Mathematical and Computer Modelling 43 (2006) 413422

www.elsevier.com/locate/mcm

Qualitative study of a model of Chagas disease

Prasenjit Das a , Debasis Mukherjee b,
a Department of Mathematics, Jadavpur University, Kolkata-700 032, India
b Department of Mathematics, Vivekananda College, Thakurpukur, Kolkata-700 063, India

Received 2 November 2005; accepted 7 November 2005

Abstract
This paper deals with the analysis of a Chagas disease model consisting of acute and chronic, resistance classes along with
vector population. Local as well as global analyses have been carried out for the model with or without resistance class. We identify
the parameter that controls the dynamics of the system. The results are also verified through numerical simulation.
c 2006 Elsevier Ltd. All rights reserved.

Keywords: Chagas disease; Infection rate; Endemic equilibrium; Global stability

1. Introduction
Chagas disease (American trypanosomiasis) is recognized as one of the major health problems in almost all
Latin American countries, especially in tropical regions. Carlos Chagas, a Brazilian physician, discovered this vectortransmitted disease around 1909 [1]. The infection is caused by the flagellate Trypanosoma (schizotrypanum) cruzi
that belongs to the Mastigophora subphylum of the phylum Sarcomastigophara. This infective agent is transmitted
horizontally to humans via blood transfusions or, more commonly, by the bite of various triatomite bugs (Triatoma
dimidiata, Triatoma nitida, etc.). During the past decades, after urban migrations, Chagas disease became frequent
in cities and a health problem in non-endemic countries also, where it can be transmitted vertically and by blood
transfusion or organ transplantation. It is a leading cause of cardiac arrhythmias, congestive heart failure, autonomic
nervous system dysfunction and sudden death in endemic areas of the American continent. Wall motion abnormalities,
either segmental or diffuse, are another important clinical feature of it [2]. Patients with this type of disease often have
chest pain which is less sensitive to esophageal distention as a prominent symptom [3]. According to the World Health
Organizations report this tropical infection emerges as the second major endemic disease after malaria [4].
Chagas disease has three stages. The acute stage follows the invasion of the bloodstream by the protozoan T. cruzi.
This stage lasts from one to two months and infected individuals may or may not show symptoms of the disease.
Young children are the population group with the highest incidence and mortality rates. After the acute phase, the
infected individuals enter the chronic stage that has a variable duration that lasts from 10 to 20 years. At its end, the
disease may follow three different paths: individuals may develop mega syndromes; others may present myocarditis
Corresponding author.

E-mail addresses: dpdas@vsnl.net (P. Das), debasis mukherjee2000@yahoo.co.in (D. Mukherjee).

c 2006 Elsevier Ltd. All rights reserved.
0895-7177/$ - see front matter
doi:10.1016/j.mcm.2005.11.002

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P. Das, D. Mukherjee / Mathematical and Computer Modelling 43 (2006) 413422

that is the terminal form with highest mortality in the group of 20 to 50 years of age. Finally, individuals may remain
asymptomatic for the rest of their lives. Individuals in this group may live an ordinary life although some may die of
sudden death associated with heart failure produced by the parasite [5].
Most persons acquire Chagas disease when feces and urine of infected triatomines (in which numerous metacyclic
forms of the parasite exist) enter into contact with either mucosa or skin. The domestic cycle results from
humanvector contact, involving the colonization of artificial ecotypes by the invertebrate vector (triatomines) and
a series of social and ecological modification. In this cycle, parasitism can cause important damage in the vertebrate
host, with high degree of morbidity and mortality frequently detected among the infected people. The interaction
between domestic and sylvatic cycles occurs as a product of different factors, the majority of them dependent on
human behaviour. The rate of vectorial transmission depends on several factors such as the density of vectors, age,
immunological conditions of the vertebrates, irritability during the vector bite, and environmental conditions [6].
Schuster and Schuab [7] proved that chronic social stress in males strongly affects the cause of infection with
T. cruzi. Urbina [8] in a review found that the presence of the parasite is a necessary and sufficient condition for
chagasic cardiomyopathy and confirmed the importance of specific etiological treatment in the management of chronic
chagasic patients. Micro epidemics of acute Chagas disease have been reported probably due to oral transmission [9].
Tarleton and Zhang [10] considered an alternative view that the primary cause of chronic Chagas disease is the failure
of the host to clear the infection, resulting in infection-induced immune-mediated tissue damage.
Previous models of Chagas disease transmission include those of Rabinovich et al. [11], Rabinovich and
Rossell [12] and Rabinovich and Himschoot [13]. Assuming a constant proportion of infective vectors but allowing
the human host population to grow exponentially with high annual growth rates, Busenberg and Vargas found that
when approaching the endemic equilibrium there are exponentially stable solutions and no oscillatory behaviour is
possible [5]. Introducing vector population dynamics under the assumption of constant host population, VelascoHernandez [1] shows the existence of an endemic equilibrium point when the basic reproductive number is greater
than one. No fluctuating behaviour is observed in this regard. Again Velasco-Hernandez [5] has considered the effects
of vector and blood transfusion transmission. The role of density dependence on the population dynamics of the vector
population is explored. Introducing the density dependence effects and vector stage-structure, limit cycle solutions are
obtained whereas on neglecting the density dependence effect there is a non-oscillatory approach to the endemic
equilibrium.
Consequently, the severity of this disease makes us interested to study the above disease through a mathematical
model, in order to know its dynamical behaviour so as to restore its further propagation by implementing several
fruitful measures. In spirit of the above works we have presented here a mathematical model with acute and chronic,
resistance classes and vector population, which was suggested by Velasco-Hernandez (personal communication). We
now investigate the dynamical behaviour of the system. Further, we identify the parameter, resistance rate (k), which
influence the dynamics.
In this paper, first we have determined both the disease-free and endemic equilibrium points for the systems.
Conditions for the stability of the disease-free equilibrium are derived. The uniqueness of the endemic equilibrium
points, together with their local and global behaviour, has been discussed. Numerical simulations have also been
carried out.
2. Model
The model considers the effect of vector transmission as opposed to horizontal transmission by blood transfusion,
and also the effect on two different infective stages, namely acute and chronic, respectively, on the existence and
stability of endemic and disease-free stages. Moreover, the model includes a resistance class that plays a vital role in
disease transmission.
We assume that the total host population and vector population remain constant in time. Let x denote the
susceptible proportion of the total population, a denote the proportion of individuals who are infected and in the
acute phase and c represent the proportion of those individuals who are infected but in the chronic phase of the
disease. Also consider the vector population divided into susceptible and infected proportions: the last is denoted by
v. Hence we get (1 v) is the proportion of susceptible vectors and 1 a c = x, the population of susceptible
hosts. Further, we assume that represents the number of bites per vector per host per unit time; is the proportion
of infected bites that gives rise to the infection and is the ratio of vector numbers to host numbers. Moreover, i is

P. Das, D. Mukherjee / Mathematical and Computer Modelling 43 (2006) 413422

415

the proportion of bites of susceptible vectors on acute and chronic infective hosts that results in infection in the vector
i = 0, 1 respectively. Let us define = and bi = i .
Moreover, we consider that infectious hosts in the acute stage may pass to the chronic stage only if they are bitten
v
again by infected vectors h+v
. Otherwise they develop resistance (ka) to the infection and do not develop the chronic
stage. Vectors can get the infection only by biting hosts in the acute and/or the chronic stage.
Hence our proposed model is as follows:
da
dt
dc
dt
dr
dt
dv
dt

= v(1 a c r ) a
= a

v
mc,
(h + v)

v
(m + k)a,
(h + v)
(1)

= ka mr,
= (1 v)(b0 a + b1 c) dv

where , h, m, d are the transmission coefficient, half saturation constant, per capita mortality rate for the host
population and per capita mortality rate for the vector population, respectively. Here all rate coefficients have
dimension time1 .
At first we consider the case when there is no resistance class, r . Then the model (1) becomes
v
da
= v(1 a c) a
ma,
dt
(h + v)
dc
v
= a
mc,
dt
(h + v)
dv
= (1 v)(b0 a + b1 c) dv.
dt

(2)

3. Existence of equilibrium points and their stability for system (2)

There exists a trivial disease-free equilibrium point of the system E 10 (0, 0, 0).
From the system of equations (2), for the equilibrium point we have
v (1 a c ) a
a

v
ma = 0
(h + v )

v
mc = 0
(h + v )

(1 v )(b0 a + b1 c ) dv = 0.

(3)
(4)
(5)

Eq. (4) implies that

c =

a v
.
m(h + v )

(6)

Putting the value of c from Eq. (6) in Eq. (5), we get



a v
(1 v ) b0 a + b1
= dv .
m(h + v )
Therefore,
a =

dv m(h + v )
.
(1 v )[b0 m(h + v ) + b1 v ]

(7)

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P. Das, D. Mukherjee / Mathematical and Computer Modelling 43 (2006) 413422

From Eqs. (3), (6) and (7) we have

(dm + d + b0 m + b1 )v 2 + (dmh + dm 2 + dm + b0 mh b0 m b1 2 )v
+ mh(dm b0 ) = 0.

(8)

Define
F(v ) = (dm + d + b0 m + b1 )v 2 + (dmh + dm 2 + dm + b0 mh b0 m b1 2 )v
+ mh(dm b0 ).
Now, F 00 (v ) = 2(dm + d + b0 m + b1 ) > 0. Therefore, F(v ) is a strictly convex function of v .
Again F(0) = mh(dm b0 ). If > dm
b0 then F(0) < 0.

Now, F(1) = md + d 2 + dmh + dm 2 + dm + dhm 2 > 0.

Hence, by the intermediate mean value theorem, we have a unique solution v (0, 1) of Eq. (8). Since
0 < v < 1, we have a > 0 and hence c > 0.
Hence we get the following theorem:
Theorem 1. Let >
a , c , v > 0.

dm
b0 .

Then there exists a unique endemic equilibrium point E 11 (a , c , v ) of system (2) with

Local Analysis
Now, the Jacobian of system (2) is as follows:


ha
v
+m
v
(1 a c)
v +

h+v
(h + v)2

v
ha
J =
m

h+v
(h + v)2
b0 (1 v)
b1 (1 v)
(b0 a + b1 c + d)

The characteristic equation of the above Jacobian matrix at the disease-free equilibrium E 10 (0, 0, 0) is (m + ){2 +
(m + d) + (md b0 )} = 0.
All three eigenvalues of above matrix are negative provided < dm
b0 . Consequently we get the following theorem:
Theorem 2. The disease-free equilibrium point E 10 (0, 0, 0) is locally asymptotically stable if <
if >

dm
b0 .

dm
b0

and is unstable

The characteristic equation of the above Jacobian matrix at E 11 (a , c , v ) is

3 + A2 + B + C = 0,

(9)

where
mc
d
A = 2m + + v +
,
a
1 v






mc
d
md
mc v
m(1 v )
c

m+
+
b0 a +
B = v + + m
+

(b0 v + b1 h)
a
1 v
1 v
a
v
h + v
and

hmb0 c (1 v ) md(v + mc
m 2 hc (1 v )(b0 a + b1 c )
mv c d
a + m)
C =
+
+
+
h + v
1 v
a v (h + v )
a (1 v )

hmc (1 v )(v + mc
m 2 (a + c )(1 v )(b0 a + b1 c )
a + m)b1

.
v (h + v )
av

P. Das, D. Mukherjee / Mathematical and Computer Modelling 43 (2006) 413422

417

If
C >0

and

AB C > 0

(10)

then all the roots of Eq. (9) have negative real parts. Hence by the RouthHurwiz criterion we get the following
theorem:
Theorem 3. Let the assumption of Theorem 1 hold. The endemic equilibrium point E 11 (a , c , v ) is locally
asymptotically stable if the inequalities (10) hold.
Global analysis
3 , are eventually
From the model formulation, it is obvious that the solutions of system (2), which initiate in R+
uniformly bounded. Thus there exists a set U as a domain of attraction, where U = {(a, c, v) : a > 0, c > 0, a + c <
1, 0 < v < 1}. We shall show that the endemic equilibrium point E 11 (a , c , v ) is globally asymptotically stable in
the set U as its domain of attraction.
Define, V (a, c, v) = 12 (a a )2 + M2 (c c )2 + 12 (v v )2 , where M is a positive constant to be chosen later.
Evidently V is a positive definite function in the region U except at E 11 , where it is zero.
The time derivative of V along the solution of (2) is

dV (a, c, v)
da
dc
dv
= (a a )
+ M(c c ) + (v v )
dt
dt
dt
 dt

v
2

+ m (a a ) m M(c c )2 (b0 a + b1 c + d)(v v )2

= v +
h+v


v
+ (a a )(c c ) v + M
h + v


a h
+ (a a )(v v ) (1 a c) + b0 (1 v )
(h + v)(h + v )


Mah
+ b1 (1 v ) .
+ (c c )(v v )
(h + v)(h + v )
Choosing M =

h+v
,

we get


dV
v
m(h + v )
= v +
+ m (a a )2
(c c )2 (b0 a + b1 c + d)(v v )2
dt
h+v



a h
+ (a a )(v v ) (1 a c) + b0 (1 v )
(h + v)(h + v )


ah
+ (c c )(v v )
+ b1 (1 v )
h+v
m(h + v )
(v + m)(a a )2
(c c )2 d(v v )2



a

+ +
+
b
(1

v
)
|a a ||v v | + { + b1 (1 v )}|c c ||v v |
0
h + v


(11)

= a11 (a a )2 a22 (c c )2 a33 (v v )2 + 2a13 |a a ||v v | + 2a23 |c c ||v v |

T
T

i.e., dV
dt X D X , where X = {|a a |, |c c |, |v v |} and D = [ai j ]33 .
)
The elements of matrix D are given by a11 = v + m, a22 = m(h+v
, a33 = d, a12 = a21 = 0,

1
a
1

a13 = a31 = 2 { + h+v + b0 (1 v )}, a23 = a32 = 2 { + b1 (1 v )}.

Here,
a
2
[ + h+v
[ + b1 (1 v )]2
+ b0 (1 v )]
if
+
< 1.
4m(h + v )d
4d(v + m)

|D| > 0

(12)

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P. Das, D. Mukherjee / Mathematical and Computer Modelling 43 (2006) 413422

Theorem 4. Suppose that the assumptions of Theorem 1 hold. If the condition (12) holds, whenever (a, c, v) Int U ,
3.
then E 11 is globally asymptotically stable with respect to all solutions initiating Int R+
Proof. Since U is a global attractor we may restrict our attention to solutions initiating in Int U . From the above
inequality, for (a, c, v) Int U , the right-hand side of (11) considered as a quadratic form in the variables
is negative definite about E 11 and so V (a, c, v) is
|a a |, |c c |, |v v | is negative definite. Hence dV (a,c,v)
dt
a Lyapunov function for (a, c, v) Int U . This completes the proof. 
Now we investigate whether the inclusion of resistance class can change the dynamics already obtained. So we
consider system (1) and analyze it in detail in Section 4.
4. Existence and stability of equilibrium points for system (1)
The system (1) has the equilibrium E 20 (0, 0, 0, 0) which is stable if < (m+k)d
and is unstable if > (m+k)d
b0
b0 .
Again by a similar fashion we may prove the existence and uniqueness of the endemic equilibrium point E 21 (a,
c,
r , v)

when > (m+k)d

and
hence
we
get
the
following
theorem:
b0
Theorem 5. Let >
a,
c,
r , v > 0.

(m+k)d
b0 .

Then there exists a unique endemic equilibrium point E 21 (a,

c,
r , v)
for system (1) with

Local analysis
We examine the characteristic equation for the linearization of system (1) at equilibrium point E 21 (a,
c,
r , v),

which is written as
4 + A1 3 + A2 2 + A3 + A4 = 0

(13)

d
where, A1 = 3m + v(1
+ h+ v ) + k + 1
v ,





(1 v)b1 ah

d
d
3md
r + c

v + 2m +
+ 3m 2 + v 2m +
+
A2 = m
a
1 v
1 v
1 v
(h + v)
2


c
a + r
+ m(1 v)b
0
+
,
h + v
v





(1 v)b
1 hm c
m v
d
(c + a + r )
2d

A3 =
m+
(r + c)
+ m v + m
m+
a
1 v
a
1 v
v(h
+ v)




c
a + r
b1 c
(1 v)
ah

(mb1 b0 v)
+ m 2 (1 v)

+
+ 2b0 ,

h + v
v
a
(h + v)
2





d
2 v(1
v)
ah

v
2 r + c
+
(mb0 kb1 ) + m v + m + k +
A4 = vm

a
1 v
h + v
(h + v)
2




md
(1 v)b
1 ah

v
m+k

+ m 2 (1 v)(
c + b0 )
+
.
1 v
v
(h + v)
2
(h + v)
2

Let us apply the RouthHurwiz criterion to the characteristic Eq. (13). The necessary and sufficient condition for the
local stability of the positive equilibrium E 21 (a,
c,
r , v)
is that all the determinants D1 = A1 , D2 = A1 A2 A3 , D3 =
A1 (A1 A3 A1 A4 ) A23 and D4 = A4 D3 are positive. Thus we have the following theorem:
Theorem 6. Let the assumption of Theorem 5 hold. If Di > 0, i = 1, 2, 3, 4 then the endemic equilibrium point
E 21 (a,
c,
r , v)
of system (1) is asymptotically stable.
Global analysis
4 , are eventually
From the model formulation, it is obvious that the solutions of system (1), which initiate in R+
uniformly bounded. Thus there exists a set U = {(a, c, r, v) : a > 0, c > 0, r > 0, a + c + r < 1, 0 < v < 1} as a

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P. Das, D. Mukherjee / Mathematical and Computer Modelling 43 (2006) 413422

domain of attraction. We shall show that the endemic equilibrium E 21 (a,

c,
r , v)
is globally asymptotically stable in
the set U as its domain of attraction.
We define W (a, c, r, v) = 12 (a a)
2 + g21 (c c)
2 + g22 (r r )2 + 21 (v v)
2 , where g1 and g2 are positive constants
to be chosen later. Evidently W is a positive definite function in the region U except at E 21 , where it is zero.
Now the time derivative of W along the solutions of system (1) is
da
dc
dr
dv
dW (a, c, r, v)
= (a a)

+ g1 (c c)

+ g2 (r r ) + (v v)

.
dt
dt
dt
dt
dt
Choosing, g1 =

h+v

v
k

we have from the above expression and from the system (1) that

dW
v
(h + v)

= v +
+ m + k (a a)
2m
(c c)
2 (b0 a + b1 c + d)(v v)
2
dt
h+v



ah

m v
2
(r r ) + (a a)(v

v)
(1 a c r )
+ b0 (1 v)

k
(h + v)(h + v)



ah
+ (c c)(v

v)

+ b1 (1 v)

h+v
and g2 =

(14)

T
T
i.e., dW
|c c|,
|r r |, |v v|}
and N = [a i j ]44 .
dt Y N Y , where Y = {|a a|,
m(h+v)

m v
, a 33 = k , a 44 = d, a 12 = a 21 = 0, a 13 = a 31 = 0,
Here, a 11 = v + m + k, a 22 =

1
a 14 = a 41 = 21 { + h+
+
b
(1

v)},

=
a

a 23 = a 32 = 0, a 34 = a 43 = 0.
0
24
42 = 2 { + b1 (1 v)},
v
Here, |N | > 0 implies that
a

[ + h+
2
[ + b1 (1 v)]
2
v + b0 (1 v)]
+
< 1.

4m(h + v)d

4d( v + m + k)

(15)

Now we can state and prove the following theorem:

Theorem 7. Suppose that the assumptions of Theorem 5 hold. If the condition (15) holds, whenever (a, c, r, v)
4.
Int U , then E 21 is globally asymptotically stable with respect to all solutions initiating in Int R+
Proof. Since U is a global attractor we may restrict our attention to solutions initiating in Int U . From the above
inequality (15), for (a, c, r, v) Int U , the right-hand side of (14) considered as a quadratic form in the variables
is negative definite about E 21 and so W (a, c, r, v)
|a a|,
|c c|,
|r r |, |v v|
is negative definite. Hence, dW (a,c,r,v)
dt
is a Lyapunov function for (a, c, r, v) Int U . This completes the proof. 
5. Discussion
Here we have considered a model of Chagas disease with or without resistance class and studied the basic
population dynamics and transmission mechanisms of the disease. The main results obtained in this paper indicate
that there is a strong tendency of the disease to reach an asymptotically stable endemic equilibrium point.
The model is studied numerically with the following set of parametric values: = .4, = 1, h = 1, m =
1 day1 , b0 = 2, b1 = 1, d = 1 day1 and = 1, = 1, h = 1, m = 1 day1 , b0 = 2, b1 = 1, d = 1 day1 .
These simulations indicate that when < dm
b0 , all trajectories of system (2) converge to the point E 10 (0, 0, 0),
whereas all the trajectories of the above system converge to the point E 11 (a , c , v ) when >
(m+k)d
b0 ,

dm
b0

[see Figs. 1

and 2]. Moreover, when <

we observed from simulation that the disease-free equilibrium of system
(1) behaves as a stable point for the choice of parametric values = 1.3, = 1, h = 1, m = 1 day1 , k =
2 day1 , b0 = 2, b1 = 1, d = 1 day1 , while the endemic equilibrium point of this system seems to be stable for
[see Figs. 3 and
= 6, = 1, h = 1, m = 1 day1 , k = 2 day1 , b0 = 2, b1 = 1, d = 1 day1 when > (m+k)d
b0
4].
From model analysis and numerical simulation we observe that when the disease-free equilibrium of system (1)
and system (2) are stable in nature then the endemic equilibrium of the corresponding system is unstable in nature.

420

P. Das, D. Mukherjee / Mathematical and Computer Modelling 43 (2006) 413422

Fig. 1. This figure shows the stability behaviour of the disease-free equilibrium of system (2).

Fig. 2. The figure represents the stability behaviour of the endemic equilibrium of system (2).

Biologically we may say that when the mortality rate for vector population is above some threshold value then the
disease-free equilibrium is stable, i.e. there is no scope to spread the disease, and when the mortality rate for the vector
population is below some threshold value then an endemic equilibrium exists, i.e. the disease spreads. Conditions for
the stability of the endemic equilibrium are found which are very difficult to interpret biologically.
Analyzing system (2), we see that the endemic equilibrium point exists for > dm
b0 and is globally asymptotically
1 (1v )]
stable for [+b
4m(h+v )d +
2

a
2
[+ h+v
+b0 (1v )]
4d(v +m)

< 1, whereas introducing the resistance class into system (2), it is

observed that the endemic equilibrium point of the system (1) exists for >
(1v)]
2

[+ h+
2
v +b0 (1v)]
4d( v+m+k)

(m+k)d
b0

and is globally asymptotically

1
+
< 1. This result reveals that the resistance rate coefficient, k, has an
stable for [+b
4m(h+v)d

important role on the existence of the endemic equilibrium point and its stability.
Hence, in brief, we may conclude that if the mortality rate for the vector population decreases then the disease
becomes endemic for a larger value of the mortality rate for the host population. Whenever resistance class is included
in the system, the endemicity of the disease depends not only on a larger value of the mortality rate for the host

P. Das, D. Mukherjee / Mathematical and Computer Modelling 43 (2006) 413422

421

Fig. 3. This figure shows the stability behaviour of the disease-free equilibrium of system (1).

Fig. 4. This figure represents the stability behaviour of the endemic equilibrium of system (1).

population but also on a larger value of the resistance rate coefficient provided the mortality rate for the vector
population remains smaller. It is observed that a class of individuals who develop permanent resistance after fighting
off an initial infection has an impact on the transmission of Chagas disease. The structure of the infection is the fact
that a high proportion of individuals infected with Chagas disease do not pass through a symptomatic acute phase;
rather, they pass directly to an asymptomatic phase comparable to the chronic stage modeled here.
Acknowledgment
The authors are grateful to the anonymous referee for his/her valuable comments in improving the paper.
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