Skip to main content
Elsevier - PMC COVID-19 Collection logoLink to Elsevier - PMC COVID-19 Collection
. 2012 Oct 17;399(2):565–575. doi: 10.1016/j.jmaa.2012.10.015

Dynamics of a model with quarantine-adjusted incidence and quarantine of susceptible individuals

Mohammad A Safi a, Abba B Gumel b,
PMCID: PMC7125820  PMID: 32287386

Abstract

A new deterministic model for the spread of a communicable disease that is controllable using mass quarantine is designed. Unlike in the case of the vast majority of prior quarantine models in the literature, the new model includes a quarantine-adjusted incidence function for the infection rate and the quarantine of susceptible individuals suspected of being exposed to the disease (thereby making it more realistic epidemiologically). The earlier quarantine models tend to only explicitly consider individuals who are already infected, but show no clinical symptoms of the disease (i.e., those latently-infected), in the quarantine class (while ignoring the quarantine of susceptible individuals). In reality, however, the vast majority of people in quarantine (during a disease outbreak) are susceptible. Rigorous analysis of the model shows that the assumed imperfect nature of quarantine (in preventing the infection of quarantined susceptible individuals) induces the phenomenon of backward bifurcation when the associated reproduction threshold is less than unity (thereby making effective disease control difficult). For the case when the efficacy of quarantine to prevent infection during quarantine is perfect, the disease-free equilibrium is globally-asymptotically stable when the reproduction threshold is less than unity. Furthermore, the model has a unique endemic equilibrium when the reproduction threshold exceeds unity (and the disease persists in the population in this case).

Keywords: Quarantine, Equilibrium, Reproduction number, Stability

1. Introduction

Quarantine (of individuals feared exposed to a communicable disease) is one of the oldest public health control measures for the spread of communicable diseases in given populations. More recently, this measure was successfully used to combat the spread of some emerging and re-emerging human and animal diseases, such as the severe acute respiratory syndrome (SARS) [1], [2], [3], [4], [5], [6], [7], [8], foot-and-mouth disease [9] and the 2009 swine influenza pandemic [10]. Mathematical models have been designed and used to gain qualitative insights into the spread of diseases in the presence of quarantine of individuals suspected of being exposed to a disease, and the subsequent isolation or hospitalization of those with clinical symptoms of the disease (see, for instance, [1], [2], [3], [4], [5], [6], [7], [8], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21]). In the aforementioned models, with the exception of the models in [2], [5], the dynamics of the quarantined susceptible individuals is not explicitly incorporated into the model (the models only count quarantined individuals who are actually latently-infected, and essentially ignore those who remain susceptible at the end of the quarantine period).

In other words, in the aforementioned models (with the exception of the models in [2], [5]) the class (or compartment) of quarantined individuals contain only those who are latently-infected (and the temporary removal of susceptible individuals from the susceptible pool is not accounted for). The justification given for this assumption (of ignoring the back-and-forth dynamics of quarantined susceptible individuals: from susceptible to quarantine and back to susceptible class if they show no disease symptoms) is that, in general, the fraction of infected contacts that can be traced and quarantined at the time of infection is very small; and that the total population is large in comparison to the size of the infected individuals [13]. In practice, however, quarantine involves the removal of all individuals suspected of being exposed to a given disease (regardless of infection status) from the rest of the population (this often involves a lot of people; the term mass quarantine is often used to describe this process). Those who show disease symptoms during quarantine are hospitalized (or isolated), and those who remain susceptible at the end of the quarantine period are returned to the susceptible class. It is, therefore, instructive to study the impact of the aforementioned assumption (of not explicitly accounting for the quarantine of susceptible individuals) on the transmission dynamics of a disease that is controllable using quarantine.

The purpose of this study is to investigate the qualitative impact of explicitly including the dynamics of quarantined susceptible individuals on the spread of a disease that is controllable by quarantine and isolation. To achieve this objective, a new deterministic model, which includes the dynamics of quarantined susceptible individuals and quarantine-adjusted incidence function, is designed and analyzed. It should be mentioned that quarantined-adjusted incidence has also been used in a number of quarantine models, such as those in [5], [14], [15], [20].

The model to be considered is that for the transmission dynamics of a communicable disease that can be controlled using quarantine and isolation, such as ebola, measles, pandemic influenza and SARS [1], [2], [3], [4], [5], [7], [8], [11], [12], [14], [19], [21]. It is based on splitting the total population at time t, denoted by N(t), into the sub-populations of non-quarantined susceptible (S(t)), quarantined susceptible (Sq(t)), non-quarantined latently-infected (i.e., infected but show no clinical symptoms of the disease) (E(t)), quarantined latently-infected (Eq(t)), non-quarantined symptomatic (I(t)), quarantined symptomatic (Iq(t)), hospitalized (H(t)) and recovered (R(t)) individuals, so that

N(t)=S(t)+Sq(t)+E(t)+Eq(t)+I(t)+Iq(t)+H(t)+R(t).

The model is given by the following system of non-linear differential equations (a flow diagram of the model is depicted in Fig. 1 ):

dSdt=Π+ψ1Sq(t)+ψ2R(t)λa(t)S(t)γS(t)μS(t),dSqdt=γS(t)rλa(t)Sq(t)(ψ1+μ)Sq(t),dEdt=λa(t)S(t)(σ1+μ)E(t),dEqdt=rλa(t)Sq(t)(σ2+μ)Eq(t),dIdt=σ1E(t)(α1+ϕ1+μ+δ1)I(t),dIqdt=σ2Eq(t)(α2+ϕ2+μ+δ2)Iq(t),dHdt=α1I(t)+α2Iq(t)(ϕ3+μ+δ3)H(t),dRdt=ϕ1I(t)+ϕ2Iq(t)+ϕ3H(t)(ψ2+μ)R(t), (1)

where λa is the infection rate given by Safi et al. [20]:

λa(t)=β{I(t)+η1E(t)+ηq[Iq(t)+η2Eq(t)]+ηhH(t)}Na(t), (2)

and Na(t) is the total actively-mixing population given by (see also [20])

Na(t)=S(t)+E(t)+I(t)+ηq[Sq(t)+Eq(t)+Iq(t)]+ηhH(t)+R(t). (3)

In (2), β is the effective contact rate, and the modification parameters 0η1,ηh<1 accounts for the assumed reduction of infectiousness of exposed and hospitalized individuals, respectively, in relation to the symptomatically-infected (infectious) individuals in the I class. Similarly, 0ηq1 accounts for the assumed reduction of infectiousness of infected quarantined individuals in relation to individuals in the I class (the parameter 0η21 represents the assumed reduction of infectiousness of exposed quarantined individuals, in the Eq class, in relation to infectious quarantined individuals in the Iq class).

Fig. 1.

Fig. 1

Flow diagram of the model.

In (3), ηq is a modification parameter that measures the efficacy of quarantine in preventing individuals in quarantine from having contact with members of the general public. If ηq=0, then quarantine is perfectly-implemented (so that individuals in the quarantine classes are not part of the actively-mixing population, and do not transmit infection).

The non-quarantined susceptible population (S) is increased by the recruitment of individuals into the community, at a rate Π. This population is reduced by infection (at the rate λa), quarantine (at a rate γ) and natural death (at a rate μ; populations in all epidemiological compartments are assumed to suffer natural death at this rate). This population is increased by the return of quarantined susceptible individuals at the end of the quarantine period (at a rate ψ1) and the loss of natural immunity by recovered individuals (at a rate ψ2). The population of quarantined susceptible individuals (Sq) is generated by the quarantine of non-quarantined susceptible individuals (at the rate γ). It is decreased by infection (at a reduced rate rλa, with 0<r<1 accounting for the efficacy of quarantine in preventing infection of quarantined susceptible individuals) and by the reversion to the non-quarantined susceptible class at the end of the quarantine period (at the rate ψ1).

Non-quarantined latently-infected individuals (E) are generated at the rate λa and decreased by the development of clinical symptoms of the disease (at a rate σ1). Similarly, the population of quarantined latently-infected individuals (Eq) is generated at the rate rλa and decreased by the development of clinical symptoms (at a rate σ2). Non-quarantined symptomatic individuals (I) are generated at the rate σ1. This population is decreased by hospitalization (at a rate α1), natural recovery (at a rate ϕ1) and disease-induced mortality (at a rate δ1). The population of quarantined symptomatic individuals (Iq) is generated at the rate σ2 and decreased by hospitalization (at a rate α2), recovery (at a rate ϕ2) and disease-induced death (at a rate δ2).

The population of hospitalized individuals (H) is generated by the hospitalization of non-quarantined and quarantined symptomatic individuals (at the rate α1 and α2, respectively). It is diminished by recovery (at a rate ϕ3) and disease-induced death (at a rate δ3<δ2<δ1). The recovered population (R) is generated at the rates ϕi(i=1,2,3) and diminished by loss of natural immunity (at the rate ψ2).

The model (1) is an extension of many of the models for quarantine published in the literature (including those in [1], [3], [4], [6], [11], [12], [13], [14], [15], [16], [17], [18]), by considering the dynamics of quarantined susceptible individuals (this entails adding the epidemiological compartments Sq,Eq and Iq), in line with the models in [2], [5]. Furthermore, the model (1) extends the model in [5] by:

  • (i)

    including a compartment for hospitalized individuals (H);

  • (ii)

    allowing for the infection of quarantined susceptible individuals (at the rate rλa; that is, unlike in [5], it is assumed that the efficacy of quarantine to prevent infection of quarantined susceptible individuals is not 100%);

  • (iii)

    allowing for disease transmission by infected quarantined and hospitalized individuals (i.e., it is assumed, unlike in [5], that quarantine and hospitalization are not 100% effective in preventing transmission by infected quarantined or hospitalized individuals).

The model (1) also extends the model in [2] by:

  • (a)

    incorporating demographic parameters (i.e., using an endemic model as against the epidemic model used in [2]);

  • (b)

    using a standard incidence function to model the infection rate (the mass action incidence function was used in [2] by assuming constant total population);

  • (c)

    allowing for the infection of quarantined susceptible individuals (quarantine was assumed to be perfect against infection in [2]);

  • (d)

    allowing for disease transmission by non-quarantined latently-infected individuals.

Furthermore, detailed qualitative analysis of the model will be carried out in this study (this is not done in [2]). The model (1) extends the quarantine models with quarantined-adjusted incidence in [15], [20], by including the dynamics of quarantined susceptible individuals (Sq) as well as adding classes for quarantined exposed (Eq) and symptomatic (Iq) individuals.

The model (1) will now be analyzed to gain insight into its dynamical features.

2. Analysis of the model

2.1. Basic properties

Since the model (1) monitors human populations, all its associated parameters are non-negative. The following basic results can be established using the method in Appendix A of [22].

Theorem 1

The variables of the model (1) are non-negative for all time. In other words, solutions of the model system (1) with positive initial data will remain positive for all time t>0 .

Lemma 1

The closed set

D={(S,Sq,E,Eq,I,Iq,H,R)R+8:S+Sq+E+Eq+I+Iq+H+RΠμ}

is positively-invariant for the model (1) .

Proof

Adding all the equations of the model (1) gives,

dNdt=ΠμN(δ1I+δ2Iq+δ3H).

Since dN/dtΠμN, it follows that dN/dt0 if NΠ/μ. Thus, a standard comparison theorem [23] can be used to show that NN(0)eμt+Πμ(1eμt). In particular, N(t)Π/μ if N(0)Π/μ. Thus, the region D is positively-invariant. Further, if N(0)>Π/μ, then either the solution enters D in finite time, or N(t) approaches Π/μ asymptotically. Hence, the region D attracts all solutions in R+8.  □

2.2. Local stability of disease-free equilibrium (DFE)

The DFE of the model (1) is given by

E0=(S,Sq,E,Eq,I,Iq,H,R)=(Π(μ+ψ1)μ(μ+ψ1+γ),Πγμ(μ+ψ1+γ),0,0,0,0,0,0). (4)

The local stability of E0 will be explored using the next generation operator method [24], [25]. Using the notation in [25], the non-negative matrix, F, of the new infection terms, and the M-matrix, V, of the transition terms associated with the model (1), are given, respectively, by

F=(βη1ν1βη2ηqν1βν1βηqν1βηhν1rβη1ν2rβη2ηqν2rβν2rβηqν2rβηhν2000000000000000),

and,

V=(k100000k2000σ10k3000σ20k4000α1α2k5),

where,

ν1=μ+ψ1μ+ψ1+ηqγ,ν2=γμ+ψ1+ηqγ,k1=σ1+μ,k2=σ2+μ,
k3=α1+ϕ1+μ+δ1,k4=α2+ϕ2+μ+δ2,k5=α3+μ+δ3.

It follows that the control reproduction number [26], [27], denoted by Rq=ρ(FV1), where ρ is the spectral radius, is given by

Rq=βν1[η1k2k3k4k5+σ1k2k4k5+ηhα1σ1k2k4]k1k2k3k4k5+rβν2[η2ηqk1k3k4k5+ηqσ2k1k3k5+ηhα2σ2k1k3]k1k2k3k4k5.

Using Theorem 2 in [25], the following result is established.

Lemma 2

The DFE of the model (1) , given by (4) , is locally-asymptotically stable (LAS) if Rq<1 , and unstable if Rq>1 .

The threshold quantity Rq measures the average number of new infections generated by a single infectious individual in a population where a certain fraction of the susceptible population is vaccinated. Lemma 2 implies that the disease can be eliminated from the community (when Rq<1) if the initial sizes of the sub-populations of the model are in the basin of attraction of the DFE (E0).

2.3. Backward bifurcation analysis

In this section, the existence of endemic equilibria (that is, equilibria where the infected compartments of the model are non-zero) of the model (1) is established. Let,

E1=(S,Sq,E,Eq,I,Iq,H,R)

represents any arbitrary endemic equilibrium point (EEP) of the model (1). Further, define

λa=β{I+η1E+ηq[Iq+η2Eq]+ηhH}Na, (5)

(the force of infection of the model (1) at steady-state). It follows, by solving the equations in (1) at steady-state, that

S=Π(rλa+ψ1+μ)r(λa)2+[r(γ+μ)+ψ1+μ]λa+(ψ1+μ)(γ+μ)γψ1,Sq=Πγr(λa)2+[r(γ+μ)+ψ1+μ]λa+(ψ1+μ)(γ+μ)γψ1,E=λaSk1,Eq=rλaSqk2,I=λaSσ1k1k3,Iq=rλaSqσ2k2k4,H=λaSσ1α1k1k3k5+rλaSqσ2α2k2k4k5,R=λaSσ1ϕ1k1k3k6+rλaSqσ2ϕ2k2k4k6+λaSσ1α1ϕ3k1k3k5k6+rλaSqσ2α2ϕ3k2k4k5k6. (6)

Substituting the expressions in (6) into (5) shows that the non-zero equilibria of the model satisfy the following quadratic equation (in terms of λa):

a0(λa)2+a1λa+a2=0, (7)

where,

a0=rk2k4(k3k5k6+k5k6σ1+k5σ1ϕ1+k6σ1α1ηh+ϕ3α1σ1),
a1=r(ηqγk1k3k4k5k6+ηqγσ2k1k3k5k6+k1k2k3k4k5k6+γσ2α2ϕ3k1k3)+r(γσ2ϕ2k1k3k5+ηhγα2σ2k1k3k6)rβ(ηhα1σ1k2k4k6+η1k2k3k4k5k6+σ1k2k4k5k6)+(ψ1+μ)(α1σ1ϕ3k2k4+σ1ϕ1k2k4k5+ηhα1σ1k2k4k6+σ1k2k4k5k6+k2k3k4k5k6),
a2=k1k2k3k4k5k6(ηqγ+ψ1+μ)(1Rq).

The endemic equilibria of the model (1) can then be obtained by solving for λa from (7), and substituting the positive values of λa into the expressions in (6). The quadratic equation (7) can be analyzed for the possibility of multiple endemic equilibria when Rq<1. It should be noted that the coefficient, a0, of the quadratic (7) is always positive and a2 is positive (negative) if Rq is less (greater) than unity. Hence, the following result is established.

Theorem 2

The model (1) has

  • (i)

    a unique endemic equilibrium if a2<0Rq>1;

  • (ii)

    a unique endemic equilibrium if ( a1<0 and a2=0 ) or a124a0a2=0;

  • (iii)

    two endemic equilibria if a2>0,a1<0 and a124a0a2>0;

  • (iv)

    no endemic equilibrium otherwise.

Thus, it is clear from Case (i) of Theorem 2 that the model (1) has a unique EEP (of the form E1) whenever Rq>1. Furthermore, Case (iii) of Theorem 2 indicates the possibility of backward bifurcation, where a LAS DFE co-exists with a LAS endemic equilibrium when the associated reproduction number Rq is less than unity (see, for instance, [28], [29], [30] for discussions on backward bifurcation) in the model (1). The epidemiological importance of the phenomenon of backward bifurcation is that the classical requirement of having Rq<1 is, although necessary, not sufficient for disease elimination. In this case, disease elimination will depend upon the initial sizes of the sub-populations of the model. Thus, the existence of backward bifurcation in the transmission dynamics of a disease makes its effective control difficult. A more rigorous proof of the backward bifurcation property of the model (1), based on using center manifold theory (see, for instance, [25], [29], [31], [32]), is given in the Appendix.

2.3.1. Non-existence of backward bifurcation

In this section, the scenario where the backward bifurcation property of the model can be lost is explored. Consider the model (1) with a perfect quarantine efficacy against infection (so that, r=0). In this case, the coefficients a0,a1 and a2 of the quadratic equation (7) reduce to a0=0,a1>0 and a20 whenever R~q=Rq|r=01. Thus, for this case, the quadratic equation (7) has one solution (λa=a2a10.) Therefore, the model (1) with a perfect quarantine has no positive endemic equilibrium whenever R~q<1. This rules out the possibility of backward bifurcation in this case (since backward bifurcation requires the existence of at least two endemic equilibria whenever R~q1 [28], [29], [30]). Furthermore, it can be shown that, for the case when r=0, the DFE (E0) of the model (1) is globally-asymptotically stable (GAS) under some conditions, as shown below.

Setting r=0 in the model (1) gives the following reduced model (it should be noted from (1) that, for the case when r=0, (Eq(t),Iq(t))(0,0) as t; hence, these variables are omitted from the asymptotic analysis of the model for the special case with r=0):

dSdt=Πλ1(t)S(t)γS(t)+ψ1Sq(t)+ψ2R(t)μS(t),dSqdt=γS(t)(ψ1+μ)Sq(t),dEdt=λ1(t)S(t)(σ1+μ)E(t),dIdt=σ1E(t)(α1+ϕ1+μ+δ1)I(t),dHdt=α1I(t)(ϕ3+μ+δ3)H(t),dRdt=ϕ1I(t)+ϕ3H(t)(ψ2+μ)R(t), (8)

with the associated force of infection λa=λ1, where

λ1=λa|r=0=β{I(t)+η1E(t)+ηhH(t)}S(t)+ηqSq(t)+E(t)+I(t)+ηhH(t)+R(t). (9)

It can be shown that the reproduction number associated with the reduced model (8), with (9), is given by

R~q=Rq|r=0=βν1(η1k3k5+σ1k5+ηhσ1α1)k1k3k5.

Define,

D1={(S,Sq,E,I,H,R)R+6:S+Sq+E+I+H+RΠμ}.

The model (8) has a DFE, given by E01=(S,Sq,0,0,0,0).

Theorem 3

The DFE ( E01 ) of the reduced model (8) , with (9) , is GAS in D1 whenever R~qν1<1 .

Proof

Consider the following Lyapunov function

F=(k5R~qν1ηhβ)E+(k5+ηhα1k3ηh)I+H,

with Lyapunov derivative (where a dot represents differentiation with respect to time) given by

F˙=(k5R~qν1ηhβ)E˙+(k5+ηhα1k3ηh)I˙+H˙=k5R~qν1ηhβ[βS(I+η1E+ηhH)S+ηqSq+E+I+ηhH+Rk1E]+(k5+ηhα1k3ηh)(σ1Ek3I)+α1Ik5Hk5R~qν1ηh(I+η1E+ηhH)k1k5R~qν1ηhβE+σ1(k5+ηhα1)k3ηhE(k5+ηhα)ηhI+α1Ik5H,since SS+ηqSq+E+I+ηhH+R in D1=[k5Rq~(η1βk1)ν1ηhβ+σ1(k5+ηhα1)k3ηh]E+(α1+k5R~qν1ηhk5+ηhα1ηh)I+k5(R~qν11)H=k5ηh(R~qν11)(I+η1E+ηhH)0whenever R~qν1<1.

Since all the parameters and variables of the model (1) are non-negative (Theorem 1), it follows that F˙0 for R~qν1 (it should be noted that ν1=SN<1) with F˙=0 if and only if E=I=H=0. Hence, F is a Lyapunov function on D1. Thus, it follows, by LaSalle’s Invariance Principle [33], that

(E(t),I(t),H(t))(0,0,0)as t. (10)

Since lim suptI(t)=0 and lim suptH(t)=0 (from (10)), it follows that, for sufficiently small ϖ>0, there exist constants M1>0 and M2>0 such that lim suptI(t)ϖ for all t>M1 and lim suptH(t)ϖ for all t>M2. Hence, it follows from the last equation of the model (8) that, for t>max{M1,M2},

R˙ϕ1ϖ+ϕ3ϖμR.

Thus, by comparison theorem [23],

R=lim suptRϕ1ϖ+ϕ3ϖμ,

so that, by letting ϖ0,

R=lim suptR0. (11)

Similarly (by using lim inftI(t)=0 and lim inftH(t)=0), it can be shown that

R=lim inftR0. (12)

Thus, it follows from (11), (12) that

R0R.

Hence,

limtR(t)=0. (13)

Similarly, it can be shown that

limtS(t)=Π(μ+ψ1)μ(μ+ψ1+γ)=S,limtSq(t)=Πγμ(μ+ψ1+γ)=Sq. (14)

Thus, by combining Eqs. (10), (13), (14), it follows that every solution of the equations of the model (8), with initial conditions in D1, approaches E0 as t (for R~qν1<1).  □

The above result shows that, for the case when the efficacy of quarantine in preventing infection is perfect (i.e., r=0), the disease can be eliminated from the community if the associated reproduction number of the model is less than unity. Furthermore, this result clearly shows that the backward bifurcation property of the model (1) is caused by the imperfect nature of the efficacy of quarantine to prevent infection (see the Appendix).

Conditions for the persistence of the disease in the population will be investigated below.

2.4. Persistence

The model system (1) is said to be uniformly-persistent if there exists a constant c such that any solution (S(t),Sq(t),E(t),Eq(t),I(t),Iq(t),H(t),R(t)) satisfies [34], [35]:

lim inftS(t)c,lim inftSq(t)c,lim inftE(t)c,lim inftEq(t)c,
lim inftI(t)c,lim inftIq(t)c,lim inftH(t)c,lim inftR(t)c,

provided that (S(0),Sq(0),E(0),Eq(0),I(0),Iq(0),H(0),R(0))D.

Theorem 4

System (1) is uniformly-persistent in D if and only if Rq>1 .

Proof

The theorem can be proved by using the approach used to prove Proposition 3.3 of [36], by applying a uniform persistence result in [34] and noting that the DFE of the model (1) is unstable whenever Rq>1 (Lemma 2).  □

The consequence of this result is that each infected variable (E,Eq,I,Iq,H) of the model will persist above a certain threshold value at steady-state, so that the disease will persist (become endemic) in the population. It should be mentioned that some other models for quarantine, which did not explicitly include the dynamics of quarantined susceptible individuals, also showed the presence of a unique endemic equilibrium and disease persistence when the associated reproduction number exceeds unity (see, for instance, [13], [17], [18]).

Conclusions

A new deterministic model for the spread of a disease in a population in the presence of quarantine is designed. A major feature of the model is that it incorporate the dynamics of quarantine-adjusted incidence and the quarantine of susceptible individuals (that is, quarantine is modeled in terms of the temporarily removal of susceptible individuals from the susceptible pool as well as the removal of new infected individuals, detected via the contact tracing of known infectious individuals). Rigorous analysis of the model reveals that it undergoes the phenomenon of backward bifurcation when the associated reproduction number (Rq) is less than unity. The presence of this phenomenon, which does not arise if the quarantine is 100% effective, implies that the effective control of the spread of the disease, using an imperfect quarantine, depends on the initial sizes of the sub-populations of the model (when Rq<1). The model has a unique endemic equilibrium whenever Rq>1. Furthermore, it is shown that the disease will persist in the population whenever Rq>1.

Acknowledgments

ABG acknowledges, with thanks, the support in part of the Natural Science and Engineering Research Council (NSERC) and Mathematics of Information Technology and Complex Systems (MITACS) of Canada. The authors are grateful to the anonymous reviewers for their constructive comments.

Submitted by Juan J. Nieto

Appendix. Proof of backward bifurcation property of model (1)

The proof is based on using center manifold theory [31], [32]. In particular, Theorem 4.1 of [32] will be used. It is convenient to make the following change of variables:

S=x1,Sq=x2,E=x3,Eq=x4,I=x5,Iq=x6,H=x7,R=x8.

Furthermore, let X=(x1,x2,x3,x4,x5,x6,x7,x8)T. Thus, the model (1) can be re-written in the form dXdt=F(X), with F=(f1,f2,f3,f4,f5,f6,f7,f8)T, as follows:

dx1dt=f1=Πβ[x5+η1x3+ηq(x6+η2x4+ηhx7)]x1x1+x3+x5+ηq(x2+x4+x6)+x7+x8+ψ1x2(μ+γ)x1,dx2dt=f2=γx1rβ[x5+η1x3+ηq(x6+η2x4+ηhx7)]x1x1+x3+x5+ηq(x2+x4+x6)+x7+x8(μ+ψ1)x2,dx3dt=f3=β(x5+η1x3+ηq[x6+η2x4+ηhx7])x1x1+x3+x5+ηq(x2+x4+x6)+x7+x8k1x3,dx4dt=f4=rβ(x5+η1x3+ηq[x6+η2x4+ηhx7])x1x1+x3+x5+ηq(x2+x4+x6)+x7+x8k2x4,dx5dt=f5=σ1x3k3x5,dx6dt=f6=σ2x4k4x6,dx7dt=f7=α1x5+α2x6k5x7,dx8dt=f8=ϕ1x5+ϕ2x6+ϕ3x7k6x8. (15)

The Jacobian of the system (15), at the associated DFE (E0), is given by

J(E0)=[M4×8U4×8],

where

M=((γ+μ)ψ1βη1x1x1+ηqx2βηqη2x1x1+ηqx2γ(ψ1+μ)rβη1x2x1+ηqx2rβηqη2x1x2+ηqx200βη1x1x1+ηqx2k1βηqη2x1x1+ηqx200rβη1x2x1+ηqx2rβηqη2x1x2+ηqx2k200σ10000σ200000000),
U=(βx1x1+ηqx2βηqx1x1+ηqx2βηhx1x1+ηqx20rβx2x1+ηqx2rβηqx2x1+ηqx2rβηhx2x1+ηqx20βx1x1+ηqx2βηqx1x1+ηqx2βηhx1x1+ηqx20rβx2x1+ηqx2rβηqx2x1+ηqx2rβηhx2x1+ηqx20k30000k400α1α2k50ϕ1ϕ2ϕ3k6).

Consider the case when Rq=1. Furthermore, suppose that β is chosen as a bifurcation parameter. Solving for β from Rq=1 gives

β=k1k2k3k4k5ν1M1+rν2M2,

where

M1=η1k2k3k4k5+σ1k2k4k5+ηhα1σ1k2k4,
M2=η2ηqk1k3k4k5+ηqσ2k1k3k5+ηhα2σ2k1k3.

The transformed system (15), with β=β, has a hyperbolic equilibrium point (i.e., the linearized system has a simple eigenvalue with zero real part, and all other eigenvalues have negative real part), so that the center manifold theory [31], [32] can be used to analyze the dynamics of (15) near β=β.

It can be shown that the right eigenvector of J(E0)|β=β, denoted by w, is given by w=(w1,w2,,w7,w8)T, where,

w1=k2w4+(μ+ψ1)w2γ,w2=[γμ(μ+γ+ψ1)][k1w3+k2w4(μ+γ)],
w5=σ1w3k3,w6=σ2w4k4,w7=α1w5+α2w6k5,
w8=ϕ1w5+ϕ2w6+ϕ3w7k6,w3>0,w4>0.

Similarly, J(E0)|β=β has a left eigenvector, v given by v=(v1,v2,,v7,v8), where,

v1=0,v2=0,v7=βηhx1v3k5(x1+ηqx2)+rβηhx1v4k5(x1+ηqx2),
v6=α2v7k4+βηqx1v3k4(x1+ηqx2)+rβηqx1v4k4(x1+ηqx2),
v5=α1v7k3+βx1v3k3(x1+ηqx2)+rβx1v4k3(x1+ηqx2),v3>0,v4>0,v8=0.

Consequently, it follows that the associated bifurcation coefficients, a and b (defined in Theorem 4.1 of [32]), are given, respectively, by

a=k,i,j=18vkwiwj2fk(0,0)xixj=(rηqv4w4ηqv3w4)(μ+σ2μ+ψ1+ηqγ)(rv4x2+v3x1)k3k4k5k6(a1+a2+a3+a4), (16)
b=k,i=18vkwi2fk(0,0)xiβ=(v3x1+rv4x2)(η1w3+η2ηqw4+w5+ηqw6+ηhw7)x1+ηqx2>0,

where

a1=k3k4k5k6w3+k3k4k5k6ηqw4,
a2=k4k5k6σ1w3+k3k5k6ηqσ2w4,
a3=k4k6ηhα1σ1w3+k3k6ηhα2σ2w4,
a4=k4k5ϕ1σ1w3+k3k5ϕ2σ2w4+k4ϕ3α1σ1w3+k3ϕ3α2σ2w4.

Since the bifurcation coefficient b is always positive, it follows (from Theorem 4.1 of [32]) that the system (15) will undergo backward bifurcation if the bifurcation coefficient a is positive. This result is summarized below.

Theorem 5

The transformed model (15) , or equivalently (1) , exhibits backward bifurcation at Rq=1 whenever the bifurcation coefficient, a , given by (16) , is positive.

It should be noted from (16) that the bifurcation coefficient a, is positive whenever

r>ηqv3w4(μ+σ2)v4(ηqw4x2)(μ+ψ1+ηqγ)+v3x1(a1+a2+a3+a4)v4(ηqw4x2)k3k4k5k6=rc.

Thus, the transformed model (15), exhibits backward bifurcation at Rq=1 whenever r>rc. Furthermore, it should be noted that for the case when quarantined susceptible individuals do not acquire infection during quarantine (i.e., r=0), the bifurcation coefficient a becomes

a=ηqv3w4(μ+σ2μ+ψ1+ηqγ)v3x1k3k4k5k6(a1+a2+a3+a4)<0

since ai>0 for i=1,,4 (since all the model parameters are non-negative). Thus, since a<0 in this case, it follows from Theorem 4.1 of [32] that the model (1) will not exhibit backward bifurcation if r=0. In other words, this study shows that the backward bifurcation property of the model (1) arises due to the infection of susceptible individuals in quarantine. This result is consistent with Theorem 3 (where it was shown that the DFE of the model (1) with r=0 is globally-asymptotically stable).

References

  • 1.Gumel A.B. Modelling strategies for controlling SARS outbreaks. Proc. Roy. Soc. Ser. B. 2004;271:2223–2232. doi: 10.1098/rspb.2004.2800. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Lipsitch M. Transmission dynamics and control of severe acute respiratory syndrome. Science. 2003;300:1966–1970. doi: 10.1126/science.1086616. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Lloyd-Smith J.O., Galvani A.P., Getz W.M. Curtailing transmission of severe acute respiratory syndrome within a community and its hospital. Proc. R. Soc. Lond. B. 2003;170:1979–1989. doi: 10.1098/rspb.2003.2481. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.McLeod R.G., Brewster J.F., Gumel A.B., Slonowsky D.A. Sensitivity and uncertainty analyses for a SARS model with time-varying inputs and outputs. Math. Biosci. Eng. 2006;3:527–544. doi: 10.3934/mbe.2006.3.527. [DOI] [PubMed] [Google Scholar]
  • 5.Mubayi A., Kribs-Zaleta C., Martcheva M., Castillo-Chavez C. A cost-based comparison of quarantine strategies for new emerging diseases. Math. Biosci. Eng. 2010;7(3):687–717. doi: 10.3934/mbe.2010.7.687. [DOI] [PubMed] [Google Scholar]
  • 6.Riley S. Transmission dynamics of etiological agent of SARS in Hong Kong: the impact of public health interventions. Science. 2003;300:1961–1966. doi: 10.1126/science.1086478. [DOI] [PubMed] [Google Scholar]
  • 7.Wang W., Ruan S. Simulating the SARS outbreak in Beijing with limited data. J. Theoret. Biol. 2004;227:369–379. doi: 10.1016/j.jtbi.2003.11.014. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.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]
  • 9.Kao R.R., Roberts M.G. Quarantine-based disease control in domesticated animal herds. Appl. Math. Lett. 1998;4:115–120. [Google Scholar]
  • 10.Sato H., Nakada H., Yamaguchi R., Imoto S., Miyano S., Kami M. When should we intervene to control the 2009 influenza A(H1N1) pandemic? Rapid Communications. Euro. Surveill. 2010;15(1) doi: 10.2807/ese.15.01.19455-en. 19455. [DOI] [PubMed] [Google Scholar]
  • 11.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]
  • 12.Day T., Park A., Madras N., Gumel A.B., Wu J. When is quarantine a useful control strategy for emerging infectious diseases? Amer. J. Epidemiol. 2006;163:479–485. doi: 10.1093/aje/kwj056. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Feng Z., Xu D., Zhao H. Epidemiological models with non-exponentially distributed disease stages and application to disease control. Bull. Math. Biol. 2007;69:1511–1536. doi: 10.1007/s11538-006-9174-9. [DOI] [PubMed] [Google Scholar]
  • 14.Hethcote H.W., Zhien M., Shengbing L. 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]
  • 15.Nuno M., Feng Z., Martcheva M., Castillo-Chavez C. Dynamics of two-strain influenza with isolation and partial cross-immunity. SIAM J. Appl. Math. 2005;65:964–982. [Google Scholar]
  • 16.Podder C.N., Gumel A.B., Bowman C.S., McLeod R.G. Mathematical study of the impact of quarantine, isolation and vaccination in curtailing an epidemic. J. Biol. Sys. 2007;15:185–202. [Google Scholar]
  • 17.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]
  • 18.Safi M.A., Gumel A.B. The effect of incidence functions on the dynamics of a quarantine/isolation model with time delay. Nonlinear Anal. RWA. 2011;12(1):215–235. doi: 10.1016/j.nonrwa.2010.06.009. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19.Webb G.F., Blaser M.J., Zhu H., Ardal S., Wu J. Critical role of nosocomial transmission in the Toronto SARS outbreak. Math. Biosci. Eng. 2004;1:1–13. doi: 10.3934/mbe.2004.1.1. [DOI] [PubMed] [Google Scholar]
  • 20.Safi M.A., Imran M., Gumel A.B. Threshold dynamics of a non-autonomous SEIRS model with quarantine and isolation. Theory Biosci. 2012;131:19–30. doi: 10.1007/s12064-011-0148-6. [DOI] [PubMed] [Google Scholar]
  • 21.Chowell G., Castillo-Chavez C., Fenimore P.W., Kribs-Zaleta C.M., Arriola L., Hyman J.M. Model parameters and outbreak control for SARS. EID. 2004;10:1258–1263. doi: 10.3201/eid1007.030647. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Thieme H.R. Princeton University Press; 2003. Mathematics in Population Biology. [Google Scholar]
  • 23.Smith H.L., Waltman P. Cambridge University Press; 1995. The Theory of the Chemostat. [Google Scholar]
  • 24.Diekmann O., Heesterbeek J.A.P., Metz J.A.J. On the definition and computation of the basic reproduction ratio R0 in models for infectious disease in heterogeneous population. J. Math. Biol. 1990;28:365–382. doi: 10.1007/BF00178324. [DOI] [PubMed] [Google Scholar]
  • 25.van den Driessche P., Watmough J. Reproduction numbers and sub-threshold endemic equilibria for compartmental models of disease transmission. Math. Biosci. 2002;180:29–48. doi: 10.1016/s0025-5564(02)00108-6. [DOI] [PubMed] [Google Scholar]
  • 26.Anderson R.M., May R.M. Springer-Verlag; Berlin, Heidelrberg, New York: 1982. Population Biology of Infectious Diseases. [Google Scholar]
  • 27.Hethcote H.W. The mathematics of infectious diseases. SIAM Rev. 2000;42:599–653. [Google Scholar]
  • 28.Elbasha E.H., Gumel A.B. Theoretical assessment of public health impact of imperfect prophylactic HIV-1 vaccines with therapeutic benefits. Bull. Math. Biol. 2006;68:577–614. doi: 10.1007/s11538-005-9057-5. [DOI] [PubMed] [Google Scholar]
  • 29.Garba S.M., Gumel A.B., Abu Bakar M.R. Backward bifurcations in dengue transmission dynamics. Math. Biosci. 2008;1:11–25. doi: 10.1016/j.mbs.2008.05.002. [DOI] [PubMed] [Google Scholar]
  • 30.Sharomi O., Podder C.N., Gumel A.B., Elbasha E., Watmough J. Role of incidence function in vaccine-induced backward bifurcation in some HIV models. Math. Biosci. 2007;2:436–463. doi: 10.1016/j.mbs.2007.05.012. [DOI] [PubMed] [Google Scholar]
  • 31.Carr J. Springer-Verlag; New York: 1981. Applications of Centre Manifold Theory. [Google Scholar]
  • 32.Castillo-Chavez C., Song B. Dynamical models of tuberculosis and their applications. Math. Biosci. Eng. 2004;1:361–404. doi: 10.3934/mbe.2004.1.361. [DOI] [PubMed] [Google Scholar]
  • 33.Hale J.K. John Wiley and Sons; New York: 1969. Ordinary Differential Equations. [Google Scholar]
  • 34.H. Freedman, S. Ruan, M. Tang, Uniform persistence and flows near a closed positively invariant set, 1994.
  • 35.Thieme H. Epidemic and demographic interaction in the spread of potentially fatal diseases in growing populations. Math. Biosci. 1992;1:99–130. doi: 10.1016/0025-5564(92)90081-7. [DOI] [PubMed] [Google Scholar]
  • 36.Li M., Graef J., Wang L., Karsai J. Global dynamics of a SEIR model with varying total population size. Math. Biosci. 1999;160:191–213. doi: 10.1016/s0025-5564(99)00030-9. [DOI] [PubMed] [Google Scholar]

Articles from Journal of Mathematical Analysis and Applications are provided here courtesy of Elsevier

RESOURCES