+εh+ε2σ22+B12KSm+3α2Im+2h2εm+1Pm+2M0λ+C1+M0α+(q+δ)KαKε11.

    Case 2. For (S,I,P)D2, it follows from (4.16) and (4.18) that

    LˆVM0(α+(q+δ)KαKS+Pε1h)+εh+ε2σ22+B12KSm+3,α2Im+2h2εm+1Pm+2=M0Pε1hh2εm+1Pm+2+C2.

    Notice that for any p>1, x0, the following inequality holds [15]:

    xξxp+ξ11p, (4.23)

    thus,

    LˆVM0Pε1hh2εm+1Pm+2+C2M0ε1h(hPm+2+(1h)1m+1)h2εm+1Pm+2+C2(h2εm+1M0ε1)Pm+2+M0ε1(1h)1+1m+1+C2M0ε1(1h)1+1m+1+C21.

    Case 3. For (S,I,P)D3, it follows from (4.16), (4.19), and (4.23) that

    LˆVM0(α+(q+δ)KαKS+ε1Ih)+εh+ε2σ22+B12KSm+3α2Im+2h2εm+1Pm+2=M0ε1Ihα2Im+2+C3M0ε1h(hIm+2+(1h)1m+1)α2Im+2+C3(α2M0ε1)Im+2+M0ε1(1h)1+1m+1+C3M0ε1(1h)1+1m+1+C31.

    Case 4. For (S,I,P)D4, it follows from (4.16) and (4.20) that

    LˆV12KSm+3+M0(α+(q+δ)KαKS+PIh)+εh+ε2σ22+Bα2Im+2h2εm+1Pm+212K(1ε1)m+3+C41.

    Case 5. For (S,I,P)D5, it follows from (4.16) and (4.21) that

    LˆVα2Im+2+M0(α+(q+δ)KαKS+PIh)+εh+ε2σ22+B12KSm+3h2εm+1Pm+2α2(1ε1)m+2+C51.

    Case 6. For (S,I,P)D6, it follows from (4.16) and (4.22) that

    LˆVh2εm+1Pm+2+M0(α+(q+δ)KαKS+PIh)+εh+ε2σ22+B12KSm+3α2Im+2h2εm+1(1ε1)m+2+C61.

    Clearly, from above all it can be obtained that for a sufficiently small ε1,

    LˆV(S,I,P)1 for all (S,I,P)R3+Dε1.

    Therefore, A2 in Lemma 4.1 is satisfied. The system (2.1) has a stable stationary distribution and the solution is ergodic by the Lemma 4.1 [14]. This completes the proof.

    Remark 4.1. The existence of the stationary distribution describes the probability equilibrium state of variables such as biomass and species abundance in the long-term evolution of ecosystems. It provides quantitative tools for key issues such as extinction risk and coexistence probability. The ultimate boundedness characterizes the dynamic resilience of an ecosystem, which refers to its ability to resist collapse or explosive growth under stochastic disturbances (environmental noise and resource fluctuations). Both of them provide theoretical basis for the analysis of ecosystems, and ultimately boundedness often lays the foundation for the existence of stationary distributions, which is a necessary but not sufficient condition for the existence of stationary distributions.

    In this section, first the dimensionality of deterministic model (3.1) is reduced. Then, the corresponding reduction stochastic model could be obtained by applying the lemma from [11]. Finally, the stochastic bifurcation is analyzed.

    In terms of the slow time t=ετ, the model (3.1) becomes the following slow system:

    {ε˙S=S(1SK)qSI=f1,ε˙I=qSIIPαIδI2=f2,˙P=P(Ih)=g. (5.1)

    Note that systems (3.1) and (5.1) are equivalent as long as ε>0.

    When ε=0 in (3.1), the following equation, which is also called the fast subsystem, could be obtained:

    {˙S=S(1SK)qSI=f1,˙I=qSIIPαIδI2=f2,˙P=0. (5.2)

    The singular perturbation theory defines the critical manifold of (3.1) as the equilibrium points of the fast subsystem (5.2), which means

    {f1=S(1SK)qSI=0,f2=qSIIPαIδI2=0. (5.3)

    By simply calculating, we get the explicit expression of critical manifold:

    M10={(S,I,P)|S=K,I=0},M20={(S,I,P)|S=(1qI)K,P=(δq2K)I+qKα}.

    For further discussion, the critical manifold is decomposed into the following branches:

    M10={(S,I,P)|S=K,I=0,P>qKα},M+10={(S,I,P)|S=K,I=0,P<qKα},M20={(S,I,P)|S=(1qI)K,P=(δq2K)I+qKα,I<1q},M+20={(S,I,P)|S=(1qI)K,P=(δq2K)I+qKα,I>1q}.

    Then, we have the following result:

    Theorem 5.1. Consider 0<ε1, where the branches M10 and M20 are normally hyperbolic attracting, and M+10 and M+20 are normally hyperbolic saddle. M10 and M20 lose their normal hyperbolicity at Q(K,0,qKα) and T(0,1q,δqα).

    Proof. Along the manifold M10, the Jacobian matrix associated with (5.3) is given by

    J10=(1qK0qKPα).

    The eigenvalues are λ11=1<0 and λ12=qKPα . By simply calculating, M10 is normally hyperbolic attracting when P>qKα and normally hyperbolic saddle when 0<P<qKα. In addition, Q(K,0,qKα) is a turning point where M10 loses its normal hyperbolicity (as Figure 1).

    Figure 1.  The critical manifold of system (3.1). The red curve is the saddle part and the blue curve is the attracting part.

    Similarly, along the manifold M20, we have

    J20=(qI1qK+q2KIqIδI).

    The eigenvalues are λ21,22=qIδI1±(δIqI+1)24(qI2(q2Kδ)+I(δ+q2K))2. By calculating, M20 is normally hyperbolic attracting when 0<I<1q and normally hyperbolic saddle when I>1q. In addition, T(0,1q,δqα) is a turning point where M20 loses its normal hyperbolicity.

    Obviously, T has no biological significance because of δqα<0. In the following, we will only discuss about point Q. Moreover, from definition, it is easy to know that slow flow doesn't exist at Q. For 0<ε1, Fenichel's theorem indicates that M10 and M20 can be perturbed to Mε10 and Mε20, which the distance to M10 and M20 is within O(ε), respectively. As ε increases, the solution trajectory fluctuates accordingly, but ultimately stabilizes at the internal equilibrium point E4, as Figure 2.

    Figure 2.  The solution trajectory of system (3.1) with increasing ε. As ε increases, the solution trajectory fluctuates accordingly, but ultimately stabilizes at the internal equilibrium point E4. (a) ε=0.1, (b) ε=0.9.

    To analyze the system (3.1), the central manifold theorem is applied to reduce the dimensionality. Using the linear transformation w=S+qKI yields the following system:

    {˙w=(wqKI)(1wK+qI)qI(wqKI)+qK(qI(wqKI)IPαIδI2),˙I=qwIq2KI2IPαIδI2,˙P=εP(Ih). (5.4)

    Let

    X=(wI), g(w,I,P)=P(Ih),
    f(w,I,P)=(f(w,I,P)f0(w,I,P))=(ww2KqKI+qwI+q2KwIq3k2I2qKIPqKαIqKδI2qwIq2KI2PIαIδI2).

    By transformation, the matrix Xf(K,0,qKα) is transformed to block-diagonal with eigenvalues 1 and 0. Hence, for sufficiently small ε and in a neighborhood of (0,qKα), the locally attracting critical manifold ^M0 and slow manifold ^Mε are as follows:

    ^M0={(w,I,P)|w=h0(I,P)},^Mε={(w,I,P)|w=h(I,P,ε),(I,P)N},

    where h0(I,P)=K(1+qI+q2KI+(1+qI+q2KI)24K(qKI+q3K2I2+qKIP+qKαI+qKδI+K))2 and h(I,P,ε) is a solution of the partial differential equation

    f(h(I,P,ε),I,P)=Ih(I,P,ε)f0(h(I,P,ε),I,P)+εPh(I,P,ε)g(h(I,P,ε),I,P),

    and N is a sufficiently small neighborhood of (I,P).

    Explicitly, we have

    h(I,P,ε)=k0+(k1I+k2ε+k3P)+(k4I2+k5IP+k6Iε+k7P2+k8Pε+k9ε2)+.

    Then, we obtain the following equation:

    h(I,P,ε)h2(I,P,ε)KqKI+qh(I,P,ε)I+q2Kh(I,P,ε)Iq3k2I2qKIPqKαIqKδI2=(k1+2k4I+k5P+k6ε)(qh(I,P,ε)Iq2KI2PIαIδI2)+εP(k3+k5I+2k7P+k8ε)(Ih).

    Through using Maple to compare coefficients, the center manifold expression to second order is

    h(I,P,ε)=k0+k1I+k4I2+k5IP+=K+qK(qKα)qK+1αI+k4I2qK(qK+1α)2IP+,

    where k4=qK(qKδαδ+αq+δ)(qKα+1)2(2qK2α+1).

    By local attractivity, it is sufficient to obtain the reduced system of system (3.1):

    {dI=(qI(k0+k1I+k4I2+k5IP)q2KI2IPαIδI2)dt,dP=εP(Ih)dt. (5.5)

    The function h(I,P,ε) satisfies h(0,qKα,0)=K. In order to make it easier to distinguish between the stochastic system and deterministic system, we use wt, It, and Pt to represent stochastic system variables here. Meanwhile, we fix a particular solution (Idett,Pdett) of the deterministic system (5.5).

    By local attractivity, the system (2.1) could be rewritten in (wt,It,Pt)-coordinates as

    {dwt=1εf(wt,It,Pt)dt+σ1εF(wt,It,Pt)dB1(t),dIt=1εf0(wt,It,Pt)dt+σ1εF0(wt,It,Pt)dB1(t),dPt=g(wt,It,Pt)dt+σ2G(wt,It,Pt)dB2(t),

    where

    (F(wt,It,Pt)F0(wt,It,Pt))=(h(It,Pt,ε)qKItIt),G(wt,It,Pt)=Pt.

    Consider the deviation ξt=wth(It,Pt,ε) of sample paths from ^Mε. It satisfies an SDE (Stochastic Differential Equation) of the form

    dξt=1ε^f(ξt,It,Pt)dt+σ1ε^F(ξt,It,Pt)dB1(t),

    and using Itˆo's formula, it shows that

    ˆf(ξt,It,Pt)=f(h(It,Pt,ε)+ξt,It,Pt)Ith(It,Pt,ε)f0(h(It,Pt,ε)+ξt,It,Pt)εPth(It,Pt,ε)g(h(It,Pt,ε)+ξt,It,Pt)+O(σ21),

    where the last term is the second-order term in Itˆo's formula. The properties of invariant manifold indicate that all terms in ˆf(ξt,It,Pt), except the last one, vanish when ξt=0. Then, we could approximate the linearization of ^f at ξt=0 by the matrix

    A(It,Pt,ε)=wtf(h(It,Pt,ε),It,Pt)Ith(It,Pt,ε)wtf0(h(It,Pt,ε),It,Pt)εPth(It,Pt,ε)wtg(h(It,Pt,ε),It,Pt)=12Kh(It,Pt,ε)+qIt+q2KIt(k1+2k4It+k5Pt)qIt.

    Since A(0,qKα,0)=wtf(K,0,qKα)=A=1, the eigenvalues of A(It,Pt,ε) have negative real parts, bounded away from zero when we take N and ε small enough. In the following, the dependence of A on ε will be ignored.

    Now approximate the dynamics of (ξt,It,Pt) by the following system:

    {dξ0t=1εA(Idett,Pdett)ξ0tdt+σ1εF0(Idett,Pdett)dB1(t),dIdett=1ε(qwIdettq2K(Idett)2IdettPdettαIdettδ(Idett)2)dt,dPdett=Pdett(Idetth)dt,

    where F0(I,P)=F(0,I,P)|Q=K is the value of the diffusion coefficient on the invariant manifold. Moreover, the process ξ0t is Gaussian with zero mean and covariance matrix X, where X obeys the equation:

    A(It,Pt,ε)X+XA(It,Pt,ε)T+F0(It,Pt)F0(It,Pt)T=0,

    through calculating, we have

    X=K22(12h(It,Pt,ε)KqIt+q2KItqIt(k1+2k4It+k5Pt)).

    As we know, all eigenvalues of A(It,Pt) have negative real parts, and there exists a locally attracting invariant manifold X=H(I,P,ε) for (I,P)N and ε small enough. Based on this invariant manifold, define the domain of concentration of paths

    B(h)={(w,I,P):(I,P)N,wh(I,P,ε),H1(I,P,ε)(wh(I,P,ε))<h2},

    and stopping times

    τB(h)=inf{t>0:(wt,It,Pt)B(h)},τN=inf{t>0:(It,Pt)N},

    where h is defined in Theorem 5.3.2 [11].

    Then, a conclusion through the Theorem 5.3.2 could be drawn that sample paths of the stochastic system (2.1) are concentrated in B(h) as long as (It,Pt) remains in N. To put it another way, it means the sample paths under stochastic condition tend to concentrate in a neighborhood of order σ1 of the invariant manifold ^Mε. Based on this result, rescale time by τ=1εt, the system could be approximated by its projection

    {dIt=1ε(qIt(k0+k1It+k4I2t+k5ItPt)q2KI2tItPtαItδI2t)dτ+σ1εItdB1(τ),dPt=Pt(Ith)dτ+σ2PtdB2(τ), (5.6)

    which is also called the reduced stochastic system.

    Remark 5.1. This method of reducing the dimensionality of the stochastic system by mapping it to the slow manifold makes the dynamical behavior of multidimensional stochastic slow-fast systems easier to analyze, while also ensuring the accuracy of the analysis. For ecosystems affected by natural stochastic noise and characterized by multiple timescales, the discussion process will not be complicated and the conclusions are more in line with reality.

    In the following, the bifurcation of the reduced system (5.6) will be discussed. First of all, there are three equilibrium points containing two boundary equilibrium points E11(0,0), E12(I12,0) where I12=q2K+δqk1+(qk1q2Kδ)24qk4(qKα)2qk4, and an internal equilibrium point E13(Ir,Pr) where Ir=h,Pr=q(k0+k1h+k4h2)q2Khαδh1k5qh. Note that 0<h<q2K+δqk1+(qk1q2Kδ)24qk4(qKα)2qk4 is an existence condition for E13.

    This subsection mainly focuses on the analysis of the internal equilibrium point E13, as it has more biological significance. Let u=ItIr, v=PtPr, and we have

    {˙u=r11u(τ)+r12v(τ)+Ψ(u(τ),v(τ))+σ1ε(u(τ)+Ir)ξ1(τ),˙v=r21v(τ)+r22v(τ)+Φ(u(τ),v(τ))+σ2(v(τ)+Pr)ξ2(τ), (5.7)

    where ξi(τ)dτ=dBi(τ),

    r11=1ε(q(k0+2k1h+3k4h2+2k5hPr2qKh)Prα2δh),r12=1ε(h+qk5h2),Ψ(u,v)=1ε(uv+k5qu2vδu2q2Ku2+qk1u2+qk4u3),r21=Pr, r22=0, Φ(u,v)=uv.

    Performing coordinate transformation u=rcosθ and v=rsinθ on system(5.7), we have

    {˙r=r(r11cos2θ+r22sin2θ+(r12+r21)sinθcosθ)+σ1εrcos2θξ1(τ)+σ2rsin2θξ2(τ),˙θ=r21cos2θr12sin2θr11sinθcosθσ1εsinθcosθξ1(τ)+σ2sinθcosθξ2(τ).

    Based on the Khasminskii limit theorem [14], if the noise intensity of white noise (σ1,σ2) is small enough, then the response process r(τ),θ(τ) weakly converges with a two-dimensional Markov diffusion process. By using the random averaging method, the following Itˆo stochastic differential equation is obtained:

    {dr=mrdt+ε11dBr+ε12dBθ,dθ=mθdt+ε21dBr+ε22dBθ, (5.8)

    where Br(τ) and Bθ(τ) are independent standard Wiener processes, (mrmθ) is the drift vector, and (ε11ε12ε21ε22) is the diffusion coefficient matrix.

    By calculating various coefficients, the parameters in (5.8) satisfy:

    mr=r2r11+58r(σ21ε+σ22),mθ=12(r21r12),ε211=38r2(σ21ε+σ22),ε222=18(σ21ε+σ22),ε212=ε221=0,

    where the average amplitude r(τ) is a one-dimensional Markov diffusion process when ε212=ε221=0. It means we could obtain the following equation:

    dr=((μ1+μ28)r+μ3r)dτ+(μ3+μ48r2)12dBr, (5.9)

    where

    μ1=12r11,μ2=5(σ21ε+σ22),μ3=12(σ21εh2+σ22P2r),μ4=3(σ21ε+σ22).

    From Pr>0, it can be seen that μ30. According to the Itˆo's differential equation, the Fokker-Planck equation of system (5.9) is:

    P(r)τ=r(((μ1+μ28)r+μ3r)P(r))+122r2(μ3+μ48r2)P(r)). (5.10)

    The initial condition is P(r,τ|r0,τ0)δ(rr0), ττ0, where P(r,τ|r0,τ0) is the transition probability density of the diffusion process r(τ). The steady-state density PST(r) is the invariant measure of r(τ), and it is the solution of the following degenerate system:

    r(((μ1+μ28)r+μ3r)P(r))+122r2((μ3+μ48r2)P(r))=0. (5.11)

    By calculating, we could obtain

    Pst=82π23Δμ2Δ3(μ4μ3)32Γ(2Δ)(Γ(12Δ))1r2(μ4r2+8μ3)Δ2, (5.12)

    where Δ=(8μ1+μ2)μ14, Γ(x)=0τx1eτdτ.

    Based on Namachivaya's theory [16], when the noise intensity approaches zero, the extreme value of Pst(r) approaches the behavior of the deterministic system. We calculate the most likely amplitude r of (5.9) so that Pst(r) has its maximum value at r, i.e.,

    dPst(r)dr|r=r=0,d2Pst(r)dr2|r=r<0,

    where r=8μ38μ1+μ2μ4, (8μ38μ1+μ2μ4<12).

    In addition, Pst(r) achieves the minimum value at r=0, which means the system (2.1) is almost unstable at the equilibrium point E13 when subjected to random excitation. According to the singular boundary theory, the system (2.1) undergoes P-bifurcation at r=r.

    Remark 5.2. Through numerical simulation, as shown in Figure 3, the position of P-bifurcation increases as μ3 increases. Figure 4(a)(d) respectively corresponds to different values of parameter μ3 in Figure 3(a). The influence of ε is also shown in Figure 3. With the increase of ε, the oscillation amplitude of x(τ) and y(τ) decreases, where the impact on x(τ) is relatively greater.

    Figure 3.  (a) The steady-state probability density Pst(r) and the position r of stochastic P-bifurcation at μ1=0.354137, μ2=0.2125, μ3=0.1,0.15,0.2,0.35, μ4=0.1275. (b) The time responses of the system (5.6) as ε changes.
    Figure 4.  (a)–(d): Images of the steady-state probability density Pst(r) using data of Table 1.
    Table 1.  The P-bifurcation probability and position in system (5.6).
    condition cond1 cond2 cond3 cond4
    r 0.54 0.66 0.76 1.016
    Psτ(r) 1.4777 1.2065 1.0448 0.7898
    μ3 0.1 0.15 0.2 0.35

     | Show Table
    DownLoad: CSV

    Remark 5.3. The existence of P-bifurcation indicates that the solution crossing the singularity Q will follow Mε+10 for a distance before being repelled, then the solution will be attracted by Mε20. By calculating, the equilibrium point E4 on Mε20 is locally asymptotically stable. Hence, the solution converges to the stable equilibrium point E4.

    In this paper, an stochastic eco-epidemiological model with multi-time scale is mainly studied through the theory analysis and numerical simulation. First, we take a dimensionless transformation to system for simplicity. Then based on the stochastic noise, the stochastic items are considered in order to be more in line with reality. Meanwhile, considering the difference in iteration speed between prey and predator, paramater ε is added to the model. The stability and bifurcation of equilibrium points on the deterministic system are discussed.

    For the system with noise, the existence and uniqueness of solutions is proven by constructing a function V, and boundedness is also obtained. Then, the C2-function ¯V and ˆV are constructed to prove the ergodic property of the solutions by the lemma from [14]. As for the slow-fast dynamics, the deterministic condition is analyzed. It is obtained that the solution crossing the singularity converges to the stable equilibrium point E4 by geometric singular perturbation theory and center-manifold reduction considering 0<ε1. Applying the theorem from [11], it could be known that sample paths of the stochastic system are concentrated in the neighborhood of the deterministic one. Finally, through calculating, P-bifurcation occurs at the singularity, and that's why there is a delay in the trajectory at the singularity of the solution. Numerical simulation verified our theoretical results.

    Compared with other eco-epidemic systems, it should be noted that the models proposed in this paper investigate dynamical behavior with multi-time scale and stochastic noises, which makes the work studied in this paper have some new and positive features. It is also interesting to consider the effects of the other types of functional response functions, which will be the subject of our further research. In practical application, the control of disease is also very significant and important. The discussion of biological control is very extensive. One direction that can be explored in the future is model predictive control. It can better tackle the scenario involving the uncertainties or disturbances, and it is worth exploring whether the model predictive control can be used to the proposed model, such as [17].

    The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.

    This study was funded by National Natural Science Foundation of China (61703083) and Regional Joint Key Project of National Natural Science Foundation (U23A20324).

    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.



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