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Co-occurring intellectual disability and substance use disorders

  • Received: 01 June 2021 Accepted: 09 June 2021 Published: 17 June 2021
  • Individuals with intellectual disabilities (ID) are an expanding population that confronts multiple disadvantages from social and environmental determinants of health. Deinstitutionalization and community integration have improved the lives of individuals with ID in many ways. However, deinstitutionalization may increase their access to alcohol and drugs and the potential for developing Substance Abuse Disorders (SUD). It is estimated that 7–8 million people in the United States with an intellectual disability (ID) suffer disproportionately from substance use problems [1]. There is a lack of empirical evidence to inform prevention and treatment efforts in this population and more research needs to be done in order to address these issues.

    Citation: Nita V Bhatt, Julie P Gentile. Co-occurring intellectual disability and substance use disorders[J]. AIMS Public Health, 2021, 8(3): 479-484. doi: 10.3934/publichealth.2021037

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  • Individuals with intellectual disabilities (ID) are an expanding population that confronts multiple disadvantages from social and environmental determinants of health. Deinstitutionalization and community integration have improved the lives of individuals with ID in many ways. However, deinstitutionalization may increase their access to alcohol and drugs and the potential for developing Substance Abuse Disorders (SUD). It is estimated that 7–8 million people in the United States with an intellectual disability (ID) suffer disproportionately from substance use problems [1]. There is a lack of empirical evidence to inform prevention and treatment efforts in this population and more research needs to be done in order to address these issues.



    Outbreaks of infectious diseases do great harm to life and fortune. The construction and research of mathematical models play an extremely important role in the prevention and control of diseases. Scholars have studied various properties of many epidemic models, such as SIR (Susceptible-Infected-Recovered), SEIR (Susceptible-Exposed-Infected-Recovered), SIRS, SIQS (Susceptible-Infected-Quarantined-Recovered), which portray different characteristics of disease transmission[1,2,3,4,5,6]. The authors in [6] studied the Hopf bifurcation and stability of a delayed SIR model. They established an epidemic model with temporary immunity and specific functional response[7], and got the well-possedness and the threshold to determine different behaviors of the model.

    When an epidemic occurs, people can learn about the transmission route of the disease, prevention measures and the government's policy on disease control from media such as the TV or Internet, so that they can take certain measures to slow down the spread of the disease, such as self-isolation, vaccination, and compliance with the government's anti-epidemic regulations. On account of the role of media information on disease control, scholars have studied the different properties of epidemic models with information intervention[8,9,10,11,12]. At present, there are mainly two ways to study the impact of information intervention on the behavior. One is to study the impact of information intervention on the contact rate[8,9,13,14], and the other is to introduce a new class with information awareness[10,11,15,16]. In [15], the following epidemic model with separate information intervention class was established:

    {.St=Λd1StβStItd2mMtSt+δRt,.It=βStIt(d1+γ+μ)It,.Rt=d2mMtSt+γIt(d1+δ)Rt,.Mt=a1It1+b1Ita2Mt, (1.1)

    where St, It, Rt denote the quantity of the susceptible class, the infected class, and the recovered class at time t, separately. Mt represents the individuals of the class with information awareness. The meanings of the parameters in model (1.1) are shown in Table 1. In addition, a2 represents the degradation rate of information, which contains the subtraction due to the natural death of M. Thus, the assumption that a2>d1 is reasonable. The whole part d2m indicates response rate; the detailed meaning of each parameter on the information and schematic diagram of the above model can be seen in [15]. All the above parameters are specified as positive.

    Table 1.  Meanings of the parameters in model (1.1).
    Parameters Meaning
    Λ The inflow rate in the population
    d1 The natural death rate
    μ Mortality due to disease
    β The contact rate between S and I
    γ The recovery rate of the infected
    δ The loss rate of immunity, turning the recovered into the susceptible
    a1, b1 The information growth rate and the saturation coefficient
    a2 The degradation rate of information
    m The rate of information interaction
    d2 The response intensity

     | Show Table
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    Reality is not immutable and often full of various uncertainties. The above deterministic model (1.1) can not reflect these uncertain factors. Therefore, the introduction of the model with stochastic noise will better reflect the reality and present more research contexts. For this reason, many scholars have studied epidemic models with various stochastic factors[17,18,19,20]. The authors have studied the nontrivial positive periodic solution and condition for extinction of the model with media coverage and white noise[18]. Bao-Shao investigated an SIRS model with Markovian switching, which is used to describe the changes of coefficients in different environments, and discussed the influence of Markovian switching on the behavior of the model. In this paper, we introduce the stochastic perturbation of white noise into the above model, whose intensity is proportional to each class, that is

    {dSt=[Λd1StβStItd2mMtSt+δRt]dt+σ1StdW1(t),dIt=[βStIt(d1+γ+μ)It]dt+σ2ItdW2(t),dRt=[d2mMtSt+γIt(d+δ)Rt]dt+σ4RtdW4(t),dMt=(a1It1+b1Ita2Mt)dt+σ3MtdW3(t). (1.2)

    Here, Wi(t),i=1,2,3,4 are mutually independent Brownian motions on probability space and σi,i=1,2,3,4 represent the intensities of the stochastic perturbations. The greater the stochastic perturbations, the deeper the impact on the system, the greater σi will be.

    In addition to physical or respiratory transmission, there is also a form of vertical transmission from an infected mother to the newborns, such as with hepatitis B and AIDS. Vertical transmission from the mother to the newborn is considered as one of the most important ways of AIDS transmission. Thus, the epidemic models possessing vertical transmission have been extensively investigated[21,22,23]. The authors in [21] proposed an epidemic model with vertical transmission where the parameter b signifies the birth rate of the population and q stands for the proportion of newborns infected after birth from infectious mothers. p=1q and d1>b0 is assumed. Therefore, pb expresses the rate of newborns who have not been infected by their mothers and become susceptible.

    Hence, introducing the above factors, including the information intervention and vertical transmission, we can obtain the following stochastic model:

    {dSt=[Λd1StβStItd2mMtSt+b(St+Rt+Mt)+pbIt+δRt]dt+σ1StdW1(t),dIt=[qbIt+βStIt(d1+γ+μ)It]dt+σ2ItdW2(t),dMt=(a1It1+b1Ita2Mt)dt+σ3MtdW3(t),dRt=[d2mMtSt+γIt(d1+δ)Rt]dt+σ4RtdW4(t). (1.3)

    The above factors not only make the model more general, but also raise the degree of difficulty of the study. The novelties of this paper are as follows: (ⅰ) An epidemic model with information intervention and vertical transmission is established; (ⅱ) a threshold is obtained to determine the different dynamics of the model and the exponential rates of three classes are studied; (ⅲ) the critical case of Δ=0, which has rarely been discussed in the literature, is investigated here.

    This paper is arranged as follows: In Section 2, some estimations of the solution are given, followed by some lemmas to be used later. Section 3 gives a rough illustration of the value for disease extinction and provides the main conclusions of the paper. Part 4 focuses on the proof of Theorem 3.1 and Proposition 3.1 in detail. Part 5 proves the persistence of the model when Δ>0 and obtains the condition that the model has a stationary distribution. Section 6 studies the critical case when Δ=0. Section 7 discusses the results of the paper and lists some examples and numerical simulations to check the previous results.

    In this paper, (Ω,F,{F}t,P) is assumed to be a complete probability space and R4+:={(a,b,c,d)|a0,b0,c0,d0} and R4,o+:={(a,b,c,d)|a>0,b>0,c>0,d>0}. ab=min{a,b}. Ps,i,m0,r and Es,i,m0,r denote the probability and expectation with initial condition (s,i,m0,r), respectively.

    For the general SDE dxt=f(xt)dt+g(xt)dW(t) and the twice-differentiable function V(x), the operator LV is defined by

    LV(x)=fTVx(x)+12tr(gTVxx(x)g). (2.1)

    In addition, the Itˆos formula can be expressed as

    dV(x)=LV(x)dt+Vx(x)Tg(xt)dW(t). (2.2)

    First of all, we are concerned with the existence and uniqueness as well as approximate scope of the solution. The following lemmas will respond to these problems.

    Lemma 2.1.

    (i) For the initial condition (s,i,m0,r)R4+, the model (1.3) has a global solution (St,It,Mt,Rt) that possesses Markov-Feller property. Moreover, the solution (St,It,Mt,Rt) will remain in R4+ with probability 1.

    (ii) Let σ=max{σ1,σ2,σ3,σ4}, for 0<ϑ<p<θ<2(d1b)σ2, there exist constants N1>0 and N2>0 satisfying

    E[(St+It+Mt+Rt)1+θ+Sϑt][(s+i+m0+r)1+θ+sϑ]eN1t+N2N1. (2.3)

    Proof. The proof of part (ⅰ) is common and omitted. Our main proof is part (ⅱ). Let V1(S,I,M,R):=(S+I+M+R)1+θ+Sϑ. Direct calculation to V1(S,I,M,R) yields to

    LV1(S,I,M,R)=(1+θ)(S+I+M+R)θ[Λ(d1b)(S+I+M+R)μI+a1I1+b1I(a2d1)M]+θ(1+θ)2(S+I+M+R)θ1[σ21S2+σ22I2+σ23M2+σ23R2]ϑSϑ1[Λd1SβSId2mMS+b(S+R+M)+pbI+δR]+ϑ(1+ϑ)σ212Sϑ(1+θ)[Λ+a1b1](S+I+M+R)θ+(1+θ)(S+I+M+R)θ1[(d1b)(S+I+M+R)2+θσ22(S2+I2+M2+R2)]ϑΛSϑ1+ϑd1Sϑ+ϑβSϑI+ϑd2mSϑM+ϑ(1+ϑ)σ212Sϑ.

    Let 0<ϑ<p<θ<2(d1b)σ2, so ϑ(1+p)p<1+ϑ and (d1b)+θσ22<0 hold true. By using Young's inequality, it has

    SϑIp1+p(Sϑ)1+pp+11+pI1+pSϑ(1+p)p+11+p(S+I+M+R)1+p,

    and

    SϑMp1+p(Sϑ)1+pp+11+pM1+pSϑ(1+p)p+11+p(S+I+M+R)1+p.

    Hence,

    LV1(S,I,M,R)=[(d1b)θσ22](1+θ)(S+I+M+R)θ+1+(1+θ)[Λ+a1b1](S+I+M+R)θϑΛSϑ1+[ϑd1+ϑ(1+ϑ)σ212]Sϑ+[ϑβ+ϑd2m]Sϑ(1+p)p+11+p[ϑβ+ϑd2m](S+I+M+R)1+p.

    Let N1=d1bθσ22, then LV1(S,I,M,R)+N1V1(S,I,M,R)N2, where

    N2=sup(S,I,M,R)R4+{N1θ(S+I+M+R)θ+1+(1+θ)[Λ+a1b1](S+I+M+R)θϑΛSϑ1+[ϑd1+ϑ(1+ϑ)σ212]Sϑ+[ϑβ+ϑd2m]Sϑ(1+p)p+11+p[ϑβ+ϑd2m](S+I+M+R)1+p+N1Sϑ}<.

    The rest of the process is standard; one can see Lemma 2.3 in [24]. Thus, (2.3) is obtained.

    Lemma 2.2. For all initial conditions (s,i,m0,r)R4+, the solution (St,It,Mt,Rt) of (1.3) satisfies

    lim supt(St+It+Mt+Rt)<,a.s., (2.4)

    hence,

    limtStt=0,limtItt=0,limtMtt=0,limtRtt=0,a.s.,limtσ1tt0SsdW1(s)=0,limtσ2tt0IsdW2(s)=0,limtσ4tt0RsdW4(s)=0,a.s. (2.5)

    Moreover, it has

    limtlnStt=0,limtlnItt0,limtlnMtt0,limtlnRtt0,a.s. (2.6)

    Proof. For (2.4), the proof is analogous to Lemma 3.1 in [22], mainly utilizing the result of Theorem 3.9 in [25], so it is omitted here. The proofs for (2.5) can be derived from (2.4) and strong law of large numbers.

    For limtlnStt0 and other formulas in (2.6), we recommend Lemma 2.3 in [26] to get a detailed proof. In addition, the property that ESϑt< will lead to lim inftlnStt0, so limtlnStt=0 is obtained.

    We will give a value in this section and roughly explain it as the threshold of the extinction or persistence of model (1.3).

    Take into account the first equation of model (1.3) on the boundary It=0, Mt=0, and Rt=0, it has

    dˉSt=[Λ(d1b)ˉSt]dt+σ1ˉStdW1(t). (3.1)

    Let ˉSut be the solution to (3.1) with the initial condition ˉS0=u. It should be noted that StˉSt,t>0 cannot be obtained by using the comparison theorem. Applying the Itˆos formula to the function ˉS1lnˉS and making use of the result in [27], there exists the unique stationary distribution π0 for (3.1) with the density

    f(x)=ˉuˉvΓ(ˉv)xˉv1eˉux,x>0,

    where ˉv=2(d1b)σ21+1, ˉu=2Λσ21, Γ() is the Gamma function. We get from the strong law of large numbers that

    limt1tt0βˉSsds=0βxf(x)dx=βΛd1b,a.s. (3.2)

    Calculating the second formula of model (1.3), it has

    lnItt=lnI0t+1tt0βSsds(d1+γ+μqb+12σ22)+σ2W2(t)t. (3.3)

    Intuitively, if lim suptlnItt<0, then limtIt=0. This leads to the results limtMt=0, limtRt=0, which will be explained in detail later. Thus, we have StˉSt if t is sufficiently large, then one can anticipate that

    limt1tt0βSsdslimt1tt0βˉSsds=βΛd1b. (3.4)

    Defining the value

    Δ:=βΛd1b(d1+γ+μqb+12σ22). (3.5)

    Hence, lim suptlnItt will tend to Δ above. If Δ<0, then lim suptlnItt will be negative, and the disease will die out. Conversely, when Δ>0, no matter how small the initial value I0 is, It tends to be large for a sufficiently long time. The above description seems simple; however, the proof requires careful and rigorous implementation.

    Now, we present the main conclusions of this paper, the proof of which will be given in the later section. Let RS0=βΛ(d1b)(d1+γ+μqb+12σ22).

    Theorem 3.1. When Δ<0, or equivalently RS0<1, the solution (St,It,Mt,Rt) with the initial condition (s,i,m0,r)R4,o+ satisfies

    limtlnItt=Δ<0,a.s., (3.6)

    (3.6) implies that the disease It becomes extinct at an exponential rate.

    Theorem 3.1 gives a condition to judge the extinction of the disease.

    Proposition 3.1. If Δ<0, let ¯Δ:=min{Δ,a2+12σ23,d1+δ+12σ24}>0 and ¯Δ1:=min{Δ,a2+12σ23}>0, then

    limtlnMtt=¯Δ1=max{Δ,(a2+σ232)},a.s., (3.7)
    limtlnRtt=¯Δ=max{Δ,(a2+12σ23),(d1+δ+σ242)},a.s. (3.8)

    Furthermore,

    limtln|StˉSt|tmax{¯Δ,(d1b+σ212)},a.s. (3.9)

    Definition 3.1. [28] The disease in model (1.3) is called to be persistent in the mean, if the following inequality holds

    lim inft1tt0I(u)du>0,a.s.

    Theorem 3.2. For the solution (St,It,Mt,Rt) with the initial condition (s,i,m0,r)R4,o+, when Δ > 0, that is, RS0>1, the disease It in model (1.3) is persistent in the mean. Moveover, the solution (St,It,Mt,Rt) has the invariant probability measure.

    Remark 3.1. According to Theorems 3.1 and 3.2, we know that the sign of Δ will judge extinction or persistence of model (1.3) and RS0 can be regarded as the reproduction number, which depicts the number of second-generation infections after a single infected one enters the population.

    In this section, we will prove Theorem 3.1 and Proposition 3.1 with the assumption that Δ<0.

    First, consider the equation

    dˉSεt=[Λ(d1b)ˉSεt+ε]dt+σ1ˉSεtdW1(t). (4.1)

    Similar to the Eq (3.1), a suitable Lyapunov function can be proved to obtain the invariant measure πε with density

    fε(s)=(2(Λ+ε)σ21)2(d1b)σ21+1Γ(2(d1b)σ21+1)x2(d1b)σ212e2(Λ+ε)σ21x,x>0.

    Lemma 4.1. Provided that Δ<0, for any ϵ>0 and H>0, there is a constant δ1>0 such that for any (s,i,m0,r)[0,H]×[0,δ1]3 (where [0,δ1]3 represents [0,δ1]×[0,δ1]×[0,δ1]), it has

    Ps,i,m0,r{limtIt=0,limtMt=0,limtRt=0}1ϵ. (4.2)

    Proof. Let (s,i,m0,r)[0,H]×[0,δ1]3. For the 0<ε1<(d1b)ˉΔ8β (ˉΔ is defined in Proposition 3.1), consider the Eq (4.1) with ε replaced by ε1, the ergodicity of solution with the initial data s denoted by ˉSε1,st leads to

    limt1tt0ˉSε1,sudu=0xfε1(x)dx=Λ+ε1d1b.

    If the initial value is not emphasized later, we still use ˉSε1t to express the solution of the equation.

    Thus, there is a constant T1 such that P(ΩH1)>1ϵ5, where

    Ωs1={ω:1tt0ˉSε1,suduΛ+ε1d1b+ˉΔ8β,tT}.

    Due to ˉSε1,stˉSε1,Ht for sH, it yields Ps(Ω1)>1ϵ5 for s[0,H].

    Because limtσiWi(t)t=0,a.s., i=1,2,3,4, it has for some constant T2, P(Ω2)>1ϵ5, where

    Ω2={ω:σiWi(t)tmin{ˉΔ8,ε1},tT2andi=1,2,3,4}.

    Assume that T=max{T1,T2}; thanks to Lemmas 2.1 and 2.2, then for some positive constants C1 and K, it has P(Ω3)>1ϵ5 and P(Ω4)>1ϵ5, where

    Ω3={ω:St(ω)C1,t>0}, (4.3)

    and

    Ω4={ω:T0βSuduK}.

    Let K above be sufficiently large such that P(Ω5)>1ϵ5. Here,

    Ω5={ω:|σiWi(t)|K,fori=1,2,3,4andtT}.

    Choose δ1 sufficiently small so that

    δ1(e2K+a1e4KT+d2m(e3K+a1e6KT)K/β+γe4KT)<ε12b+pb+δ, (4.4)

    and

    δ1max{C2,C3}<ε12b+pb+δ. (4.5)

    Here, C2 and C3 will be determined in (4.11) and (4.12), respectively, later.

    Let the stopping time be defined as

    τ=inf{t:maxt>0{It,Mt,Rt}ε12b+pb+δ}.

    From the second equation, we get

    It=I0exp{t0βSudu(d1+γ+μqb+12σ22)t+σ2W2(t)}. (4.6)

    Similarly, the third and fourth equations of (1.3) result in

    Mt=Ψ1(t)[M0+t0a1Iu1+b1IuΨ11(u)du] (4.7)

    and

    Rt=Ψ2(t)[R0+t0(d2mSuMu+γIu)Ψ12(u)du], (4.8)

    where Ψ1(t)=exp{(a2+σ232)t+σ3W3(t)} and Ψ2(t)=exp{(d1+δ+σ242)t+σ4W4(t)}.

    Hence, we get from (4.6) that for almost every ωΩ4Ω5 and t[0,Tτ], it has

    ItI0eT0βSudu+σ2W2(u)I0e2Kδ1e2Kε12b+pb+δ.

    Moreover, the expression of Ψ1(t) leads to that for ωΩ5,

    exp{(a2+σ232)tK}Ψ1(t)exp{(a2+σ232)t+K},t[0,Tτ].

    Thus, when ω5i=4,

    Ψ1(t)t0a1Iu1+b1IuΨ11(u)dut0a1I0e2Ke(a2+σ232)t+σ3W3(t)e(a2+σ232)uσ3W3(u)duδ1a1e4KT. (4.9)

    Due to (4.4), it has

    Mt=Ψ1(t)M0+Ψ1(t)t0a1Iu1+b1IuΨ11(u)dueKδ1+δ1a1e4KTε12b+pb+δ. (4.10)

    In the same way, for t[0,Tτ] on 5i=4,

    Ψ2(t)t0d2mSuMuΨ12(u)dut0d2mδ1[eK+a1e4KT]Sue(d1+δ+σ242)(tu)+σ3W3(t)σ3W3(u)dud2mδ1[eK+a1e4KT]e2KK/β,

    and

    Ψ2(t)t0γIuΨ12(u)duT0γI0e2Ke2Kduδ1γe4KT.

    Thus, it yields from (4.8) and (4.4) that

    RteKR0+d2mδ1[eK+a1e4KT]e2KK/β+δ1γe4KTδ1[eK+d2m(e3K+a1e6KT)K/β+γe4KT]ε12b+pb+δ.

    Hence, for (s,i,m0,r)[0,H]×[0,δ1]3 on almost every ω5i=4, we have

    τT.

    Next, we shall prove the assertion τ= for almost every ω5k=1Ωk.

    First, when t[T,τ], it has SvˉSε1v for all v[0,t] by comparison principle; then for almost ω5k=1Ωk,

    It=I0exp{t0βSudu(d1+γ+μqb+12σ22)t+σ2W2(t)}I0exp{t0βˉSε1udu(d1+γ+μqb+12σ22)t+σ2W2(t)}I0exp{β(Λ+ε1d1b)t+ˉΔ8t(d1+γ+μqb+12σ22)t+ˉΔ8t}I0exp{Δt+2ˉΔ8t+βε1d1bt}I0e(Δ+3ˉΔ8)tδ1e5ˉΔ8t,(s,i,m0,r)[0,H]×[0,δ1]3.

    One can rewrite Mt on tT that

    Mt=Ψ1(t)[M0+T0a1Iu1+b1IuΨ11(u)du+tTa1Iu1+b1IuΨ11(u)du].

    For almost every ωΩ2, exp{(a2+σ232)t18ˉΔt}Ψ1(t)exp{(a2+σ232)t+18ˉΔt} is obtained and

    Ψ1(t)tTa1Iu1+b1IuΨ11(u)due(a2+σ232)t+18ˉΔttTa1I0e5ˉΔ8ue(a2+σ232+18ˉΔ)uduδ1a1a2+σ23212ˉΔe38ˉΔt,on2i=1Ωi.

    Therefore, there exists a positive constant C2 satisfying

    Mte(a2+σ23218ˉΔ)t[m0+T0a1I0e2Ke(a2+σ232)u+Kdu]+δ1a1a2+σ23212ˉΔe38ˉΔt(δ1+a1δ1e3Ke(a2+σ232)TT)e(a2+σ23218ˉΔ)t+δ1a1a2+σ23212ˉΔe38ˉΔtδ1C2e38ˉΔt,

    where

    C2=a1a2+σ23212ˉΔ+1+a1e3Ke(a2+σ232)TT. (4.11)

    Similarly, rewriting the expression of Rt (4.8) yields

    Rt=Ψ2(t)[R0+T0(d2mSuMu+γIu)Ψ12(u)du]+Ψ2(t)tT(d2mSuMu+γIu)Ψ12(u)du.

    For almost all ωΩ2, we have

    e(d1+δ+σ242)t18ˉΔtΨ2(t)e(d1+δ+σ242)t+18ˉΔt.

    For almost all ω3i=1Ωi and t>T, it has

    Ψ2(t)tTd2mSuMuΨ12(u)due(d1+δ+σ242)t+18ˉΔttTd2mC1δ1C2e38ˉΔue(d1+δ+σ242+18ˉΔ)uduδ1d2mC1C2d1+δ+σ24214ˉΔe18ˉΔt.

    Similar to the proof of Mt, it has

    Ψ2(t)tTγIuΨ12(u)duγI0d1+δ+σ24212ˉΔe38ˉΔt.

    Thus,

    Rte(d1+δ+σ242)t+18ˉΔt[δ1+d2mδ1(e3K+a1e6KT)K/β+δ1γe4KT]+δ1d2mC1C2d1+δ+σ24214ˉΔe18ˉΔt+γδ1d1+δ+σ24212ˉΔe38ˉΔtδ1C3e18ˉΔt,

    where

    C3=d2mC1C2d1+δ+σ24214ˉΔ+γd1+δ+σ24212ˉΔ+1+d2m(e3K+a1e6KT)K/β+γe4KT. (4.12)

    Assume that n is an integer with n>T. We get from the estimation of It, Mt and Rt for t[0,nτ] and almost every ω5k=1Ωk that

    Itδ1ε12b+pb+δ,Mtδ1C2ε12b+pb+δ,

    and

    Rtδ1C3ε12b+pb+δ.

    These results imply nτ on almost every ω5k=1Ωk. On the basis of arbitrariness of n, the assertion τ= is obtained. In addition, from the estimation of It, Mt, and Rt, one has

    limtlnItt5ˉΔ8,limtlnItt3ˉΔ8,limtlnIttˉΔ8.

    This will lead to the (4.2) for any initial condition (s,i,m0,r)[0,H]×[0,δ1]3 on almost 5k=1Ωk with P(5k=1Ωk)1ϵ.

    The subsequent proof of Theorem 1 is analogue to that of Theorem 2.2 in [29], so it is omitted here.

    Now, we provide the proof of the Proposition 3.1. From (3.6), we get that for any small ϵ1, there exist positive random variables ξ1, ξ2 satisfying that for t>0,

    ξ1e(Δϵ1)tItξ2e(Δ+ϵ1)t.

    Due to the expression of Ψ1(t), it yields

    limtlnΨ1(t)t=(a2+σ232),a.s.

    This means there exist random variables ξ3>0, ξ4>0 satisfying that for t>0,

    ξ3e(a2+σ232+ϵ1)tΨ1(t)ξ4e(a2+σ232ϵ1)t.

    By virtue of (4.7) and the increasing property of a1I1+b1I with respect to I, it yields

    Mtξ3e(a2+σ232+ϵ1)tm0+ξ3e(a2+σ232+ϵ1)tt0a1ξ1e(Δϵ1)uξ4(1+b1ξ1e(Δϵ1)u)e(a2+σ232ϵ1)uduξ3e(a2+σ232+ϵ1)tm0+ξ3a1ξ1ξ4(1+b1ξ1)(Δ+a2+σ2322ϵ1)[e(Δ3ϵ1)te(a2+σ232+ϵ1)t].

    Thus,

    lim inftlnMtt¯Δ14ϵ1.

    Similarly, we can get that

    lim suptlnMtt¯Δ1+4ϵ1.

    Therefore, one obtains that for almost every ω5k=1Ωk, (3.7) holds true by the arbitrariness of ϵ1.

    Due to Lemma 2.2 and (3.7), it has limtlnStMtt=¯Δ1, which leads to there being random variables ξ5>0 and ξ6>0 satisfying

    ξ5e(¯Δ1ϵ1)tStMtξ6e(¯Δ1+ϵ1)t.

    Moreover, there are random variables ξ7>0 and ξ8>0 such that

    ξ7e(d1+δ+σ242+ϵ1)tΨ2(t)ξ8e(d1+δ+σ242ϵ1)t.

    Thus, we get from (4.8) that

    ξ7e(d1+δ+σ242+ϵ1)t[R0+1ξ8t0(d2mξ5e(¯Δ1ϵ1)u+γξ1e(Δϵ1)u)e(d1+δ+σ242ϵ1)udu]Rtξ8e(d1+δ+σ242ϵ1)t[R0+1ξ7t0(d2mξ6e(¯Δ1+ϵ1)u+γξ2e(Δ+ϵ1)u)e(d1+δ+σ242+ϵ1)udu]. (4.13)

    Hence, it has

    lim suptlnRttmax{¯Δ1,(d1+δ+σ242)}+4ϵ1,lim inftlnRttmax{¯Δ1,(d1+δ+σ242)}4ϵ1.

    This implies that (3.8) holds.

    For the convergence rate of the solution St with initial data (s,i,m0,r) of (1.3) to the solution ˉSt with initial data s of (3.1), take into account the equation

    d(ˉStSt)=[(d1b)(ˉStSt)+βStIt+d2mMtStpbItbMt(b+δ)Rt]dt+σ1(ˉStSt)dW1(t). (4.14)

    Let Ψ3(t):=exp{(d1b+σ212)t+σ1W1(t)}, then utilizing the constant variation method, we can obtain

    ˉStSt=Ψ3(t)t0[βSuIu+d2mMuSupbIubMu(b+δ)Ru]Ψ13(u)du. (4.15)

    This means

    Ψ3(t)t0[pbIu+bMu+(b+δ)Ru]Ψ13(u)duˉStStΨ3(t)t0[βSuIu+d2mMuSu]Ψ13(u)du. (4.16)

    By (3.6) and Lemma 2.2, there is a random variable ξ9>0 such that

    StItξ9e(Δ+ϵ1)t. (4.17)

    Let Δ1:=max{ˉΔ,(d1b+σ212)}, and Δ2>Δ1. For a sufficiently small ϵ1, Δ2>Δ1+3ϵ1 can be satisfied. The expression of Ψ3(t) implies that there exist random variables ξ10>0 and ξ11>0 such that

    ξ10e(d1b+σ212+ϵ1)tΨ3(t)ξ11e(d1b+σ212ϵ1)t.

    Similar to the method in (4.12), we can get from (4.16) that

    ˉStStξ11ξ10e(d1b+σ212ϵ1)tt0[βξ9e(Δ+d1b+σ212+2ϵ1)u+d2mξ6e(¯Δ1+d1b+σ212+2ϵ1)u]du.

    Applying L'Hospital rule means

    limtˉStSteΔ2t0.

    Likewise, we can get that limtˉStSteΔ2t0. Thus, (3.9) is obtained.

    In this section, we shall prove Theorem 3.2, which studies the condition of persistence in the mean and the invariant probability measure of the model (1.3). First, we prove the disease persistence in Subsection 5.1.

    For C1 in (4.3), define V2(I)=lnI, V3=ˉSS and

    V4(S,I,M)=V2(I)+βd1bV3+βd2mC1(d1b)a2M. (5.1)

    Direct calculation by Ito's formula yields that

    dV4=LV4dt+βσ1d1b(ˉSS)dW1(t)σ2dW2(t)+βd2mC1σ3(d1b)a2MdW3(t), (5.2)

    where

    LV4=1I[βSI(d1+γ+μqb)I]+σ222+βd1b[(d1b)(ˉSS)+βSI]+βd1b[d2mMS(b+δ)RbMpbI]+βd2mC1(d1b)a2(a1I1+b1Ia2M)βS+(d1+γ+μqb+σ222)β(ˉSS)+β2d1bSI+βd2mMSd1b+βd2mC1a1(d1b)a2Iβd2mC1d1bMβˉS+(d1+γ+μqb+σ222)+β2C1d1bI+βd2mC1a1(d1b)a2IΔ+β2C1d1bI+βd2mC1a1(d1b)a2Iβ(ˉSΛd1b). (5.3)

    Here, we use (4.3) and (4.14). Hence, integrating for (5.2) from 0 to t and dividing it by t, we have

    V4(St,It,Mt)V4(S0,I0,M0)tΔ+(β2C1d1b+βd2mC1a1(d1b)a2)1tt0Isdsβtt0ˉSsds+βΛd1bσ2W2(t)t+βσ1d1b1tt0(ˉSsSs)dW1(s)+βd2mC1σ3(d1b)a21tt0MsdW3(s).

    Then, taking the limit, for Δ>0, using the results in Lemma 2.2 and the expression of V4 as well as the ergodicity of ˉS, yields

    (β2C1d1b+βd2mC1a1(d1b)a2)limt1tt0IsdsΔ, (5.4)

    which signifies the disease in model (1.3) is persistent in the mean.

    Next, we prove the invariant probability measure of the model (1.3) under the condition of Δ>0.

    Let σ2=max{σ21,σ22,σ23,σ24}. Define a function by

    F(S,I,M,R):=H2V4(S,I,M)+V5(S,I,M,R)lnSlnMlnR, (5.5)

    where the function V4 is defined in (5.1), V5(S,I,M,R)=11+a(S+I+M+R)1+a, a(0,1) satisfies

    d1baσ22>0, (5.6)

    and the constant H2 is to be explained later.

    Notice that the function F(S,I,M,R) is continuous, and thus in the interior of R4+, it has the minimum value F(S0,I0,M0,R0). So, a nonnegative function ˜F(S,I,M,R) can be defined by

    ˜F(S,I,M,R)=F(S,I,M,R)F(S0,I0,M0,R0).

    By calculation to V5, it has

    LV5(S+I+M+R)a[Λ(d1b)S(d1b)IμI(a2b)M(d1b)R+a1b1]+a(S+I+M+R)a12(σ21S2+σ22I2+σ23M2+σ24R2)(Λ+a1b1)(S+I+M+R)a(d1baσ22)(S+I+M+R)a+1N112(d1baσ22)(S+I+M+R)a+1, (5.7)

    where N1=sup(S,I,M,R)R4+[(Λ+a1b1)(S+I+M+R)a12(d1baσ22)(S+I+M+R)a+1]< by (5.6).

    Meanwhile,

    L(lnS)=1S[Λd1SβSId2mMS]1S[b(S+R+M)+pbI+δR]+12σ21ΛS+d1+σ212+βI+d2mM,
    L(lnM)=1M[a1I1+b1Ia2M]+σ232a1IM(1+b1I)+a2+σ232,

    and

    L(lnR)=1R[d2mMS+γI(d1+δ)R]+σ242d2mMSRγIR+d1+δ+σ242γIR+d1+δ+σ242.

    Hence, let N2=2d1+a2+δ+σ21+σ23+σ242,

    L˜F(S,I,M,R,ˉS)H2[Δ+β2C1d1bI+βd2mC1a1(d1b)a2I]+N1+N212(d1baσ22)(S+I+M+R)a+1ΛS+βI+d2mMa1IM(1+b1I)γIRH2[β(ˉSβd1b)]=:˜F1(S,I,M,R)H2[β(ˉSβd1b)]. (5.8)

    We define the function f1(S,I,M,R):=12(d1baσ22)(S+I+M+R)a+1 for convenience. Let the constants Ni(i=3,4,5) be defined as follows,

    N3:=sup(S,I,M,R)R4+{f1+H2[Δ+β2C1d1bI+βd2mC1a1(d1b)a2I]+βI+d2mM},N4=sup(S,I,M,R)R4+{f1(S,I,M,R)+βI+d2mM},

    and

    N5:=sup{S1ϵ2}×(I,M,R)R3+{H2[Δ+β2C1d1bI+βd2mC1a1(d1b)a2I]12f1+βI+d2mM}.

    It is easy to see that Ni<(i=3,4,5). Let the constant ϵ2 be sufficiently small and H2 sufficiently large such that

    Δ+β2C1d1bϵ2+βd2mC1a1(d1b)a2ϵ2<0, (5.9)
    Λϵ2+N1+N2+N31, (5.10)
    H2(Δ+β2C1d1bϵ2+βd2mC1a1(d1b)a2ϵ2)+N1+N2+N41, (5.11)
    a1ϵ2(1+b1ϵ2)+N1+N2+N31, (5.12)
    γϵ2+N1+N2+N31, (5.13)

    and

    d1baσ2241εa+12+N1+N2+N51. (5.14)

    For the ϵ2 above, define the bounded set E as the following form,

    E:={(S,I,M,R):ϵ2S1ϵ2,ϵ2I1ϵ2,ϵ22R1ϵ22,ϵ22M1ϵ22}.

    The following will suffice to prove L˜F1(S,I,M,R)1 in the domain R4+E. Note that R4+E could be divided into eight sub-regions Eci, i=1,...,8:

    Ec1={(S,I,M,R)R4+:S<ϵ2},Ec2={(S,I,M,R)R4+:I<ϵ2},Ec3={(S,I,M,R)R4+:M<ϵ22,Iϵ2},Ec4={(S,I,M,R)R4+:R<ϵ22,Iϵ2},Ec5={(S,I,M,R)R4+:S>1ϵ2},Ec6={(S,I,M,R)R4+:I>1ϵ2},Ec7={(S,I,M,R)R4+:M>1ϵ22,Ec8={(S,I,M,R)R4+:R>1ϵ22}.

    (ⅰ) When (S,I,M,R)Ec1, it follows from (5.8) and (5.10) that

    ˜F1(S,I,M,R)ΛS+N1+N2+N3Λϵ2+N1+N2+N31.

    (ⅱ) When (S,I,M,R)Ec2, it yields from (5.8) and (5.11) that

    ˜F1(S,I,M,R)H2(Δ+β2C1d1bϵ2+βd2mC1a1(d1b)a2ϵ2)+N1+N2+N41.

    (ⅲ) When (S,I,M,R)Ec3, (5.8) and (5.12) lead to

    ˜F1(S,I,M,R)a1IM(1+b1I)+N1+N2+N3a1ϵ2(1+b1ϵ2)+N1+N2+N31.

    (ⅳ) When (S,I,M,R)Ec4, it follows from (5.8) and (5.13) that

    ˜F1(S,I,M,R)γIR+N1+N2+N3γϵ2+N1+N2+N31.

    (ⅴ) When (S,I,M,R)Ec5, we know from (5.8) and (5.14) that

    ˜F1(S,I,M,R)d1baσ224Sa+1+N1+N2+N5d1baσ2241εa+12+N1+N2+N51.

    The cases in Ec6, Ec7, Ec8 are similar to that in Ec5, which we will omit here. Hence, the assertion that L˜F1(S,I,M,R)1 in R4+E is obtained.

    Meanwhile, by the continuity of ˜F1(S,I,M,R) and the compactness of E, there is a constant H3>0 such that ˜F1(S,I,M,R)H3 for (S,I,M,R)E. Thus, it yields

    E(˜F(S0,I0,M0,R0))tE(˜F(St,It,Mt,Rt))E(˜F(S0,I0,M0,R0))t=1tt0E[L˜F(Su,Iu,Mu,Ru)]du1tt0˜F1(Su,Iu,Mu,Ru)duH2β1tt0[(˜SuΛd1b)]du.

    By using the ergodicity of ˉSt, it has

    0lim inft1tt0˜F1(Su,Iu,Mu,Ru)du=lim inft1tt0(˜F1(Su,Iu,Mu,Ru)I{(S,I,M,R)E}+˜F1(Su,Iu,Mu,Ru)I{(S,I,M,R)Ec})dulim inft1tt0H3P({(Su,Iu,Mu,Ru)E})+(1)P({(Su,Iu,Mu,Ru)Ec})dulim inft1tt0[(1+H3)P{(Su,Iu,Mu,Ru)E}1]du.

    This means

    lim inft1tt0P(u,(S0,I0,M0,R0),E)du11+H3. (5.15)

    Therefore, due to the compactness of E and (5.15), model (1.3) has the invariant probability measure by exploiting Theorem 2 in [30].

    This section will deal with the case of Δ=0, which is a critical one that has been less investigated in literature.

    Theorem 6.1. For the model (1.3) with initial condition (s,i,m0,r)R4,o+, if Δ=0 and d1b+μba1a2> 0, then

    limt1tt0I(u)du=0,a.s. (6.1)

    Proof. We prove it by contradiction. Assume that (St,It,Mt,Rt) has the invariant measure m on R4,o+. Thus, it can be concluded by the ergodicity that for any m measurable function g,

    limt1tt0g(Su,Iu,Mu,Ru)du=R4,o+g(s,i,m,r)m(ds,di,dm,dr). (6.2)

    Hence, there exist positive constants h1 and h2 such that

    limt1tt0Iudu=R4,o+im(ds,di,dm,dr)=h1>0,

    and

    limt1tt0Rudu=R4,o+rm(ds,di,dm,dr)=h2>0.

    Integrating for the second equation of (1.3) and using (2.4) as well as Lemma 2.2 leads to

    limt1tt0(βSuIu(d1+γ+μqb)Iu)du+limt1tt0σ2IudW2(u)=limtItit=0. (6.3)

    Thus, limt1tt0βSuIudu=(d1+γ+μqb)limt1tt0Iudu.

    Utilizing the same method yields to

    limt1tt0d2mMuSudu=limt1tt0(γIu+(d1+δ)Ru)du, (6.4)

    and

    limt1tt0a2Mudu=limt1tt0a1Iu1+b1Iudulimt1tt0a1Iudu. (6.5)

    For (4.14), it has

    limt1tt0[(d1b)(ˉSuSu)+βSuIu+d2mMuSupbIubMu(b+δ)Ru]du=limtˉStStt=0, (6.6)

    Substituting (6.3)–(6.5) into the above equation yields

    0=limt1tt0[(d1b)(ˉSuSu)+βSuIu+d2mMuSupbIubMu(b+δ)Ru]dulimt1tt0[(d1b)(ˉSuSu)+(d1b+μba1a2)Iu+(d1b)Ru]du.

    Then,

    limt1tt0(ˉSuSu)du1d1blimt1tt0[(d1b+μba1a2)Iu+(d1b)Ru]du1d1b[(d1b+μba1a2)h1+(d1b)h2=:h3>0. (6.7)

    Therefore, we have

    limtlnItt=limtlnI0+σ2W2(t)t+limt1tt0(βSu(d1+γ+μqb+σ222))du=limt1tt0(βˉSu(d1+γ+μqb+σ222))dulimt1tt0β(ˉSuSu)duΔβh3=βh3<0,a.s.

    Consequently, P{limtIt=0}=1, which contradicts the hypothesis at the beginning of this proof.

    From the analysis above, we see that Δ could be used to determine the different dynamical behavior of the model. In the deterministic model without stochastic noise, if Δ>0, then the disease will persist. When the noise σ2 is large enough, Δ<0 can always hold, which means the disease shall be extinct by Theorem 3.1. This reveals that stochastic noise contributes to the extinction of disease.

    If b=0 and q=0, that is, there is no vertical transmission, the model (1.3) we discuss in this paper becomes the one in [16]. The authors in [16] obtained the value RS0 to decide the persistence and stationary distribution of the model with information intervention. However, compared with the value RS1 in this paper, there is an additional term μ1maa0b in RS0, which makes the value RS0 smaller. In fact, this term can be eliminated by establishing appropriate functions. Due to the two terms μ1maa0b in RS0 and 12σ2, there is a greater gap between the value RS to judge extinction and the value RS0 to determine persistence. This article gets the same value that determines both behaviors. In addition, we also obtain more detailed estimates of I, M, and R when Δ<0.

    In addition, our model is more complex and general than that in [22]. If there is no Mt and Rt class, model (1.3) will degenerate into the model similar to that in [22]. For the two-dimensional model there, the author obtained the values RS0 and ˜RS0 for deciding the extinction (˜RS0<1) and the existence of stationary distribution (RS0>1), which are different. In our paper, a new function is built to acquire the same threshold that determines different properties.

    Moreover, we see from the expression of Δ that qb will make Δ larger, and when Δ>0, the disease will spread by Theorem 3.2. Therefore, it is proposed that women should avoid to get pregnant during the period of infection for the sake of maternal and child health, which will reduce the vertical transmission rate and be beneficial for disease control.

    In what follows, we will enumerate some examples to check the conclusions reached in the previous section.

    Example 7.1. In order to verify the conclusion of Theorem 3.1, let Λ=0.12, d1=0.05, β=0.16, a1=0.12, b1=0.12, a2=0.5, b=0.02, p=0.4, μ=0.02, δ=0.35, γ=0.45, m=1.2, σ1=0.4, σ2=0.6, σ3=0.2 and σ4=0.1, thus, the parameter Δ=0.048<0, the disease will die out; see Figure 1(a) with the initial condition S0=2.1, I0=1.2, M0=0, R0=1.2. While in the deterministic model without noise, the value Δ=0.132>0, the disease is persistent; see Figure 1(b). Figure 1(b) shows the trajectories of various parts of the model, indicating that the disease is persistent, while Figure 1(a) shows that the disease is extinct without noise.

    Figure 1.  (a) The trajectory of model (1.3) taking values in Example 7.1; (b) the trajectory of model (1.3) with values in Example 6.1 without stochastic noise.

    Example 7.2. Let Λ=0.12, d1=0.06, d2=0.8, β=0.08, a1=0.12, b1=1, a2=0.25, b=0.03, p=0.4, μ=0.04, δ=0.35, γ=0.55, m=0.15, σ1=0.3, σ2=0.4, σ3=0.2 and σ4=0.1 such that Δ<0.392. According to the results of Proposition 3.1, limtlnRtt=0.27, limtlnRtt=0.27 and limtln|StˉSt|t0.075; see Figure 2.

    Figure 2.  The trajectory of model (1.3) with values in Example 7.2 and the same initial values as in Example 7.1: (a) the trajectory of lnRtt, (b) the trajectory of lnMtt, and (c) the trajectory of ln|StˉSt|t.

    Example 7.3. Let Λ=0.12, β=0.2 and γ=0.45; other parameters are the same as those in Example 7.2. Thus, Δ=0.7213>0. We know from Theorem 3.2 that the disease in model (1.3) is persistent in the mean; see Figure 3.

    Figure 3.  The trajectory of It and Mt in model (1.3) with values in Example 7.3.

    Example 7.4. Now, we discuss the influence of information intervention factor on the behavior of model (1.3). Suppose that m=0.5, d2=0.8, and other parameters are the same as those in Example 6.2. First, let a1=0 a2=0, that is, there is no Mt class, then Δ=0.7563>0 and the disease will spread. The trajectory of susceptible class St is shown in Figure 4(a). When a1=0.9, a2=0.3, and σ3=0.2, the class Mt affected by the information intervention exists and makes themselves as uninfected as possible through different measures, such as self-isolation or vaccination, which will reduce the size of the susceptible population to varying degrees. Figure 4(b) shows the trajectory of Mt and St, where the trajectory of St is slightly smaller than that of St in Figure 4(a).

    Figure 4.  (a) The trajectory of St in model (1.3) taking values in Example 7.4; (b) the trajectory of St and Mt in model (1.3) with values in Example 7.4.

    Example 7.5. Next, to verify the conclusion of Theorem 6.1, let Λ=0.12, d1=0.06, β=0.2, a1=0.2, b1=1, a2=0.25, b=0.02, p=0.4, μ=0.047, δ=0.4, γ=0.5, m=0.15, σ1=0.08, σ2=0.1, σ3=0.5 and σ4=0.05; thus, the parameter Δ=0 and d1b+μba1a2>0, and the disease will not be persistent in the mean. See Figure 5 with the initial condition S0=2.1, I0=1.2, M0=0, and R0=1.2. (a) is the sample path of model (1.3) and (b) represents the trajectory of 1tt0Isds.

    Figure 5.  (a) The sample path of (1.3) with values in Example 7.5; (b) the trajectory of 1tt0Isds in (1.3) with values in Example 7.5.

    The dynamic behavior of a stochastic epidemic model with information intervention and vertical transmission was the concern of this paper. The threshold to judge the extinction and persistence of the disease is obtained. When Δ=βΛd1b(d1+γ+μqb+12σ22)<0, the three classes It, Mt, and Rt appearing in the model go extinct at an exponential rate, and the susceptible class St almost surely converges to the solution of the boundary equation exponentially. When Δ>0, the disease in the model is persistent in the mean. Besides, the existence of invariant probability measure under this condition is proved by constructing proper Lyapunov functions. In addition, the critical case of Δ=0 is also investigated and it is found that the disease will not be persistent in the mean under some conditions. Several discussions are presented to explain the results and some numerical examples are proposed to verify the obtained results.

    A few other issues are worth further studies. This paper analyzes the model with a bilinear incidence rate, while a nonlinear one can be applied to a wider range of circumstances. Therefore, it will be more generic to generalize the model to one with nonlinear incidence. We consider, in this paper, that the stochastic noise is continuously characterized by white noise, and the introduction of more noises such as Markovian switching and Lˊevy noise will enable the model to be more realistic. Further research can be conducted on optimizing strategies for some control and prevention measures. We leave these issues for future investigations.

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

    This research was supported by the Jiangxi Province High level and High skilled Leading Talent Training Project, the Science and Technology projects of Jiangxi Province Education Department (No. GJJ212716) and the National Key R & D Program of China (No. 2023YFC3008902).

    The authors declare that they have no competing interests.



    Conflict of interest



    The authors declare no conflicts of interest.

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