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. 2015 Dec 3;449:145–159. doi: 10.1016/j.physa.2015.10.055

Impulsive vaccination and dispersal on dynamics of an SIR epidemic model with restricting infected individuals boarding transports

Jianjun Jiao a, Shaohong Cai a,, Limei Li b
PMCID: PMC7126619  PMID: 32288097

Abstract

To understand the effect of impulsive vaccination and restricting infected individuals boarding transports on disease spread, we establish an SIR model with impulsive vaccination, impulsive dispersal and restricting infected individuals boarding transports. This SIR epidemic model for two regions, which are connected by transportation of non-infected individuals, portrays the evolvement of diseases. We prove that all solutions of the investigated system are uniformly ultimately bounded. We also prove that there exists globally asymptotically stable infection-free boundary periodic solution. The condition for permanence is discussed. It is concluded that the approach of impulsive vaccination and restricting infected individuals boarding transports provides reliable tactic basis for preventing disease spread.

Keywords: SIR model, Impulsive vaccination, Impulsive dispersal, Infection-free, Permanence

Highlights

  • An SIR epidemic model with restricting infected individuals boarding transports was investigated.

  • Impulsive vaccination and dispersal are considered, which are more reasonable.

  • Two thresholds are obtained for Infection-free of the system.

1. Introduction

The work of Kermack and McKendick  [1] was the fundamental study of epidemic models described by nonlinear differential equations. In this field, epidemic models have recently attracted much attention of mathematical epidemiologists and are perceived as significant  [2], [3], [4], [5], [6], [7]. Wang, Takeuchi and Liu  [8] studied a multi-group SVEIR epidemic model with distributed delay and vaccination. Sun and Shi  [9] considered a multigroup SEIR model with nonlinear incidence of infection and nonlinear removal functions between compartments. To understand the effect of transport-related infection on disease spread, Cui, Takeuchi and Saito  [10] proposed the spreading disease with transport-related infection. Takeuchi, Liu and Cui  [11] investigated the global dynamics of SIS models with transport-related infection, their conclusions implied that transport-related infection on disease can make the disease endemic even if all the isolated regions are disease free. Yan and Zou  [12] considered two control variables representing the quarantine and isolation strategies for SARS epidemics, they gave a theoretical interpretation to the practical experiences that the early quarantine and isolation strategies are critically important to control the outbreaks of epidemic. Chowell and Castillo-Chavez  [13] used the uncertainly and sensitivity analysis of the basic reproductive number R0 to assess the role that the model parameters play in outbreak control. Quarantine and isolation measures have been widely used to control the spread of diseases such as yellow fever, smallpox, measles, ebola, pandemic influenza, diphtheria, plague, cholera, and, more recently, severe acute respiratory syndrome (SARS)  [14], [15], [16], [17], [18], [19]. Xie, et al.  [20] simultaneously use two kinds of measures: expand the treatment ranges of suspected case and limit population flows freely to suppress the diffusion of SARS effectively. Gong et al.  [21] showed that the SARS may fluctuate with import of SARS infectiousness from outside Beijing, weakness of quarantine, more social activities and so on.

Different types of vaccination policies and strategies combining pulse vaccination policy, treatment, pre-outbreak vaccination or isolation have already been introduced by many referees  [22], [23], [24], [25], [26], [27], [28], [29], [30], [31]. The pulse vaccination strategy (PVS) consists of repeated application of vaccine at discrete time with equal interval in a population in contrast to the traditional constant vaccination  [22], [23]. At each vaccination time a constant fraction of the susceptible population is vaccinated successfully. Since 1993, attempts have been made to develop mathematical theory to control infectious diseases using pulse vaccination  [22]. Compared to the proportional vaccination models, the study of pulse vaccination models is in its infancy  [23]. The control of childhood viral infections by pulse vaccination strategy is discussed by Nokes and Swinton  [24], [25]. Stone et al.  [26] presented a theoretical examination of the pulse vaccination strategy in the SIR epidemic model. d’Onofrio  [27] investigated the application of the pulse vaccination policy to eradicate infectious disease for SIR and SEIR epidemic models.

Theories of impulsive differential equations have been introduced into population dynamics lately  [32], [33], [34], [35], [36], [37], [38]. Impulsive equations are found in almost every domain of applied science and have been studied in many investigation  [38], [39], [40], [41], they generally describe phenomena which are subject to steep or instantaneous changes. The theories of population dynamical system and its application have been achieved many good results. However, the oasis vegetation degradation combining with dynamical system has been considered very little. In this paper, we will investigate an impulsive dispersal on SIR model with restricting infected individuals boarding transports. We expect to obtain some dynamical properties of the investigated system. We also expect that impulsive dispersal will provides reliable tactic for controlling epidemic.

The organization of this paper is as follows. In Section  2, we introduce the model and background concepts. In Section  3, some important lemmas are presented. We give the globally asymptotically stable conditions of the infection-free boundary periodic solution of System (2.2), and the permanent condition of System (2.2). In Section  4, a brief discussion is given to conclude this work.

2. The model

Inspired by the above discussion, we establish an SIR model with impulsive vaccination, impulsive dispersal and restricting infected individuals boarding transports.

{dS1(t)dt=λ1d1S1(t)β1S1(t)I1(t)1+α1I1(t),dI1(t)dt=β1S1(t)I1(t)1+α1I1(t)(r1+d1+b1)I1(t),dR1(t)dt=r1I1(t)d1R1(t),dS2(t)dt=λ2d2S2(t)β2S2(t)I2(t)1+α2I2(t),dI2(t)dt=β2S2(t)I2(t)1+α2I2(t)(r2+d2+b2)I2(t),dR2(t)dt=r2I2(t)d2R2(t),}t(n+l)τ,t(n+1)τ,S1(t)=D(S2(t)S1(t)),I1(t)=0,R1(t)=D(R2(t)R1(t)),S2(t)=D(S1(t)S2(t)),I2(t)=0,R2(t)=D(R1(t)R2(t)),}t=(n+l)τ,nZ+,S1(t)=μ1S1(t),I1(t)=0,R1(t)=μ1S1(t),S2(t)=μ2S2(t),I2(t)=0,R2(t)=μ2S2(t),}t=(n+1)τ,nZ+, (2.1)

here Si(t), Ii(t) and Ri(t) represent the number of susceptible,infected, recovered individuals in city i(i=1,2) at time t. It is assumed that we adopt the fixed number of offspring, denoted by λi(i=1,2), joins into the susceptible class per unit time in city i(i=1,2). The natural death rate is assumed as the same constant di(i=1,2) for the susceptible,infected, recovered individuals in city i(i=1,2). Disease is transmitted with the incidence rate, that is, the number of new cases of infection per unit time

βiSiIi1+αiIi,i=1,2,

with city i=1,2. The transmission rate with city i is a constant βi(i=1,2). αi is a nonnegative constant representing the half saturation constant with city i(i=1,2). The infected individuals in city i(i=1,2) suffer an extra disease-related death with constant rate bi(i=1,2). ri(i=1,2) is the recovery rate of the infected individuals in city i(i=1,2). By boarding transports, the susceptible and recovered individuals of city i leave to city j(ij,i,j=1,2) with a dispersal rate 0<D<1 at moment t=(n+l)τ,nZ+. The susceptible is successfully vaccinated with μi(i=1,2) in city i(i=1,2) at moment t=(n+1)τ,nZ+.

Because Ri(t)(i=1,2) do not affect the other equations of (2.1), we can simplify system (2.1) and restrict our attention to the following system

{dS1(t)dt=λ1d1S1(t)β1S1(t)I1(t)1+α1I1(t),dI1(t)dt=β1S1(t)I1(t)1+α1I1(t)(r1+d1+b1)I1(t),dS2(t)dt=λ2d2S2(t)β2S2(t)I2(t)1+α2I2(t),dI2(t)dt=β2S2(t)I2(t)1+α2I2(t)(r2+d2+b2)I2(t),}t(n+l)τ,t(n+1)τ,S1(t)=D(S2(t)S1(t)),I1(t)=0,S2(t)=D(S1(t)S2(t)),I2(t)=0,}t=(n+l)τ,nZ+,S1(t)=μ1S1(t),I1(t)=0,S2(t)=μ2S2(t),I2(t)=0,}t=(n+1)τ,nZ+. (2.2)

3. The lemmas

The solution of (2.1), denote by X(t)=(S1(t),I1(t),R1(t),S2(t),I2(t),R2(t))T, is a piecewise continuous function X:R+R+6, X(t) is continuous on (nτ,(n+l)τ] and ((n+l)τ,(n+1)τ], nZ+ and X(nτ+)=limtnτ+X(t), X((n+l)τ+)=limt(n+l)τ+X(t) exist. Obviously the global existence and uniqueness of solutions of (2.1) is guaranteed by the smoothness properties of f, which denotes the mapping defined by right-side of system (2.1) (see Lakshmikantham  [39]).

Let V:R+×R+6R+, then V is said to belong to class V0, if

  • (i)

    V is continuous in (nτ,(n+l)τ]×R+6 and ((n+l)τ,(n+1)τ]×R+6, for each zR+6,nZ+, V(nτ+,z)=lim(t,y)(nτ+,z)V(t,y), V((n+l)τ+,z)=lim(t,y)((n+l)τ+,y)V(t,y) exist.

  • (ii)

    V is locally Lipschitzian in z.

Definition 3.1

VV0, then, for (t,z)(nτ,(n+l)τ]×R+6 and ((n+l)τ,(n+1)τ]×R+6, the upper right derivative of V(t,z) with respect to the impulsive differential system (2.1) is defined as

D+V(t,z)=lim suph01h[V(t+h,z+hf(t,z))V(t,z)].

It can easily be obtained from the following lemma.

Lemma 3.2

Suppose X(t) is a solution of (2.1)   with X(0+)0 , then X(t)0 for t0 and further X(t)>0(t0) for X(0+)>0 .

Lemma 3.3 [39]

Let the function mPC[R+,R] ​satisfy the inequalities

{m(t)p(t)m(t)+q(t),tt0,ttk,k=1,2,,m(tk+)dkm(tk)+bk,t=tk, (3.1)

where p,qPC[R+,R] and dk0,bk are constants, then

m(t)m(t0)t0<tk<tdkexp(t0tp(s)ds)+t0<tk<t(tk<tj<tdjexp(t0tp(s)ds))bk+t0ts<tk<tdkexp(stp(σ)dσ)q(s)ds,tt0.

Now, we show that all solutions of (2.1) are uniformly ultimately bounded.

Lemma 3.4

There exists a constant M>0 such that Si(t)M,Ii(t)M,Ri(t)M(i=1,2) for each solution (S1(t),I1(t),R1(t),S2(t),I2(t),R2(t)) of   (2.1)   with all t large enough.

Proof

Define

V(t)=S1(t)+I1(t)+R1(t)+S2(t)+I2(t)+R2(t),

and d=min{d1,d2}. Then tnτ,t(n+l)τ, we have

D+V(t)+dV(t)=λ1+λ2i=12[(did)Si(t)+(did)Ii(t)+(did)Ri(t)]i=12biIi(t)λ1+λ2.

When t=nτ,V(nτ+)=S1(nτ+)+I1(nτ+)+R1(nτ+)+S2(nτ+)+I2(nτ+)+R2(nτ+)=S1(nτ)+I1(nτ)+R1(nτ)+S2(nτ)+I2(nτ)+R2(nτ)=V(nτ). When t=(n+l)τ,V((n+l)τ+)=S1((n+l)τ+)+I1((n+l)τ+)+R1((n+l)τ+)+S2((n+l)τ+)+I2((n+l)τ+)+R2((n+l)τ+)=S1((n+l)τ)+I1((n+l)τ)+R1((n+l)τ)+S2((n+l)τ)+I2((n+l)τ)+R2((n+l)τ)=V((n+l)τ). By Lemma 3.3, for t(nτ,(n+1)τ], we have

V(t)V(0)exp(dt)+0t(λ1+λ2)exp(d(ts))ds=V(0)exp(dt)+λ1+λ2d(1exp(dt))λ1+λ2d,as  t.

So V(t) is uniformly ultimately bounded. Hence, by the definition of V(t), we have there exists a constant M>0 such that Si(t)M,Ii(t)M,Ri(t)M(i=1,2) for t large enough. The proof is complete.

If Ii(t)=0(i=1,2), we have the following subsystem of (2.2)

{dS1(t)dt=λ1d1S1(t),dS2(t)dt=λ2d2S2(t),}t(n+l)τ,t(n+1)τ,S1(t)=D(S2(t)S1(t)),S2(t)=D(S1(t)S2(t)),}t=(n+l)τ,S1(t)=μ1S1(t),S2(t)=μ2S2(t),}t=(n+1)τ,n=1,2. (3.2)

We can easily obtain the analytic solution of (3.2) between pulses as follows

{S1(t)={1d1[λ1(λ1d1S1(nτ+))ed1(tnτ)],t[nτ,(n+l)τ),1d1[λ1(λ1d1S1((n+l)τ+))ed1(t(n+l)τ)],t[(n+l)τ,(n+1)τ),S2(t)={1d2[λ2(λ2d2S2(nτ+))ed2(tnτ)],t[nτ,(n+l)τ).1d2[λ2(λ2d2S2((n+l)τ+))ed2(t(n+l)τ)],t[(n+l)τ,(n+1)τ). (3.3)

Considering the third and fourth equations of (3.2), we have

{S1((n+l)τ+)=1Dd1[λ1(λ1d1S1(nτ+))ed1lτ]+Dd2[λ2(λ2d2S2(nτ+))ed2lτ],S2((n+l)τ+)=Dd1[λ1(λ1d1S1(nτ+))ed1lτ]+1Dd2[λ2(λ2d2S2(nτ+))ed2lτ]. (3.4)

Considering the fifth and sixth equations of (3.2), we also have

{S1((n+1)τ+)=1μ1d1[λ1(λ1d1S1((n+l)τ+))ed1(1l)τ],S2((n+1)τ+)=1μ2d2[λ2(λ2d2S2((n+l)τ+))ed2(1l)τ]. (3.5)

Substituting (3.4) into (3.5), we have the stroboscopic map of (3.2)

{S1((n+1)τ+)=(1μ1)(1D)ed1τS1(nτ+)+(1μ1)De[d1(1l)+d2l]τS2(nτ+)+(1μ1)×[λ1(1ed1lτ)(1(1D)ed1(1l)τ)d1+Dλ2(1ed2lτ)ed1(1l)τd2],S2((n+1)τ+)=(1μ2)De[d1l+d2(1l)]τS1(nτ+)+(1μ2)(1D)ed2τS2(nτ+)+(1μ2)×[Dλ1(1ed1lτ)ed2(1l)τd1+λ2(1ed2lτ)(1(1D)ed2(1l)τ)d2]. (3.6)

(3.5) has one fixed point as

{S1=(1A1)BAA2(1A1)(1B2)A2B1>0,S2=B1BA(1B2)(1A1)(1B2)A2B1>0, (3.7)

where

A1=(1μ1)(1D)ed1τ<1,
B1=(1μ1)De[d1(1l)+d2l]τ<1,
A2=(1μ2)De[d1l+d2(1l)]τ<1,
B2=(1μ2)(1D)ed2τ<1,
A=(1μ1)×[λ1(1ed1lτ)(1(1D)ed1(1l)τ)d1+Dλ2(1ed2lτ)ed1(1l)τd2]>0,
B=(1μ2)×[Dλ1(1ed1lτ)ed2(1l)τd1+λ2(1ed2lτ)(1(1D)ed2(1l)τ)d2]>0.

Lemma 3.5

The unique fixed point (S1,S2) of   (3.6)   is globally asymptotically stable.

Proof

For convenience, we make a notation as (S1n,S2n)=(S1(nτ+),S2(nτ+)). The linear form of (3.6) can be written as

(S1n+1S2n+1)=M(S1nS2n). (3.8)

Obviously, the near dynamics of (S1,S2) is determined by linear system (3.6). The stabilities of (S1,S2) ​are determined by the eigenvalue of M less than 1. If M satisfies the Jury criteria  [22], we can know the eigenvalue of M less than 1,

1trM+detM>0. (3.9)

We can easily know that (S1,S2) is unique fixed point of (3.6), and

M=(A1B1A2B2). (3.10)

For

1trM+detM=1(A1+B2)+(A1B2A2B1)=(1A1)(1B2)A2B1=[(1(1μ1)ed1τ)+(1μ1)Ded1τ][(1(1μ2)ed2τ)+(1μ2)Ded2τ](1μ1)(1μ2)D2e(d1+d2)τ=[1(1μ1)ed1τ][1(1μ2)ed2τ]+[1(1μ1)ed1τ](1μ2)Ded2τ+[1(1μ2)ed2τ](1μ1)Ded1τ>0.

From Jury criteria, (S1,S2) is locally stable. Because the fixed point (S1,S2) of (3.6) is unique, then, it is globally asymptotically stable. This completes the proof.

Lemma 3.6

The periodic solution (S1(t)˜,S2(t)˜) of System   (3.2)   is globally asymptotically stable, where

{S1(t)˜={1d1[λ1(λ1d1S1)ed1(tnτ)],t[nτ,(n+l)τ),1d1[λ1(λ1d1S1)ed1(t(n+l)τ)],t[(n+l)τ,(n+1)τ),S2(t)˜={1d2[λ2(λ2d2S2)ed2(tnτ)],t[nτ,(n+l)τ).1d2[λ2(λ2d2S2)ed2(t(n+l)τ)],t[(n+l)τ,(n+1)τ), (3.11)

here S1 and S2 are determined as   (3.7) , S1 and S2 are defined as

{S1=1Dd1[λ1(λ1d1S1)ed1lτ]+Dd2[λ2(λ2d2S2)ed2lτ],S2=Dd1[λ1(λ1d1S1)ed1lτ]+1Dd2[λ2(λ2d2S2)ed2lτ]. (3.12)

4. The dynamics

Theorem 4.1

If

D<12, (4.1)

and

maxi=1,2βidi[λiτ+λidiSidi(edilτ1)+λidiSidi(ediτedilτ)](ri+di+bi)τ<0, (4.2)

hold, the infection-free boundary periodic solution (S1(t)˜,0,S2(t)˜,0) of   (2.2)   is globally asymptotically stable, where Si(i=1,2) and Si(i=1,2) are defined as   (3.7), (3.12) .

Proof

First, we prove the local stability of the infection-free boundary periodic solution (S1(t)˜,0,S2(t)˜,0) of (2.2). Defining S11(t)=S1(t)S1(t)˜,S12(t)=S2(t)S2(t)˜,I1(t)=I1(t),I2(t)=I2(t), then we have the following linearly similar system for (2.2) which is concerning one periodic solution (S1(t)˜,0,S2(t)˜,0)

(dS11(t)dtdI1(t)dtdS12(t)dtdI2(t)dt)=(d1β1S1(t)˜000β1S1(t)˜(r1+d1+b1)0000d2β2S2(t)˜000β2S2(t)˜(r2+d2+b2))(S11(t)I1(t)S12(t)I2(t)).

It is easy to obtain the fundamental solution matrix

Φ(t)=(exp(d1t)1000exp(0t(β1S1(s)˜(r1+d1+b1))ds)0000exp(d2t)2000exp(0t(β2S2(s)˜(r2+d2+b2))ds)).

There is no need to calculate the exact form of i(i=1,2), as they are not required in the analysis that follows. The linearization of the fifth, sixth, seventh and eighth equations of (2.2) is

(S11(nτ+)I1(nτ+)S12(nτ+)I2(nτ+))=(1D0D00100D01D00001)(S11(nτ)I1(nτ)S12(nτ)I2(nτ)).

The linearization of the ninth, tenth, eleventh and twelfth equations of (2.2) is

(S11(nτ+)I1(nτ+)S12(nτ+)I2(nτ+))=(1μ10000100001μ200001)(S11(nτ)I1(nτ)S12(nτ)I2(nτ)).

The stability of the periodic solution (S1(t)˜,0,S2(t)˜,0) is determined by the eigenvalues of

M=(1D0D00100D01D00001)(1μ10000100001μ200001)Φ(τ),

where are

λ1=(1μ1)(1D)ed1τ<1,

and

λ2=|(1D)(K1+K3)+(1D)2(K1+K3)24(12D)K1K32||(1D)(K1+K3)+(1+D)2(K1+K3)22||(K1+K3)2|,

and

λ3=(1μ2)(1D)ed2τ<1,

and

λ4=|(1D)(K1+K3)(1D)2(K1+K3)24(12D)K1K32||(1D)(K1+K3)(1D)2(K1K3)22|=|(1D)(K1+K3)(1D)2(K1K3)22|(1D)max{K1,K3},

where K1=e0τ[β1S1(t)˜(r1+d1+b1)]dt and K3=e0τ[β2S2(t)˜(r2+d2+b2)]dt. According to condition (4.1), (4.2) and the Floquet theory  [39], i.e. 

exp[0τ(βiSi(t)˜(ri+di+bi))dt]<1(i=1,2),

then,

λ2|(K1+K3)2|<1,

and

λ4(1D)max{K1,K3}<1,

hold, the infection-free boundary periodic solution (S1(t)˜,0,S2(t)˜,0) of (2.2) is locally stable.

In the following, we will prove the global attraction. Choose a ε>0 such that

ρi=exp[0τ(βi(Si(t)˜+ε)(ri+di+bi))dt]<1(i=1,2).

From the first and third equations of (2.2), we notice that dSi(t)dtλidiSi(t)(i=1,2). Then, we consider following impulsive comparative differential equation

{dS21(t)dt=λ1d1S21(t),dS22(t)dt=λ2d2S22(t),}t(n+l)τ,t(n+1)τ,S21(t)=D(S22(t)S21(t)),S22(t)=D(S21(t)S22(t)),}t=(n+l)τ,S21(t)=μ1S21(t),S22(t)=μ2S22(t),}t=(n+1)τ. (4.3)

From Lemma 3.6 and comparison theorem of impulsive equation (see theorem 3.1.1 in Ref.  [39]), we have S1(t)S21(t), S2(t)S22(t) and S21(t)S1(t)˜, S22(t)S2(t)˜, as t. Then

{S1(t)S21(t)S1(t)˜+ε,S2(t)S22(t)S2(t)˜+ε, (4.4)

for all t large enough. For convenience, we may assume (4.4) holds for all t0. From (2.2) and (4.4), we get

dIi(t)dt[βi(Si(t)˜+ε)(ri+di+bi)]Ii(t)(i=1,2). (4.5)

So Ii((n+1)τ)Ii(nτ+)exp[nτ(n+1)τ(βi(Si(S)˜+ε)(ri+di+bi))ds](i=1,2). Hence Ii(nτ)Ii(0+)ρin(i=1,2) and Ii(nτ)0(i=1,2) as n, therefore Ii(t)0(i=1,2) as t.

Next, we will prove that Si(t)Si(t)˜(i=1,2) as t. For ε1>0, there must exist a t0>0 such that 0<Ii(t)<ε1(i=1,2) for all tt0. Without loss of generality, we may assume that 0<Ii(t)<ε1 for all t0. For system (2.2) we have

λi(di+βiε11+αiε1)Si(t)dSi(t)dtλidixi(t)(i=1,2), (4.6)

then we have S31(t)S1(t)S21(t), S32(t)S2(t)S22(t) and S31(t)S31(t)˜,S32(t)S32(t)˜, S21(t)S1(t)˜,S22(t)S2(t)˜ as t. While (S31(t),S32(t)) and (S21(t),S22(t)) are the solutions of

{dS31(t)dt=λ1(d1+β1ε11+α1ε1)S31(t),dS32(t)dt=λ2(d2+β2ε11+α2ε1)S32(t),}t(n+l)τ,t(n+1)τ,S31(t)=D(S32(t)S31(t)),S32(t)=D(S31(t)S32(t)),}t=(n+l)τ,S31(t)=μ1S31(t),S32(t)=μ2S32(t),}t=(n+1)τ, (4.7)

and

{dS21(t)dt=λ1d1S21(t),dS22(t)dt=λ2d2S22(t),}t(n+l)τ,t(n+1)τ,S21(t)=D(S22(t)S21(t)),S22(t)=D(S21(t)S22(t)),}t=(n+l)τ,S21(t)=μ1S21(t),S22(t)=μ2S22(t),}t=(n+1)τ (4.8)

respectively.

{S31(t)˜={1(d1+β1ε11+α1ε1)[λ1(λ1(d1+β1ε11+α1ε1)S31)e(d1+β1ε11+α1ε1)(tnτ)],t[nτ,(n+l)τ),1(d1+β1ε11+α1ε1)[λ1(λ1(d1+β1ε11+α1ε1)S31)e(d1+β1ε11+α1ε1)(t(n+l)τ)],t[(n+l)τ,(n+1)τ),S32(t)˜={1(d2+β2ε11+α2ε1)[λ2(λ2(d2+β2ε11+α2ε1)S32)e(d2+β2ε11+α2ε1)(tnτ)],t[nτ,(n+l)τ).1(d2+β2ε11+α2ε1)[λ2(λ2(d2+β2ε11+α2ε1)S32)e(d2+β2ε11+α2ε1)(t(n+l)τ)],t[(n+l)τ,(n+1)τ), (4.9)

here S31 and S32 are determined as

{S31=(1A31)B3A3A32(1A31)(1B32)A32B31>0,S32=B31B3A3(1B32)(1A31)(1B32)A32B31>0, (4.10)

and S31 and S32 are defined as

{S31=1D(d1+β1ε11+α1ε1)[λ1(λ1(d1+β1ε11+α1ε1)S31)e(d1+β1ε11+α1ε1)lτ]+D(d2+β2ε11+α2ε1)[λ2(λ2(d2+β2ε11+α2ε1)S32)e(d2+β2ε11+α2ε1)lτ],S32=D(d1+β1ε11+α1ε1)[λ1(λ1(d1+β1ε11+α1ε1)S31)e(d1+β1ε11+α1ε1)lτ]+1D(d2+β2ε11+α2ε1)[λ2(λ2(d2+β2ε11+α2ε1)S32)e(d2+β2ε11+α2ε1)lτ], (4.11)

where

A31=(1μ1)(1D)e(d1+β1ε11+α1ε1)τ<1,
B31=(1μ1)De[(d1+β1ε11+α1ε1)(1l)+(d2+β2ε11+α2ε1)l]τ<1,
A32=(1μ2)De[(d1+β1ε11+α1ε1)l+(d2+β2ε11+α2ε1)(1l)]τ<1,
B32=(1μ2)(1D)e(d2+β2ε11+α2ε1)τ<1,
A3=(1μ1)×[λ1(1e(d1+β1ε11+α1ε1)lτ)(1(1D)e(d1+β1ε11+α1ε1)(1l)τ)(d1+β1ε11+α1ε1)+Dλ2(1e(d2+β2ε11+α2ε1)lτ)e(d1+β1ε11+α1ε1)(1l)τ(d2+β2ε11+α2ε1)]>0,
B3=(1μ2)×[Dλ1(1e(d1+β1ε11+α1ε1)lτ)e(d2+β2ε11+α2ε1)(1l)τ(d1+β1ε11+α1ε1)+λ2(1e(d2+β2ε11+α2ε1)lτ)(1(1D)e(d2+β2ε11+α2ε1)(1l)τ)(d2+β2ε11+α2ε1)]>0.

For any ε2>0, there exists a t1,t>t1 such that

S31(t)˜ε2<S1(t)<S1(t)˜+ε2,

and

S32(t)˜ε2<S2(t)<S2(t)˜+ε2.

Let ε10, so we have

S1(t)˜ε2<S1(t)<S1(t)˜+ε2,

and

S2(t)˜ε2<S2(t)<S2(t)˜+ε2,

for t large enough, which implies S1(t)S1(t)˜ and S2(t)S2(t)˜ as t. This completes the proof.

The next work is to investigate the permanence of system (2.2).

Definition 4.2

System (2.2) is said to be permanent if there are constants m,M>0 (independent of initial value) and a finite time T0 such that for all solutions (S1(t),I1(t),S2(t),I2(t)) with all initial values S1(0+)>0,I1(0+)>0,S2(0+)>0,I2(0+)>0, mS1(t)M,mI1(t)M,mS2(t)M,mI2(t)M, hold for all tT0. Here T0 may depend on the initial values (S1(0+),I1(0+),S2(0+),I2(0+)).

Theorem 4.3

If

mini=1,2βidi[λiτ+λidiSidi(edilτ1)+λidiSidi(ediτedilτ)](ri+di+bi)τ>0, (4.12)

holds, system (2.2)   is permanent. Where Si(i=1,2) and Si(i=1,2) are defined as   (3.7), (3.12) .

Proof

Suppose (S1(t),I1(t),S2(t),I2(t)) is a solution of (2.2) with S1(0)>0,I1(0)>0,S2(0)>0,I2(0)>0. By Lemma 3.4, we have proved there exists a constant M>0 such that S1(t)M,I1(t)M,S2(t)M,I2(t)M, for t large enough. From system (2.2), we know Ii(t)>Ii(0+)e(ri+di+bi)t(i=1,2) for all t large enough. Thus, we only need to find m1>0 and ε3 such that Ii(t)m1(i=1,2) for t large enough. Otherwise, we can select m2>0 small enough, and prove Ii(t)<m2(i=1,2) cannot hold for t0. By the condition (4.12), we can obtain

σi=βi(di+βim21+αim2)[λiτ+λi(di+βim21+αim2)S4i(di+βim21+αim2)(e(di+βim21+αim2)lτ1)+λi(di+βim21+αim2)S4i(di+βim21+αim2)(e(di+βim21+αim2)τe(di+βim21+αim2)lτ)](ri+(di+βim21+αim2)+bi)τβiε3τ>0,

with S4i(i=1,2) and S4i(i=1,2) are defined as (4.16), (4.17). Then,

{dS1(t)dt>λ1(d1+β1m21+α1m2)S1(t),dS2(t)dt>λ2(d1+β2m21+α2m2)S2(t),}t(n+l)τ,t(n+1)τ,S1(t)=D(S2(t)S1(t)),S2(t)=D(S1(t)S2(t)),}t=(n+l)τ,S1(t)=μ1S1(t),S2(t)=μ2S2(t),}t=(n+1)τ. (4.13)

By Lemmas 3.6, we have S1(t)S41(t), S2(t)S42(t) and S41(t)S41(t)¯,S42(t)S42(t)¯,t, where (S41(t),S42(t)) is the solution of

{dS41(t)dt=λ1(d1+β1m21+α1m2)S41(t),dS42(t)dt=λ2(d2+β2m21+α2m2)S42(t),}t(n+l)τ,t(n+1)τ,S41(t)=D(S42(t)S41(t)),S42(t)=D(S41(t)S42(t)),}t=(n+l)τ,S41(t)=μ1S41(t),S42(t)=μ2S42(t),}t=(n+1)τ, (4.14)

with

{S41(t)¯={1(d1+β1m21+α1m2)[λ1(λ1(d1+β1m21+α1m2)S31)e(d1+β1m21+α1m2)(tnτ)],t[nτ,(n+l)τ),1(d1+β1m21+α1m2)[λ1(λ1(d1+β1m21+α1m2)S31)e(d1+β1m21+α1m2)(t(n+l)τ)],t[(n+l)τ,(n+1)τ),S42(t)¯={1(d2+β2m21+α2m2)[λ2(λ2(d2+β2m21+α2m2)S32)e(d2+β2m21+α2m2)(tnτ)],t[nτ,(n+l)τ).1(d2+β2m21+α2m2)[λ2(λ2(d2+β2m21+α2m2)S32)e(d2+β2m21+α2m2)(t(n+l)τ)],t[(n+l)τ,(n+1)τ), (4.15)

here S41 and S42 are determined as

{S41=(1A41)B4A4A42(1A41)(1B42)A42B41>0,S42=B41B4A4(1B42)(1A41)(1B42)A42B41>0, (4.16)

and S41 and S42 are defined as

{S41=1D(d1+β1m21+α1m2)[λ1(λ1(d1+β1m21+α1m2)S41)e(d1+β1m21+α1m2)lτ]+D(d2+β2m21+α2m2)[λ2(λ2(d2+β2m21+α2m2)S32)e(d2+β2m21+α2m2)lτ],S42=D(d1+β1m21+α1m2)[λ1(λ1(d1+β1m21+α1m2)S31)e(d1+β1m21+α1m2)lτ]+1D(d2+β2m21+α2m2)[λ2(λ2(d2+β2m21+α2m2)S32)e(d2+β2m21+α2m2)lτ], (4.17)

where

A41=(1μ1)(1D)e(d1+β1m21+α1m2)τ<1,
B41=(1μ1)De[(d1+β1m21+α1m2)(1l)+(d2+β2m21+α2m2)l]τ<1,
A42=(1μ2)De[(d1+β1m21+α1m2)l+(d2+β2m21+α2m2)(1l)]τ<1,
B42=(1μ2)(1D)e(d2+β2m21+α2m2)τ<1,
A4=(1μ1)×[λ1(1e(d1+β1m21+α1m2)lτ)(1(1D)e(d1+β1m21+α1m2)(1l)τ)(d1+β1m21+α1m2)+Dλ2(1e(d2+β2m21+α2m2)lτ)e(d1+β1m21+α1m2)(1l)τ(d2+β2m21+α2m2)]>0,
B4=(1μ2)×[Dλ1(1e(d1+β1m21+α1m2)lτ)e(d2+β2m21+α2m2)(1l)τ(d1+β1m21+α1m2)+λ2(1e(d2+β2m21+α2m2)lτ)(1(1D)e(d2+β2m21+α2m2)(1l)τ)(d2+β2m21+α2m2)]>0.

Therefore, there exist T1>0 and ε3>0 such that

S1(t)S41(t)S41(t)¯ε3,

and

S2(t)S42(t)S42(t)¯ε3.

Then,

dIi(t)dt[βi(S4i(t)¯ε3)(ri+di+bi)]Ii(t)(i=1,2), (4.18)

for tT1. Let N1N and N1τ>T1. Integrating (4.18) on (nτ,(n+1)τ),nN1, we have

Ii((n+1)τ)Ii(nτ+)exp(nτ(n+1)τ[βi(S4i(t)¯ε3)(ri+di+bi)]dt)=Ii(nτ)eσi(i=1,2),

then Ii((N1+k)τ)Ii(N1τ+)ekσi, as k, which is a contradiction to the boundedness of Ii(t). Hence, there exists a t1>0 such that Ii(t)m1(i=1,2).

Thus, we can obtain dSi(t)dt>λi(di+βiM1+αiM)Si(t)(i=1,2). Then, the following comparatively impulsive differential equation is

{dS51(t)dt=λ1(d1+β1M1+α1M)S51(t),dS52(t)dt=λ2(d2+β2M1+α1M)S51(t),}t(n+l)τ,t(n+1)τ,S51(t)=D(S52(t)S51(t)),S52(t)=D(S51(t)S52(t)).}t=(n+l)τ,S51(t)=μ1S51(t),S52(t)=μ1S52(t).}t=(n+1)τ. (4.19)

Similar to Lemma 3.6, we have

{S51(t)˜={1(d1+β1M1+α1M)[λ1(λ1(d1+β1M1+α1M)S51)e(d1+β1M1+α1M)(tnτ)],t[nτ,(n+l)τ),1(d1+β1M1+α1M)[λ1(λ1(d1+β1M1+α1M)S51)e(d1+β1M1+α1M)(t(n+l)τ)],t[(n+l)τ,(n+1)τ),S52(t)˜={1(d2+β2M1+α2M)[λ2(λ2(d2+β2M1+α2M)S32)e(d2+β2M1+α2M)(tnτ)],t[nτ,(n+l)τ).1(d2+β2M1+α2M)[λ2(λ2(d2+β2M1+α2M)S32)e(d2+β2M1+α2M)(t(n+l)τ)],t[(n+l)τ,(n+1)τ), (4.20)

here S51 and S52 are determined as

{S51=(1A51)B5A5A52(1A51)(1B52)A52B51>0,S52=B51B4A5(1B52)(1A51)(1B52)A52B51>0, (4.21)

and S51 and S52 are defined as

{S51=1D(d1+β1M1+α1M)[λ1(λ1(d1+β1M1+α1M)S51)e(d1+β1M1+α1M)lτ]+D(d2+β2M1+α2M)[λ2(λ2(d2+β2M1+α2M)S52)e(d2+β2M1+α2M)lτ],S52=D(d1+β1M1+α1M)[λ1(λ1(d1+β1M1+α1M)S51)e(d1+β1M1+α1M)lτ]+1D(d2+β2M1+α2M)[λ2(λ2(d2+β2M1+α2M)S52)e(d2+β2M1+α2M)lτ], (4.22)

where

A51=(1μ1)(1D)e(d1+β1M1+α1M)τ<1,
B51=(1μ1)De[(d1+β1M1+α1M)(1l)+(d2+β2M1+α2M)l]τ<1,
A52=(1μ2)De[(d1+β1M1+α1M)l+(d2+β2M1+α2M)(1l)]τ<1,
B52=(1μ2)(1D)e(d2+β2M1+α2M)τ<1,
A5=(1μ1)×[λ1(1e(d1+β1M1+α1M)lτ)(1(1D)e(d1+β1M1+α1M)(1l)τ)(d1+β1M1+α1M)+Dλ2(1e(d2+β2M1+α2M)lτ)e(d1+β1M1+α1M)(1l)τ(d2+β2M1+α2M)]>0,
B5=(1μ2)×[Dλ1(1e(d1+β1M1+α1M)lτ)e(d2+β2M1+α2M)(1l)τ(d1+β1M1+α1M)+λ2(1e(d2+β2M1+α2M)lτ)(1(1D)e(d2+β2M1+α2M)(1l)τ)(d2+β2M1+α2M)]>0.

For any ε4 small enough, we obtain

S51(t)>S51(t)˜ε4,

and

S52(t)>S52(t)˜ε4.

From the comparison theorem of impulsive differential equation, we have

S1(t)>S51(t)>S51(t)˜ε4>(S51(t)+S51(t))ε4=m51,

and

S2(t)>S52(t)>S52(t)˜ε4>(S52(t)+S52(t))ε4=m52,

i.e.  S1(t)>m51 and S2(t)>m52. This completes the proof.

Corollary 4.4

If

mini=1,2βidi[λiτ+λidiSidi(edilτ1)+λidiSidi(ediτedilτ)](ri+di+bi)τ>0, (4.23)

holds, system   (2.1)   is permanent. Where Si(i=1,2) and Si(i=1,2) are defined as   (3.7), (3.12) .

5. Discussion

In this paper, we establish an SIR model with impulsive dispersal,vaccination and restricting infected individuals boarding transports. This SIR epidemic model for two regions, which are connected by transportation of non-infected individuals, portrays the evolvement of diseases. We prove that all solutions of the investigated system are uniformly ultimately bounded. From (4.1) and (4.2), if maxi=1,2βidi[λiτ+λidiSidi(edilτ1)+λidiSidi(ediτedilτ)](ri+di+bi)τ<0 holds, the infection-free boundary periodic solution (S1(t)˜,0,0,S2(t)˜,0,0) of system (2.1) is globally asymptotically stable. From (4.12) or (4.23), if mini=1,2βidi[λiτ+λidiSidi(edilτ1)+λidiSidi(ediτedilτ)](ri+di+bi)τ>0 holds, system (2.1) is permanent. It is concluded that the approach of impulsive vaccination and restricting infected individuals boarding transports provides reliable tactic basis for preventing disease spread. In the real world, after the etiology the way of propagating, the effective methods of medical control of a new disease are clarified in terms of medical science, the combining vaccination and social control policy are effective methods to reduce the number of infected people. So our works will pay an important role to study new epidemic model with vaccination, impulsive dispersal and restricting infected individuals boarding transports.

Competing interests

The authors declare that they have no competing interest. All authors have read and approved the final manuscript.

Footnotes

Supported by National Natural Science Foundation of China (11361014, 10961008).

Contributor Information

Jianjun Jiao, Email: jiaojianjun05@126.com.

Shaohong Cai, Email: caishaohong2014@126.com.

References

  • 1.Kermack W., McKendick A. Contributions to the mathematical theory of epidemics I. Proc. Soc. A. 1927;115:700–721. doi: 10.1007/BF02464423. [DOI] [PubMed] [Google Scholar]
  • 2.Muroya Yoshiaki, Kuniya Toshikazu, Wang Jinliang. Stability analysis of a delayed multi-group SIS epidemic model with nonlinear incidence rates and patch structure. J. Math. Anal. Appl. 2015;425:415–439. [Google Scholar]
  • 3.Enatsu Y., Nakata Y., Muroya Y. Lyapunov functional techniques for global stability analysis of a delayed SIRS epidemic model. Nonlinear Anal. Real World Appl. 2012;13:2120–2133. [Google Scholar]
  • 4.Faria T. Global dynamics for Lotka- Volterra systems with infinite delay and patch structure. Appl. Mat. Comput. 2014;245:575–590. [Google Scholar]
  • 5.Guo H., Li M.Y., Shuai Z. Global stability of the endemic equilibrium of multigroup SIR epidemic models. Can. Appl. Soc. 2008;136:2793–2802. [Google Scholar]
  • 6.Kuniya T., Muroya Y. Global stability of a multi-group SIS epidemic models concerning population migration. Discrete Contin. Dyn. Syst. 2014;103:1105–1118. [Google Scholar]
  • 7.Shu H., Fan D., Wei J. Global stability of multi-group SEIR epidemic models with distributed delays and nonlinear transmission. Nonlinear Anal. Real World Appl. 2012;13:1581–1592. [Google Scholar]
  • 8.Wang J., Takeuchi Y., Liu S. A multi-group SVEIR epidemic model with distributed delay and vaccination. Int. J. Biomath. 2012;5:1260001. [Google Scholar]
  • 9.Sun R., Shi J. Global stability of multigroup epidemic model with group mixing and nonlinear incidence rates. Appl. Math. Comput. 2011;218:280–286. [Google Scholar]
  • 10.Cui J., Takeuchi Y., Saito Y. Spreading disease with transport-related infection. J. Theoret. Biol. 2006;239:376–390. doi: 10.1016/j.jtbi.2005.08.005. [DOI] [PubMed] [Google Scholar]
  • 11.Takeuchi Y., Liu X., Cui J. Global dynamics of SIS models with transport-related infect. J. Math. Anal. Appl. 2007;329:1460–1471. [Google Scholar]
  • 12.Yan X., Zou Y. Optimal and sub-optimal quarantine and isolation control in SARS epidemics. Math. Comput. Modelling. 2008;47:235–245. doi: 10.1016/j.mcm.2007.04.003. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Chowell G. Model parameters and outbreak control for SARS. Emerg. Infect. Diseases. 2004;10(7):1258–1263. doi: 10.3201/eid1007.030647. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Chowell G., Hengartner N.W., Castillo-Chavez C., Fenimore P.W., Hyman J.M. The basic reproductive number of ebola and the effects of public health measures: the cases of Congo and Uganda. J. Theoret. Biol. 2004;1:119–126. doi: 10.1016/j.jtbi.2004.03.006. [DOI] [PubMed] [Google Scholar]
  • 15.Hethcote H.W., Ma Z., Liao S. Effects of quarantine in six endemic models for infectious diseases. Math. Biosci. 2002;180:141–160. doi: 10.1016/s0025-5564(02)00111-6. [DOI] [PubMed] [Google Scholar]
  • 16.Safi M.A., Gumel A.B. Global asymptotic dynamics of a model for quarantine and isolation. Discrete Contin. Dyn. Syst. Ser. B. 2010;14:209–231. [Google Scholar]
  • 17.Anderson R.M., May R.M. Springer-Verlag; Berlin, Heidelberg, New York: 1982. Population Biology of Infectious Diseases. [Google Scholar]
  • 18.Anderson R.M., May R.M. Oxford University; London, New York: 1991. Infectious Diseases of Humans: Dynamics and Control. [Google Scholar]
  • 19.Hethcote H.W. The mathematics of infectious diseases. SIAM Rev. 2000;42:599–653. [Google Scholar]
  • 20.Xie Zh. Simulation research of SARS control strategy in China: prevention and control measure’s effect comparison. J. Syst. Simul. 2004;16:2667–2672. [Google Scholar]
  • 21.Gong J. Simulation and analysis of control of severe acute respiratory syndrome. J. Remote Sens. 2003;7:260–265. [Google Scholar]
  • 22.Jury E.L. Wiley; New York: 1974. Inners and Stability of Dynamics System. [Google Scholar]
  • 23.Gakkhar S., Negi K. Pulse vaccination in SIRS epidemic model with non-monotonic incidence rate. Chaos Solitons Fractals. 2008;35:626–638. [Google Scholar]
  • 24.Zhou Y., Liu H. Stability of periodic solutions for an SIS model with pulse vaccination. Math. Comput. Modelling. 2003;38:299–308. [Google Scholar]
  • 25.Nokes D.J., Swinton J. The control of childhood viral infections by pulse vaccination. IMA J. Math. Appl. Med. Biol. 1995;12:29–53. doi: 10.1093/imammb/12.1.29. [DOI] [PubMed] [Google Scholar]
  • 26.Stone L., Shulgin B., Agur Z. Theoretical examination of the pulse vaccination policy in the SIR epidemic models. Math. Comput. Modelling. 2000;31:207–215. [Google Scholar]
  • 27.d’Onofrio A. Stability properties of vaccination strategy in SEIR epidemic model. Math. Biosci. 2002;179:57–72. doi: 10.1016/s0025-5564(02)00095-0. [DOI] [PubMed] [Google Scholar]
  • 28.Gaoa Shujing, Chen Lansun, Nieto Juan J., Torres Angela. Analysis of a delayed epidemic model with pulse vaccination and saturation incidence. Vaccine. 2006;24:6037–6045. doi: 10.1016/j.vaccine.2006.05.018. [DOI] [PubMed] [Google Scholar]
  • 29.Bachy M., Boudet F., Boureau M. Electric pulses increase the immunogenicity of an influenza DNA vaccine injected intramuscularly in the mouse. Vaccine. 2001;19:1688–1693. doi: 10.1016/s0264-410x(00)00406-0. [DOI] [PubMed] [Google Scholar]
  • 30.Scheerlinck J.P., Karlis J., Tjelle T.E., President P.J., Mathiesen I., Newton S.E. In vivo electroporation improves immune rersponses to DNA vaccination in sheep. Vaccine. 2004;22:1820–1825. doi: 10.1016/j.vaccine.2003.09.053. [DOI] [PubMed] [Google Scholar]
  • 31.Zhao Y.G., Peng B., Deng H. Anti-HBV immune responses in rhesus macaques elicited by electroporation mediated DNA vaccination. Vaccine. 2006;24:897–903. doi: 10.1016/j.vaccine.2005.08.093. [DOI] [PubMed] [Google Scholar]
  • 32.Meng X., Chen L. Permance and global stability in an impulsive Lotka–Volterra N-species competitive system with both discrete delays and continuous delays. Int. J. Biomath. 2008;1:179–196. [Google Scholar]
  • 33.Jiao J. An appropriate pest management SI model with biological and chemical control concern. Appl. Math. Comput. 2008;196:285–293. [Google Scholar]
  • 34.Jiao J., Chen L. Global attractivity of a stage-structure variable coefficients predator–prey system with time delay and impulsive perturbations on predators. Int. J. Biomath. 2008;1:197–208. [Google Scholar]
  • 35.Jiao J. A delayed stage-structured predator–prey model with impulsive stocking on prey and continuous harvesting on predator. Appl. Math. Comput. 2008;195:316–325. [Google Scholar]
  • 36.Jiao J. Analysis of a stage-structured predator–prey system with birth pulse and impulsive harvesting at different moments. Nonlinear Anal. RWA. 2011;12:2232–2244. [Google Scholar]
  • 37.Jiao J. Dynamics of a stage-structured predator–prey model with prey impulsively diffusing between two patches. Nonlinear Anal. RWA. 2010;11:2748–2756. [Google Scholar]
  • 38.Xu R. Global stability and Hopf bifurcation of a predator–prey model with stage structure and delayed predator response. Nonlinear Dynam. 2012;67:1683–1693. [Google Scholar]
  • 39.Lakshmikantham V. World Scientific; Singapor: 1989. Theory of Impulsive Differential Equations. [Google Scholar]
  • 40.Liu X., Chen L. Complex dynamics of Holling II lotka-Volterra predator–prey system with impulsive perturbations on the predator. Chaos Solitons Fractals. 2003;16:311–320. [Google Scholar]
  • 41.Chen L., Meng X., Jiao J. Biological dynamics. Science. 2009 (in Chinese) [Google Scholar]

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