Mathematical Modeling

September 11, 2013 15:35 WSPC/S0218-3390 129-JBS 1350023
Journal of Biological Systems

Vol. 21, No. 3 (2013) 1350023 (25 pages)
c World Scientific Publishing Company
DOI: 10.1142/S021833901350023X
MODELING AND ANALYSIS OF AN SEIR MODEL

WITH DIFFERENT TYPES OF NONLINEAR
TREATMENT RATES
B. DUBEY∗,§ , ATASI PATRA∗,¶ , P. K. SRIVASTAVA‡,

and UMA S. DUBEY†,∗∗
∗Department of Mathematics
†Department of Biological Sciences
Birla Institute of Technology and Science, Pilani
Pilani-333031, India
‡Department of Mathematics
Indian Institute of Technology

Patna-800013, India
§balram.dubey@gmail.com
¶atasimaths@gmail.com
pksri09@gmail.com
∗∗uma@pilani.bits-pilani.ac.in
Received 18 July 2012

Accepted 20 August 2013
Published 16 September 2013
In this study, an SEIR epidemic model is proposed for treatment of infectives considering
the development of acquired immunity in recovered individuals. We employed two dif-
ferent types of treatment functions. Stability analysis for disease-free as well as endemic
equilibria is performed. It is observed that the existence of unique endemic equilibrium
depends on the basic reproductive number R0 as well as on treatment rate. Numerical
simulations are performed on the proposed models to support and analyze theoretical
findings.
Keywords: SEIR Model; Holling’s Type III and IV Treatment Rates; Stability Analysis.
1. Introduction
The wide spread and frequent occurrence of many communicable diseases are
intriguing health care workers and policy makers all over the globe. In order to
control or to eradicate a disease, complete understanding of the dynamics of the
disease progression is required. In one way it can be achieved through mathematical
modeling, which has been successfully used to understand various aspects of many
diseases and to suggest its control.1–4 It has thereby emerged as an important tool
in epidemiology.
§ Corresponding author.
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Dubey et al.
Since the pioneer work of Kermack and McKendrick,5,6 a lot of work has been
done to understand the infectious diseases. In these models, the entire population is
assumed to be divided into compartments of susceptible individuals (S), infectious
individuals (I) and removed or recovered individuals (R). Susceptible individuals are
those who are healthy and do not have any infection. Individuals who are infected
with the disease and are capable to transfer it to susceptible via contacts are called
Infectious individuals. As time progresses, infectious individuals loose the infectiv-
ity, and move to removed or recovered compartment. These recovered individuals
are immune to infectious microbes and thus do not acquire the disease again.
For certain diseases, on contact with infected individuals, susceptibles may not
immediately become infectious. Rather there is latency and after this latent period
they become infectious and can spread infection to susceptible individuals. These
individuals who are exposed to disease pathogen but are yet to become infectious are
classified as Exposed (E). The model along with exposed individuals corresponds
to SEIR type.4,7–12
Epidemic models with exposed class have been well studied in literature.9,11,13,14
Li et al.9 analyzed the global stability of an SEIR epidemic model considering con-
stant immigration and infectious force in exposed, infected and recovered class. Li
and Muldowney10 considered the global dynamics of an SEIR model with a nonlin-
ear incident rate using the geometric method. Liu et al.11 studied an epidemiological
model with nonlinear incidence rate instead of bilinear incidence. They investigated
rich dynamics of the model and established that the clearance of disease depends not
only on parameters but also on its initial values. They also showed that for some
parametric values periodic solution may exist through Hopf bifurcation. Green-
halgh13 studied dynamical properties of the model first with constant infection rate
and then with density-dependent infection rate together with density-dependent
death rate. It was observed that in case of constant contact, for disease persistence,
there is only one threshold parameter while in case of density-dependent contact
there exists three threshold conditions. They also found Hopf birfucation in later
case. Korobeinikov15 established global stability for SEIR models with nonlinear
incidence by constructing a suitable Lyapunov function.
Greenhalgh16 considered an SEIR model with density-dependent death rate and
constant infection rate. They found that the system possess three equilibria: (i)
when the population becomes extinct, (ii) when the disease is eradicated and (iii)
when the disease is present within the population. They found that it is possible
for this third equilibrium to exist and be locally unstable. They found, numerically,
the occurrence of cycles of disease incidence with varying amplitude for different
parametric values. Li et al.17 established the global stability of SEIR model with
varying total population size and they further studied an SEIR model with vertical
transmission in a constant population and incidence term in the form of bilinear
mass action.18
Li et al.19 classified the individuals in infected class into the early and later
stages of infectives according to infection progression. The global stability of the
1350023-2
Modeling and Analysis of an SEIR Model
disease-free equilibrium and the local stability of the endemic equilibrium are estab-
lished. Further, the global stability of the endemic equilibrium is obtained when
infection is not fatal. Mukhopadhyay and Bhattacharyya20 considered distinct inci-
dence rates for the exposed and the infected populations in an SEIS model, which
they further extended, to account for the nonhomogeneous mixing, by consider-
ing the effect of diffusion on different population subclasses. The diffusive model
is analyzed using matrix stability theory and conditions for Turing bifurcation are
derived. Acedo et al.21 obtained an exact global solution using modal expansion infi-
nite series for the classical SIRS model. They showed that for real initial conditions
the modal expansion series present a convergent behavior.
In recent years, classical epidemiological models with add-on of certain new
factors such as different treatment plans, quarantine, vaccination, bacteria, etc. have
been investigated7,12,22–29 as treatment and isolation or quarantine are important
ways to control spread of the disease. Bai and Zhou7 studied global properties of an
SEIRS epidemic model with periodic vaccination and seasonal contact rate. Elbasha
et al.23 studied the qualitative dynamics of an SIRS model with vaccination, with
waning natural and vaccine-induced immunity and found that model undergoes
backward bifurcation depending upon the protection level of the vaccine. Hu et al.24
considered an epidemic model with standard incidence rate and treatment rate of
infectious individuals. Here the treatment rate is taken to be capacity dependent.
Further, it is proportional to the number of infectives below the capacity and a
constant when the number of infectives exceed the capacity. The existence and
stability of equilibria are found to be dependent on both basic reproduction number
and the capacity for treatment. For small capacity, a bistable endemic equilibria
has been determined.
Ghosh et al.30 proposed an SIS model for carrier-dependent infectious diseases
caused by direct contact of susceptibles with infectives as well as by carriers by
assuming the growth of both the human and the carrier populations logistic. They
also assumed that the density of carrier population increases with the increase
in the cumulative density of discharges by the human population into the envi-
ronment. They found that if the growth of carrier population caused by conducive
household discharges increases, the spread of the infectious disease increases. Ghosh
et al.31 investigated an SIS model for bacterial infectious disease where the growth
of human population is logistic. They concluded from the analysis that the spread
of the infectious disease increases when the growth of bacteria caused by conducive
environmental discharge due to human sources increases. Naresh et al.32 proposed
and analyzed a nonlinear mathematical model for the spread of carrier-dependent
infectious diseases in a population with variable size structure and they studied
the role of vaccination. It is assumed here that the susceptible becomes infected
by direct contact with infectives and/or by the carrier population present in the
environment. They obtained a threshold condition, in terms of vaccine-induced
reproduction number which is, if less than one, the disease dies out in the absence
of carriers provided the vaccine efficacy is high enough, and otherwise the infection
1350023-3
Dubey et al.
persists in the population. The model also exhibits backward bifurcation when the
vaccine-induced reproduction number is equal to one. They have also shown that
the constant immigration of susceptible makes the disease more endemic. Naresh
et al.33 proposed and analyzed a nonlinear mathematical model and studied the
spread of HIV/AIDS in a population of varying size with immigration of infectives.
They found that the disease is always persistent if the direct immigration of infec-
tives is allowed in the community. Further, in the absence of inflow of infectives,
the endemicity of the disease is found to be higher if pre-AIDS individuals also
interact sexually in comparison to the case when they do not take part in sexual
interactions. Thus, if the direct immigration of infectives is restricted, the spread
of infection can be slowed down. Naresh et al.34 further developed an SIR model
with nonlinear incidence rate and time delayed. They established the existence and
stability of the possible equilibria in terms of a certain threshold conditions and
basic reproduction number.
Gerberry and Milner35 proposed an SEIQR model for childhood disease consid-
ering quarantined class (infectious individuals who are isolated from further con-
tacts for some time, usually the length of infection period). They found that the
inclusion of quarantined class in the classical SIR model for childhood disease can
be responsible for self-sustained oscillations. Recently, Liu et al.36 investigated the
application of pulse vaccination strategy to prevent and control some infectious
diseases. This is described by age-structured SIR model in which susceptible and
recovered individuals are structured by chronological age, while infected individuals
are structured by infection age.
It is known that the capacity of any community for treatment of a disease
is limited, Wang and Ruan27 considered a SIR epidemic model with constant
removal rate (i.e. the recovery from infected subpopulation per unit time) as given
below:

r, I > 0
h(I) =
0, I = 0.
Then they performed stability analysis and showed that this model exhibits various
bifurcations. Zhang and Suo29 modified the removal rate to Holling type II:
βI
h(I) = , I ≥ 0; β, γ > 0.
1 + γI
They discussed the stability of equilibria and established that the model exhibits
Bogdanov–Takens bifurcation, Hopf bifurcation and Homoclinic bifurcation.
It may be noted that although various types of epidemiological models have
been studied and analyzed, SEIR model with different removal rates of Holling
type III and type IV are yet to be studied. Here in this paper we consider an
SEIR type model with these two different removal rates to account for the different
treatment capacity of the community. In fact in Holling type II, for any outbreak
1350023-4
of the disease its treatment capacity is first very low and then grows slowly with
improvement of hospital’s condition, availability of effective drugs, etc. Further,
when number of infected individuals is very large, the treatment capacity reaches
to its maximum due to limited treatment facilities. This condition pertains to newly
emergent diseases whose treatment is very limited.
In the present paper, we have considered the following two types of removal rate
functions:
Case I: Holling type III

βI 2
h(I) = , I ≥ 0, β, γ > 0.
1 + γI 2
Case II: Holling type IV
βI
h(I) = I2
, I ≥ 0, β, a, b > 0.
a +I +b
Holling type III defines the condition in which removal rate first grows very fast
initially with increase in infectives and then it grows slowly and finally settles
down to maximum saturated value. After this any increase in infectives will not
affect the removal rate. This condition pertains to a known disease which has re-
emerged and has available treatment modalities. Whereas in Holling type IV, the
removal/treatment rate initially grows with growth of infectives and reaches the
maximum and then starts decaying. Such a situation may arise due to limitation
in availability of treatment for large number of infected individuals. When supplies
of treatment (medicine, immunization, etc.) are depleted, then in spite of high
number of infectives the available treatment becomes very low. This case may arise
when there is re-emergence and spread of disease in place of limited treatment
facilities.
In this paper, we have considered an SEIR epidemic model with Holling type
III removal rate function. We have then discussed the positivity, boundedness and
stability of the model system. Further, the removal rate function is modified to
Holling type IV and corresponding stability analysis is performed. A brief analysis
is also presented when the treatment rate function is of Holling type II. Finally,
numerical simulations are carried out to support the analytical findings.
2. Mathematical Model
We consider an SEIR model with removal of infectious population via treatment,
assuming perpetual immunity of removed individual. As mentioned in the introduc-
tion we shall consider two different removal rate functions (treatment functions).
We assume that the total population is divided into four compartments of Suscep-
tible (S), Exposed (E), infectious (I) and Recovered (R) classes. Let susceptibles
be recruited in population at a constant rate A and δ0 be the natural death rate
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Dubey et al.
for the population in all classes. The susceptibles become infected on contact with
infected individuals. This interaction is considered to be of mass action type. α is
the rate at which susceptible is exposed to the infection. Upon infection the suscep-
tible individuals move to exposed class and only after latency they become infective
and move to infectious class. Let δ1 be the rate at which an individual leaves the
exposed class and becomes infective i.e., δ11 is the latency period. The infectious
individuals are assumed to leave via natural- and disease-related death as well as
natural recovery. Let δ2 be natural recovery rate of the infectious individuals and
hence δ12 is the infectious period. Let δ3 be the death rate of the infectious individual
due to infection. Removal of infectious individual is also made by treatment using
removal rate function. Let h(I) be recovery rate of the infectious subpopulation
through treatment which we consider of following two types: Holling type III and
Holling type IV. The schematic diagram of the interacting subpopulations is shown
in Fig. 1.
Here we assume that after recovery the individuals become immunized and
hence they are no longer susceptible to it. This happens because acquired immune
response leads to development of immunological memory and therefore individual
is not infected from the same disease again and does not enter the susceptible
population.
Keeping the above assumptions in mind, the mathematical model can be gov-
erned by the following system of ordinary differential equations:
dS
= A − δ0 S − αSI ,
dt
dE
= −δ0 E − δ1 E + αSI ,
dt
dI
= −δ0 I − δ2 I + δ1 E − δ3 I − h(I), (2.1)
dt
dR
= δ2 I − δ0 R + h(I),
dt
S(0) > 0, E(0) ≥ 0, I(0) ≥ 0, R(0) ≥ 0.
Fig. 1. Schematic diagram of the interacting populations.
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Since removed class R does not have any effect on the dynamics of S, E and I class,
we shall study following reduced system:
dS
= A − δ0 S − αSI ,
dt
dE
= −δ0 E − δ1 E + αSI ,
dt (2.2)
dI
= −δ0 I − δ2 I + δ1 E − δ3 I − h(I),
dt
S(0) > 0, E(0) ≥ 0, I(0) ≥ 0.
Note that the dynamical properties of R are completely determined once we know
those of S, E and I i.e., all the property of system (2.1) can be drawn from those
of system (2.2). Hence, we shall focus our study on the model system (2.2).
In the following, considering the saturated removal rate and supposing the
removed individuals with perpetual immunity, the SEIR epidemic models are for-
mulated for two different treatment rate functions. We study both the cases one
by one.
Case I: Holling type III
We take
βI 2
h(I) = , I ≥ 0, β, γ > 0.
1 + γI 2
It is easy to see that the treatment rate h(I) is a continuously differentiable
increasing function of I and
(i) h(0) = 0,
(ii) h (I) > 0,
β
(iii) limI→∞ h(I) = γ,
where βγ is the maximal treatment capacity of some community.

Thus, in this case model (2.2) takes the form as:
dS
= A − δ0 S − αSI ,
dt
dE
= −δ0 E − δ1 E + αSI ,
dt (2.3)
2
dI βI
= −δ0 I − δ2 I + δ1 E − δ3 I − ,
dt 1 + γI 2
S(0) > 0, E(0) ≥ 0 and I(0) ≥ 0.
It is well known that the dynamics of a disease is closely related to the stability of
the equilibrium points of mathematical models. In classical epidemiological models,
there usually exists two equilibrium points: a disease-free equilibrium and a unique
1350023-7
Dubey et al.
endemic equilibrium. The stability of the disease-free equilibrium is determined

by a threshold parameter R0 , known as the basic reproductive number, i.e., the
disease-free equilibrium is asymptotically stable if R0 < 1, while it is unstable if
R0 > 1. Biologically, the disease can be cured if R0 < 1, and it persists if R0 > 1.
In the next section, we present the stability analysis of model (2.3).
3. Stability Analysis
First of all, we analyze model (2.3) which has been obtained from model (2.1)
taking h(I) as mentioned in Case I. In the following lemma, we establish a region
of attraction for model system (2.3). The proof of this lemma is similar to that of
Freedman and So,37 Shukla and Dubey38 and hence is omitted.
Lemma 3.1. The set Ω = {(S, E, I) : S > 0, E ≥ 0, I ≥ 0, S + E + I ≤ δ0 }

A
is a
positively invariant region of system (2.3).
The above lemma shows that all solutions of our model (2.3) are non-negative
and bounded. Thus, the model is biologically well behaved.
In the following, we discuss the existence of equilibria. We note that model
(2.3) has one disease-free equilibrium P0 ( δA0 , 0, 0) and one endemic equilibrium
P ∗ (S ∗ , E ∗ , I ∗ ). The disease-free equilibrium P0 always exists. For the existence
of endemic equilibrium P ∗ , we note that S ∗ , E ∗ and I ∗ are the positive solutions
of the following algebraic equations:
A
S= , (3.1a)
δ0 + αI
AαI
E= , (3.1b)
(δ0 + δ1 )(δ0 + αI)
βI 2
−(δ0 + δ2 + δ3 )I + δ1 E − = 0. (3.1c)
1 + γI 2
Substituting the value of E from Eq. (3.1b) in Eq. (3.1c), we get a cubic equation
of the form:
KI 3 + LI 2 + MI + N = 0, (3.2)
where
K = pqαγ, L = pqγδ0 − δ1 Aαγ + βqα, M = pqα + βqδ0 ,
N = pqδ0 − δ1 Aα, p = δ0 + δ2 + δ3 , q = δ0 + δ1 .
We note that Eq. (3.2) has a real positive root I ∗ if the following inequalities hold:
αβ
1 < R0 < 1 + , (3.3)
pδ0 γ
δ1 Aα
where R0 = δ0 pq is the basic reproductive number.
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Knowing the value of I ∗ , the values of S ∗ and E ∗ can then be computed from
(3.1a) and (3.1b), respectively. This shows that the endemic equilibrium P ∗ exists
under condition (3.3).
Remark: If R0 exceeds the upper bound given by (3.3) for the existence of endemic
equilibrium, then there may exist more than one endemic equilibrium points. How-
ever, in this paper we are concentrating on the existence of unique equilibrium and
its stability.
Now we study the local and global stability behavior of the above two equilibria.
To study the local stability behavior of the equilibria of model system (2.3), we
compute the variational matrices corresponding to each equilibrium point.
Let M0 be the variational matrix corresponding to P0 . Then we have
 
−δ0 0 −αA/δ0
M0 =  0 −q αA/δ0 .
0 δ1 −p
From the above matrix, we note that one eigenvalue of M0 is −δ0 (which is negative)
and other two eigenvalues have negative real parts if only if R0 < 1. Thus we can
state the following theorem.
Theorem 3.1. The disease-free equilibrium point P0 ( δA0 , 0, 0) is locally asymptot-

ically stable if R0 < 1 and is a saddle point with two-dimensional stable manifold
and one-dimensional unstable manifold if R0 > 1.
Now the variational matrix M ∗ corresponding to P ∗ is given by

 
−(δ0 + αI ∗ ) 0 −αS ∗
 αI ∗ −q αS ∗ 
M∗ =  .
2βI ∗
0 δ1 −p − (1+γI ∗2 )2
The characteristic equation of M ∗ is given by
λ3 + A1 λ2 + B1 λ + C1 = 0,
where
2βI ∗
A1 = δ0 + αI ∗ + p + q + ,
(1 + γI ∗2 )2

2βI ∗
B1 = p + (δ0 + αI ∗ + q) + q(δ0 + αI ∗ ) − αδ1 S ∗ ,
(1 + γI ∗2 )2

∗ 2βI ∗
C1 = q(δ0 + αI ) p + − αδ0 δ1 S ∗ .
(1 + γI ∗2 )2
By the Routh–Hurwitz criteria, all eigenvalues of M ∗ will have negative real parts
if and only if
A1 > 0, C1 > 0 and A1 B1 > C1 .
We note that A1 is always positive and thus we can state the following theorem.
1350023-9
Dubey et al.
Theorem 3.2. The endemic equilibrium P ∗ (S ∗ , E ∗ , I ∗ ) is locally asymptotically

stable iff the following inequalities hold :
C1 > 0 and A1 B1 > C1 . (3.4)
In the next theorem, we are able to find sufficient conditions for P ∗ to be globally
asymptotically stable.
Theorem 3.3. Let the following inequalities hold in Ω:

γA2 < δ02 , (3.5a)
(k1 αA + k2 δ0 δ1 )2 < k1 k2 δ02 q(p + k ∗ ), (3.5b)
where k1 , k2 and k ∗ are given in Appendix A.
Then P ∗ is globally asymptotically stable with respect to all solutions initiating

in the interior of the positive octant Ω (for proof, see Appendix A).
We note that if γ and A are small enough and β is large enough, then conditions
(3.5a) and (3.5b) are satisfied. When γ decreases and β increases, the treatment rate
h(I) increases. This implies that by decreasing γ and by increasing β, the treatment
rate can be increased and the system can be made globally asymptotically stable.
It may also be noted that by decreasing the recruitment rate A the possibility of
the system to be globally asymptotically stable is more plausible.
The above analysis shows that as the treatment is increased, the endemic equilib-
rium which was previously locally asymptotically stable will be globally asymptoti-
cally stable. The local stability shows that the disease persists in the neighborhood
of endemic equilibrium. It does not give any information outside the neighborhood.
The global stability shows that the disease persists in a finite region Ω.
βI 2
From Eq. (3.1c), it can easily be seen that as the treatment rate h(I) = 1+γI 2
increases, the equilibrium level of infectives decreases, and consequently from

Eqs. (3.1a) and (3.1b) it follows that equilibrium level of susceptibles increases
whereas the equilibrium level of exposed individuals decreases. Thus, we conclude
that higher level of treatment would cause reduced level of infection in the popula-
tion which in turn would lead to lesser number of people getting exposed and more
number of people susceptible.
Case II: Holling type IV
Now we shall take
βI
h(I) = I2
, I ≥ 0, β, a, b > 0.
a +I +b
We note that h(I) is continuously differentiable function which satisfies:
(i) h(0) = 0,
2
β(b− Ia )
(ii) h (I) = 2 > 0 if A2 < δ02 ab and h (I) < 0 if A2 > δ02 ab,
( Ia
+I+b)2
βI
(iii) lima→∞ h(I) = I+b .
1350023-10
In this case we have the following system:

dS
= A − δ0 S − αSI ,
dt
dE
= −δ0 E − δ1 E + αSI ,
dt (3.6)
dI βI
= −δ0 I − δ2 I + δ1 E − δ3 I − I2
,
dt a +I +b
S(0) > 0, E(0) ≥ 0 and I(0) ≥ 0.
It can easily be verified that model system (3.6) has a disease-free equilibrium
P¯0 ( δA0 , 0, 0), which always exists and an unique endemic equilibrium P̄ (S̄, Ē, I)
¯
which exists if the following inequalities hold:
1 < R1 < αm ,
αδ1 A
where R1 = is the basic reproduction number for model system (3.6) and
δ0 q(p+ βb )

p(δ0 + αa) 1
αm = min , [p(δ0 + αb) + αβ] .
δ0 (p + βb ) δ0 (p + βb )
By the Routh–Hurwitz criteria, the following results can be established immedi-
ately.
Theorem 3.4. The disease-free equilibrium P̄0 is locally asymptotically stable
if R1 < 1 and is a saddle point (with two-dimensional stable manifold and one-
dimensional unstable manifold) if R1 > 1.
¯ is locally asymptotically
Theorem 3.5. The endemic equilibrium point P̄ (S̄, Ē, I)
stable iff the following inequalities hold :
A2 > 0, C2 > 0 and A2 B2 > C2 , (3.7)

where
A2 = δ0 + αI¯ + p + q + J,
¯ − αδ1 S̄,
¯ + J) + q(δ0 + αI)
B2 = q(p + J) + (δ0 + αI)(p
¯
C2 = (δ0 + αI)q(p + J) − δ0 δ1 αS̄, and
¯2

β(b − Ia )
J= = h (I).
¯
I¯2 ¯ 2
( + I + b)
a
Remark: If I¯2 < ab, then A2 > 0.

We have the following result for the global stability of endemic equilibrium P̄ .
Theorem 3.6. Let the following inequalities hold in Ω:
A2 < δ02 ab, (3.8a)
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Dubey et al.
bδ0
I¯ < , (3.8b)
A
(k3 αA + k4 δ0 δ1 )2 < k3 k4 δ02 q(p + k̄), (3.8c)
where k3 , k4 and k̄ are given in Appendix B.

Then P̄ is globally asymptotically stable with respect to all solutions initiating
in the interior of the positive octant Ω.
From the above theorem, we note that by decreasing the recruitment rate A
of the susceptible population, conditions (3.8a) and (3.8b) can be made satisfied.
By increasing the values of parameters a and β, the treatment rate h(I) can be
increased and in such a case condition (3.8c) may be satisfied. This shows that
by decreasing A and by increasing a and β, the system can be made globally
asymptotically stable. Again as in the case of Holling type III recovery, it can
be seen from the equilibrium analysis of model (3.6) that the infected individuals
will settle down at a lower equilibrium level and susceptible individuals at higher
equilibrium level by increasing the treatment rate.
Remark: Holling type II functional response is a special case of Holling type IV.
It may be noted that if a is very large enough, then the treatment rate function
h(I) = I 2 βI βI
reduces to h(I) = I+b βI
= 1+γI , where γ = 1b and it has been studied
a +I+b
without exposed class by Zhang and Suo.29 However, we shall mention briefly the
βI
results obtained for model (2.2) when h(I) = 1+γI . In such a case, model (2.2) has
two equilibrium points, namely, P̃0 ( δA0 , 0, 0) and P̃ ∗ (B̃ ∗ , Ñ ∗ , Ẽ ∗ ).
The equilibrium point P̃0 ( δA0 , 0, 0) is
(i) locally asymptotically stable if R2 < 1, and

(ii) unstable if R2 > 1,
αAδ1
where R2 = δ0 q(p+β) is the basic reproduction number for model (2.2) in the case
of Holling type II treatment rate.
The equilibrium point P̃ ∗ (B̃ ∗ , Ñ ∗ , Ẽ ∗ ) exists if the following inequalities hold:
α p
1 < R2 < + .
γδ0 P +β
Under an analysis similar to the previous cases, we can state the following results.
Theorem 3.7. The equilibrium point P̃ ∗ (B̃ ∗ , Ñ ∗ , Ẽ ∗ ) is locally asymptotically sta-

ble iff
C0 > 0 and A0 B0 > C0 ,
1350023-12
where
β
A0 = (δ0 + p + q + αI˜∗ ) + > 0,
(1 + γ I˜∗ )2

β ∗ β
B0 = q p + ˜
+ (δ0 + αI ) p + + q(δ0 + αI˜∗ ) − αδ1 S̃ ∗ ,
(1 + γ I˜∗ )2 (1 + γ I˜∗ )2

β
C0 = (δ0 + αI˜∗ ) q p + − αδ1 S̃ ∗ + δ1 α2 S̃ ∗ I˜∗ .
(1 + γ I˜∗ )2
Theorem 3.8. The equilibrium point P̃ ∗ (B̃ ∗ , Ñ ∗ , Ẽ ∗ ) is globally asymptotically

stable if the condition holds in Ω:
2
A β
l 1 α + l 2 δ1 < l1 l2 q p + ,
δ0 1 + γ I˜∗
where
(α0 + αI˜∗ )q 2α2 A2
l1 = , l2 = .
2α2 I˜∗2 δ02 (δ0 + αI˜∗ )(p + β
1+γ I˜∗
)
4. Numerical Simulations
In order to illustrate the results obtained in previous sections, we performed com-
puter simulations using MATLAB 6.1. We chose the following set of values of param-
eters (other set of parameters may also exist)
A = 7.0, δ0 = 0.02, δ1 = 0.2, δ2 = 0.025,
δ3 = 0.03, α = 0.003, β = 0.3, γ = 0.04
with initial conditions
S(0) = 210.0, E(0) = 10.0, I(0) = 8.0. (4.1)
For the above set of values of parameters, it can easily be seen that condition
(3.3) for the existence of the interior equilibrium P ∗ (S ∗ , E ∗ , R∗ ) is satisfied. Thus,
P ∗ (S ∗ , E ∗ , R∗ ) exists and it is given by
S ∗ = 252.0905, E ∗ = 8.9009, I ∗ = 2.5893.
It may further be noted that both the inequalities in Eq. (3.4) are satisfied for the
set of values of parameters given in (4.1). This shows that the interior equilibrium
P ∗ is locally asymptotically stable.
Now we present the simulation results of model (2.3) in Figs. 2–5, and the
comparative results of models (2.3) and (3.6) in Figs. 6–8. The behavior of S, E
and I with respect to time t are plotted in Fig. 2 from which we note that the
trajectories approach to the endemic equilibrium P ∗ (252.0905, 8.9009, 2.5893). It
1350023-13
Dubey et al.
255 11
250 10.5
245
10
240
9.5
235
E→
S→
230 9
225
8.5
220
8
215
7.5
210
205 7
0 100 200 300 400 500 0 100 200 300
time → time →
(a) (b)
5.5
4.5
I→
3.5
2.5
2
0 100 200 300
time →
(c)
Fig. 2. (a) Susceptible individuals, (b) exposed individuals and (c) infected individuals approach-
ing endemic equilibrium P ∗ (252.0905, 8.9009, 2.5893).
may also be noted here that conditions (3.5a) and (3.5b) in Theorem 3.3 are not
satisfied for the set of values of parameters chosen in (4.1). Since conditions (3.5a)
and (3.5b) are sufficient (not necessary) for P ∗ to be globally asymptotically stable,
no conclusion can be drawn at this stage regarding global stability behavior of P ∗ .
It may be noted from Fig. 2(a) that the number of susceptible individuals
increases sharply with time till a steady state is acquired. This increase in sus-
ceptible individuals is dependent on the recruitment rate (A) that is greater than
the decline caused due to its natural death rate and infection. In Fig. 2(b), it is
1350023-14
IV 1
IV 2
IV 3
IV 4
IV 5
20
IV 6
15
I →
10
0
0
100 0
20
200 40
60
S→ 300 80 E →
Fig. 3. Global stability of P∗

= (14.9409, 1.8118, 1.0105). Trajectories initiating at different
initial values (IV) as mentioned in text approach and enter the infected steady state P ∗ .
260 6
250 α = 0.003
5.5 α = 0.0035
α = 0.004
240 α = 0.0045
5 α = 0.005
230 α = 0.0055
4.5
S Population
220
I Population
210 4
200
3.5
190
3
180
2.5
170
160 2
0 50 100 150 200 250 300 350 400 450 500 0 50 100 150 200 250 300 350 400 450 500
time → time →
(a) (b)
Fig. 4. (a) and (b) Effect of variation in α on the solution trajectories of susceptible and infectious
populations.
observed that the exposed individuals initially decrease and then increase to get
stabilized at a higher level. The initial decrease in the number of exposed individ-
uals is due to either natural death or transfer of the exposed individuals to the
infected class. Whereas later the increase in exposed individuals takes place when
there are large number of infected people in the population. Figure 2(c) shows a
1350023-15
Dubey et al.
150 8
β=0.00 β=0.26
β=0.28
7 β=0.30
β=0.32
100 6
Infectives
Infectives
5
50 4
0 2
0 100 200 300 400 500 0 100 200 300 400 500
t time
(a) (b)
Fig. 5. (a) and (b) Behavior of infectives without and with treatment.
150 150
β=0.00 β=0.00
β=0.32 β=0.32
β=15.0 β=15.0
100 100
Infectives
Infectives
50 50
0 0
0 100 200 300 400 500 0 100 200 300 400 500
time time
(a) (b)
Fig. 6. (a) and (b) Effect of different treatment on infectives with Holling type III (a) and Holling
type IV (b) removal rate function.
sharp decline in number of infected individuals followed by enhancement and set-

tlement at an elevated level. The decrease in the number of infected individuals is
due to natural death, disease-induced death or natural recovery from the disease.
Moreover, many of these infected individuals also respond to treatment. But some
exposed individuals also enter the infected class, thus the equilibrium value settles
down at a relatively elevated level.
Now we choose another set of values of parameters as given below.
A = 1.2, δ0 = 0.05, δ1 = 0.2, δ2 = 0.003,
(4.2)
δ3 = 0.03, α = 0.03, β = 0.3, γ = 0.00027.
With the above set of values of parameters, we note that the interior equilibrium
P ∗ (S ∗ , E ∗ , I ∗ ) exists and it is given by
S ∗ = 14.9409, E ∗ = 1.8118, I ∗ = 1.0105.
1350023-16
60 90
(250, 10, 8) (250, 10, 8)

(250, 10, 15) 80 (250, 10, 15)
(250, 10, 25) (250, 10, 25)
50
70
40 60
25 25
I Population
I Population
20 50 20
30 15 15
10
10
5 40
−5 0 5 10 15
0 5 10 15 20
20 30
20
10
10
0 0
0 50 100 150 200 250 300 0 50 100 150 200 250 300
time → time →
(a) (b)
Fig. 7. (a) and (b) Effect of removal rate functions on infected population (I) with Holling type
III (a) and Holling type IV (b) removal rates for different initial values. The small inset windows
in both Figs. 7(a) and 7(b) represent trajectories for initial period.
250 250
(250, 10, 8)
(250, 10, 8) (250, 10, 15)
(250, 10, 15) (250, 10, 25)
(250, 10, 25)
200 200
S Population
S Population
150 150
100 100
50 50
0 0
0 50 100 150 200 250 300 0 50 100 150 200 250 300
time → time →
(a) (b)
Fig. 8. (a) and (b) Effect of removal rate functions on susceptible population (S) with Holling
type III (a) and Holling type IV (b) removal rates for different initial values.
1350023-17
Dubey et al.
It may be noted here that the value of γ in Eq. (4.2) is much more smaller than
its value in Eq. (4.1). Thus, for the values of parameters chosen in Eq. (4.2), the
treatment rate is high in comparison to the treatment rate corresponding to the
values of parameters chosen in Eq. (4.1).
It can easily be seen that all conditions of Theorems 3.2 and 3.3 are satisfied for
the set of values of parameters given in (4.2). This shows that P ∗ is locally as well as
globally asymptotically stable. We also plotted trajectories starting with different
initial values (IV). Trajectories in green starts at IV1 = (210, 10, 6), red starts at
IV2 = (150, 20, 5), blue starts at IV3 = (250, 2, 20), black starts at IV4 = (25, 2, 20)
and magenta starts at IV5 = (20, 2, 5). We note that all the trajectories (see Fig. 3)
approach and enter P ∗ = (14.9409, 1.8118, 1.0105).
We studied the effect of variation in infection rate α for the set of values
of parameters given in Eq. (4.1). The corresponding trajectories are plotted in
Figs. 4(a) and 4(b). Figure 4(a) shows that S decreases as α increases. It seems that
the point at which final equilibrium attained depends on the rate of infection (infec-
tivity). If α is in a smaller range, then S increases with respect to time and settles
down at its equilibrium level for a fixed α. This implies that in a given population
when the infection rate is less, then more people are susceptible. This may be due to
the fact that the recruitment rate is much higher than the decline due to conversion
to exposed class. When α increases beyond a certain level, initially S decreases and
after certain time it starts increasing and then attains its steady state. This could be
happening because at high infectivity more people would get converted to exposed
class as compared to the people getting recruited in susceptible class. The decline
in susceptible class may take place because the infected individuals who have recov-
ered would also develop acquired immunity and thus no longer be susceptible to the
re-infection by the same causative agent. An initial decline in susceptible followed
by a slight increase in type III recovery may also be due to the fact that as the
number of infected increases, the treatment increases and subsequently the recovery
rate also increases. This forces the number of infected to decrease and therefore an
increase in susceptible. Besides this, some new member will also be recruited by
birth to susceptible class and thus settles down at a slightly elevated level.
From Fig. 4(b), we note that I increases as α increases. If α is large enough, then
I initially increases rapidly and after showing an oscillatory behavior it obtains its
equilibrium level. This would happen because as the rate of infection increases there
would be a sudden increase in the number of infected people (because of conver-
sion from susceptible). This number is subsequently brought down due to effective
treatment which controls the situation and keeps the population in a steady state.
This steady state is attained at a higher value in diseases with higher infectivity
and limited treatment such as AIDS. In such cases a large number of people may
get infected.
If the rate of infection is small, I settles down at a lower value of steady state
after showing oscillatory behavior. When infectivity is less, then obviously lesser
1350023-18
people will get infected initially but gradually with time the number of infected
people will built up till it attains a steady state. Note that the final steady state
depends upon both infectivity as well as treatment. But in case of mild infections
the number of people getting infected will remain relatively low, thus settling at
lower value. It may be noted that the legends for Figs. 4(a) and 4(b) are same.
Figure 5(a) shows the behavior of infectives with respect to time t in the absence
of any treatment (β = 0). From this figure we note that the number of infected
individuals increase very fast, then decrease and settle down at a relatively higher
equilibrium level. This decrease may be due to the recovery of infected individ-
uals by the immune response of the body. Since only immune response is not
enough to control the infection, thus infected individuals settle down at a rela-
tively higher equilibrium level. Figure 5(b) shows the effect of treatment rate β
on the infectious population I with respect to time t. This figure shows that I
decreases as the treatment rate β increases. It is also observed that the number
of infectious populations initially decreases for some time and with little increase
it settles down at its equilibrium level. This is due to the fact that as the disease
is not getting totally eradicated it will persist in the population but at a much
lower level. This pattern observed here may be due to treatment as well as immune
response.
The effect of treatment in the case of Holling type III and IV recovery are shown
in Figs. 6(a) and 6(b), respectively. Figure 6(a) shows that as the treatment rate
increases, the number of infected individuals decreases and it tends to zero at high
treatment rate (β = 15). Figure 6(b) shows that I decreases as β increases. If β
is high (β = 15), in the case of type IV recovery the infected individuals show
an oscillatory behavior and finally it settles down at a higher equilibrium level as
compared to the type III recovery. It may be noted here that in case of type III
recovery [see Fig. 6(a)], the number of infectives has drastically declined to almost
zero for intermediate and high treatment values whereas when the treatment is very
less, then the infected population stabilizes at a relatively high level. In contrast to
this in type IV recovery [see Fig. 6(b)], when the treatment is low or intermediate
the infectives have settled down at a high value. But when the treatment is high,
then the infectives have stabilized at a lower level but not negligible (unlike type III
recovery). This is because in Holling type III, the treatment persists at saturation
level and therefore the number of infectives declines to almost zero at intermedi-
ate and high levels of treatment but remains persistent at low level of treatment.
Whereas in Holing type IV, the treatment itself declines (due to resource limitation)
after attaining a maximum value, and thus the infection is never cleaned from the
population.
The dynamics of infectious population with Holling type III and IV treatment
rates are presented in Figs. 7(a) and 7(b), respectively. For Holling type III treat-
ment rate we chose γ = 0.05 and then for Holling type IV treatment rate we choose
β = 15, a = 150, b = 75, keeping all other parameters same as in Eq. (4.1). We
1350023-19
Dubey et al.
plotted the solution trajectories initiating from different initial points: S(0) = 250,
E(0) = 10 and for I(0) we choose 8, 15 and 25, respectively. It may be noted
from Fig. 7(a) that for smaller initial value of infectious populations (I(0) = 8),
the infectious individuals first decrease and then settle to steady state whereas for
I(0) = 25, infectious individuals first decrease and show some transient oscillation
before settling to its steady state. In order to show the initial pattern of infectious
population clearly, we plotted the trajectories for first 20 days in a separate window
box. The initial difference in behavior when the initial population size is high may
be attributed to the fact that in this condition because of higher population density
more people will contact disease leading to increased infection in population. But
with time this gradually decays and settles down at the equilibrium level. But for
low initial population size, there is only a decline in the infectives before reaching
to its steady state in the case of Holling type III treatment rate. Further, in the
case of Holling type IV treatment rate [see Fig. 7(b)] it is observed that infected
population shows oscillations before settling to steady state. As noted from the
window box in Fig. 7(b), if the number of initially infected individuals is small,
then there is an increase in the infected population at first, whereas when initially
infected population is more, then infected population first decreases and then fol-
low the pattern of transient oscillations and finally settles down at its equilibrium
level. Here the situation is slightly different from Holling type III treatment func-
tion. In the case of Holling type IV treatment function, in both small and large
population sizes at initial time, there is an oscillatory behavior before settling to
equilibrium.
We also plotted the behavior of susceptible population, in case of Holling type
III and IV treatment rates for the same set of parameter and initial values as above,
in Figs. 8(a) and 8(b), respectively. We note that in case of Holling III treatment
rate the susceptible population first decays and reaches to minima and then finally
increases to reach and enter the steady state value for all lower, intermediate and
higher population density at initial time [see Fig. 8(a)]. Further in case of Holling
type IV treatment we note that before reaching the steady state, susceptible pop-
ulation shows transient oscillations for all the three initial values [see Fig. 8(b)].
It may further be noted that the behavior of susceptible population is reversed of
the infectious population in both Holling type III and IV treatment functions. This
emphasizes the fact that susceptible population upon infection gets converted to
infectious population, and thus increase in one leads to decrease in another and
vice versa. The susceptible population first declines before attaining steady state
for Holling type III and IV treatment functions whereas the infectious population
first increases in the case of both Holling type III and IV treatment function.
5. Conclusions
In this paper, an SEIR mathematical model is proposed and analyzed. This model
consists of four variables, namely, susceptible, exposed, infectious and recovered
1350023-20
individuals. This paper is, in fact, the generalization of the work29 by introducing
exposed class in the model and by taking two different types of treatment rates.
Zhang and Suo29 studied an SIR model by taking the treatment rate in the form of
Holling type II. We have considered two different types of treatment rates for the
infected individuals by taking in the form of Holling type III and IV. In both the
types of treatment functions, the basic reproduction number R0 and R1 are reported
with the characteristic: in the case of Holling type III treatment rate, the disease
persists if 1 < R0 < 1 + pδαβ
0γ
and in the case of Holling type IV treatment rate, the
disease persists if 1 < R1 < αm . In both the cases, the model has been analyzed
using stability theory of ordinary differential equations. Criteria for the disease-
free equilibrium point and the endemic equilibrium point to be locally and globally
asymptotically stable are obtained. It has been shown that in the case of Holling
type III recovery the disease-free equilibrium point is locally asymptotically stable
if the basic reproduction number R0 < 1 and unstable if R0 > 1. Similar results are
obtained in the case of Holling type IV recovery function. It has also been found
that under certain conditions, the endemic equilibrium can also be made locally
as well as globally asymptotically stable. The model of Zhang and Suo29 is further
generalized in the case of Holling type II treatment function by taking into account
the exposed class. Computer simulation has also been performed to investigate the
dynamics of interacting subpopulations.
It has been observed that the number of infectives as well as susceptibles in
all three cases (Holling types II, III and IV) depend upon the treatment function
but do so in a variable manner. In Holling type II, the treatment slowly increases,
then attains its peak and finally settles down at its saturation value. This case is
applicable when availability of treatment is poor including newly emergent diseases.
In such a case a large proportion of population may get infected as in the case of
highly infectious diseases such as HIV.
In Holling type III, the treatment initially increases fast, then increases slowly,
attains its peak and is finally stabilized. For different initial values, the infected
population shows different patterns. This indicates that the dynamics of infected
population depends on the parameters as well as initial values. Here the quan-
tum of infection (prevalence of disease as well as the new infection) depends upon
the maximum treatment capacity in the community. The infectivity is high when
the treatment is low and vice versa. Our numerical experiment also shows that
in case of Holling type III treatment rate function, the susceptible individuals first
decrease and attain its minimum value and then start increasing to enter the steady
state.
In the case of Holling type IV, the treatment increases slowly, attains its peak
and then decreases to zero. Here the infected population initially increases and then
shows transient oscillations and finally it is stabilized at a much lower equilibrium
level. This pertains to the situation when the disease has been brought under control
by an effective treatment. In case of Holling type IV treatment rate function, the
1350023-21
Dubey et al.
susceptible individuals first show transient oscillations and then settle down at its
equilibrium level.
Acknowledgments
The authors are thankful to the anonymous referees for their valuable sug-
gestions that lead to a definite value addition in the paper. The first author
(BD) gratefully acknowledges the support received by UGC, New Delhi, Grant
No. F.510/2/DRS/2010 (SAP-I) and the second author (AP) acknowledges the
support received from DST Grant No. SR/WOS-A/MS-21/2011(G).
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Appendix A. Proof of Theorem 3.3

Consider the following positive definite function about P ∗ :
1 1 1
V (t) = (S − S ∗ )2 + k1 (E − E ∗ )2 + k2 (I − I ∗ )2 , (A.1)
2 2 2
where k1 and k2 are positive constants to be chosen suitably later on. Differentiat-
ing V with respect to time t along the solutions of model (2.3), a little algebraic
manipulation yields:
dV 1 1
= − a11 (S − S ∗ )2 + a12 (S − S ∗ )(E − E ∗ ) − a22 (E − E ∗ )2
dt 2 2
1 1
− a11 (S − S ∗ )2 + a13 (S − S ∗ )(I − I ∗ ) − a33 (I − I ∗ )2
2 2
1 1
− a22 (E − E ∗ )2 + a23 (E − E ∗ )(I − I ∗ ) − a33 (I − I ∗ )2 , (A.2)
2 2
where

∗ β(I + I ∗ )
a11 = δ0 + αI > 0, a22 = k1 q > 0, a33 = k2 p + ,
(1 + γI 2 )(1 + γI ∗2 )
a12 = k1 αI ∗ , a13 = −αS, a23 = k1 αS + k2 δ1 .

dV
Sufficient conditions for dt to be negative definite are that the following inequalities
hold:
a212 < a11 a22 , (A.3)
a213 < a11 a33 , (A.4)
a223 < a22 a33 . (A.5)
q(δ0 +αI ∗ )
If we choose k1 = 2α2 I ∗2
, then the condition (A.3) is automatically satisfied.
If we choose
2α2 A2
k2 = ,
δ02 (δ0 + αI ∗ )(p + k ∗ )
where
βI ∗ δ02
k∗ = ,
(1 + γI ∗2 )(δ02 + γA2 )
then (3.5a) ⇒ (A.4). We also note that (3.5b) ⇒ (A.5). This shows that V is a
Lyapunov function with respect to all solutions initiating in the interior of the
positive octant Ω, proving the theorem.
Appendix B. Proof of Theorem 3.6

We take the following positive definite function about the equilibrium point P̄
1 1 1
V̄ (t) = (S − S̄)2 + k3 (E − Ē)2 + k4 (I − I)
¯ 2. (B.1)
2 2 2
1350023-24
Under an analysis similar to the proof of Theorem 3.3 as given in Appendix A and
by choosing
q(δ0 + αI)¯ 2α2 A2
k3 = and k4 = 2 ¯ + k̄) and
2α2 I¯ δ (δ0 + αI)(p
0
AI¯
β(b − aδ 0
)
k̄ = ¯2 2
,
( Ia + I¯ + b)( aδ
A
2 + δ
A
0
+ b)
0
it can be cheeked that V̄ is a Lyapunov’s function under conditions (3.8a) and

(3.8b) and hence the theorem follows.
1350023-25

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September 11, 2013 15:35 WSPC/S0218-3390 129-JBS 1350023

Journal of Biological Systems

MODELING AND ANALYSIS OF AN SEIR MODEL

B. DUBEY∗,§ , ATASI PATRA∗,¶ , P. K. SRIVASTAVA‡,

Indian Institute of Technology

Received 18 July 2012

Modeling and Analysis of an SEIR Model

Modeling and Analysis of an SEIR Model

Case I: Holling type III

Fig. 1. Schematic diagram of the interacting populations.

Modeling and Analysis of an SEIR Model

where βγ is the maximal treatment capacity of some community.

endemic equilibrium. The stability of the disease-free equilibrium is determined

Lemma 3.1. The set Ω = {(S, E, I) : S > 0, E ≥ 0, I ≥ 0, S + E + I ≤ δ0 }

Modeling and Analysis of an SEIR Model

Theorem 3.1. The disease-free equilibrium point P0 ( δA0 , 0, 0) is locally asymptot-

Now the variational matrix M ∗ corresponding to P ∗ is given by

Theorem 3.2. The endemic equilibrium P ∗ (S ∗ , E ∗ , I ∗ ) is locally asymptotically

Theorem 3.3. Let the following inequalities hold in Ω:

Then P ∗ is globally asymptotically stable with respect to all solutions initiating

increases, the equilibrium level of infectives decreases, and consequently from

Modeling and Analysis of an SEIR Model

In this case we have the following system:

A2 > 0, C2 > 0 and A2 B2 > C2 , (3.7)

Remark: If I¯2 < ab, then A2 > 0.

where k3 , k4 and k̄ are given in Appendix B.

The equilibrium point P̃0 ( δA0 , 0, 0) is

(i) locally asymptotically stable if R2 < 1, and

Theorem 3.7. The equilibrium point P̃ ∗ (B̃ ∗ , Ñ ∗ , Ẽ ∗ ) is locally asymptotically sta-

C0 > 0 and A0 B0 > C0 ,

Modeling and Analysis of an SEIR Model

Theorem 3.8. The equilibrium point P̃ ∗ (B̃ ∗ , Ñ ∗ , Ẽ ∗ ) is globally asymptotically

Modeling and Analysis of an SEIR Model

Fig. 3. Global stability of P∗

sharp decline in number of infected individuals followed by enhancement and set-

Modeling and Analysis of an SEIR Model

(250, 10, 8) (250, 10, 8)

Modeling and Analysis of an SEIR Model

Modeling and Analysis of an SEIR Model

Modeling and Analysis of an SEIR Model

Appendix A. Proof of Theorem 3.3

a12 = k1 αI ∗ , a13 = −αS, a23 = k1 αS + k2 δ1 .

Appendix B. Proof of Theorem 3.6

Modeling and Analysis of an SEIR Model

it can be cheeked that V̄ is a Lyapunov’s function under conditions (3.8a) and

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