Processing math: 100%
Research article Special Issues

Transmission dynamics of cholera with hyperinfectious and hypoinfectious vibrios: mathematical modelling and control strategies

  • Received: 02 February 2019 Accepted: 25 April 2019 Published: 16 May 2019
  • Cholera is a common infectious disease caused by Vibrio cholerae, which has different infectivity. In this paper, we propose a cholera model with hyperinfectious and hypoinfectious vibrios, in which both human-to-human and environment-to-human transmissions are considered. By analyzing the characteristic equations, the local stability of disease-free and endemic equilibria is established. By using Lyapunov functionals and LaSalleos invariance principle, it is verified that the global threshold dynamics of the model can be completely determined by the basic reproduction number. Numerical simulations are carried out to illustrate the corresponding theoretical results and describe the cholera outbreak in Haiti. The study of optimal control helps us seek cost-effective solutions of time-dependent control strategies against cholera outbreaks, which shows that control strategies, such as vaccination and sanitation, should be taken at the very beginning of the outbreak and become less necessary after a certain period.

    Citation: Jiazhe Lin, Rui Xu, Xiaohong Tian. Transmission dynamics of cholera with hyperinfectious and hypoinfectious vibrios: mathematical modelling and control strategies[J]. Mathematical Biosciences and Engineering, 2019, 16(5): 4339-4358. doi: 10.3934/mbe.2019216

    Related Papers:

    [1] Yoichi Enatsu, Yukihiko Nakata . Stability and bifurcation analysis of epidemic models with saturated incidence rates: An application to a nonmonotone incidence rate. Mathematical Biosciences and Engineering, 2014, 11(4): 785-805. doi: 10.3934/mbe.2014.11.785
    [2] Fang Zhang, Wenzhe Cui, Yanfei Dai, Yulin Zhao . Bifurcations of an SIRS epidemic model with a general saturated incidence rate. Mathematical Biosciences and Engineering, 2022, 19(11): 10710-10730. doi: 10.3934/mbe.2022501
    [3] Thomas Torku, Abdul Khaliq, Fathalla Rihan . SEINN: A deep learning algorithm for the stochastic epidemic model. Mathematical Biosciences and Engineering, 2023, 20(9): 16330-16361. doi: 10.3934/mbe.2023729
    [4] Guo Lin, Shuxia Pan, Xiang-Ping Yan . Spreading speeds of epidemic models with nonlocal delays. Mathematical Biosciences and Engineering, 2019, 16(6): 7562-7588. doi: 10.3934/mbe.2019380
    [5] Yang Chen, Wencai Zhao . Dynamical analysis of a stochastic SIRS epidemic model with saturating contact rate. Mathematical Biosciences and Engineering, 2020, 17(5): 5925-5943. doi: 10.3934/mbe.2020316
    [6] Andrei Korobeinikov, Philip K. Maini . A Lyapunov function and global properties for SIR and SEIR epidemiological models with nonlinear incidence. Mathematical Biosciences and Engineering, 2004, 1(1): 57-60. doi: 10.3934/mbe.2004.1.57
    [7] Jack Farrell, Owen Spolyar, Scott Greenhalgh . The effect of screening on the health burden of chlamydia: An evaluation of compartmental models based on person-days of infection. Mathematical Biosciences and Engineering, 2023, 20(9): 16131-16147. doi: 10.3934/mbe.2023720
    [8] Tahir Khan, Fathalla A. Rihan, Muhammad Ibrahim, Shuo Li, Atif M. Alamri, Salman A. AlQahtani . Modeling different infectious phases of hepatitis B with generalized saturated incidence: An analysis and control. Mathematical Biosciences and Engineering, 2024, 21(4): 5207-5226. doi: 10.3934/mbe.2024230
    [9] Shuixian Yan, Sanling Yuan . Critical value in a SIR network model with heterogeneous infectiousness and susceptibility. Mathematical Biosciences and Engineering, 2020, 17(5): 5802-5811. doi: 10.3934/mbe.2020310
    [10] Roberto A. Saenz, Herbert W. Hethcote . Competing species models with an infectious disease. Mathematical Biosciences and Engineering, 2006, 3(1): 219-235. doi: 10.3934/mbe.2006.3.219
  • Cholera is a common infectious disease caused by Vibrio cholerae, which has different infectivity. In this paper, we propose a cholera model with hyperinfectious and hypoinfectious vibrios, in which both human-to-human and environment-to-human transmissions are considered. By analyzing the characteristic equations, the local stability of disease-free and endemic equilibria is established. By using Lyapunov functionals and LaSalleos invariance principle, it is verified that the global threshold dynamics of the model can be completely determined by the basic reproduction number. Numerical simulations are carried out to illustrate the corresponding theoretical results and describe the cholera outbreak in Haiti. The study of optimal control helps us seek cost-effective solutions of time-dependent control strategies against cholera outbreaks, which shows that control strategies, such as vaccination and sanitation, should be taken at the very beginning of the outbreak and become less necessary after a certain period.


    In the modeling of infectious diseases, incidence rate and recovery rate are two important factors that affect the dynamical behavior of the models. The bilinear incidence rate βSI are frequently used to describe the epidemic transmission process, where β is the transmission rate, S and I represent the numbers of susceptible and infective respectively. But, it is unrealistic when the number of infective individuals is large. To study the cholera epidemic spread in Bari in 1973, Capasso and Serio [1] proposed a saturated incidence rate:

    βSI1+αI, (1.1)

    where βI describes the infection force of the disease, 11+αI measures the inhibition effect from the behavioral change of the susceptible individuals as the number of infected gradually increases.

    In classical epidemic models, the recovery rate is usually assumed to be proportional to the number of infected, which means that medical resources are plentiful for the infectious diseases [2]. In fact, when diseases break out, medical resources tend to be scarce [3,4,5]. In order to study the influence of hospital beds on infectious diseases, the following nonlinear recovery rate function [5] is proposed by Shan and Zhu:

    γ(b,I)=γ0+b(γ1γ0)b+I, (1.2)

    where γ0 and γ1 are the minimum and maximum per-capita recovery rates respectively, b denotes the number of hospital beds. An SIR model with (1.2) is studied, and it is found that backward bifurcation, saddle-node bifurcation, Hopf bifurcation and cusp type of Bogdanov-Takens bifurcation of codimension 3 will happen with different values of b [5].

    Cui et al. studied an SIR epidemic model (system (1.3)) with saturate incidence rate and nonlinear recovery rate [6]. It is proved that when the number of hospital beds is small enough, system (1.3) can take place backward bifurcation, saddle-node bifurcation and Hopf bifurcation.

    S(t)=ΛβSI1+αIμS,I(t)=βSI1+αIμIϵIγ(b,I)I,R(t)=γ(b,I)IμR, (1.3)

    where S(t),I(t),R(t) are the numbers of susceptible, infected, recovered at time t respectively, γ(b,I) is defined in (1.2). Besides, Λ is the birth rate; the interpretations of β and α are the same as in [1]; μ denotes the natural death rate; ϵ represents the disease-induced death rate.

    To describe the heterogeneity of contact, complex networks are therefore incorporated into the epidemic models. Li and Yousef studied a network-based SIR epidemic model with saturated treatment function [7]. Huang and Li studied the complex dynamical properties of a network-based SIS epidemic model with saturated treatment function [8]. A condition which can determine the direction of bifurcation at R0=1 is derived in [7,8]. Wang and Yang [9] employed an edge-compartmental approach which can reduce the dimension of a mean-field vector-borne model to research the global dynamics of the system. Wang and Yang [10] proposed a degree-edge-mixed SIS model and used a novel geometric method to completely investigate the stability of feasible equilibrium. Based on the SIR model [7], Yang et al. adopted the edge-compartmental approach to prove the existence of backward bifurcation and deeply analyzed the local stability of each endemic equilibrium [11].

    To our knowledge, few people combined saturated incidence rate and nonlinear recovery rate to discuss the dynamics of network-based epidemic models. So the research of this paper is still valuable, the highlights are summarized as follows:

    A new network-based SIR epidemic model is established and then reduced to a degree-edge-mixed model by an edge-compartmental approach;

    A necessary and sufficient condition which determines the existence of backward bifurcation at R0=1 is derived;

    The stability of the feasible endemic equilibrium is proved by a geometric approach.

    We know that time delay exists in the epidemic spreading, Jiang and Zhou [12] studied the influence of time delay on epidemic spreading under limited resources. They found that time delay can induce first-order, continuous and hybrid phases and a small resources amount can effectively control the spread of infectious diseases if the delay exceeds a threshold. The stability of nonlinear systems with time delay has been studied in the literature [13,14,15,16,17]. Yang et al. obtained the existence of a positive periodic solution for neutral-type integral differential equation arising in epidemic model with time-varying delay [18]. Of course, we do not consider the delay factor in our paper, which will be a worthy of attention and research work.

    The structure of this paper is as follows. In Section 2, a new SIR epidemic model is proposed on complex networks. Besides, the dimension of the system is reduced by the edge-compartmental method. In Section 3, the existence and stability of the disease-free equilibrium and endemic equilibrium are studied. The results of numerical simulations are given in Section 4. Lastly, conclusions and discussions are presented in Section 5.

    In this section, we extend model (1.3) to the network. Furthermore, disease-induced death rate is not considered and the susceptible individuals will not be infected once vaccinated. The other parameters are exactly the same as in system (1.3) and we show the interpretation of the parameters in Table 1 for better visualization. All the nodes are classified into n groups and the nodes in the same group have the same degree. Suppose that Sk(t),Ik(t),Rk(t) be the densities of susceptible, infected, recovered with degree k at time t respectively. So, the specific mean-field equations of network-based SIR model are as follows:

    Sk(t)=ΛβkSk(t)θ(t)1+αθ(t)μSk(t)ηSk(t),Ik(t)=βkSk(t)θ(t)1+αθ(t)μIk(t)(γ0+b(γ1γ0)b+θ(t))Ik(t),Rk(t)=(γ0+b(γ1γ0)b+θ(t))Ik(t)μRk(t)+ηSk(t), (2.1)

    with θ(t) is the probability that any given edge is connected to an infected node, assume the network is uncorrelated, then

    θ(t)=1knk=1kp(k)Ik(t),

    where p(k) is the probability that a node is connected to k other nodes and k=nk=1kp(k) denotes the mean degree of the network. It is supposed that newborns are balanced by deaths, that is Λ=μ.

    Table 1.  Definition of parameters.
    Parameter Definition
    μ The birth rate / The death rate
    β Transmission rate of infected individuals
    α The saturated coefficient
    b The number of hospital beds
    γ0 The minimum per-capita recovery rate
    γ1 The maximum per-capita recovery rate
    η Proportion that has been vaccinated

     | Show Table
    DownLoad: CSV

    Inspired by the edge-compartmental method [9,10,11], we can rewrite system (2.1) as the following degree-edge-mixed model:

    Sk(t)=μβkSk(t)θ(t)1+αθ(t)μSk(t)ηSk(t),θ(t)=βkθ(t)1+αθ(t)nk=1k2p(k)Sk(t)μθ(t)(γ0+b(γ1γ0)b+θ(t))θ(t). (2.2)

    Remark 1. The dimension of degree-edge-mixed model (2.2) is much lower than system (2.1). So the process of analysis presented in this paper will be relatively concise.

    Lemma 1. If θ(0)>0,Sk(0)>0, then for all kN and tR+, we have Sk(t)>0,θ(t)>0.

    Proof. Firstly, we prove that θ(t)>0 for all t>0. From the (n+1)th equation of system (2.2), we have θ(t)=θ(0)et0z(τ)dτ,z(t)=βk(1+αθ(t))nk=1k2p(k)Sk(t)μγ0b(γ1γ0)b+θ(t). Since θ(0)>0, we can deduce θ(t)>0 for all t>0.

    Note that Sk(0)>0, in view of the continuity of Sk(t), we can find a small δ>0, such that Sk(t)>0 for t(0,δ). Now we demonstrate that Sk(t)>0 for all t>0. If not, we may assume that there exists t0δ>0, s.t. Sk(t0)=0 and Sk(t)>0 for t(0,t0). Thus, from the first n equation of system (2.2), we can obtain Sk(t0)=μ>0. This leads to Sk(t)<0 for some t(0,t0), which is apparently a contradiction. Therefore, Sk(t)>0 for all t>0.

    Remark 2. From the result of Lemma 1 and the fact Sk(t)+Ik(t)+Rk(t)=1, we can assert that Ω:={(S1,S2,,Sn,θ)0<Sk(t)1,0θ(t)<1} is a positive invariant set of system (2.2).

    System (2.2) has a unique disease-free equilibrium given by E0=(μμ+η,μμ+η,,μμ+η,0)Rn+1. Linearizing the (n+1)th equation of system (2.2) at E0 yields

    θ(t)=(βμk2(μ+η)kμγ1)θ(t). (3.1)

    Solving Eq (3.1) by a constant variation method, we can build the following equation:

    θ(t)=θ(0)e(μ+γ1)t+βμk2(μ+η)kt0e(μ+γ1)(st)θ(s)ds.

    Using the approach introduced in [19], we can calculate the basic reproduction number R0 by taking Laplace transform:

    R0=βμk2(μ+η)k+0e(μ+γ1)tdt=βμk2(μ+η)(μ+γ1)k,

    where k2=nk=1k2p(k).

    The local and global stability of the disease-free equilibrium E0 will be proved in this subsection.

    Theorem 1. If R0<1, the disease-free equilibrium E0 of system (2.2) is locally asymptotically stable, whereas if R0>1,E0 is unstable.

    Proof. Linearizing system (2.2) at E0 yields to

    Sk(t)=(μη)Sk(t)βkμμ+ηθ(t),θ(t)=(βμk2(μ+η)kμγ1)θ(t). (3.2)

    Furthermore, the Jacobian matrix of Eq (3.2) is

    J(E0)=(μη00βμμ+η0μη02βμμ+η00μηnβμμ+η000βμk2(μ+η)kμγ1)(n+1)×(n+1).

    Obviously, λ=(μ+η) is n-multiple negative eigenvalue. So, the stability of E0 is determined by the following eigenvalue:

    λ=βμk2(μ+η)kμγ1=(μ+γ1)(R01).

    Therefore, all eigenvalues of the Jacobian matrix J(E0) are negative when R0<1, and hence, E0 is locally asymptotically stable. By contrast, if R0>1,E0 is unstable.

    Next, we will prove the global stability of the disease-free equilibrium E0.

    Theorem 2. Denote ^R0 =β(b+1)k2(μ+bμ+γ0+bγ1)k, if ^R01, then E0 is globally asymptotically stable.

    Proof. Let a Lyapunov function V(t)=θ(t), then

    V(t)=βθ(t)k(1+αθ(t))nk=1k2p(k)Sk(t)μθ(t)(γ0+b(γ1γ0)b+θ(t))θ(t)βk2kθ(t)μθ(t)(γ0+b(γ1γ0)b+θ(t))θ(t)=[βk2kμγ0b(γ1γ0)b+1b(γ1γ0)(1θ(t))(b+1)(b+θ(t))]θ(t)[βk2kμγ0b(γ1γ0)b+1]θ(t)=[μ+γ0+b(γ1γ0)b+1](^R01)θ(t),

    if ^R0 <1, V(t)0; if ^R0 =1, then V(t)b(γ1γ0)(1θ(t))(b+1)(b+θ(t))θ(t)0. The equality holds if and only if θ(t)=0. Hence, we can conclude that the disease-free equilibrium E0 is globally asymptotically stable if ^R01.

    Remark 3. Because γ0<γ1, so R0=μ(μ+bμ+γ0+bγ1)(μ+η)(μ+bμ+γ1+bγ1)^R0<^R0.

    Remark 4. If ^R0<1, that is R0<μ(μ+bμ+γ0+bγ1)(μ+η)(μ+bμ+γ1+bγ1)<1, then E0 is globally asymptotically stable.

    Remark 5. It seems that the condition R0<1 is not sufficient to ensure the global asymptotic stability of E0. So system (2.2) may exist backward bifurcation at R0=1 which will be proved later.

    The existence of feasible positive equilibrium will be proved in this subsection.

    Theorem 3. If R0>1, system (2.2) admits at least an endemic equilibrium.

    Proof. Assume that E=(Sk,θ),k=1,2,,n, is an endemic equilibrium of system (2.2), then E should satisfy

    0=μβkSkθ1+αθμSkηSk,0=βθk(1+αθ)nk=1k2p(k)Skμθ(γ0+b(γ1γ0)b+θ)θ. (3.3)

    Then we can obtain Sk=μ(1+αθ)βkθ+(μ+η)(1+αθ),k=1,2,,n. Substituting Sk into the (n+1)th equation of (3.3), then we can get a self-consistency equation:

    F(θ):=μ+γ0+b(γ1γ0)b+θβknk=1k2p(k)μβkθ+(μ+η)(1+αθ)=0. (3.4)

    Since R0>1,F(0)<0,F(1)>0, using the Immediate Value Theorem, we can conclude that Eq (3.4) has at least one positive root in (0,1). This implies that system (2.2) admits at least an endemic equilibrium.

    Remark 6. If R01, then F(0)0,F(1)>0, we can not conclude whether system (2.2) exists endemic equilibrium by the method of the Immediate Value Theorem. However, we already know that E0 is not globally asymptotically stable, so system (2.2) may also exist endemic equilibrium when R01. In other words, the system may take place backward bifurcation at R0=1 which will be proved in Theorem 4.

    Next, we will derive a necessary and sufficient condition which determines the existence of backward bifurcation at R0=1.

    Theorem 4. System (2.2) exists backward bifurcation at R0=1 if and only if b<ˆb; the system undergoes forward bifurcation if and only if b>ˆb, where

    ˆb=μ(γ1γ0)k22(μ+γ1)[μαk22+(μ+γ1)kk3],k3=nk=1k3p(k).

    Proof. The endemic equilibrium should satisfy Eq (3.4). Replacing β by (μ+η)(μ+γ1)kR0μk2 and we can obtain the following equation:

    μ+γ0+b(γ1γ0)b+θ(μ+η)(μ+γ1)R0nk=1k2p(k)μQ0=0, (3.5)

    where Q0=(μ+η)(μ+γ1)kkθR0+(μ+η)(1+αθ)μk2.

    If we keep in mind that θ is a function of R0, then the direction of bifurcation is depended on the sign of θR0|(R0,θ)=(1,0). More exactly, if θR0|(R0,θ)=(1,0)<0, then backward bifurcation occurs at R0=1. Conversely, the forward bifurcation happens.

    Next, taking the derivative of Eq (3.5) associated with R0 by the implicit function theorem, then yields to the following equation:

    b(γ1γ0)θR0(b+θ)2+(μ+η)(μ+γ1)[nk=1k2p(k)(R0Q1μQ0)Q20]=0, (3.6)

    where Q1=μ(μ+η)[(μ+γ1)kkθ+(μ+γ1)kkθR0R0+μαk2θR0].

    Substituting (R0,θ)=(1,0) into Eq (3.6), we can obtain the following equation by simple calculation and arrangement:

    θR0|(R0,θ)=(1,0)=bμ(μ+γ1)k22b(μ+γ1)2kk3+bμα(μ+γ1)k22μ(γ1γ0)k22.

    Thus if

    θR0|(R0,θ)=(1,0)<0b<μ(γ1γ0)k22(μ+γ1)[μαk22+(μ+γ1)kk3].

    The same holds true also for the other proposition.

    Remark 7. It is a fact that the number of hospital beds does play a key role in determining whether there is a backward bifurcation at R0=1. More precisely, if b is small enough to satisfy the result of Theorem 4, backward bifurcation will occur. In this case, there will also exist endemic equilibrium even if R0<1 (see Figure 2(b)). That is to say, R0<1 is not sufficient to eradicate the diseases from the population, which is unfavorable to the control of infectious diseases.

    Figure 1.  The time evolutions of θ(t) with different initial conditions θ(0)=0.001×i,i=1,2,,20. (a) ^R0=0.8933<1. (b) R0=1.5008>1..
    Figure 2.  (a) The time evolutions of θ(t) with different initial conditions θ(0)=0.001×i,i=1,2,,20. (b) The backward bifurcation diagrams in the R0θ-plane with different values of b..

    Otherwise, when b is big enough, forward bifurcation will take place at R0=1. In this case, E0 will be globally asymptotically stable when R0<1. This also shows the existence of the threshold for the number of hospital beds. When the relevant departments provide enough hospital beds such that b>ˆb, infectious diseases can be completely eliminated if R0<1.

    From the above discussions, we can summarize the following results.

    Corollary 1. For system (2.2),

    (1) if R0<1 and

    (a) b<ˆb, there exists two endemic equilibria;

    (b) b>ˆb, there is no endemic equilibrium.

    (2) when R0=1, if b<ˆb, then there exists a unique endemic equilibrium; otherwise, there is no endemic equilibrium.

    (3) if R0>1, the endemic equilibrium always exist (see Theorem 3) and the number of endemic equilibrium is associated with the value of b (see Figure 3).

    Figure 3.  Bifurcation diagrams in the R0θ-plane with different values of b. Forward bifurcation takes place at R0=1 for each subgraph.

    In this subsection, we will use a geometric approach to prove the local stability of the endemic equilibrium. Linearizing system (2.2) at E yields

    Sk(t)=(μηβkθ1+αθ)Sk(t)βkSk(1+αθ)2θ(t),θ(t)=βθk(1+αθ)nk=1k2p(k)Sk(t)+(βk(1+αθ)2nk=1k2p(k)Skμγ0b2(γ1γ0)(b+θ)2)θ(t). (3.7)

    And hence the characteristic equation can be expressed as follows:

    (λ+μ+η+βkθ1+αθ)xk+βkSk(1+αθ)2y=0,βθk(1+αθ)nk=1k2p(k)xk+(λ+μ+γ0+b2(γ1γ0)(b+θ)2βk(1+αθ)2nk=1k2p(k)Sk)y=0, (3.8)

    where (xk,y) is the eigenvector that correspond to eigenvalue λ. From the first equation of (3.8), we can obtain

    xk=βkSkyβkθ(1+αθ)+(λ+μ+η)(1+αθ)2,k=1,2,,n.

    Substituting xk into the second equation of (3.8) leads to

    H(λ)y=0,

    where H(λ)=βknk=1k3p(k)βSkθβkθ(1+αθ)2+(λ+μ+η)(1+αθ)3+λ+μ+γ0+b2(γ1γ0)(b+θ)2βknk=1k2p(k)Sk(1+αθ)2.

    If y=0, then λ=μηβkθ1+αθ<0. Otherwise, when y0, then H(λ)=0. Since

    βkSkθ1+αθ=μμSkηSk,Sk=μ(1+αθ)βkθ+(μ+η)(1+αθ),βknk=1k2p(k)Sk1+αθ=μ+γ0+b(γ1γ0)b+θ, (3.9)

    and hence

    H(λ)=βknk=1k2p(k)(μμSkηSk)βkθ(1+αθ)+(λ+μ+η)(1+αθ)2+λ+βknk=1k2p(k)Sk1+αθb(γ1γ0)θ(b+θ)2βknk=1k2p(k)μβkθ(1+αθ)+(μ+η)(1+αθ)2=βknk=1k2p(k)(μμSkηSk)βkθ(1+αθ)+(λ+μ+η)(1+αθ)2+λb(γ1γ0)θ(b+θ)2+βknk=1k2p(k)μβkθ+(μ+η)(1+αθ)βknk=1k2p(k)μβkθ(1+αθ)+(μ+η)(1+αθ)2=βknk=1k2p(k)(μμSkηSk)βkθ(1+αθ)+(λ+μ+η)(1+αθ)2+λb(γ1γ0)θ(b+θ)2+βknk=1k2p(k)μαθβkθ(1+αθ)+(μ+η)(1+αθ)2. (3.10)

    Besides, taking the derivative of F associated with θ, we can have:

    F(θ)=b(γ1γ0)(b+θ)2+βknk=1k2p(k)μ(βk+(μ+η)α)(βkθ+(μ+η)(1+αθ))2=βknk=1k2p(k)μ(βkSkθ1+αθ+(μ+η)αSkθ1+αθ)(βkθ+(μ+η)(1+αθ))2Skθ1+αθb(γ1γ0)(b+θ)2=βknk=1k2p(k)μμSkηSk+(μ+η)αSkθ1+αθθ(βkθ+(μ+η)(1+αθ))b(γ1γ0)(b+θ)2=βknk=1k2p(k)(μμSkηSk)(1+αθ)+(μ+η)αSkθθ(βkθ(1+αθ)+(μ+η)(1+αθ)2)b(γ1γ0)(b+θ)2=βknk=1k2p(k)μμSkηSk+μαθθ(βkθ(1+αθ)+(μ+η)(1+αθ)2)b(γ1γ0)(b+θ)2. (3.11)

    Therefore, we can obtain that

    H(0)=βknk=1k2p(k)μμSkηSk+μαθβkθ(1+αθ)+(μ+η)(1+αθ)2b(γ1γ0)θ(b+θ)2=θF(θ). (3.12)

    Theorem 5. When F(θ)<0, then E is unstable; when F(θ)>0, then E is locally asymptotically stable.

    Proof. When F(θ)<0, since H(0)=θF(θ)<0,limλ+H(λ)=+, by the Intermediate Value Theorem, we can conclude that the equation H(λ)=0 has at least one positive real solution, so E is unstable.

    When F(θ)>0, we rewrite the equation H(λ)=0 as the following equation:

    ˆH(λ)=βknk=1k2p(k)(μμSkηSk)nikL(λ,i,θ)+βknk=1k2p(k)μαθβkθ(1+αθ)+(μ+η)(1+αθ)2nk=1L(λ,k,θ)+(λb(γ1γ0)θ(b+θ)2)nk=1L(λ,k,θ)=0, (3.13)

    where L(λ,k,θ)=βkθ(1+αθ)+(λ+μ+η)(1+αθ)2. Suppose Eq (3.13) has a solution λ with Reλ0, then since

    |ˆH(λ)|ˆH(Reλ)ˆH(0)=nk=1L(0,k,θ)H(0)=nk=1L(0,k,θ)θF(θ),

    if F(θ)>0, we can conclude that |ˆH(λ)|>0, this contradicts with the fact ˆH(λ)=0. So Eq (3.13) has no solution with nonnegative real parts. Therefore, when F(θ)>0,E is locally asymptotically stable.

    Corollary 2. If R0<1 and b<ˆb, system (2.2) exists two endemic equilibria, the one with smaller value is unstable; the other one with larger value is locally asymptotically stable.

    Proof. If R0<1 and b<ˆb, there exists two endemic equilibria (see Corollary 1). For the endemic equilibrium with smaller value, since F(θ)<0 (see Figure 2(b)), then E is unstable; and for the endemic equilibrium with larger value, since F(θ)>0, so E is locally asymptotically stable.

    Next, numerical simulations will be presented to validate the previous theoretical results. Our simulations are based on the scale-free network with p(k)=ξk2.5,k=1,2,,100, and the constant ξ is chosen so that the equation 100k=1p(k)=1 holds. For better visualization, we present the values of the parameters in Table 2.

    Table 2.  Parameter values of numerical simulations.
    Parameter Figure 1(a) Figure 1(b) Figure 2(a) Figure 2(b) Figure 3 Figure 4(a) Figure 4(b)
    μ 0.02 0.02 0.01 0.01 0.01 0.02 0.02
    β 0.006 0.03 0.009 0.03 0.03
    α 10 10 10 10 10 0/3/6/9/12 10
    b 0.03 0.03 0.003 0.003/0.005/0.007/0.009/0.011 0.0165/0.017/0.0175/0.018 0.03 0/0.003/0.006/0.009/0.012
    γ0 0.03 0.03 0.005 0.005 0.005 0.03 0.03
    γ1 0.09 0.09 0.08 0.08 0.08 0.09 0.09
    η 0.008 0.008 0.008 0.008 0.008 0.008 0.008

     | Show Table
    DownLoad: CSV

    Firstly, we verify the stability of the disease-free equilibrium E0. According to the selected parameter values, we can calculate R0=0.3002,^R0=0.8933. It is known that E0 is globally asymptotically stable from the result of Theorem 2. As seen in Figure 1(a), limt+θ(t)=0. Therefore, this does support the global stability of E0.

    In Figure 1(b), we can obtain R0=1.5008>1 and hence model (2.2) exists endemic equilibrium. Observing the simulation results, we can see that all trajectories move towards to a positive constant and the unique endemic equilibrium could be stable. However, when R0>1, model (2.2) can exhibit more complex dynamics (see Figure 3).

    Secondly, we will verify that system (2.2) may exist endemic equilibrium when R0<1. The parameter values as shown in Table 2, since R0=0.4280<1,^R0=4.5545>1, therefore E0 is not globally asymptotically stable from the result of Theorem 2. From Figure 2(a), it can be observed that the trajectories partially converge to zero or partially move towards to a positive level which corresponds to different initial conditions. Therefore, the initial infectious density must be controlled to a lower level for the control of the diseases. The result of the co-existence of two locally asymptotically stable equilibria is named as the bistable phenomenon.

    Different values of b are taken to show the bifurcation diagrams. In Figure 2(b), backward bifurcation occurs at R0=1 when b<ˆb=0.016. Besides, the larger the value of b, the smaller the depth of backward bifurcation. In Figure 3, the parameters are the same as those given in Figure 2, except for the value of b. It can be seen that forward bifurcation occurs at R0=1 for each subgraph. The reason is that although the values of b are different, they are all bigger than ˆb. Hence, the numerical simulation results are consistent with the theoretical results of Theorem 4.

    At the same time, we can observe that the shapes of the bifurcation curves are different from Figure 3. For example, the endemic equilibrium curve has an "S shape" when b=0.017. That is to say, backward bifurcation takes place at a certain value of R0. And the situation results in the existence of three endemic equilibria. So, the number of endemic equilibrium is uncertain when R0>1.

    Lastly, we will investigate the effect of α and b on diseases transmission through numerical simulations. The parameters in Figure 4 are the same as those in Figure 1(b) and R0=1.5008>1. From Figure 4, we can observe that the larger α or b, the value of θ(t) at steady state will be smaller, which means that the final density of infected individuals will also be smaller. This indicates that the behavioral change of individuals can indeed suppress the spread of the diseases. Besides, enriching the adequate hospital beds is also important for the control of the diseases.

    Figure 4.  The time evolutions of θ(t) with initial condition θ(0)=0.01. (a) α=3×(i1), (b) b=0.003×(i1),i=1,2,,5.

    Many scholars proved that the number of hospital beds plays an important role in the occurrence of bifurcation [5,6,20,21,22], but most of them studied the homogeneously mixed models. In [6], Cui et al. obtained a quadratic equation with respect to I and discussed the existence and classification of equilibrium from the algebraic perspective. The condition for the existence of backward bifurcation is proved by reducing system (1.3) into the center manifold. In this paper, a network-based SIR epidemic model which is the extension of model (1.3) is proposed. Using the edge-compartmental approach, we reduced the dimension of the system. It is proved that when θR0|(R0,θ)=(1,0)<0b<ˆb, backward bifurcation will occur at R0=1. The method is different from the approach in [6]. Moreover, the condition which determines the direction of bifurcation at R0=1 is related to the network structure.

    It is also possible that system (2.2) exists multiple endemic equilibria when R0>1 (see Figure 3). In conclusion, the condition R0<1 is not enough to guarantee the global asymptotic stability of E0, and R0>1 does not confirm the uniqueness of endemic equilibrium. In addition, we established a relationship between the local stability of endemic equilibrium and the tangent slope of the epidemic curve. It is observed that the larger α or b can reduce the endemic level (see Figure 4). Therefore, the effect from the individual behavioral change should not be ignored and the hospital beds should be adequately provided in the process of controlling the infectious diseases.

    However, whether system (2.2) can exhibit more complex dynamical behavior such as Hopf, saddle-node, transcritical and Bogdanov-Takens bifurcation are not discussed. At present, the bifurcation theory on networks is still less. It will be interesting and important to solve the problem and we leave this for future work.

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

    Research Project Supported by National Nature Science Foundation of China (Grant Nos. 12071445, 12271519), the Fundamental Research Program of Shanxi Province (Grant Nos. 20210302123031, 202203021211091), the Science and Technology Innovation Program of higher education in Shanxi Province (Grant No. 2023L436).

    The authors declare there is no conflict of interest in this paper.



    [1] Cholera Fact Sheets, World Health Organization, August 2017. Available from: https://www.who.int/en/news-room/fact-sheets/detail/cholera.
    [2] J. H. Tien and D. J. D. Earn, Multiple transmission pathways and disease dynamics in a waterborne pathogen model, Bull. Math. Biol., 72 (2010), 1506–1533.
    [3] X. Zhou and J. Cui, Threshold dynamics for a cholera epidemic model with periodic transmission rate, Appl. Math. Model., 37 (2013), 3093–3101.
    [4] D. Posny, J. Wang, Z. Mukandavire, et al., Analyzing transmission dynamics of cholera with public health interventions, Math. Biosci., 264 (2015), 38–53.
    [5] Y. Wang and J. Cao, Global stability of general cholera models with nonlinear incidence and removal rates, J. Frankl. Inst., 352 (2015), 2464–2485.
    [6] J. P. Tian and J. Wang, Global stability for cholera epidemic models, Math. Biosci., 232 (2011), 31–41.
    [7] D. M. Hartley, J. G. Morris and D. L. Smith, Hyperinfectivity: A critical element in the ability of V. cholerae to cause epidemics? PLoS Med., 3 (2006), 63–69.
    [8] R. L. M. Neilan, E. Schaefer, H. Gaff, et al., Modeling optimal intervention strategies for cholera, Bull. Math. Biol., 72 (2010), 2004–2018.
    [9] Z. Mukandavire, S. Liao, J. Wang, et al., Estimating the reproductive numbers for the 2008–2009 cholera outbreaks in Zimbabwe, PNAS, 108 (2011), 8767–8772.
    [10] T. K. Sengupta, R. K. Nandy, S. Mukhopadhyay, et al., Characterization of a 20-kDa pilus protein expressed by a diarrheogenic strain of non-O1/non-O139 vibrio cholerae, FEMS Microbiol. Lett., 160 (1998), 183–189.
    [11] C. T. Codec ¸o, Endemic and epidemic dynamics of cholera: the role of the aquatic reservoir, BMC Infect. Dis., 1 (2001), 1–14.
    [12] C. Modnak, A model of cholera transmission with hyperinfectivity and its optimal vaccination control, Int. J. Biomath., 10 (2017), 1750084.
    [13] A.P.Lemos-Paião, C.J.SilvaandD.F.M.Torres, A cholera mathematical model with vaccination and the biggest outbreak of world's history, AIMS Mathematics, 3 (2018), 448–463.
    [14] J. K. Hale and S. Verduyn Lunel, Introduction to Functional Differential Equations, 1st edition, Springer-Verlag, New York, 1993.
    [15] P. van den Driessche and J. Watmough, Reproduction numbers and sub-threshold endemic equilibria for compartmental models of disease transmission, Math. Biosci., 180 (2002), 29–48.
    [16] O. Sharomi and T. Malik, Optimal control in epidemiology, Ann. Oper. Res., 251 (2017), 55–71.
    [17] J. K. K. Asamoah, F. T. Oduro, E. Bonyah, et al., Modelling of rabies transmission dynamics using optimal control analysis, J. Appl. Math., 12 (2017), 1–23.
    [18] L. Cesari, Optimization-Theory and Applications. Problems with ordinary differential equations, in: Applications of Mathematics, vol. 17, Springer-Verlag, New York, 1983.
    [19] W. H. Fleming and R. W. Rishel, Deterministic and Stochastic Optimal Control, 1st edition, Springer-Verlag, New York, 1975.
    [20] L. Pontryagin, V. Boltyanskii, R. Gramkrelidze, et al., The Mathematical Theory of Optimal Processes, John Wiley & Sons, 1962.
    [21] C. J. Silva and D. F. M. Torres, Optimal control for a tuberculosis model with reinfection and post-exposure interventions, Math. Biosci., 244 (2013), 154–164.
    [22] M. McAsey, L. Mou and W. Han, Convergence of the forward-backward sweep method in optimal control, Comput. Optim. Appl., 53 (2012), 207–226.
    [23] O. Zakary, A. Larrache, M. Rachik, et al., Effect of awareness programs and travel-blocking operations in the control of HIV/AIDS outbreaks: a multi-domains SIR model, Adv. Differ. Equ., 2016 (2016), 169.
    [24] C. Modnak, J. Wang and Z. Mukandavire, Simulating optimal vaccination times during cholera outbreaks, Int. J. Biomath., 7 (2014), 1450014.
    [25] J. Wang and C. Modnak, Modeling cholera dynamics with controls, Canadian Appl. Math. Quart., 19 (2011), 255–273.
    [26] D.S.Merrell, S.M.Butler, F.Qadri, et al., Host-induced epidemic spread of the cholera bacterium, Nature, 417 (2002), 642–645.
    [27] S. Lenhart and J. T. Workman, Optimal control applied to biological models, Chapman & Hall/CRC Press, Boca Raton, 2007.
    [28] Global Task Force on Cholera Control, Cholera Country Profile: Haiti, World Health Organization, May 2011. Available from: https://www.who.int/cholera/countries/HaitiCountryProfileMay2011.pdf.
    [29] A. P. Lemos-Paião, C. J. Silva and D. F.M. Torres, An epidemic model for cholera with optimal control treatment, J. Comput. Appl. Math., 318 (2017), 168–180.
  • Reader Comments
  • © 2019 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Metrics

Article views(5398) PDF downloads(922) Cited by(17)

Figures and Tables

Figures(5)  /  Tables(2)

Other Articles By Authors

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog