Dynamical behaviors of an Echinococcosis epidemic model with distributed delays

  • Received: 26 July 2016 Accepted: 09 March 2017 Published: 01 October 2017
  • MSC : Primary: 37N25, 93D30; Secondary: 92B05

  • In this paper, a novel spreading dynamical model for Echinococcosis with distributed time delays is proposed. For the model, we firstly give the basic reproduction number R0 and the existence of a unique endemic equilibrium when R0>1. Furthermore, we analyze the dynamical behaviors of the model. The results show that the dynamical properties of the model is completely determined by R0. That is, if R0<1, the disease-free equilibrium is globally asymptotically stable, and if R0>1, the model is permanent and the endemic equilibrium is globally asymptotically stable. According to human Echinococcosis cases from January 2004 to December 2011 in Xinjiang, China, we estimate the parameters of the model and study the transmission trend of the disease in Xinjiang, China. The model provides an approximate estimate of the basic reproduction number R0=1.23 in Xinjiang, China. From theoretic results, we further find that Echinococcosis is endemic in Xinjiang, China. Finally, we perform some sensitivity analysis of several model parameters and give some useful measures on controlling the transmission of Echinococcosis.

    Citation: Kai Wang, Zhidong Teng, Xueliang Zhang. Dynamical behaviors of an Echinococcosis epidemic model with distributed delays[J]. Mathematical Biosciences and Engineering, 2017, 14(5&6): 1425-1445. doi: 10.3934/mbe.2017074

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  • In this paper, a novel spreading dynamical model for Echinococcosis with distributed time delays is proposed. For the model, we firstly give the basic reproduction number R0 and the existence of a unique endemic equilibrium when R0>1. Furthermore, we analyze the dynamical behaviors of the model. The results show that the dynamical properties of the model is completely determined by R0. That is, if R0<1, the disease-free equilibrium is globally asymptotically stable, and if R0>1, the model is permanent and the endemic equilibrium is globally asymptotically stable. According to human Echinococcosis cases from January 2004 to December 2011 in Xinjiang, China, we estimate the parameters of the model and study the transmission trend of the disease in Xinjiang, China. The model provides an approximate estimate of the basic reproduction number R0=1.23 in Xinjiang, China. From theoretic results, we further find that Echinococcosis is endemic in Xinjiang, China. Finally, we perform some sensitivity analysis of several model parameters and give some useful measures on controlling the transmission of Echinococcosis.


    1. Introduction

    Echinococcosis, which is often referred to as a hydatid disease, is a parasitic disease that affects both humans and other mammals, such as sheep, dogs, rodents and horses [3]. There are three different forms of Echinococcosis found in humans, each of which is caused by the larval stages of different species of the tapeworm of genus Echinococcus. The first of the three and also the most common form found in humans is cystic Echinococcosis, which is caused by Echinococcus granulosus. The second is alveolar Echinococcosis, which is caused by Echinococcus multilocularis and the third is polycystic Echinococcosis, which is caused by Echinococcus vogeli and very rarely, Echinococcus oligarthus. Alveolar and polycystic Echinococcosis are rarely diagnosed in humans and are not as widespread as cystic Echinococcosis. Thus, we focus on cystic Echinococcosis in this paper.

    Echinococcus granulosus is an extremely small tapeworm, only 4-6 mm in length in its adult stage. This stage occurs in carnivore "definitive hosts, " generally dogs, wolves, coyotes, or wild dogs [17]. When mature, the adult tapeworm produces eggs that are passed in feces of the infected carnivore. The eggs contaminate foliage or vegetation which may be eaten by grazing animals, the "intermediate hosts, " generally ruminants such as sheep, goats, or cattle, although an extremely wide range of potential intermediate hosts exists. After the intermediate host ingests tapeworm eggs, the eggs hatch into tiny embryos in the small intestine of that host. These small mobile forms penetrate the intestinal mucosa, enter the circulatory tract, and are then transported via the bloodstream to various filtering organs in that host. The embryo lodges in those organs and there develops into a larval cystic form termed the "hydatid cyst". Eventually a thick wall develops around the hydatid cyst, and numerous tiny tapeworm heads are produced via asexual division within "brood capsules" from the germinal lining of each hydatid cyst. If parts of the viscera containing hydatid cysts are eaten by suitable carnivore hosts, then the tiny protoscolices are liberated from the brood capsules, evaginate their head region with its suckers and hooks, and move actively to eventually attach to the intestinal mucosa. There they grow within approximately 40 days to the adult stage to the tapeworm, which is then capable of producing eggs. Humans act as intermediate hosts for Echinococcus granulosus, and are infected when they ingest tapeworm eggs from the definitive host. The eggs may be eaten in foods such as vegetables, fruits or herbs, or drunk in contaminated water. The life cycle of Echinococcus granulosus is shown in Figure 1.

    Figure 1. Life cycle of Echinococcus granulosus.

    China is one of the countries in the world which have the most serious Echinococcosis. A national survey of important parasitic diseases in 2004 showed that the average prevalence of Echinococcosis in epidemic areas was about 1.08%. About 380000 people in the country are infected. During 2004-2008, China's 27 provinces and municipalities had Echinococcosis case reports, and 98.2% of reported cases distributed in Xinjiang, Inner Mongolia, Sichuan, Tibet, Gansu, Qinghai, Ningxia. At least 66 million people in China are threatened by Echinococcosis [20].

    Echinococcosis is widely distributed and highly endemic in Xinjiang, China. Between 2004 and 2011, a total of 6086 human Echinococcosis cases were reported in Xinjiang, China (see Figure 2 [22]).

    Figure 2. Monthly new reported Echinococcosis cases in Xinjinag from 2004 to 2011.

    The average infection rates in sheep, cattle and dogs were 54.20%, 15.21% and 24.52%, respectively [9]. During 2008-2009, Xinjiang, China supervising agency for animal epidemic prevention examined Echinococcosis infection of liver and lung samples of cattle and sheep in fix point slaughter houses (see Table 2 [11]). Meanwhile, Echinococcus granulosus infection for dogs was also examined in various parts of Xinjiang, China (see Table 2 [23]).

    Table 1. Infection of cattle and sheep liver/lung in Xinjiang, China.
    Region Infection rate
    Sheep Cattle
    Northern Xinjiang Ili 70% 41%
    Tacheng 63% 25%
    Altay 65.8% 27%
    Changji 50.78% 9.23%
    Southern Xinjiang Kashgar 47% -
    Hotan 25% 18%
    Kezilesu Kirgiz Autonomous Prefecture 38% 6.2%
    Aksu 50.3% 6.29%
    Bayingolin Mongolia Autonomous Prefecture 60.3% 12.3%
    Eastern Xinjiang Hami 42% 17%
    Turpan 36% 16.68%
     | Show Table
    DownLoad: CSV
    Table 2. Infection of dog in Xinjiang, China.
    Region Infection rate
    Northern Xinjiang Ili 70%
    Tacheng 63%
    Altay 65.8%
    Changji 50.78%
    Southern Xinjiang Kashgar 47%
    Hotan 25%
    Kezilesu Kirgiz Autonomous Prefecture 38%
    Aksu 50.3%
    Bayingolin Mongolia Autonomous Prefecture 60.3%
    Eastern Xinjiang Hami 42%
    Turpan 36%
     | Show Table
    DownLoad: CSV

    Mathematical modeling is an important method of studying the spread of infectious disease qualitatively and quantitatively. Models can be used to understand how an infectious disease spreads in the real world, and how various complexities affect the dynamics. There have been some modeling studies on different aspects of Echinococcosis, and most of them are statistical models. A base-line survey was carried out on the transmission dynamics of Echinococcus granulosus, Taenia hydatigena and Taenia ovis in sheep in Uruguay by Cabrera et al. in [4]. The Echinococcus granulosus was only relative stable and the basic reproduction ratio was estimated about 1.2 in an endemic steady state. The effects of the different transmission levels of the parasites on potential control strategies were discussed. Torgerson et al. [16] examined the abundance and prevalence of infection of Echinococcus granulosus in cattle and sheep in Kazakhstan. Maximum likelihood techniques were used to define the parameters and their confidence limits in the model and the negative binomial distribution was used to define the error variance in the observed data. Lahmar et al. [8] examined the abundance and prevalence of infection of Echinococcus granulosus in camels in Tunisia.

    Recently, dynamic models of Echinococcosis have been discussed in [19,21]. The work [19] proposed a deterministic model to study the transmission dynamics of Echinococcosis in Xinjiang, China. The results demonstrated that the dynamics of the model were completely determined by the basic reproductive number R0. The authors showed that Echinococcosis was endemic in Xinjiang, China with the current control measures. In [21] two mathematical models, the baseline model and the intervention model, were proposed to study the transmission dynamics of Echinococcosis. Applying these mathematical models to Qinghai Province, China, the authors showed that the infection of Echinococcosis was in an endemic state. In [19,21], the authors considered the density of Echinococcus eggs as a compartment in their models. However, it is hard to obtain the parameters of Echinococcus eggs in actual epidemiological surveys. To solve this problem, we take Echinococcus eggs in the environment as vectors and propose a novel spreading model for Echinococcosis with distributed time delays in this paper. We will evaluate the basic reproduction number R0 and analyze the dynamical behaviors of the model. According to human Echinococcosis cases from January 2004 to December 2011 in Xinjiang, China, we will estimate the parameters of the model and study the transmission trend of the disease in Xinjiang, China. We will also carry out some sensitivity analysis of the basic reproduction number R0 in terms of various model parameters. Finally, we shall suggest some strategies for control Echinococcosis infection in Xinjiang, China.

    The article is organized as follows. The model is presented in Section 2. The basic properties on the positivity and boundedness of solutions, computation of the basic reproduction number and the existence of endemic equilibrium for the model are discussed in Section 3. In Section 4, we establish the global stability of the disease-free equilibrium for the model. In Section 5, we will apply the theory of permanence for infinite-dimensional systems to obtain the permanence of the model. The global stability theorem of the endemic equilibrium is stated and proved in Section 6. In Section 7, we estimate the parameters of the model and study the transmission trend of the disease in Xinjiang, China. A brief discussion is given in Section 8.


    2. Model formulation

    Based on the transmission mechanism of Echinococcosis, we consider dogs being the definitive hosts, livestock being the intermediate hosts, humans represented as an accidental intermediate hosts respectively.

    The dogs population is subdivided into two classes: the susceptible population and the infected population denoted by SD(t) and ID(t), respectively. For livestock population, we separate the total livestock population into two classes: susceptible and infectious denoted by SL(t) and IL(t), respectively. Humans are infected when they ingest tapeworm eggs from the definitive host. We separate the total population into three classes: susceptible, exposed and infectious denoted by SH(t), EH(t) and IH(t), respectively.

    To model the Echinococcosis infection delay from infected livestock to susceptible dogs, we let τ be the random variable that describes the time between infection offal thrown in the environment and eaten by dogs with a probability distribution f1(τ). h1 denotes the average survival time of larval cysts into the infection offal thrown in the environment. Here, f1: [0,h1][0,+) is continuous on [0,h1] satisfying h10f1(τ)dτ=1. When infection offal was dropped in the environment at time th1, the number of infected dogs at time t is given by

    β1SD(t)h10f1(τ)IL(tτ)dτ.

    To model the Echinococcosis infection delay from infected dogs to susceptible livestock, we let τ be the random variable that is the time between eggs produced by infected dogs and ingestion by susceptible livestock with a probability distribution f2(τ). h2 describes average life expectancy for Echinococcus eggs. f2(τ) is assumed to be non-negative and continuous on [0,h2] satisfying h20f2(τ)dτ=1. When infected dogs produced Echinococcus eggs at time th2, the number of infected livestock at time t is given by

    β2SL(t)h20f2(τ)ID(tτ)dτ.

    Humans act as an accidental intermediate host for Echinococcosis. Thus, similarly to the infection of livestock, the number of infected human at time t is given by

    β3SH(t)h20f3(τ)ID(tτ)dτ,

    where f3(τ) is a probability distribution. Because the range of movement for humans and livestock is different, we choose distribution function in different forms. Hence, distribution f3(τ) is different from f2(τ). Similarly, f3(τ) is assumed to be non-negative and continuous on [0,h2] satisfying h20f3(τ)dτ=1.

    Based on the above discussions, a dynamical model of Echinococcosis with distributed time delays can be written as:

    {dSD(t)dt=A1β1SD(t)h10f1(τ)IL(tτ)dτd1SD(t)+σID(t),dID(t)dt=β1SD(t)h10f1(τ)IL(tτ)dτ(d1+σ)ID(t),dSL(t)dt=A2β2SL(t)h20f2(τ)ID(tτ)dτd2SL(t),dIL(t)dt=β2SL(t)h20f2(τ)ID(tτ)dτd2IL(t),dSH(t)dt=A3β3SH(t)h20f3(τ)ID(tτ)dτd3SH(t)+γIH(t),dEH(t)dt=β3SH(t)h20f3(τ)ID(tτ)dτ(d3+ω)EH(t),dIH(t)dt=ωEH(t)(d3+μ+γ)IH(t). (1)

    All parameters in model (1) are assumed to be positive constants. For the dog population, A1 describes the annual recruitment rate; d1 is the natural death rate; σ denotes the recovery rate of transition from infected to non-infected dogs, including natural recovery rate and recovery due to anthelmintic treatment; For the livestock population, A2 is the annual recruitment rate; d2 is the death rate; For human population, A3 is the annual recruitment rate; d3 is the natural death rate; μ is the disease-related death rate; 1/ω denotes the incubation period of infected individuals; γ denotes the recovery rate.

    Motivated by biological background of model (1), the initial conditions for model (1) are given as follows

    {SD(θ)=ϕ1(θ), ID(θ)=ϕ2(θ), SL(θ)=ϕ3(θ), IL(θ)=ϕ4(θ),SH(θ)=ϕ5(θ), EH(θ)=ϕ6(θ), IH(θ)=ϕ7(θ), (2)

    where ϕ=(ϕ1,ϕ2,,ϕ7)C([h,0],R7+), h=max{h1,h2}. In this paper, for any integer n>0 we denote by C([h,0],Rn+) the Banach space of all continuous functions ϕ:[h,0]Rn+ with sup-norm ϕ=suphθ0|ϕ(θ)|.


    3. Basic properties

    For any ε>0, we define the region Γε as follows.

    Γε={(SD,ID,SL,IL,SH,EH,IH)R7+, SD+IDA1d1+ε,SL+ILA2d2+ε,SH+EH+IHA3d3+ε}.

    Firstly, on the positivity and ultimate boundedness of solutions for model (1), we have the following result.

    Lemma 3.1. ( i ) The solution of model (1) with initial conditions (2) satisfy (SD(t),ID(t),SL(t),IL(t),SH(t),EH(t),RH(t))>0 for all t>0.

    ( ii ) All solutions of model (1) with initial conditions (2) ultimately turn into the region Γε as t.

    The proof of Lemma 3.1 is simple, we hence omit it here.

    Remark 3.2. According to Lemma 3.1, all feasible solutions of model (1) enter or remain in the region Γε as t is large enough. Therefore, the dynamics of model (1) can be considered only in Γε.

    Simple algebraic calculation shows that model (1) always has a disease-free equilibrium E0=(S0D,0,S0L,0,S0H,0,0), where

    S0D=A1d1,S0L=A2d2,S0H=A3d3.

    Following the idea in [24,18], we can introduce the basic reproduction number for model (1) as follows

    R0=β1β2A1A2d1d22(d1+σ).

    Remark 3.3. To better understand the basic reproduction number, we rewrite it as

    R0=A2d21d1+σβ2A1d11d2β1.

    The biological meaning of R0 can be interpreted as follows, near the disease free equilibrium, the total number of livestock reaches at a stable state A2/d2 and every livestock will be susceptible. Then susceptible livestock is infected by infectious dogs over its expected infectious period 1/(d1+σ) with probability β2. Furthermore, the total number of dogs reaches stable state A1/d1 and every dog will be susceptible, which is infected by infectious livestock over its expected infectious period 1/d2 with probability β1. The square root arises from the two 'generations' required for an infected dogs or livestock to 'reproduce' itself.

    It can be proved that if R0>1 then model (1) has a unique endemic equilibrium E(SD,ID,SL,IL,SH,EH,IH), where

    SD=d2(d1+σ)(A1β2+d1d2)β2d1(β1A2+d1d2+d2σ),ID=β1β2A1A2d1d22(d1+σ)d1β2(β1A2+d1d2+d2σ)=d22(d1+σ)β2(β1A2+d1d2+d2σ)(R201),SL=d1(β1A2+d1d2+d2σ)β1(A1β2+d1d2),IL=β1β2A1A2d1d22(d1+σ)d2β1(A1β2+d1d2)=d1d2(d1+σ)β1(A1β2+d1d2)(R201),SH=A3(d3+ω)(d3+μ+γ)(β3ID+d3)(d3+ω)(d3+μ+γ)γωβ3ID,EH=β3SHID(d3+ω),IH=ωβ3SHID(d3+ω)(d3+μ+γ).

    Therefore, we finally have the following theorem.

    Theorem 3.4. ( i ) Model (1) always has a disease-free equilibrium E0.

    ( ii ) Model (1) has a unique endemic equilibrium E if and only if R0>1.


    4. Global stability of E0

    Regarding the stability of the disease-free equilibrium E0, we have the following result.

    Theorem 4.1. If R0<1, then the disease-free equilibrium E0 of model (1) is globally asymptotically stable in Γε.

    Proof. Notice that the last three equations are independent of the first four equations, we start by considering the first four equations,

    {dSD(t)dt=A1β1SD(t)h10f1(τ)IL(tτ)dτd1SD(t)+σID(t),dID(t)dt=β1SD(t)h10f1(τ)IL(tτ)dτ(d1+σ)ID(t),dSL(t)dt=A2β2SL(t)h20f2(τ)ID(tτ)dτd2SL(t),dIL(t)dt=β2SL(t)h20f2(τ)ID(tτ)dτd2IL(t). (3)

    Since R0<1, it follows that

    d22(d1+σ)β2A2(R201)=β1A1d1d22(d1+σ)β2A2<0.

    Hence, there is a small enough constant ε>0 such that

    β1(A1+d1ε)d1d22(d1+σ)β2(A2+d2ε)<0.

    Let (SD(t),ID(t),SL(t),IL(t),SH(t),EH(t),IH(t)) be any solution of model (1) in Γε. Then,

    SD(t)A1d1+ε, SL(t)A2d2+εfor allt0.

    Consider the following Lyapunov functional

    V(t)=ID(t)+β1h10f1(τ)ttτSD(u+τ)IL(u)dudτ+d2(d1+σ)β2(A2+d2ε)(IL(t)+β2h20f2(τ)ttτSL(u+τ)ID(u)dudτ),

    calculating the derivative of V(t) along the solution of system (3), we have

    ˙V(t)=β1SD(t)h10f1(τ)IL(tτ)dτ(d1+σ)ID(t)+β1IL(t)h10f1(τ)SD(t+τ)dτβ1SD(t)h10f1(τ)IL(tτ)dτ+d2(d1+σ)β2(A2+d2ε)(β2SL(t)h20f2(τ)ID(tτ)dτd2IL(t)+β2ID(t)h20f2(τ)SL(t+τ)dτβ2SL(t)h10f1(τ)ID(tτ)dτ)=(d1+σ)ID(t)+β1IL(t)h10f1(τ)SD(t+τ)dτ+d2(d1+σ)β2(A2+d2ε)(d2IL(t)+β2ID(t)h20f2(τ)SL(t+τ)dτ)(d1+σ)ID(t)+β1(A1d1+ε)IL(t)+d2(d1+σ)β2(A2+d2ε)(d2IL(t)+β2(A2d2+ε)ID(t))=(β1(A1+d1ε)d1d22(d1+σ)β2(A2+d2ε))IL(t)0.

    Let E={(SD,ID,SL,IL):˙V=0}. Then, we have E{(SD,ID,SL,IL):IL=0}. Let ME be the largest invariant set with respect to system (3) and let further (SD(t),ID(t),SL(t),IL(t)) be any solution of system (3) which retains in M for all tR, then (SD(t),ID(t),SL(t),IL(t)) is defined and bounded on tR.

    Since M{(SD,ID,SL,IL):IL=0}, we have IL(t)0. Furthermore, from the fourth equation of system (3), we have SL(t)h20f2(τ)ID(tτ)dτ0. Therefore, we have

    dSD(t)dt=A1d1SD(t)+σID(t)dID(t)dt=(d1+σ)ID(t),dSL(t)dt=A2d2SL(t).

    Solving second equation, we have

    ID(t)=ID(0)exp((d1+σ)t)for alltR.

    Hence, ID(t)0. Otherwise, ID(t) will be unbounded on R.

    Since

    SD(t)=A1d1+SD(0)exp(d1t)for alltR,

    then we also have SD(0)0. Otherwise SD(t) will be unbounded on R. Therefore SD(t)A1/d1. Similarly, we can obtain SL(t)A2/d2. Finally, we have (SD(t),ID(t),SL(t),IL(t))=(A1/d1,0,A2/d2,0). This shows that M{(A1/d1,0,A2/d2,0)}. By the LaSalle invariance principle, (A1/d1,0,A2/d2,0) of system (3) is globally asymptotically stable.

    Next, we consider the last three equations

    {dSH(t)dt=A3β3SH(t)h20f3(τ)ID(tτ)dτd3SH(t)+γIH(t),dEH(t)dt=β3SH(t)h20f3(τ)ID(tτ)dτ(d3+ω)EH(t),dIH(t)dt=ωEH(t)(d3+μ+γ)IH(t). (4)

    Since ID(t)0 as t, we obtain that EH(t)0 as t by the second equation of system (4). Furthermore, from the third equation of system (4) we also have IH(t)0 as t. Lastly, from the first equation of system (4) we finally have that SH(t)A3/d3 as t. Therefore, (A3/d3,0,0) is globally attractive with respect to system (4). Thus, according to the theory of asymptotic autonomous system [15], we finally obtain that the disease-free equilibrium E0 is globally asymptotically stable for model (1) when R0<1. This completes the proof of Theorem 4.1.


    5. Permanence

    In this section, we will apply the theory of persistence for infinite-dimensional dynamical system from [7] to obtain the permanence of model (1).

    Let X be a complete metric space with metric d. Suppose that T(t):XX,t0, is a C0-semigroup on X. For any xX, the positive orbit γ+(x) through x is defined as γ+(x)={T(t)x:t0}, and its ω-limit set is ω(x)={yX: there is a time sequence tk such that limkT(tk)x=y}. Let X0 and X0 be two nonempty subsets such that X=X0X0 and X0X0=. Further, we assume that C0-semigroup T on X satisfies

    T(t):X0X0,T(t):X0X0.

    We denote T0(t)=T(t)|X0 and T0(t)=T(t)|X0. We further assume that there is a global attractor A0 for T0 in X0, and let

    ˜A0={ω(x):xA0}.

    Furthermore, the definitions of the compactness, point dissipativity and the uniform persistence for C0-semigroup T on X, and the definitions of the isolated invariance and acyclic covering for a subset AX, can be found in Kuang [7].

    Now, we state the following lemma, which can be found in ([7], Theorem 2.4).

    Lemma 5.1. Assume that

    ( i ) there is a t00 such that T(t) is compact in X for t>t0;

    ( ii ) T(t) is point dissipative in X;

    ( iii ) ˜A0 is isolated and has an acyclic covering M=ki=1Mi.

    Then T(t) is uniform persistent if and only if

    Ws(Mi)X0=,i=1,2,,k,

    where Ws(Mi)={xX:ω(x),ω(x)Mi} is the stable set of Mi.

    In the following, as an application of this lemma, we establish the result on the permanence of model (1).

    Theorem 5.2. If R0>1, then model (1) is permanent.

    Proof. We firstly prove the permanence of system (3). To apply Lemma 5.1, we choose space X=C([h,0],R4+), and sets X0 and X0 are defined by

    X0={(ϕ1,ϕ2,ϕ3,ϕ4)X:ϕ2(θ)>0 or ϕ4(θ)>0 for some θ[h,0]},X0={(ϕ1,ϕ2,ϕ3,ϕ4)X:ϕ2(θ)0, ϕ4(θ)0 for all θ[h,0]}.

    Denote ϕ=(ϕ1,ϕ2,ϕ3,ϕ4) and x=(SD,ID,SL,IL). Let x(t,ϕ)=(SD(t,ϕ),ID(t,ϕ),SL(t,ϕ),IL(t,ϕ)) be the solution of system (3) with initial value ϕ at t=0. We define C0-semigroup T(t) in Lemma 5.1 as follows

    T(t)ϕ=xt(ϕ),ϕX,t0,

    where xt(ϕ)=x(t+s,ϕ) with s[h,0].

    Now, we verify that all the conditions of Lemma 5.1 are satisfied.

    Firstly, we show that X0 and X0 are positively invariant sets. Let ϕ=(ϕ1,ϕ2,ϕ3,ϕ4)X0, from system (3) we can obtain

    SD(t,ϕ)SD(0,ϕ)exp(β1t0h10f1(τ)IL(sτ,ϕ)dτdsd1t),ID(t,ϕ)=e(d1+σ)t{ID(0,ϕ)+t0β1SD(ρ,ϕ)h10f1(τ)IL(ρτ,ϕ)dτe(d1+σ)ρdρ},SL(t,ϕ)SL(0,ϕ)exp(β2t0h20f2(τ)ID(sτ,ϕ)dτdsd2t),IL(t,ϕ)=ed2t{IL(0,ϕ)+t0β2SL(ρ,ϕ)h20f2(τ)ID(ρτ,ϕ)dτed2ρdρ} (5)

    for all t>0. Obviously, SD(t,ϕ)0 and SL(t,ϕ)0 for all t0. If there is a t1>0 such that ID(t1)=0 and IL(t1)=0, then from (5) we can obtain ID(0,ϕ)=IL(0,ϕ)=0 and for any s[0,t1]

    h20f2(τ)ID(sτ,ϕ)dτ=0,h10f1(τ)IL(sτ,ϕ)dτ=0.

    Hence, we have ϕ2(θ)=ϕ4(θ)=0 for all θ[h,0]. This leads to a contradiction with ϕ=(ϕ1,ϕ2,ϕ3,ϕ4)X0. Therefore, ID(t,ϕ)>0 and IL(t,ϕ)>0 for all t0. This shows that xt(ϕ)=(SDt(ϕ),IDt(ϕ),SLt(ϕ),ILt(ϕ))X0 for all t0. This implies that X0 is positively invariant.

    Let ϕ=(ϕ1,ϕ2,ϕ3,ϕ4)X0. Since ϕ2=ϕ4=0, by the existence and uniqueness theorem of solutions for the functional differential equations, we have

    ID(t,ϕ)0,IL(t,ϕ)0for allt0.

    From this, we obtain that X0 also is positively invariant.

    Denote by ω(ϕ) the ω-limit set of the solution of model (3) starting at t=0 with initial value ϕX. Let

    Ω={ω(ϕ):ϕX0},E0=(A1d1,0,A2d2,0).

    Restricting system (3) to X0, we obtain

    {dSD(t)dt=A1d1SD(t)dSL(t)dt=A2d2SL(t). (6)

    It is easy to verify that system (6) has a unique equilibrium (A1/d1,A2/d2), which is globally asymptotically stable. Therefore, we have Ω={E0}, and E0 is a covering of Ω, which is isolated (since E0 is the unique equilibrium) and is acyclic (since there exists no solution in X0 which links E0 to itself). It remains to show that

    Ws(E0)X0=, (7)

    where Ws(E0) denotes the stable manifold of E0. Suppose that (7) does not hold, then there exists a solution (SD(t),ID(t),SL(t),ID(t)) of model (3) with initial conditions in X0, such that

    limtSD(t)=A1d1,  limtID(t)=0,  limtSL(t)=A2d2,  limtIL(t)=0. (8)

    Since R0=β1β2A1A2d1d22(d1+σ)>1, we can choose a small enough constant ϵ>0 such that A1/d1ϵ>0, A2/d2ϵ>0 and

    Rϵ0β1β2(A1d1ϵ)(A2d2ϵ)d1d22(d1+σ)>1.

    For this ϵ>0, by (8), there exists a t1>0 such that

    SD(t)>A1d1ϵ,SL(t)>A2d2ϵfor alltt1.

    Hence, by system (3), we have

    dID(t)dtβ1(A1d1ϵ)h10f1(τ)IL(tτ)dτ(d1+σ)ID(t),dIL(t)dtβ2(A2d2ϵ)h20f2(τ)ID(tτ)dτd2IL(t)

    for all tt1. Consider the following auxiliary system

    dU(t)dt=β1(A1d1ϵ)h10f1(τ)V(tτ)dτ(d1+σ)U(t),dV(t)dt=β2(A2d2ϵ)h20f2(τ)U(tτ)dτd2V(t). (9)

    Let (U(t),V(t)) be the solution of system (9) with initial conditions U(t1+θ)=ID(t1+θ) and V(t1+θ)=IL(t1+θ) for all θ[τ,0], by the comparison theorem of functional differential equations([12], Chapter 5, Theorem 1.1) we have

    ID(t)U(t),IL(t)V(t)for alltt1.

    From (8), we further have

    limtU(t)=0,limtV(t)=0. (10)

    Consider the following auxiliary function

    W(t)=W1(t)+d1+σβ2(A2d2ϵ)W2(t),

    where

    W1(t)=U(t)+β1(A1d1ϵ)h10f1(τ)ttτV(ρ)dρdτ

    and

    W2(t)=V(t)+β2(A2d2ϵ)h20f2(τ)ttτU(ρ)dρdτ.

    Then, from (10) we have

    limtW(t)=0.

    Calculating the derivative of W(t) along the solution of system (9), we have

    ˙W(t)=˙W1(t)+d1+σβ2(A2d2ϵ)˙W2(t)=β1(A1d1ϵ)[1d1d22(d1+σ)β1β2(A1d1ϵ)(A2d2ϵ)]V(t)=β1(A1d1ϵ)(11(Rϵ0)2)V(t)>0.

    Therefore, W(t) increases as t increases. This shows that W(t) does not tend to zero as t, which leads a contradiction. Therefore, (7) holds and system (3) satisfies all conditions of Lemma 2. Therefore, system (3) is permanent. Then there exists a constant η>0 such that lim inftID(t)>η. For any positive number ε<η, there is a T>0 such that ID(t)>ηε, for all tT.

    Next, we prove that system (4) is also permanent. From system (4), we have

    dSH(t)dtA3(β3(ηε)+d3)SH,for all tT+h,

    it follows that

    lim inftSH(t)A3β3(ηε)+d3.

    Using a similar argument as above, we can obtain that

    lim inftEH(t)β3A3(ηε)(d3+ω)(β3(ηε)+d3)

    and

    lim inftSH(t)β3ωA3(ηε)(d3+ω)(β3(ηε)+d3)(d3+μ+γ).

    This implies that model (1) is permanent.


    6. Global stability of E

    In this section, we will obtain the stability of endemic equilibrium of model (1). We will use the theory of cooperative systems to prove the global stability of system.

    Consider the functional differential equations

    dx(t)dt=f(xt) (11)

    where f:URn is a continuously differentiable map on the open subset U of Cr. Denote x(t,ϕ) for the unique solution of (11) satisfying x0=ϕ and let [0,σϕ] be its maximal interval of existence. Now we have the following lemma, which can be found in ([26], Theorem 3.2).

    Lemma 6.1. Let f:C+τRn be a continuously differentiable cooperative map, and let F:Rn+Rn be defined by F(x)=f(ˆx), xRn+. Assume that

    (1) for any ϕC+τ with ϕi(0)=0, fi(ϕ)0 and f maps bounded sets into bounded sets;

    (2) f:C+τRn is sublinear, i.e., for any α(0,1), ϕC+r, f(αϕ)>αf(ϕ), and F:Rn+R is strictly sublinear, i.e., for any α(0,1), xRn+ with x0, F(αx)>αF(x);

    (3) f(ˆ0)=0, df(ˆ0) satisfies (R), and for any xRn+, DF(x) is irreducible.

    (a) If s(DF(0))0, then ˆ0 is globally asymptotically stable for (11) with respect to c+r;

    (b) If s(DF(0))>0, then either

        ( i ) for any ϕC+r{ˆ0}, limtxt(ϕ)=+, or alternatively,

        ( ii ) (11) admits a unique positive steady state ˆx with ˆx0 and ˆx is globally asymptotically stable with respect to C+r{ˆ0}.

    We further have the following result on the stability of the endemic equilibrium.

    Theorem 6.2. If R0>1, then endemic equilibrium E of model (1) is globally asymptotically stable.

    Proof. We still start by considering system (3). It is easily proved that SD(t)+ID(t)A1/d1 and SL(t)+IL(t)A2/d2 as t. Therefore, in system (4) we can represent SD(t) and SL(t) by A1/d1ID(t) and A2/d2SL(t), respectively, then system (3) reduces to the following system with two equations:

    {dID(t)dt=β1(A1d1ID(t))h10f1(τ)IL(tτ)dτ(d1+σ)ID(t),dIL(t)dt=β2(A2d2IL(t))h20f2(τ)ID(tτ)dτd2IL(t). (12)

    By Lemma 3.1, the dynamics of system (12) can be focused on the following restricted region

    Ω={(ID,IL):0IDA1d1, 0ILA2d2}.

    We will use Lemma 6.1 to prove the global stability of system (12). We only need to verify all assumptions in Lemma 6.1 for system (12). Consider the following equation

    dx(t)dt=f(xt)

    where x(t)=(ID(t),IL(t))T and f:C([h,0],R2+)R2 is defined by

    f(ϕ)=(f1(ϕ)f2(ϕ))=(β1(A1d1ϕ1(0))tth1f1(ts)ϕ2(s)ds(d1+σ)ϕ1(0)β2(A2d2ϕ2(0))tth1f2(ts)ϕ1(s)dsd2ϕ2(0)).

    Let

    F(x)=(F1(x1,x2)F2(x1,x2))=(β1(A1d1x1)x2(d1+σ)x1β2(A2d2x2)x1d2x2).

    For any ϕ, ψC([h,0],R2+), we have

    df1(ψ)ϕ=β1ϕ1(0)tth1f1(ts)ψ2(s)ds+β1(A1d1ψ1(0))tth1f1(ts)ϕ2(s)ds(d1+σ)ϕ1(0),df2(ψ)ϕ=β2ϕ2(0)tth2f2(ts)ψ1(s)ds+β2(A2d2ψ2(0))tth2f2(ts)ϕ1(s)dsd2ϕ2(0).

    Hence, for any ψ(0)(0,A1/d1) and ϕC([h,0],R2+) with ϕ(0)=0, we have

    df1(ψ)ϕ=β1(A1d1ψ1(0))tth1f1(ts)ϕ2(s)ds>0

    and

    df2(ψ)ϕ=β2(A2d2ψ2(0))tth2f2(ts)ϕ1(s)ds>0,

    which imply that f is a cooperative map. For any ϕC([h,0],R2+) with ϕ(0)=0, we have

    f1(ϕ)=β1A1d1tth1f1(ts)ϕ2(s)ds0,f2(ϕ)=β2A2d2tth1f2(ts)ϕ1(s)ds0.

    It is easy to see from the expression of f that f maps bounded sets in C([h,0],R2+) into bounded sets in R2+. For any α(0,1) and ϕC([h,0],R2+) we have

    f1(αϕ)=β1(A1d1αϕ1(0))tth1f1(ts)αϕ2(s)ds(d1+σ)αϕ1(0)β1(A1d1ϕ1(0))tth1f1(ts)αϕ2(s)ds(d1+σ)αϕ1(0)=αf1(ϕ).

    Using the same argument, we can show that f2(αϕ)αf2(ϕ). Therefore, the functional f is sublinear. For xR2+ with x0, we have

    F1(αx)=β1(A1d1αx1)αx2(d1+σ)αx1>α[β1(A1d1x1)x2(d1+σ)x1]=αF1(x)

    and

    F2(αx)=β2(A2d2αx2)αx1d2αx2>α[β2(A2d2x2)x1d2x2]=αF2(x).

    This shows that F is strictly sublinear. Since f(ˆ0)=0 and for any ϕC([h,0],R2+),

    df1(ˆ0)ϕ=β1A1d1tth1f1(ts)ϕ2(s)ds(d1+σ)ϕ1(0),df2(ˆ0)ϕ=β2A2d2tth2f2(ts)ϕ1(s)dsd2ϕ2(0),

    it is easy to see that df(ˆ0) satisfies assumption (R) in [26]. By computing DF(x), we have

    DF(x)=((d1+σ)β1A1d1x2β1(A1d1x1)β2(A2d2x2)d2β2A2d2x1).

    Clearly, DF(x) is irreducible for xΩ. Since

    DF(0)=((d1+σ)β1A1d1β2A2d2d2),

    the characteristic equation of DF(0) is

    det(λIDF(0))=λ2+a1λ+a0=0,

    where

    a1=d1+d2+σ,a0=d2(d1+σ)β1β2A1A2d1d2=d2(d1+σ)(1R20).

    When R0>1, we have a0<0. Hence, s(DF(0)):=max{Reλ:det(λIDF(0))=0}>0. By Lemma 6.1, one can conclude that the equilibrium (ID,IL) of system (12) is globally asymptotically stable. According to the theory of asymptotic autonomous systems [15], we further obtain that endemic equilibrium (SD,ID,SL,IL) is globally attractive for system (3).

    Next, when t, the limiting system of equation (4) is

    {dSH(t)dt=A3β3SHIDd3SH+γIH,dEH(t)dt=β3SHID(d3+ω)EH,dIH(t)dt=ωEH(d3+μ+γ)IH. (13)

    Let U(t)=SH(t)SH, V(t)=IH(t)IH, W(t)=EH(t)EH, we can transform equation (13) into the following system

    {dU(t)dt=(β3ID+d3)U(t)+γV(t),dW(t)dt=β3IDU(t)(d3+ω)W(t),dV(t)dt=ωW(t)(d3+μ+γ)V(t). (14)

    The Jacobian matrix of equation (14) at (0,0,0) is

    J|(0,0,0)=(β3IDd30γβ3ID(d3+ω)00ω(d3+μ+γ)).

    The characteristic equation is

    ϕ(λ)=λ3+a2λ2+a1λ+a0=0,

    where

    a2=3d3+β3ID+ω+μ+γ,a1=(β3ID+d3)(d3+ω)+(β3ID+d3)(d3+μ+γ)+(d3+ω)(d3+μ+γ),a0=(β3ID+d3)(d3+ω)(d3+μ+γ)β3IDωγ.

    It is clear that a0,a1,a2>0, and by simple computation, we have

    a1a2a0=6d3ωγ+2ωμγ+4d3μγ+6d3ωμ+6β3IDd3ω+6β3IDd3μ+6β3IDd3γ+2β3IDωμ+2β3IDωγ+2β3IDμγ+2β23ID2d3+8β3IDd23+β23ID2ω+β3IDω2+β23ID2μ+β3IDμ2+β23ID2γ+β3IDγ2+8d33+8d23ω+8d23μ+8d23γ+2d3ω2+2d3μ2+2d3γ2+ω2μ+ωμ2+ω2γ+ωγ2>0.

    Hence, by Routh-Hurwitz criteria, all roots of ϕ(λ)=0 have negative real parts. Furthermore, by the stability theory of linear differential equations, it follows that (0,0,0) is globally attractive for equation (14). Therefore, (SH,EH,IH) is also globally attractive for equation (13). According to theory of asymptotic autonomous systems [15], we finally obtain that endemic equilibrium E(SD,ID,SL,IL,SH,EH,IH) of model (1) is globally asymptotically stable.


    7. Numerical simulations

    In this section, we shall estimate the parameters of model (1) and study the transmission trend of the disease in Xinjiang, China. From Xinjiang Center for Disease Control and Prevention (Xinjiang CDC) [22], we have obtained the monthly numbers of reported Echinococcosis cases from January 2004 to December 2011 (see Figure 2).

    As an illustration, we take the parameters in Table 3 and give a few necessary comments:

    Table 3. Parameters and their values (unit: month−1).
    Parameters Value Comments Source
    A1 1.34×104 recruitment rate for dog [25]
    d1 0.0067 dog natural mortality rate [1]
    β1 6.3×1010 livestock to dog transmission rate fitting
    σ 1/6 recovery rate from infected to non-infected dogs [13]
    A2 8.7×106 recruitment rate for livestock [10]
    d2 0.0275 livestock mortality rate assumption
    β2 2.8×108 parasite egg-to-livestock transmission rate fitting
    h1 1/3 survival time of larval cysts into the infection offal [6]
    h2 1.17 average life expectancy for Echinococcus eggs [17]
    A3 2×104 human annual birth population [2]
    d3 0.0012 human natural mortality rate [14]
    ω 1/(14×12) human incubation period [13]
    μ 0.0793% human disease-related death rate [5]
    γ 0.0625 treatment/recovery rate assumption
    β3 2.96×1012 parasite egg-to-human transmission rate fitting
     | Show Table
    DownLoad: CSV

    (a) The number of dogs in Xinjiang, China was estimated to be 2 millions in 2004 [25]. The average life expectancy of dogs was 12.5 years [1]. Thus, d1=1/(12.5×12)=0.0067. We estimated the capacity of dogs in Xinjiang, China to be 2 millions. Thus, A12000000×0.0067=1.34×104. The adult Echinococcus granulosus resided in the small bowel of the dogs and its life expectancy was about 5-6 months [13]. We select 6 months. So, the recovery rate σ=1/6.

    (b) According to China Statistical Yearbook [10], the recruitment rate A2 for livestock population was estimated to be 8.7×106 and the mortality rate of livestock d2 was estimated to be 0.0275.

    (c) The average survival time of larval cysts into the infection offal thrown in the environment is assumed to be 7-10 days [6]. We select h1=1/3. Life expectancy is assumed to be 35 days for parasite eggs [17]. So h2=35/30=1.17.

    (d) The average life expectancy of people in Xinjiang Uygur Autonomous Region of China was 71.12 years in 2005 [14]. We take it as the current average life expectancy. Thus, d3=1/(71.12×12)=0.0012. According to the data of the Sixth Census of China [2], human annual birth population in Xinjiang, China was 2.4×105, that is A3=(2.4×105)/12=2×104. The incubation period of Echinococcosis can be months to years or even decades. We select 14 years [13].

    (e) The parameters β1, β2 and β3 are obtained by fitting the model to data. We first apply the Runge-Kutta method to obtain the numerical expression formula of model (1) with parameters β1, β2 and β3, then by the least-square estimation the estimation values of β1, β2 and β3 are given through MATLAB implementation.

    The numerical simulation of the model on the number of human Echinococcosis cases is shown in Figure 3. We can predict the general tendency of the epidemic in a long term according to the current situation, which is presented in Figure 4. It shows that the number of human Echinococcosis cases will increase steadily in the next 6 or 7 years, then reach the peak (about 120) in 2017 and begin a slow decline, and finally become stable.

    Figure 3. The comparison between the reported human Echinococcosis cases in Xinjiang, China from January 2004 to December 2011 and the simulation of IH(t) from the model. The initial values used in the simulations were SD(0)=2×106, ID(0)=8×105, SL(0)=8.4×108, IL(0)=5.7×107, SH(0)=1.96×107, EH(0)=1500, IH(0)=4.
    Figure 4. The tendency of the human Echinococcosis cases IH(t) in short and long times.

    Moreover, with these parameter values, we can roughly estimate the basic reproduction number R0=1.23 for model (1) under the current circumstances in Xinjiang, China. This indicates that human Echinococcosis is endemic in Xinjiang, China: it stabilizes and is approaching its equilibrium. Therefore, if no further effective prevention and control measures are taken, the disease will not vanish. From Figure 5, we can see that when R0<1 the number of Echinococcosis humans IH(t) tends to 0. On the contrary, when R0>1, IH(t) tends to a stable equilibrium. We can see that R0 is really the threshold for the establishment of the disease and the number of infections increases with the increase of R0.

    Figure 5. The tendency of the human Echinococcosis cases IH(t) with different values of R0. When β1=3.3×1010(lower curve) and 6.3×1010, and the values of other parameters in Table 3 do not change, R0=0.9932 and 1.2321, respectively.

    Next, to find better control strategies for Echinococcosis infection, we perform some sensitivity analysis to determine the influence of parameters A1, d1, σ and β1 on R0. From Figure 6 we can see that R0 decreases if A1 decreases, or d1 increases, or σ increases, or β1 decreases. From Figure 6(a), it is obvious that when A1 is less than 6500, R0 can be less than 1. However, the recruitment rate of dogs can achieve 13400 in Xinjiang, China. This indicates that human Echinococcosis in Xinjiang, China cannot be eradicated if recruitment rate of dogs cannot be controlled under 6500. From Figure 6(d), we can see that when β1 is less than 3.5×1010, R0 can be less than 1. In order to decrease the parameter β1, we have the following measures. Dogs should be barred from slaughter houses and should not be fed uncooked offal. Infection carcasses and offal should be burned or buried. The parameter σ can be increased through increasing the frequency of dog anthelmintic.

    Figure 6. The influence of parameters on R0. (a) versus A1; (b) versus d1; (c) versus β1; (d) versus σ. Other parameter values in Table 3 do not change.

    8. Discussion

    In this paper, in order to understand how Echinococcosis spreads in the real world and forecast the disease trends, we propose a novel spreading model for Echinococcosis with distributed time delays. We calculated the basic reproduction number R0. The mathematical results show that the dynamics of the model is completely determined by R0. If R0<1, the disease-free equilibrium is globally asymptotically stable, and if R0>1, the model is permanence and endemic equilibrium is globally asymptotically stable.

    With suitable parameter values, we estimated the basic reproduction number to be R0=1.23 in Xinjiang, China for model (1). Moreover, sensitivity analysis demonstrates that Echinococcosis can be controlled with several strategies which can change four parameters A1, d1, β1 and σ(see Figure 6). From Figure 3 we can see that our model matches the trend of monthly data for human Echinococcosis cases well. However, model (1) cannot simulate the oscillations of the data. Therefore, extension of our framework to include the stochastic disturbance is an interesting future work. We hope this work would lead to a better understanding of transmission of Echinococcosis.


    Acknowledgments

    This research was supported by the The Natural Science Foundation of Xinjiang [2015211C031].


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