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Research article Special Issues

Characterization of recycled Inconel 718 metal powder for assessing its reusability in the laser powder bed fusion process

  • Received: 10 November 2021 Revised: 23 January 2022 Accepted: 10 February 2022 Published: 23 February 2022
  • Additive manufacturing technologies such as laser powder bed fusion (LPBF) provide unprecedented abilities to manufacture complex 3-D parts and structures; however, the process produces leftover metal powder that is often unused, resulting in significant cost and disposal overhead. Towards this end, to ensure the ability to recycle the unused powder that is typically found within the build volume and in the overflow compartments of LPBF systems, a thorough chemical and structural analysis is required. Such an analysis will help in determining the extent of recyclability and reusability of the unused powder. For these purposes, characterization of recycled powder for Inconel 718 was performed in this work as a function of build-cycle to compare and contrast the evolution in physical and chemical properties such as particle size distribution, morphology, and composition. We note that the analysis was carried out for 21 build-cycles. Characterization of the particle size distribution and circularity was performed using traditional scanning electron microscopy methods and that information was later compared to measurements of surface profile using coherent scanning interferometry. Reusability was assessed using these results in conjunction with chemical analysis of the powder that was carried out using energy dispersive X-ray spectroscopy. For the extent of build-cycles considered in this work, it was seen that the physical and chemical changes in the recycled powder were will within accepted limits for powder usage and that with appropriate measures, recycled powder can be re-incorporated for subsequent builds without compromise in the powder quality. This study provides a pathway for greatly reducing powder consumption and thus cost during the LPBF process.

    Citation: Susana J. Castillo, Anna Hayes, Greg Colvin, Barrett G. Potter, Rongguang Liang, Krishna Muralidharan. Characterization of recycled Inconel 718 metal powder for assessing its reusability in the laser powder bed fusion process[J]. Clean Technologies and Recycling, 2022, 2(1): 32-46. doi: 10.3934/ctr.2022002

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  • Additive manufacturing technologies such as laser powder bed fusion (LPBF) provide unprecedented abilities to manufacture complex 3-D parts and structures; however, the process produces leftover metal powder that is often unused, resulting in significant cost and disposal overhead. Towards this end, to ensure the ability to recycle the unused powder that is typically found within the build volume and in the overflow compartments of LPBF systems, a thorough chemical and structural analysis is required. Such an analysis will help in determining the extent of recyclability and reusability of the unused powder. For these purposes, characterization of recycled powder for Inconel 718 was performed in this work as a function of build-cycle to compare and contrast the evolution in physical and chemical properties such as particle size distribution, morphology, and composition. We note that the analysis was carried out for 21 build-cycles. Characterization of the particle size distribution and circularity was performed using traditional scanning electron microscopy methods and that information was later compared to measurements of surface profile using coherent scanning interferometry. Reusability was assessed using these results in conjunction with chemical analysis of the powder that was carried out using energy dispersive X-ray spectroscopy. For the extent of build-cycles considered in this work, it was seen that the physical and chemical changes in the recycled powder were will within accepted limits for powder usage and that with appropriate measures, recycled powder can be re-incorporated for subsequent builds without compromise in the powder quality. This study provides a pathway for greatly reducing powder consumption and thus cost during the LPBF process.



    1. Introduction

    Since Kermack and McKendrick [13] proposed the classical deterministic compartmental model (called SIR model) to describe epidemic outbreaks and spread, mathematical models have become important tools in analyzing the spread and control of infectious diseases, see [1,2,5,9,11,12,20,21,27] and references therein. The number of infected individuals used in these models is usually calculated via data in the hospitals. However, some studies on influenza show that some individuals of the population who are infected never develop symptoms, i.e. being asymptomatically infective. The asymptomatically infected individuals will not go to hospital but they can infect the susceptible by contact, then progress to the recovered stage, see for instance [3,14,22]. Hence, using the data from hospitals to mathematical models to assess the epidemic will underestimate infection risks.

    On the other hand, seasonality is very common in ecological and human social systems (cf. [26]). For example, variation patterns in climate are repeated every year, birds migrate according to the variation of season, opening and closing of schools are almost periodic, and so on. These seasonal factors significantly influence the survival of pathogens in the environment, host behavior, and abundance of vectors and non-human hosts. A number of papers have suggested that seasonality plays an important role in epidemic outbreaks and the evolution of disease transmissions, see [4,6,8,9,16,17,19,21,28]. However, it is still challenging to understand the mechanisms of seasonality and their impacts on the dynamics of infectious diseases.

    Motivated by the above studies on asymptomatic infectivity or seasonality, we develop a compartmental model with asymptomatic infectivity and seasonal factors in this paper. This model is a periodic discontinuous differential system. We try to establish the theoretical analysis on the periodic discontinuous differential systems and study the dynamics of the model. This will allow us to draw both qualitative and quantitative conclusions on the effect of asymptomatic infectivity and seasonality on the epidemic.

    The rest of the paper is organized as follows. In section 2, we formulate the SIRS model with asymptomatic infective and seasonal factors, then discuss the existence and regularity of non-negative solutions for this model. In section 3, we define the basic reproduction number R0 for the model, give the evaluation of R0 and investigate the threshold dynamics of the model (or the uniformly persistent of the disease). It is shown that the length of the season, the transmission rate and the existence of asymptomatic infection affect the basic reproduction number R0. In section 4, we study the global dynamics of the model ignoring seasonal factor. We prove that there is a unique disease-free equilibrium and the disease always dies out when R01; while when R0>1 there is an endemic equilibrium which is global stable if the recovering rates of asymptomatic infective and symptomatic infective are close. A brief discussion is given in the last section.


    2. Model formulation

    In this section, we first extend the classic SIRS model to a model which incorporates with the asymptomatic infective and seasonal features of epidemics, and then study the regularity of solutions of the model.

    Because there are asymptomatically infectious and symptomatically infectious individuals in the evolution of epidemic, the whole population is divided into four compartments: susceptible, asymptomatically infectious, symptomatically infectious and recovered individuals. More precisely, we let S, Ia, Is and R denote the numbers of individuals in the susceptible, asymptomatic, symptomatic and recovered compartments, respectively, and N be the total population size. Let R+=[0,+), Z+ be the set of all nonnegative integers, and ω>0 be given as the period of the disease transmissions. In addition to the assumptions of the classical SIRS model, we list the following assumptions on seasonal factors, asymptomatic infectivity and symptomatic infectivity.

    (A1) Due to the opening and closing of schools or migration of birds, each period of the disease transmission is simply divided into two seasons with high and low transmission rates, which are called high season J2 and low season J1, respectively. The seasonality is described by a piecewise constant function with high transmission rate β2 in J2 and low transmission rate β1 in J1, respectively, where J1=[mω,mω+(1θ)ω) and J2=[mω+(1θ)ω,(m+1)ω). Here mZ+, and 0<θ<1 which measures the fraction of the high season to the whole infection cycle.

    (A2) There are two classes of infective individuals: asymptomatically infective ones and symptomatically infective ones. Both of them are able to infect susceptible individuals by contact. A fraction μ of infective individuals proceeds to the asymptomatically infective compartment and the remainder (i.e. a fraction 1μ of infective individuals) goes directly to the symptomatically infective compartment. And the asymptomatically infective and symptomatically infective individuals recover from disease at rate ra and rs, respectively.

    (A3) The symptomatically infective individuals will get treatment in hospital or be quarantined. Hence, the symptomatic infective individuals reduce their contact rate by a fraction α.

    Based on these assumptions, the classical SIRS model can be extended to the following system

    {˙S(t)=dN(t)dS(t)β(t)S(t)(Ia(t)+αIs(t))+σR(t),˙Ia(t)=μβ(t)S(t)(Ia(t)+αIs(t))(d+ra)Ia(t),˙Is(t)=(1μ)β(t)S(t)(Ia(t)+αIs(t))(d+rs)Is(t),˙R(t)=raIa(t)+rsIs(t)(d+σ)R(t), (2.1)

    where N(t)=S(t)+Ia(t)+Is(t)+R(t), all parameters d, α, σ, μ, ra and rs are nonnegative, and

    β(t)={β1, tJ1=[mω,mω+(1θ)ω),β2, tJ2=[mω+(1θ)ω,(m+1)ω).

    Parameters β2 and β1 are the rates of contact transmission of the disease in high season and low season respectively for which β2β10. Besides, d is both the birth rate and death rate, α, 0α1, is the fraction of the symptomatically infective individuals reducing their contact rate with susceptible, the fraction of infective individuals becoming asymptomatically infective μ satisfies 0μ1, parameter σ is the rate of recovered population loss of the immunity and reentering the susceptible group, and ra and rs are the rates of asymptomatic infective and symptomatic infective recovering with immunity, respectively. Note that the transmission rate β(t) is a piecewise function or a step function. This idea has appeared in some literatures such as [19,24,15,10].

    From the biological point of view, we focus on the solutions of system (2.1) with initial conditions

    S(0)=S00,Ia(0)=Ia00,Is(0)=Is00,R(0)=R00 (2.2)

    in the first octant R4+.

    Note that

    ˙N(t)=˙S(t)+˙Ia(t)+˙Is(t)+˙R(t)0, tJ1 or tJ2.

    Hence, N(t)=S0+Ia0+Is0+R0, which is a constant for almost all tR+. Since the total population does not change by the assumption, we let

    S(t)+Ia(t)+Is(t)+R(t)N

    for almost all tR+. Therefore, system (2.1) with the initial conditions (2.2) in R4+ can be reduced to

    {˙S=(d+σ)(NS)β(t)S(Ia+αIs)σ(Ia+Is),˙Ia=μβ(t)S(Ia+αIs)(d+ra)Ia,˙Is=(1μ)β(t)S(Ia+αIs)(d+rs)Is,S(0)=S0,Ia(0)=Ia0,Is(0)=Is0,P0=(S0,Ia0,Is0)D0, (2.3)

    where D0R3+ and

    D0:={(S,Ia,Is)|S0,Ia0,Is0, 0S+Ia+IsN}. (2.4)

    Clearly, the right hand side of system (2.3) is not continuous on the domain R+×D0. We claim that the solution of system (2.3) exists globally on the interval R+=[0,+) and is unique.

    Theorem 2.1. For any P0D0, system (2.3) has a unique global solution φ(t,P0)=(S(t,P0),Ia(t,P0),Is(t,P0)) in R+, which is continuous with respect to t and all parameters of this system.

    Moreover, φ(t,P0)D0 for any tR+ and the solution φ(t,P0) is differentiable with respect to P0, where some derivatives are one-sided if P0 is on the domain boundary.

    Proof. Assume that φ(t,P0) is a solution of system (2.3). We first consider the two systems

    {˙S=(d+σ)(NS)βiS(Ia+αIs)σ(Ia+Is),˙Ia=μβiS(Ia+αIs)(d+ra)Ia,˙Is=(1μ)βiS(Ia+αIs)(d+rs)Is,S(t)=S,Ia(t)=Ia,Is(t)=Is,P=(S,Ia,Is)R3+ (2.5)

    in the domain R+×R3+, i=1,2, respectively.

    It is clear that for each i the solution of system (2.5) exists and is unique on its maximal interval of existence, and the solution of system (2.5) is differentiable with respect to the initial value P by the fundamental theory of ordinary differential equations.

    Note that the bounded closed set D0 in R3+ is a positive compact invariant set of system (2.5) since the vector field of system (2.5) on the boundary D0 of D0 is directed toward to the interior of D0 or lies on D0, where

    D0={(S,Ia,Is): (S,Ia,Is)R3+,S=0, 0Ia+IsN}{(S,Ia,Is): (S,Ia,Is)R3+,Is=0, 0S+IaN}{(S,Ia,Is): (S,Ia,Is)R3+,Ia=0, 0S+IsN}{(S,Ia,Is): (S,Ia,Is)R3+,S+Is+Ia=N}.

    Therefore, the solution of system (2.5) exists globally for any PD0R3+, and these solutions are in D0 for all t>0.

    Let ϕi(t,t,P) for i=1,2 be the solution semiflow of the following system

    {˙S=(d+σ)(NS)βiS(Ia+αIs)σ(Ia+Is),˙Ia=μβiS(Ia+αIs)(d+ra)Ia,˙Is=(1μ)βiS(Ia+αIs)(d+rs)Is,ϕi(t,t,P)=P, PD0, (2.6)

    respectively, that is, ϕi(t,t,P)=(S(t,t,P),Ia(t,t,P),Is(t,t,P)) for tt is the solution of system (2.6) with the initial condition ϕi(t,t,P)=(S,Ia,Is)D0, respectively.

    It follows that the solution φ(t,P0) for t0 of system (2.3) can be determined uniquely by induction. For simplicity, we let sm=(m1)ω and tm=sm+(1θ)ω for mZ+. Hence,

    [0,)=m=1[sm,sm+1]=m=1([sm,tm][tm,sm+1]),

    and φ(t,P0) can be written as follows.

    φ(t,P0)={ϕ1(t,s1,P0)whent[s1,t1],ϕ2(t,t1,ϕ1(t1,s1,P0))whent[t1,s2],...ϕ1(t,sm,um)whent[sm,tm],ϕ2(t,tm,vm)whent[tm,sm+1], (2.7)

    where um and vm are determined by letting u1=P0, v1=ϕ1(t1,s1,u1) and

    um=ϕ2(sm,tm1,vm1),vm=ϕ1(tm,sm,um)form2.

    This implies that the solution φ(t,P0) of system (2.3) exits globally in R+ and is unique for any P0D0, and it is continuous with respect to t and all parameters.

    By the expression (2.7), it is easy to see that the solution φ(t,P0) lies in D0 for all t0 and φ(t,P0) is differentiable with respect to P0. The proof is completed.

    Theorem 2.1 tells us that system (2.3) is ω-periodic with respect to t in R+×D0, and it suffices to investigate the dynamics of its associated period map P on D0 for the dynamics of system (2.3), where

    P: D0D0,P(P0)=φ(ω,P0)=ϕ2(ω,(1θ)ω,ϕ1((1θ)ω,0,P0)), (2.8)

    which is continuous in D0.


    3. Basic reproduction number and threshold dynamics

    In epidemiology, the basic reproduction number (or basic reproduction ratio) R0 is an important quantity, defined as the average number of secondary infections produced when an infected individual is introduced into a host population where everyone is susceptible. It is often considered as the threshold quantity that determines whether an infection can invade a new host population and persist. Detailedly speaking, if R0<1, the disease dies out and the disease cannot invade the population; but if R0>1, then the disease is established in the population. There have been some successful approaches for the calculations of basic reproduction number for different epidemic models. For example, Diekmann et al [7] and van den Driessche and Watmough [23] presented general approaches of calculating R0 for autonomous continuous epidemic models. And for periodic continuous epidemic models, Wang and Zhao in [25] defined the basic reproduction number. To our knowledge, there is no theoretic approach to calculate the basic reproduction number for periodic discontinuous epidemic models such as system (2.3). In this section, we use the idea and some notations given in [25] to define and calculate the basic reproduction numbers for system (2.3), and discuss the uniform persistence of the disease and threshold dynamics.

    We define X to be the set of all disease-free states of system (2.3), that is

    X={(S,Ia,Is): 0SN,Ia=Is=0}.

    Clearly, the disease-free subspace X is positively invariant for system (2.3). It can be checked that the period map P(P0) in X has a unique fixed point at (N,0,0), which is a unique disease-free equilibrium (N,0,0) of system (2.3), denoted by E0. We now consider a population near the disease-free equilibrium E0.

    For simplicity, we let x=(S,Ia,Is)T, and for i=1,2 set

     Fi=(0000μβiNαμβiN0(1μ)βiNα(1μ)βiN):=(000Fi),Vi=(d+σβiN+σαβiN+σ0d+ra000d+rs):=(d+σbi0V).

    Then the linearized system of (2.3) at E0 can be rewritten as

    dxdt=(F(t)V(t))x, (3.1)

    where F(t)=χJ1(t)F1 +χJ2(t)F2 , V(t)=χJ1(t)V1+χJ2(t)V2, and

    χJi(t)={1 as tJi,0 as tJi.

    System (3.1) is a piecewise continuous periodic linear system with period ω in tR+. In order to determine the fate of a small number of infective individuals introduced into a disease-free population, we first extend system (3.1) from tR+ to tR, and introduce some new notations. When t+m=(J1J2)=(,+), we set I(t)=(Ia(t),Is(t))T, and

    F(t)=χJ1(t)F1 +χJ2(t)F2=(μNβ(t)αμNβ(t)(1μ)Nβ(t)α(1μ)Nβ(t)),

    where

    β(t)={β1, tJ1=[mω,mω+(1θ)ω),β2, tJ2=[mω+(1θ)ω,(m+1)ω), mZ.

    Clearly, F(t) is a 2×2 piecewise continuous periodic matrix with period ω in R, and it is non-negative. And

    V=((d+ra)00(d+rs)),

    which is cooperative in the sense that the off-diagonal elements of V are non-negative.

    Let Y(t,s), ts, be the evolution operator of the linear system

    dI(t)dt=VI(t). (3.2)

    Since V is a constant matrix, for each sR the matrix Y(t,s) satisfies

    ddtY(t,s)=VY(t,s), ts, Y(s,s)=E2, (3.3)

    where E2 is a 2×2 identity matrix, and Y(t,s)=eV(ts). Hence, the monodromy matrix ΦV(t) of system (3.2) is Y(t,0), that is,

    ΦV(t)=eVt=(e(d+ra)t00e(d+rs)t),

    where d, ra and rs are positive numbers.

    We denote 1 the 1-norm of vectors and matrices. Thus, there exist K>0 and κ>0 such that

    Y(t,s)1Keκ(ts), ts, sR.

    From the boundedness of F(t), i.e. F(t)1<K1, it follows that there exists a constant K1>0 such that

    Y(t,ta)F(ta)1KK1eκa, tR, a[0,+). (3.4)

    We now consider the distribution of infected individuals in the periodic environment. Assume that I(s) is the initial distribution of infected individuals in infectious compartments. Then F(s)I(s) is the distribution of new infections produced by the infected individuals who were introduced at time s. Given ts, then Y(t,s)F(s)I(s) is the distribution of those infected individuals who were newly infected at time s and still remain in the infected compartments at time t. Thus, the integration of this distribution from to t

    tY(t,s)F(s)I(s)ds=0Y(t,ta)F(ta)I(ta)da

    gives the distribution of cumulative new infections at time t produced by all those infected individuals introduced at times earlier than t.

    Let Cω=C(R,R2) be the ordered Banach space of ω-periodic continuous functions from R to R2, which is equipped with the norm c,

    I(s)c=maxs[0,ω]I(s)1,

    and the generating positive cone

    C+ω={I(s)Cω: I(s)0, sR}.

    Define a linear operator L: CωCω by

    (LI)(t)=tY(t,s)F(s)I(s)ds=0Y(t,ta)F(ta)I(ta)da. (3.5)

    It can be checked that the linear operator L is well defined.

    Lemma 3.1. The operator L is positive, continuous and compact on Cω.

    Proof. Since Y(t,s)=eV(ts) and F(t) is a nonnegative bounded matrix, we get that L(C+ω)C+ω. This implies that the linear operator L is positive.

    We now prove the continuity of L. For each tR, we have

    LI(t)1=0Y(t,ta)F(ta)I(ta)da1=j=0(j+1)ωjωY(t,ta)F(ta)I(ta)da1j=0(j+1)ωjωY(t,ta)F(ta)I(ta)1daj=0(j+1)ωjωKK1eκaI(ta)1daωKK1j=0eκωjIc

    by (3.4). Hence,

    LI(t)c=maxt[0,ω]LI(t)1ωKK1j=0eκωjIc,

    which implies that L is continuous and uniformly bounded since j=0eκωj is convergent.

    In the following we prove the compactness of L. We first claim that LI(t) is equicontinuous. Consider I(t)Cω and t1,t2[0,ω] with t1<t2. Then

    LI(t2)LI(t1)1=t2Y(t2,s)F(s)I(s)dst1Y(t1,s)F(s)I(s)ds1=t2(Y(t2,s)Y(t1,s))F(s)I(s)ds+t2t1Y(t1,s)F(s)I(s)ds1t2Y(t2,s)Y(t1,s)1F(s)1I(s)1ds+t2t1Y(t1,s)1F(s)1I(s)1dsωY(t2,s)Y(t1,s)1F(s)1I(s)1ds+t2t1Keκ(t1s)F(s)1I(s)1dseVt2eVt110i=(i+1)ωiωK1eVs1I(s)1ds+t2t1Keκ(t1s)K1I(s)1ds0i=e˜d1(i+1)ωK1IceVt2eVt11+KK1eκωIc(t2t1),

    where ˜d1=max{d+ra,d+rs}.

    Notice that 0i=eN(i+1) is convergent and eVt is continuous on [0,ω]. Thus, if {I(t)} is bounded, for ϵ>0 there exists a δ>0 such that LI(t2)LI(t1)c<ϵ as |t2t1|<δ. This implies that {(LI)(t)} are equicontinuous. According to Ascoli-Arzela theorem, we know that L is compact. The proof of this lemma is completed.

    L is called the next infection operator, and the spectral radius of L can be defined as the basic reproduction number (or ratio)

    R0:=ρ(L) (3.6)

    of system (2.3).

    Following [25], we consider how to calculate R0 and whether the basic reproduction ratio (or number) R0 characterizes the threshold of disease invasion, i.e., the disease-free periodic solution (N,0,0) of system (2.3) is locally asymptotically stable if R0<1 and unstable if R0>1.

    It is clear that the disease-free periodic solution (N,0,0) of system (2.3) is locally asymptotically stable if all characteristic multipliers of periodic system (3.1) are less than one, and it is unstable if at least one of the characteristic multipliers of periodic system (3.1) is greater than one. By straightforward calculation, we obtain that the characteristic multipliers of periodic system (3.1) consist of e(d+σ)ω and the eigenvalues of the following matrix

    ΦFV(ω)=e(F2V)θωe(F1V)(1θ)ω,

    where

    FiV=(μβiN(d+ra)αμβiN(1μ)βiNα(1μ)βiN(d+rs)),  i=1,2.

    Note that e(d+σ)ω<1 because d+σ>0. Therefore, all characteristic multipliers of periodic system (3.1) are less than one if and only if the largest eigenvalue of ΦFV(ω), denoted by ρ(ΦFV(ω)), is less than one (i.e. ρ(ΦFV(ω))<1), and at least one of the characteristic multipliers of periodic system (3.1) is greater than one if and only if ρ(ΦFV(ω))>1, here ρ(ΦFV(ω)) is called the spectral radius of matrix ΦFV(ω).

    On the other hand, it is easy to check that all assumptions (A2)-(A7) in [25] are valid for system (3.1) except the assumption (A1). Using the notations in [25], we define a matrix Vε=VεP, here P=(1111) and ε is a very small positive number. Thus, Vε is cooperative and irreducible for each tR. Let Yε(t,s) be the evolution operator of the linear system (3.3) with V replaced by Vε. For some small ε0, as ε[0, ε0) we can define the linear operator Lε by replacing Y(t,s) in (3.5) with Yε(t,s) such that the operator Lε is positive, continuous and compact on Cω. Let Rε0:=ρ(Lε) for ε[0, ε0).

    By the proof of Theorem 2.1, we know that the solutions of the following system

    dxdt=(F(t)Vε)x (3.7)

    are continuous with respect to all parameters. Thus,

    limε0ΦFVε(ω)=ΦFV(ω),

    where ΦFVε(ω) is the monodromy matrix of system (3.7), and ΦFV(ω) is the monodromy matrix of system (3.7) as ε=0.

    According to the continuity of the spectrum of matrices, we have

    limε0ρ(ΦFVε(ω))=ρ(ΦFV(ω)).

    From Lemma 3.1, we use the similar arguments in [25] to the two linear operator Lε and L, and obtain that

    limε0Rε0=R0.

    We now easily follow the arguments in [25] to characterize R0. Let Wλ(t,s),ts be the fundamental solution matrix of the following linear periodic system

    dwdt=(V+F(t)λ)w,

    where the parameter λ(0,+). Consider an equation of λ

    ρ(Wλ(ω,0))=1. (3.8)

    Then R0 can be calculated as follows.

    Theorem 3.2. ( i ) If equation (3.8) has a solution λ0>0, then λ0 is an eigenvalue of L, which implies that R0>0;

    ( ii ) If R0>0, then λ=R0 is the only solution of equation (3.8);

    ( iii ) R0=0 if and only if ρ(Wλ(ω,0))<1 for all positive λ.

    Note that ρ(W1(ω,0))=ρ(ΦFV(ω)). Using similar arguments in [25], we can prove that the basic reproduction ratio (or number) R0 can characterize the threshold of disease invasion.

    Theorem 3.3. ( i ) R0>1 if and only if ρ(ΦFV(ω))>1;

    ( ii ) R0=1 if and only if ρ(ΦFV(ω))=1;

    ( iii ) R0<1 if and only if ρ(ΦFV(ω))<1.

    Hence, the disease-free periodic solution (N,0,0) of system (2.3) is locally asymptotically stable if R0<1, and it is unstable if R0>1.

    To save space, the proofs of the above theorems are omitted. From Theorem 3.3, we can see that R0 is a threshold parameter for local stability of the disease-free periodic solution (N,0,0). We next show that R0 is also a threshold parameter for dynamics of system (2.3) in D0.

    Theorem 3.4. When R0<1, solutions (S(t),Ia(t),Is(t)) of system (2.3) with initial points in D0 satisfies

    limt+(S(t),Ia(t),Is(t))=(N,0,0).

    And the disease-free periodic solution (N,0,0) of system (2.3) is globally asymptotically stable in D0.

    Proof. In the invariant pyramid D0 as shown in (2.4), we consider a subsystem by the last two equations of system (2.3)

    {˙Ia(t)=μβ(t)S(Ia+αIs)(d+ra)Iaμβ(t)N(Ia+αIs)(d+ra)Ia,˙Is(t)=(1μ)β(t)S(Ia+αIs)(d+rs)Is(1μ)β(t)N(Ia+αIs)(d+rs)Is. (3.9)

    Thus, the auxiliary system of (3.9) is

    {˙Ia(t)=μβ(t)N(Ia+αIs)(d+ra)Ia,˙Is(t)=(1μ)β(t)N(Ia+αIs)(d+rs)Is, (3.10)

    which is a periodic linear discontinuous system with period ω. The periodic map associated with system (3.10) is defined by ΦFV(ω), which is a linear continuous map.

    When R0<1, we have ρ(ΦFV(ω))<1, which implies that (0,0) is a globally asymptotically stable solution of system (3.10).

    Note that systems (3.9) and (3.10) are cooperative. Using the similar arguments in [18], we can prove that the comparison principle holds. Hence,

    limt+(Ia(t),Is(t))=(0,0).

    So, for arbitrarily small constant ε>0, there exists T>0 such that Ia(t)+αIs(t)<ε as t>T. From the first equation of system (2.3), we have

    ˙S=dNdSβ(t)S(Ia+αIs)+σ(NSIaIs)>dNdSβ2Sε.

    Therefore, lim inft+S(t)dNd+β2ε. Let ε0, we have

    lim inft+S(t)N.

    On the other hand, S(t)N in D0, which admits

    limt+S(t)=N.

    In summary, we have limt+(S(t),Ia(t),Is(t))=(N,0,0). Moreover, from Theorem 3.3 we know that (N,0,0) of system (2.3) is globally asymptotically stable.

    In the following, we show that the disease is uniformly persistent when R0>1.

    Theorem 3.5. If R0>1, 0<μ<1 and 0<αβ1, then there exists a constant δ0>0 such that every solution (S(t),Ia(t),Is(t)) of system (2.3) with initial values in D0 satisfies

    lim inft+Ia(t)δ0,lim inft+Is(t)δ0.

    Proof. Since system (2.3) is ω-periodic with respect to t in R+×D0, it suffices to investigate the dynamics of its associated period map P defined by (2.8) on D0 for the dynamics of system (2.3), where the map P is continuous. Clearly, P(D0)D0. Define

    X0={(S,Ia,Is)D0:Ia>0,Is>0}, X0=D0X0.

    Set

    M={P0X0:Pk(P0)X0,k0},

    which is a positive invariant set of P in X0. We claim

    M={(S,0,0):0SN}. (3.11)

    In fact, {(S,0,0):0SN}M by (2.8). On the other hand, for any P0X0{(S,0,0):0SN}, that is, either Ia0=0,Is0>0,S00 or Ia0>0,Is0=0,S00. In the case Ia0=0,Is0>0,S0>0 (resp. Ia0>0,Is0=0,S0>0), we calculate by the last two equations of system (2.3) and obtain that

    Ia(0)=μαβ(0)S(0)Is(0)>0 (resp.  Is(0)=(1μ)β(0)S(0)Ia(0)>0),

    if 0<μ<1 and 0<αβ1. This implies that Pk0(P0)X0{(S,0,0):0SN} for some k00 since the subsystem by the last two equations of system (2.3) is cooperative. If S(0)=0,Ia0=0,Is0>0 (or S(0)=0,Ia0>0,Is0=0), then S(0)=(d+σ)NσIs(0)>0 (or S(0)=(d+σ)NσIa(0)>0), which leads that Pk1(P0)X0{(S,0,0):0SN} for some k10. Therefore, (3.11) is proved and M is the maximal compact invariant set of P in X0.

    Note that E0(N,0,0) is the unique fixed point of P in M and it is an attractor of P in M by the first equation of (2.3). Since R0>1, the stable set Ws(E0) of E0 satisfies that Ws(E0)X0=.

    Applying [29,Theorem 1.3.1], we obtain that P is uniformly persistent with respect to (X0,X0). Moreover, from [29,Theorem 3.1.1], it can see that the conclusion of this theorem is true. The proof is completed.


    4. Global dynamics of system (2.3) without seasonal force

    In this section, we study the effects of asymptomatic infection on the dynamics of system (2.3) if there are not seasonal factors, that is, β1=β2=β. Then system (2.3) becomes

    {˙S=(d+σ)(NS)βS(Ia+αIs)σ(Ia+Is),˙Ia=μβS(Ia+αIs)(d+ra)Ia,˙Is=(1μ)βS(Ia+αIs)(d+rs)Is (4.1)

    in the domain R3+.

    By the formula (3.6), we let β1=β2 and obtain the basic reproduction number R0 of system (4.1) as follows.

    R0=βN(μd+ra+α(1μ)d+rs), (4.2)

    which is consistent with the number calculated using the approach of basic reproduction number in [7] and [23].

    From the expression (4.2), we can see that there is still the risks of infectious disease outbreaks due to the existence of asymptomatic infection even if all symptomatically infective individuals have been quarantined, that is, α=0. This provides an intuitive basis for understanding that the asymptomatically infective individuals promote the evolution of epidemic.

    In the following we study the dynamics of system (4.1). By a straightforward calculation, we obtain the existence of equilibria for system (4.1).

    Lemma 4.1. System (4.1) has the following equilibria in R3+.

    ( i ) If R01, then system (4.1) has a unique equilibrium, which is the disease-free equilibrium E0(N,0,0).

    ( ii ) If R0>1 and 0<μ<1, then system (4.1) has two equilibria: the disease-free equilibrium E0(N,0,0) and the endemic equilibrium E1(S,Ia,Is) in the interior of D0, where S=NR0, Ia=μ(d+σ)(d+rs)N(d+ra)(d+rs)+σ(d+μrs)+σra(1μ)(11R0), Is=(1μ)(d+ra)μ(d+rs)Ia.

    ( iii ) If R0>1 and μ=0, then system (4.1) has two equilibria: the disease-free equilibrium E0(N,0,0) and the asymptomatic-free equilibrium E2(S2,0,Is2), where S2=NR0, Is2=d+σd+σ+rsN(11R0).

    ( iv ) If R0>1 and μ=1, the system (4.1) has two equilibria: the disease-free equilibrium E0(N,0,0) and the symptomatic-free equilibrium E3(S3,Ia3,0), where S3=NR0, Ia3=d+σd+σ+raN(11R0).

    We now discuss the local stability and topological classification of these equilibria in R3+, respectively. We first study the disease-free equilibrium E0(N,0,0) and have the following lemma.

    Lemma 4.2. The disease-free equilibrium E0(N,0,0) of system (4.1) in R3+ is asymptotically stable if R0<1; E0(N,0,0) is a saddle-node with one dimensional center manifold and two dimensional stable manifold if R0=1; and E0(N,0,0) is a saddle with two dimensional stable manifold and one dimensional unstable manifold if R0>1.

    Proof. A routine computation shows that the characteristic polynomial of system (4.1) at E0 is

    f1(λ)=(λ+d+σ)(λ2a1λ+a0), (4.3)

    where a0=(d+ra)(d+rs)(1R0),

    a1=(d+ra)(βNμd+ra1)+(d+rs)(αβN1μd+rs1).

    It is clear that (d+σ)<0 is always one root of (4.3). We consider three cases, R0<1, R0=1 and R0>1, to discuss the other roots of (4.3).

    If R0<1, then a1<0 and a0>0 by βNμd+ra<R0 and βNα(1μ)d+rs<R0. Thus, three roots of (4.3) have negative real parts, which leads to the local asymptotical stability of the disease-free equilibrium E0.

    If R0=1, then a0=0 and a1<0. Hence, the characteristic equation f1(λ)=0 has three roots: λ1=(d+σ)<0, λ2=a1<0 and λ3=0. For calculating the associated eigenvectors vi of λi, i=1,2,3, we consider J(E0) with respect to μ in three cases: (ⅰ) 0<μ<1, (ⅱ) μ=0 and (ⅲ) μ=1, and we can obtain that E0 is a saddle-node with one dimensional center manifold and two dimensional stable manifold by tedious calculations of normal form.

    Summarized the above analysis, we complete the proof of this lemma.

    From Lemma 4.1 and Lemma 4.2, we can see that system (4.1) undergoes saddle-node bifurcation in a small neighborhood of E0(N,0,0) as R0 increases passing through R0=1.

    About the endemic equilibria, we have the following local stability.

    Lemma 4.3. The endemic equilibrium E1(S,Ia,Is) of system (4.1) is asymptotically stable if R0>1 and 0<μ<1; the asymptomatic-free equilibrium E2(S2,0,Is2) of system (4.1) is asymptotically stable if R0>1 and μ=0; and the symptomatic-free equilibrium E3(S3,Ia3,0) of system (4.1) is asymptotically stable if R0>1 and μ=1.

    Proof. Either μ=0 or μ=1, it is easy to compute the eigenvalues of the Jacobian matrix of system (4.1) at E2 or E3, respectively, and find that all eigenvalues have negative real parts. Hence, E2(S2,0,Is2) or E3(S3,Ia3,0) is asymptotically stable if R0>1, respectively.

    After here we only prove that E1(S,Ia,Is) is asymptotically stable if R0>1 and 0<μ<1. To make the calculation easier, we use the change of variables

    S=(d+rs)μβˆS, Ia=(d+rs)βˆIa,  Is=(d+rs)βˆIs, dt=dτ(d+rs),

    which reduces system (4.1) into the following system,

    {dSdτ=N1d1Sσ1Iaσ1IsS(Ia+αIs),dIadτ=rIa+S(Ia+αIs),dIsdτ=Is+μ1S(Ia+αIs), (4.4)

    where

    N1=N(d+σ)μβ/(d+rs)2, d1=(d+σ)/(d+rs),σ1=σμ/(d+rs), r=(d+ra)/(d+rs), μ1=(1μ)/μ

    and for simplicity we denote ˆS,ˆIa,ˆIs by S,Ia,Is respectively.

    When R0>1, the disease-free equilibrium E0(N,0,0) and endemic equilibrium E1(S,Ia,Is) of system (4.1) are transformed into the disease-free equilibrium ˆE0(N1/d1,0,0) and endemic equilibrium ˆE1(ˆS,ˆIa,ˆIs) of system (4.4) respectively, where

    ˆS=N1/d1ˆR0, ˆIa=N1σ1+rσ1μ1+r(11ˆR0), ˆIs=μ1rIa.

    Notice that ˆR0:=N1d1(1r+αμ1)>1 if and only if R0>1.

    The characteristic equation of system (4.4) at ˆE1 is

    f2(λ)=det(λIJ(ˆE1))=λ3+ξ2λ2+ξ1λ+ξ0,

    where

    ξ2={σ1+rσ1μ1+r+r2μ1ασ1+r3μ21ασ1+r3μ1α+d1σ1μ1rα+d1σ1μ21r2α+N1+d1σ1+d1rσ1μ1+2N1μ1rα+r2μ21α2N1}/{(σ1+rσ1μ1+r)(rμ1α+1)},ξ1=d1(1+r2μ1α)/(rμ1α+1)+(σ1μ1+1+r+σ1)(rμ1α+1)ˆIa,ξ0=N1μ1rα+N1rd1=rd1(ˆR01).

    It can be seen that all coefficients ξj of polynomial f2(λ) are positive if ˆR0>1, where j=0,1,2. Moreover, we claim that ξ2ξ1ξ0>0. In fact,

    ξ2ξ1ξ0=c0+c1ˆIa+c2(ˆIa)2,

    where

    c0= d1(1+r2μ1α)(r2μ1α+d1μ1rα+1+d1)(rμ1α+1)2,c1= d1μ21rασ1+r3μ1α+r2μ1ασ1+2d1r2μ1α+d1σ1μ1rα+σ1μ1 +d1σ1μ1+1+2d1+d1σ1+r(d1σ1μ1)+μ1rα(d1σ1),c2= (rμ1α+1)2(σ1μ1+1+r+σ1).

    It is easy to see that c0>0 and c2>0. Note that d1σ1μ1=d+σμd+rs>0 and d1σ1=d+σ(1μ)d+rs>0 since 0<μ<1. This implies that c1>0. Moreover, ˆIa>0 yields that ξ2ξ1ξ0>0 and what we claimed is proved.

    By the Routh-Hurwitz Criterion, we know that all eigenvalues of the characteristic polynomial f2(λ) have negative real parts. Thus, the endemic equilibrium ˆE1 of system (4.4) is asymptotically stable. This leads that the endemic equilibrium E1(S,Ia,Is) of system (4.1) is also asymptotically stable.

    From Lemma 4.2 and Lemma 4.3, we can see that R0 is the threshold quantity of local dynamics of system (4.1) in R3+. By Theorem 2.1, we only need to consider system (4.1) for its global dynamics in D0. The following theorems will show that R0 is also the threshold quantity of global dynamics of system (4.1) in D0.

    Theorem 4.4. If R01, then the disease-free equilibrium E0(N,0,0) of system (4.1) is globally asymptotically stable in D0.

    The proof of this theorem can be finished by constructing a Liapunov function

    L(S,Ia,Is)=Ia(t)+d+rad+rsαIs(t)

    in D0. For the sake of simplicity, we omit the details.

    Theorem 4.5. If R0>1 and μ=0 (resp. μ=1), then E2(S2,0,Is2) (resp. E3(S3,Ia3,0)) attracts all orbits of system (4.1) in D0 except both E0(N,0,0) and a positive orbit γ in its two dimensional stable manifold, where

    γ={(S,Ia,Is)D0: Ia=0, Is=0, 0<S<N}.

    Proof. We first prove the case that R0>1 and μ=0. When μ=0, system (4.1) becomes

    {˙S=(d+σ)(NS)βS(Ia+αIs)σ(Ia+Is),˙Ia=(d+ra)Ia,˙Is=βS(Ia+αIs)(d+rs)Is. (4.5)

    It is clear that limt+Ia(t)=0. Hence, the limit system of system (4.5) in D0 is

    {˙S=(d+σ)(NS)αβSIsσIs,˙Is=αβSIs(d+rs)Is (4.6)

    in D1={(S,Is): 0SN, 0IsN}, which has two equilibria: (N,0) and (S2,Is2). Equilibrium (N,0) is a saddle and (S2,Is2) is locally asymptotically stable if R0>1.

    In the following we prove that (S2,Is2) attracts all orbits of system (4.6) in D1 except both (N,0) and its one dimensional stable manifold.

    Let x=S+σαβ and y=Is. Then system (4.6) becomes

    {˙x=(d+σ)(N+σαβ)(d+σ)xαβxy,˙y=αβxy(d+rs+σ)y. (4.7)

    Hence, (x0,y0)=(S2+σαβ,Is2) is the unique positive equilibrium of system (4.7) if R0>1. Consider the Liapunov function of system (4.7)

    V(x,y)=12(xx0)2+x0(yy0y0lnyy0)

    in ˜D1={(x,y): σαβxN+σαβ, 0yN}. It is clear that V(x,y)0 and V(x,y)=0 if and only if x=x0 and y=y0 in ˜D1. And

    dV(x(t),y(t))dt|(4.7)=(xx0)2(αβy+d+σ)0

    in ˜D1.

    By LaSalle's Invariance Principle, we know that (x0,y0) attracts all orbits of system (4.7) in ˜D1 except both equilibrium (N+σαβ,0) and its one dimensional stable manifold {(x,y): y=0,0<x<N+σαβ}. This leads to the conclusion, E2(S2,0,Is2) attracts all orbits of system (4.1) in D0 except both E0(N,0,0) and a positive orbit γ if R0>1 and μ=0.

    Using the similar arguments, we can prove that E3(S3,Ia3,0) attracts all orbits of system (4.1) in D0 except both E0(N,0,0) and a positive orbit γ if R0>1 and μ=1.

    Theorem 4.6. If R0>1, 0<μ<1 and ra=rs, then the endemic equilibrium E1(S,Ia,Is) attracts all orbits of system (4.1) in D0 except E0(N,0,0).

    Proof. Let I=Ia+αIs,   N1=S+Ia+Is. Then under the assumption ra=rs=r, system (4.1) in D0 can be written as

    {˙S=(d+σ)NσN1dSβSI,˙I=˜μSI(d+r)I,˙N1=(d+σ)N(d+r+σ)N1+rS (4.8)

    in ˜D0:={(S,I,N1)|S0,I0, NN10}, where ˜μ=(μ+α(1μ))β.

    Thus, equilibrium E1(S,Ia,Is) of system (4.1) becomes equilibrium ˜E1(S,I,N1) of system (4.8) and ˜E1 is locally asymptotically stable, where I=Ia+αIs,N1=S+Ia+Is.

    Applying a typical approach of Liapunov functions, we define

    g(x)=x1lnx,

    and construct a Liapunov function of system (4.8)

    V1(S,I,N1)=ν12(SS)2+ν2Ig(II)+ν32(N1N1)2,

    where arbitrary constants ν1>0, ν2=ν1βS/˜μ and ν3=ν1σ/r. Note that g(x)g(1)=0 for all x>0 and the global minimum g(x)=0 is attained if and only if x=1. Thus, V1(S,I,N1)0 and V1(S,I,N1)=0 if and only if S=S, I=I and N1=N1 in ˜D0.

    The derivative of V1 along the trajectories of system (4.8) is

    dV1(S,I,N1)dt=ν1dS2(x1)2ν3(d+r+σ)N12(z1)2ν1βS2Iy(x1)20,

    where x=SS,  y=II,  z=N1N1.

    Note that the only compact invariant subset of the set {(S,I,N1): dV1(S,I,N1)dt=0} is the singleton ˜E1(S,I,N1) in ˜D0. Consequently, we can conclude that E1(S,Ia,Is) is globally asymptotically stable and attracts all orbits of system (4.1) in D0 except E0(N,0,0).

    From Theorem (4.6) and the continuity of solutions with respect to parameters ra and rs, we obtain the following results.

    Theorem 4.7. If R0>1 and 0<μ<1, then the endemic equilibrium E1(S,Ia,Is) is globally asymptotical stable in the interior of D0 for 0<|rsra|1.


    5. Discussion

    In this paper, we established a compartmental SIRS epidemic model with asymptomatic infection and seasonal factors. In our model, we divided the period of the disease transmission into two seasons. In fact, it can be divided into n seasons for any given nZ+. Compared with continuous periodic systems, our piecewise continuous periodic model can provide a straightforward method to evaluate the basic reproduction number R0, that is to calculate the spectral radius of the matrix ΦFV(ω)=e(F2V)θωe(F1V)(1θ)ω. It is shown that the length of the season, the transmission rate and the existence of asymptomatic infective affect the basic reproduction number R0, and there is still the risks of infectious disease outbreaks due to the existence of asymptomatic infection even if all symptomatically infective individuals have been quarantined, that is, α=0. This provides an intuitive basis for understanding that the asymptomatically infective individuals and the disease seasonal transmission promote the evolution of the epidemic. And theoretical dynamics of the model allow us to predict outcomes of control strategies during the course of the epidemic.


    Acknowledgments

    We are very grateful to Prof. Shigui Ruan and the anonymous referees for their valuable comments and suggestions, which led to an improvement of our original manuscript.

    The first author was supported by the National Natural Science Foundation of China (No. 11431008), and has received funding from the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement (No. 655212). The second author was supported by the National Natural Science Foundation of China (No. 11431008 & 11371248). The third author was supported by the National Natural Science Foundation of China (No. 11521061 & 11231001).




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