Nonlinear Dyn
DOI 10.1007/s11071-010-9805-4
O R I G I N A L PA P E R
Effect of delay on a predator–prey model with parasitic
infection
Pei Yongzhen · Li Shuping · Li Changguo
Received: 13 November 2009 / Accepted: 9 August 2010
© Springer Science+Business Media B.V. 2010
Abstract In the paper an eco-epidemic system with
delay and parasitic infection in the prey is investigated.
The conditions for asymptotic stability of steady states
are derived and the length of the delay preserving
the stability is also estimated. Further, the criterion
for existence of Hopf-type small amplitude periodic
oscillations of the predator and prey biomass is de-
rived. Numerical results indicate that the delay does
not affect the stability of the system in the process
but makes all populations oscillate more intensively.
In addition, the results show that the recovery makes
the levels of the infected prey and the predator be-
come lower but makes the sound prey higher in limit
time.
Keywords Time delay · Parasitic infection ·
Asymptotic stability · Bifurcation · Oscillations
P. Yongzhen () · L. Shuping
School of Science, Tianjin Polytechnic University,
Tianjin 300160, China
e-mail: pppyongzhen@163.com
P. Yongzhen
e-mail: peiyongzhen@sina.com
L. Changguo
Department of Basic Science of Institute of Military
Traffic, Tianjin 300161, China
1 Introduction
Infectious diseases can have regulating effects not only
on their host population but also on other species their
host interacts [1–3]. Ecologists and epizootiologists
alike become increasingly interested in the structuring
effects of parasites and pathogens within food webs
and multiple-species communities [4, 5]. In particu-
lar, diseases in a prey–predator system have received
significant interest in recent years. Mukherjee [6] an-
alyzed a prey–predator system in which some mem-
bers of the prey population and all predators are sub-
jected to infection by a parasite. Frank and Kirsten
[7] considered the invasion of a resident predator–
prey system by an infectious disease with frequency-
dependent transmission spreading within the predator
population. Martcheva [8] investigated the impact of
predation on the coexistence and competitive exclu-
sion of pathogen strains in the prey. Xiao and Chen
[9] proposed a system of retarded function differential
equations as a predator–prey model with disease in the
prey in which there is a time delay due to gestation of
predator. Hadeler and Freedman [10] developed and
analyzed a predator–prey model in which both species
are subjected to parasitism.
Numerous studies have shown that predators take
a disproportionate number of prey infected by para-
sites [11–13]. The review of Holmes and Bethel [14]
contains many examples in which the parasite changes
the external features or behavior of the prey, so that
infected preys are more vulnerable to predation. Dis-

eases in animals caused by macroparasites are often
more complicated, since the severity of the disease
usually depends on the parasitic load in the animal.
Hudson et al. [15] formulated models for macropara-
sitic infections in red grouse and looked at situations
in which parasitic infections of the prey made them
more vulnerable to predation. Packer et al. [16] exam-
ined the effects on prey population sizes of predator re-
moval in models of microparasitic and macroparasitic
infections with a constant predator population size.
Although many authors proposed and studied dif-
ferent predator–prey models in presence of disease,
they ignored the recovery of infective individuals. In
an SIS model, susceptible individuals become infec-
tive after contact with infective individuals. Infective
individuals return to the susceptible class after an in-
fective period. Models of this type not only form a
basis for most other epidemiological models, but are
directly applicable to gonorrhea and other sexually
transmitted diseases or bacterial infections where ex-
posed individuals typically become infective within 24
hours and do not gain immunity to the disease once the
infection is passed [17]. Recently, Venturino [18] con-
sidered similar SI and SIS models with disease spread
among the prey. Hethcote [19] has shown the effects
of the greater vulnerability to predation of the infected
prey in SIS models. As far as SIS models were con-
cerned, authors supposed that the recovery and infec-
tion arose simultaneously [20–24]. It seems reason-
able to assume that the recovery of the infective prey
after infection will not be instantaneous, but mediated
by some discrete time lag required for the infectious
period.
However, the consequences of prey infection with
delay are examined both empirically and theoretically
relatively rarely (see the review [25]). In this paper we
consider a time-delayed predator–prey model with an
infectious disease circulating in the prey population,
namely the SIS model. In order to investigate how the
predation process influences the epidemics, we con-
sider the simple case when the predator mainly eats
the infected prey. This is in accordance with the fact
that the infected individuals are less active and can be
caught more easily, or the behavior of the prey indi-
viduals is modified such that they live in parts of the
habitat which are accessible to the predator (fish and
aquatic snails staying close to water surface, snails
staying on the top of the vegetation rather than under
the plant cover) [26]. Peterson and Page [27] have in-
P. Yongzhen et al.
dicated that wolf attacks on moose are more often suc-
cessful if the moose is heavily infected by Echinococ-
cus granulosus.
This paper is organized as follows. In the next sec-
tion we establish the model discussed in this paper and
obtain the condition the interior equilibrium exists. In
Sect. 3 the condition for asymptotic stability of steady
state is derived. The length of the delay preserving the
stability is also estimated. The criterion for existence
of Hopf-type small amplitude periodic oscillations of
the predator and prey biomass is obtained. In Sect. 4
numerical simulations are given and a brief conclusion
is given at last.
2 The mathematical model
In this section we shall consider an eco-epidemiologi-
cal system consisting of three species, namely, the
sound prey (which is susceptible), the infected prey
(which becomes infective by some viruses) and the
predator population. Although with high disease mor-
tality rate, some animals, say roe and antelope, can still
recover from foot-and-mouth disease. When incorpo-
rating the recovery of the infected prey with the length
of the infectious period, the model with delay is ex-
pressed as
dS(t)
= α − μ1 S(t) − βS(t)I (t) + γ I (t − τ ),
dt
dI (t)
= βS(t)I (t) − μ2 I (t) − γ I (t)
dt
(2.1)
σ P (t)I (t)
− ,
1 + I (t)
dP (t) σ P (t)I (t)
= − μ3 P (t),
dt 1 + I (t)
We make the following assumptions for our models
(Fig. 1):
(H1 ): Assume that the total prey population is com-
posed of two population classes: the class of sus-
ceptible prey, denoted by S(t), and the class of
the infected prey, denoted by I (t). The size of
predator population denoted by P (t).
(H2 ): Assume that the recruitment rate of the prey
population (it includes immigrants and the new-
borns that are assumed to be susceptible) is de-
noted by α. And the natural death rates of sus-
ceptible prey, infected prey and predator are de-
noted by μ1 , μ2 and μ3 , respectively.
Effect of delay on a predator–prey model with parasitic infection

Fig. 1 The transfer

diagram for model (2.1)

(H3 ): Assume that the disease is spread among the three equations of (2.1), one gets
prey population only and the disease is not ge-
netically inherited. The incidence is assumed d(S(t) + I (t) + P (t))
to be the simple mass action incidence βSI , dt
where β > 0 is called the transmission coeffi- = α − μ1 S(t) − μ3 P (t)
cient. The constant γ is a recovery rate, i.e. rate  
+ γ I (t − τ ) − (μ2 + γ )I (t)
with which individuals move from the infected
 
class to the susceptible. The infected popula- ≤ α − μ S(t) + P (t)
tions have a temporary infectious period τ , after  
, + γ I (t − τ ) − (μ2 + γ )I (t)
which the recovered infective revert to the sus-
ceptible class.
where μ = min{μ1 , μ3 }. We consider the following
(H4 ): Assume that the predator eats only the infected
prey with Holling-type response function. The comparison equation:
σI
term 1+I is the capturing of the predator on d(s(t) + p(t))  
the infective prey and also the assimilation of = α − μ s(t) + p(t) ,
dt
the predator from the infective prey capturing,
where σ is the maximum capture rate for the in- and
fective preys. In real ecological sense the cap-
ture and assimilation should not be the equal al- d(i(t))
= γ i(t − τ ) − (μ2 + γ )i(t).
ways the assimilation is lesser than grazing. But dt
for mathematical simplicity we have considered
It follows that
the grazing and assimilation rates equal.
 
The initial conditions for system (2.1) are lim s(t) + p(t) = α/μ.
t→∞
   
φ1 (θ ), φ2 (θ ), ϕ(θ ) ∈ C+ = C [−τ, 0], R3+ , Again by Lemma 2.1 [9], we obtain that limt→∞ i(t) =
φi (0) > 0, ϕ(0) > 0, i = 1, 2, 0. That is, for a positive constant ε0 , i(t) < ε0 holds
for t large enough. Hence for t large enough,
where R3+ = {(S, I, P ) ∈ R3 : S ≥ 0, I ≥ 0,
P ≥ 0}. Therefore, all the standard results on exis- .
s(t) + i(t) + p(t) < α/μ + ε0 = M.
tence, uniqueness and continuous dependence on ini-
tial condition of solutions are evidently satisfied. For By the comparison theorem and non-negativity of
the boundedness of solutions we state the following S(t), I (t) and P (t), we get a positively invariant box
lemma.
= {(S, I, P ) ∈ R3+ : 0 ≤ S ≤ M, 0 ≤ I ≤ M, 0 ≤
P ≤ M} in R3+ such that all solutions with non-
Lemma 2.1 There exists a positively invariant box negative initial conditions approach
as t → ∞. The

= {(S, I, P ) ∈ R3+ : 0 ≤ S ≤ M, 0 ≤ I ≤ M, 0 ≤
proof of Lemma 2.1 is complete. 
P ≤ M} in R3+ such that all solutions with non-
negative initial conditions approach
as t → ∞,
where M is a positive constant. 2.1 Boundary equilibria and their local stability

Proof It is obvious that S(t) ≥ 0, I (t) ≥ 0, P (t) ≥ We start the mathematical analysis by looking at the
0 for non-negative initial conditions. Adding up the equilibria on the boundary of region
and at their
 P. Yongzhen et al.

local stability. Denote (1) Clearly, λ = 0 is not a root of (2.3).

(2) Let f (λ) = λ2 + a0 λ − b0 e−λτ + c0 . From the fact
βα
R1 = , f (0) > 0 and f  (λ) > 0 for λ > 0, it is obtained
μ1 (μ2 + γ ) that (2.3) has no positive real root.
2μ2 (μ2 + γ )[βα − μ1 (μ2 + γ )] (3) It is sufficient to show that (2.3) does not admit a
R2 = ,
(βα − μ1 γ )2 purely imaginary root. In fact, if λ = iω (ω > 0)
σ [βα − μ1 (μ2 + γ )] is a root of (2.3), then by separating the real and
R3 = . imaginary parts we have
μ3 [βμ2 + βα − μ1 (μ2 + γ )]
The system (2.1) has two equilibria on the boundary −ω2 − b0 cos ωτ + c0 = 0 (2.4)
of region
. One is E10 = ( μα1 , 0, 0), the other one is
and
E20 = (S̄, I¯, 0) = ( μ2β+γ , βα−μβμ
1 (μ2 +γ )
2
, 0) if R1 > 1.
Then the following results on the stability of equilibria a0 ω + b0 sin ωτ = 0. (2.5)
E10 and E20 are obtained.
Squaring both sides of (2.4) and (2.5) and adding,
Theorem 2.1 The boundary equilibrium E10 is lo- we have
cally asymptotically stable if R1 < 1. The boundary
 
equilibrium E20 is also locally asymptotically sta- ω4 + a02 − 2c0 ω2 + c02 − b02 = 0. (2.6)
ble, but E10 is unstable if R2 < 1 < R1 , R3 < 1 and
μ2 > γ . Let y = ω2 > 0, then we can write (2.6) as
 
Proof The Jacobian matrix of the model (2.1) at E10 F (y) = y 2 + a02 − 2c0 y + c02 − b02 = 0, (2.7)
are
⎛ ⎞ Noting that c02 − b02 > 0, we have F (0) > 0. Fur-
−μ1 − βα −λτ
μ1 + γ e 0 ther, according to R2 < 1, we can obtain a02 −
⎜ ⎟
J (E10 ) = ⎝ 0 βα
μ1 − μ2 − γ 0 ⎠. 2c0 > 0. We conclude that F (y) = 0 for y = ω2
0 0 −μ3 is impossible.
(4) It is easy to show that (2.3) has no imaginary root
Obviously, E10 is locally asymptotically stable if R1 < whose real part is positive. Otherwise there is an
1. Likewise, the Jacobian matrix of the model (2.1) at imaginary root λ = α + iβ with α > 0. Without
E20 is any loss of generality, we consider β > 0. Then
⎛ ⎞
−μ1 − β I¯ −β S̄ + γ e−λτ 0 we take the real and imaginary parts of (2.3),
⎜ β I¯ β S̄ − μ2 − γ − 1+σ I¯ ⎟ namely
J (E20 ) = ⎝ I¯ ⎠.
σ I¯
0 0 1+I¯
− μ3 α 2 − β 2 + a0 α + c0 = b0 e−ατ cos(βτ ),

Computing directly, the characteristic equation is 2αβ + a0 β = −b0 e−ατ sin(βτ ).


σ I¯   Hence α 2 − β 2 + a0 α + c0 + 2αβ + a0 β =
λ− + μ3 λ2 + a0 λ − b0 e−λτ + c0 = 0, b0 e−ατ [cos(βτ ) − sin(βτ )] which implies that
1+I ¯
(2.2)  
(α − β)2 + a0 (α + β) + c0  ≤ 2b0 .
where a0 = β I¯ + μ1 , b0 = βγ I¯, c0 = β I¯β S̄ and β S̄ −
μ2 − γ = 0 are used. Furthermore, by the positivity of a0 , b0 , c0 , α and
σ I¯ β, we get c0 < 2b0 . However, from μ2 > γ , we
From R3 < 1 it is easy to see that λ1 = 1+ I¯
−
μ3 < 0. So we only have to show that all roots of have c0 > 2b0 . This is a contradiction.
In view of our above discussions, all roots of (2.3)
λ2 + a0 λ − b0 e−λτ + c0 = 0 (2.3)
have negative real parts. The proof of the theorem is
have negative real parts. completed. 
Effect of delay on a predator–prey model with parasitic infection

Parallel conclusions are given in the following (2.1) becomes:

corollary.
du(t)
= −(μ1 + βI ∗ )u(t) − βS ∗ v(t) + γ v(t − τ ),
Corollary 2.1 The boundary equilibrium E10 is lo- dt
cally asymptotically stable provided that γ > βα−μμ1
1 μ2
. dv(t)
= βI ∗ u(t) −
μ3
(βS ∗ − μ2 − γ )v(t)
The boundary equilibrium E20 is also locally asymp- dt σ
(3.1)
totically stable, but E10 is unstable provided that − μ3 w(t),
 dw(t) σ − μ3
σ < μ3 1 +
βμ2
, = (βS ∗ − μ2 − γ )v(t).
βα − μ1 (μ2 + γ ) dt σ
 
βα − μ1 μ2 We compute the eigenvalues of the Jacobian matrix
γ < min μ2 , , at this equilibrium. The eigenvalues satisfy the charac-
μ1
teristic equation:
and
D(λ, τ ) = λ3 + aλ2 + bλ + c + gλe−λτ = 0, (3.2)
(μ2 + γ )[βγ − μ1 (μ2 + γ )] 1
< .
(βα − μ1 γ )2 2μ2 where
μ3
a = (μ1 + βI ∗ ) − (βS ∗ − μ2 − γ ),
σ
3 Qualitative analysis of the interior equilibrium
μ3
with time delay b= (βS ∗ − μ2 − γ )(σ − μ3 )
σ
μ3
Next we are interested in the existence of the inte- − (μ1 + βI ∗ )(βS ∗ − μ2 − γ ) + β 2 S ∗ I ∗ > 0,
σ
rior equilibrium of system (2.1) which is given by μ3
E(S ∗ , I ∗ , P ∗ ), where c= (βS ∗ − μ2 − γ )(σ − μ3 )(μ1 + βI ∗ ) > 0,
σ
α(σ − μ3 ) + γ μ3 g = −βγ I ∗ < 0.
S∗ = ,
μ1 (σ − μ3 ) + βμ3
μ3 We note that λ = 0 is a root (3.2) if and only if c = 0.
I∗ = ,
σ − μ3
3.2 Non-existence of delay induced instability
∗ (βS ∗ − μ2 − γ )(1 + I ∗ )
P = .
σ
To find the conditions for non-existence of delay in-
Clearly, the interior equilibrium E is feasible if R1 > 1 duced instability, we use the following theorem.
and R3 > 1 (that is σ > μ3 (1 + βα−μβμ 2
1 (μ2 +γ )
)). Thus
we see that the existence of interior equilibria depends Theorem 3.1 The necessary and sufficient conditions
on the threshold value of the predator capture of. So for E to be asymptotically stable for all τ ≥ 0 are
the interior equilibrium of the system (2.1) exists if (i) The real parts of all the roots of D(λ, 0) = 0 are
the predator capture the infected prey exceeded certain negative.
threshold value. all real m and any τ ≥ 0, D(mi, τ ) = 0 where
(ii) For √
i = −1.
3.1 Characteristic equation
Here D(λ, 0) = 0 has roots with negative real parts
To investigate the stability of the interior equilibrium provided the system (2.1) is locally asymptotically sta-
E, we have derived the characteristic equation for the ble.
linearization of the model (2.1) near its equilibrium Now for m = 0, D(0, τ ) = c = 0. For m = 0,
E(S ∗ , I ∗ , P ∗ ). Let u(t), v(t) and w(t) be the prospec- D(mi, τ ) = −im3 − am2 + ibm + c + igme−imτ . As-
tive linearized variables of this model. Then system sume the equation D(im, τ ) = 0 holds and separating
 P. Yongzhen et al.

the real and imaginary parts we get initial conditions. Then the system (3.1) can be written
as follows
gm sin mτ + (c − am2 ) = 0,
du(t)
= a1 u(t) + a2 v(t) + a3 v(t − τ ),
gm cos mτ + (bm − m3 ) = 0. dt
dv(t)
Squaring and adding the above two equations we get = b1 u(t) + b2 v(t) + b3 w(t), (3.5)
dt
    dw(t)
m6 + a 2 − 2b m4 + b2 − 2ac − g 2 m2 + c2 = 0.(3.3) = c1 v(t),
dt
Let m2 = n. Substituting into (3.3), we obtain the fol- where
lowing equation
a1 = −(μ1 + βI ∗ ), a2 = −βS ∗ ,
n + An + Bn + C = 0,
3 2
a3 = γ , b1 = βI ∗ ,
μ3
where b2 = − (βS ∗ − μ2 − γ ), b3 = −μ3 ,
σ
A = a 2 − 2b, σ − μ3
c1 = (βS ∗ − μ2 − γ ).
σ
B = b2 − 2ac − g 2 ,
Let ū(s), v̄(s) and w̄(s) be the Laplace transform of
C = c2 > 0.
u(t), v(t) and w(t), respectively. Taking the Laplace
transformation of the system (3.5), we have
By Routh–Hurwitz criterion, we can obtain Re n < 0,
which is contradictive. Therefore the sufficient condi- (s − a1 )ū(s) = a2 v̄(s) + a3 v̄(s)e−sτ
tions for the non-existence of real numbers satisfying
D(mi, τ ) = 0 can be expressed by the sufficient con- + a3 e−sτ K(s) + u(0),
(3.6)
ditions for non-existence of a real n as (s − b2 )v̄(s) = b1 ū(s) + b3 w̄(s) + v(0),
A > 0, B > 0 and AB − C > 0. (3.4) s w̄(s) = c1 v̄(s) + w(0),
0
Thus, all the propositions of the above theorem are where K(s) = −τ e−st v(t) dt.
satisfied if inequalities (3.4) hold and we have the fol- The inverse Laplace transform of ū(s) will have
lowing theorem. terms which exponentially increase with time if ū(s)
has poles with positive real parts. In order for
Theorem 3.2 If A > 0, B > 0, and AB − C > 0, then E(S ∗ , I ∗ , P ∗ ) to be locally asymptotically stable, it
is necessary and sufficient that all poles of ū(s) have
interior equilibrium E is asymptotically stable for all
negative real parts. We shall employ the Nyquist crite-
τ ≥ 0.
rion which states that if s is the arc length of a curve
encircling the right half place, the curve ū(s) will en-
3.3 Length of delay to preserve stability circle the origin a number of times equal to the differ-
ence between the number of poles and the number of
In this section, we assume that in absence of delay the zeroes of ū(s) in the right half plane.
interior equilibrium E is locally asymptotically sta- By Freedman et al. [28], we know that the condi-
ble. By continuity and for sufficiently small τ > 0, tion for local asymptotic stability of the interior equi-
all eigenvalues of (3.2) have negative real parts pro- librium E(S ∗ , I ∗ , P ∗ ) is given
vided one can guarantee that no eigenvalue with posi-
tive real part bifurcates from infinity (which could hap- Im F (iν0 ) > 0, (3.7a)
pen since it is a retarded system). For stability analy- Re F (iν0 ) = 0, (3.7b)
sis we require the Nyquist criterion [28]. To do so, we
consider the system (3.1) and the space of real valued in which F (s) = s 3 + as 2 + bs + c + gse−sτ + c, ν0
continuous functions defined on (τ, ∞) satisfying the is the smallest positive root of (3.7b).
Effect of delay on a predator–prey model with parasitic infection

Now F (iν0 ) = −iν03 − aν02 + ibν0 + c + Then (3.4) will be satisfied and the Nyquist criterion
igν0 (cos ν0 τ − i sin ν0 τ ), the condition (3.7) in our holds for 0 ≤ τ ≤ τ+ , where
case becomes 1
−B1 + (B12 + 4A1 η1 ) 2
τ+ = .
ν03 − bν0 < gν0 cos ν0 τ , 2A1
aν02 − c = gν0 sin ν0 τ . Here τ+ is the estimate of the length of delay for which
the stability is preserved. Hence we can state the fol-
To get an estimate on the length of delay, we utilize lowing result.
the following conditions:
Theorem 3.3 There exists a τ+ such that A1 τ 2 +
ν − bν < gν cos ντ ,
3
(3.8a) B1 τ − η1 < 0 holds for 0 ≤ τ ≤ τ+ . Then τ+ is the
maximum value (length of delay) of τ for which the
aν 2 − c = gν sin ντ . (3.8b)
interior equilibrium E is asymptotically stable.
Therefore, the interior equilibrium E will be stable
3.4 Preservation of stability and bifurcation results
if the inequality (3.8a) holds at ν = ν0 , where ν0 is the
smallest positive root of (3.8b). We shall now estimate Let us consider τ = 0 and assume λ = μ + iν in (3.2).
an upper bound ν+ of ν0 , which would be independent Then separating the real and imaginary parts, we get a
of τ . Then we estimate τ so that (3.8a) holds for all system of transcendental equations as follows
values of ν0 ≤ ν ≤ ν+ , and hence in particular at ν =  
ν0 . Maximizing gν sin ντ subject to | sin ντ | ≤ 1 and μ3 − 3μν 2 + a μ2 − ν 2 + bμ + c + gμ cos ντ e−μτ
| cos ντ | ≤ 1, then we obtain
+ gν sin ντ e−μτ = 0,
(3.12)
aν 2 − c ≤ |g|ν. (3.9) 3μ2 ν − ν 3 + 2aμν + bν − gμ sin ντ e−μτ

Thus the unique positive solution of aν 2 − |g|ν − + gν cos ντ e−μτ = 0.

c = 0 denoted by ν+ is always greater or equal to
We are interested to know the change of stability
ν0 . From the inequality (3.9), one gets ν0 ≤ ν+ if
of the interior equilibrium E which will occur at the
ν+ = |g|+(|g|2a+4ac) . Here we can see that ν+ is in-
2 1/2
values of τ for which μ = 0 and ν = 0. Then (3.12)
dependent of τ . Now we need to estimate τ so that becomes
(3.8a) holds for all ν0 ≤ ν ≤ ν+ . We can rewrite (3.8a)
as a ν̂ 2 − c = g ν̂ sin ν̂ τ̂ ,
ν̂(ν̂ 2 − b) = g ν̂ cos ν̂ τ̂ .
ν 2 < b + g cos ντ . (3.10)
Now eliminating τ̂ , we have
Now substituting ν 2 from (3.8b) to (3.10) and rear-    
ranging, we get ν̂ 6 + a 2 − 2b ν̂ 4 + b2 − 2ac − g 2 ν̂ 2 + c2 = 0.
(3.13)
ag(1 − cos ντ ) + gν sin(ντ ) < ag + ab − c. (3.11)
In order to establish Hopf-bifurcation at τ = τ̂ , we
Using the estimates sin ντ < ντ and 1 − cos ντ = need to analyze dμ dτ (τ̂ ) where μ(τ̂ ) = 0. If this deriv-
2 ≤ 2 ν τ , rearranging, we obtain
1 2 2
2 sin2 ντ ative is positive (negative), then clearly a stabilization
(destabilization) cannot take place at that value of τ̂ .
A1 τ 2 + B1 τ < η1 , Differentiating the system (3.12) with respect to τ and
setting τ = τ̂ , μ = 0 and ν = ν̂, we get
where
dμ dν
1 ξ (τ̂ ) + η (τ̂ ) = M,
A1 = |ag|ν+ 2
, B1 = |g|ν+
2
, dτ dτ
(3.14)
2 dμ dν
−η (τ̂ ) + ξ (τ̂ ) = N,
η1 = ag + ab − c. dτ dτ
 P. Yongzhen et al.

dμ
where and clearly dτ has the same sign as that of ξ M − ηN.
Now

ξ = 3ν̂ 2 − b + g ν̂ τ̂ sin ν̂ τ̂ − g cos ν̂ τ̂ ,

ξ M − ηN = 2ag ν̂ 3 sin ν̂ τ̂
η = 2a ν̂ − g sin ν̂ τ̂ − g ν̂ τ̂ cos ν̂ τ̂ ,  
+ 3g ν̂ 4 − bg ν̂ 2 cos ν̂ τ̂ − g 2 ν̂ 2
M = g ν̂ 2 cos ν̂ τ̂ ,   
= ν̂ 2 3ν̂ 4 + 2 a 2 − 2b ν̂ 2
N = −g ν̂ 2 sin ν̂ τ̂ .  
+ b2 − 2ac − g 2 > 0

Solving the system (3.14) gives provided A > 0, B > 0.

Let
dμ ξ M − ηN
= 2
dτ ξ + η2 ψ(z) = z3 + Az2 + Bz + C,

Fig. 2 (a)–(c) Time series. (d) Phase portrait

Effect of delay on a predator–prey model with parasitic infection

which is the left-hand side of (3.13) with ν̂ 2 = z; then
ψ(ν̂ 2 ) = 0. Hence, if ν̂ is the smallest positive root of
(3.13), then dμ
dτ > 0 at τ = τ̂ and stability cannot take
place at these values of τ, also we have
Theorem 3.4 If A > 0, B > 0 and AB − C < 0, then
there exists τ̂ > 0 such that the interior equilibrium
E possesses a Hopf-bifurcation as τ increases and
passes through τ̂ .

dψ  2  ξ 2 + η2 dμ 4 Numerical solutions
ν̂ = (τ̂ ) > 0,
dz ν 2 dτ
Our focus so far has been on the dynamic behavior of
2 −c
two epidemic models. We verify our results by com-
where τ̂ = ν̂1 arctan ν̂(aν̂ν̂2 −b) + nπ
ν̂
, n = 0, 1, 2, . . . . puter simulation.
Thus, the smallest τ̂ is given by τ̂0 = Firstly, we show the effect of recovery on the pop-
1 a ν̂ 2 −c
ν̂
arctan ν̂(ν̂ 2 −b)
. Hence by the Hopf-bifurcation the- ulations. Let α = 2.5, μ1 = 0.2, β = 0.2, μ2 = 0.5,
orem (cf. [29]) we have the following result. σ = 0.6, μ3 = 0.3, τ = 1. Choose γ = 0, γ = 0.3,

Fig. 3 (a)–(c) Time series. (d) Phase portrait


γ = 0.6 which implies that there are different recovery
rates. Then, with S(0) = 1, I (0) = 2, P (0) = 0.1, sys-
tems (2.1) are numerically solved for the above choice
of parameters and time series and phase portrait are
shown in Figs. 2(a), 2(b), 2(c) and Fig. 2(d), respec-
tively. Figure 2 indicates that the recovery makes the
levels of the infected prey and the predator become
lower, but makes the sound prey higher in limit time.
Secondly, we will show the effect of time delay.
Let α = 2.5, μ1 = 0.2, β = 0.5, γ = 0.7, μ2 = 0.5,
σ = 0.6, μ3 = 0.03. Choose τ = 0, τ = 1. Then sys-
tems (2.1) are numerically solved for the above choice
of parameters with S(0) = 1, I (0) = 2, P (0) = 2 in
Fig. 3 which indicates that the time delay does not
affect the stability of the system in the process, but
makes all populations oscillate more intensively.
5 Conclusions
Considering that the consequences of prey infection
with delay are examined both empirically and theoret-
ically relatively rarely, a time-delayed predator–prey
model with an infectious disease circulating in the
prey population is investigated. We derive the condi-
tions for asymptotic stability of the steady states. The
length of the delay preserving the stability is also es-
timated. The criterion for existence of periodic oscil-
lations of the predator and prey biomass is derived.
The delay does not affect the stability of the system in
the process but makes all populations oscillate more
intensively. All analytical results are interpreted eco-
logically. Numerical results indicate that the recovery
makes the levels of the infected prey and the predator
become lower but makes the sound prey higher in limit
time.
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