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A Mathematical Model for Meningitis Disease

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 A Mathematical Model for Meningitis Disease
Ibrahim M. ELmojtaba
1 and Salma O.A.ADAM
2

1 Department of Mathematics and Statistics, College of Sciences, Sultan Qaboos University, P.O.Box

36, Muscat, Oman

2 School of Management Studies - Math/Statistics Unit, Ahfad University for Women, Sudan

1 elmojtaba@squ.edu.om
2 salmaomar24u@gmail.com , so.adam@auw.edu.sd

Abstract.

In this paper we present a mathematical model to study the dynamics of the meningitis disease.
Studies show that this disease can kill in a few hours (even with treatment) a percentage of
10% of the infected population, and 20% of the survivors will have disabilities.
We used an SVCIRS model in order to understand the eects of a vaccine in a small community
of human population. In this model we distinguished between the recovered with disabilities
and the recovered without disabilities. The model is governed by a set of six ordinary dif-
ferential equations. We used mathematical analysis to study the eects of the vaccine. We
presented some numerical results for dierent scenarios. Our model suggest that the disease
can be controlled if the vaccine uptake rate is high.

Keywords: Mathematical Model, Meningitis, Basic Reproduction Number R0 , Stability

Analysis, Simulation.

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Red Sea University Journal of Basic and Applied Science
Vol(2) Special Issue (2) April-2017
1 I NTRODUCTION
M ENINGITIS is inflammation of the
meninges, the covering of the brain
and spinal cord. It is most often caused
by infection (bacterial, viral, or fungal),but
can also be produced by chemical irritation,
subarachnoid haemorrhage, cancer and other
conditions [1]. Epidemic of bacterial meningitis
are most likely to occur in sub-Saharan Africa,
in an area known as the "meningitis belt"
contains 26 countries.This epidemic region
stretches from Senegal in the west to Ethiopia
in the east.
In Africa Neisseria Meningitis group A is
responsible for the majority of epidemics,
every year bacterial meningitis epidemics
affect more than 450 million people living
in the 26 countries of the African meningitis
belt. In this area over 800,000 cases were
reported in the years (1996-2010), of this cases
10% resulted in deaths, with another 10-20%
developing neurological Sequelae.
Neisseria meningitidis only infects human;
there is no animal reservoir, it spreads by
person-to-person contact through respiratory
droplets of infected people or throat secretions
even with appropriate treatment around
10% of patients die. The case fatality rate
can be between 3% and 10% in developed
countries as high as 20% in African countries,
and up to 20% of survivors have serious
permanent health problems as a result of the
disease (deafness, epilepsy, cerebral palsy,
speech disorders, loss of limbs, and mental
retardation). There is no immunity after
infection. Approximately on average, 10% of
the population at any time carry the germs for
days, weeks, or months. Neisseria meningitidis
are conducive to spreading of Overcrowding
and climatic conditions such as dry seasons
or prolonged drought and dust storms. The
disease mainly affects young children, but it’s
also common in older and young adults [4],
[9], [8], [14].
In 2010, a new meningococcal A conjugate
vaccine was introduced in some African’s
countries with the total of 20 million persons 1
to 29 years of age vaccinated. In 2011 and 2012
the number of persons were immunized is
ISSN: 1858-7658 (Online)
ISSN: 1858-7690 (Print)
increased across the other African’s countries.
2 M ODEL F ORMULATIONS
In this model we divided the population(N )
into six categories, susceptible individuals
those who are susceptible to infection(S), vac-
cinated individual those who are have im-
munity from the vaccine(V ), carrier individ-
ual those who are carry to infection but they
have not sign of disease(C), Infected individ-
ual those who are they have infection and
are still infected(I), Recovered individual with-
out disability those who are recovered after
treatment(R1 ), and Recovered individual with
disability those who are recovered after treat-
ment but they have disability(R2 ), hence
N (t) = S(t) + V (t) + C(t) + I(t) + R1 (t) + R2 (t).
It is assumed that susceptible individuals are
recruited into the population at a constant rate
Λ(immigration only) and we consider they are
increased by the loss of immunity cussed by
vaccine wanes at a rate (ωV ) or infection after
the recovered and become susceptible again
at a rate (ψ(R1 + R2 ))and so we consider the
susceptible individual they decreased by natu-
ral death at a rate (µS), those people moving
to class V after the vaccination at the vaccine
uptake rate (θS), and by infection they moving
to class C at a rate (βτ S NI ) and to class I at a
rate (β(1−τ )S NI ), where β it’s transmission rate
and τ it’s Proportion moving to I without first
passing through C. We consider the vaccinated
individual increased by vaccination of suscep-
tible individuals at a vaccine uptake rate(θs).
Since the vaccine does not confer immunity
to all vaccine recipients, vaccinated individuals
may become infected, but at a lower rate than
unvaccinated so the vaccinated individual de-
creased by infection and moving to class I at a
rate (β(1−γ)V NI ), where γ it’s Vaccine efficacy ,
by waning of vaccine based immunity moving
to class S at the vaccine wanes rate (ωV ), and
by natural death at a rate (µV ). And so on of
the rest of the compartments. The interaction
between six categories of the population are
shown in Figure 1
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Vol(2) Special Issue (2) April-2017 ISSN: 1858-7690 (Print)
µ µ 3 M ODEL ANALYSIS
 3.1 Local stability of the disease-free equi-
C R1 librium E0
β(1 − τ )
σ The disease-free equilibrium (DFE) of the
Λ ψ
χρ above system is given by
δ
ψ
µ S R2 µ
E0 = (S, V, C, I, R1 , R2 ) =
ω βτ χ(1 − ρ)  
θ Λ(µ + ω) θΛ
, , 0, 0, 0, 0
µ(θ + µ + ω) µ(θ + µ + ω)
V β(1 − γ) I In order to study the local stability of the
µ
DFE we have to find the the basic reproduc-
µ+α
tion number R0 . It is defined as the basic
Fig. 1: Schematic representation of the reaction reproduction number is the average number
between the population categories of secondary infections produced when one
infected individual is introduced into a virgin
population.
Theorem 1: If R0 < 1 the E0 is stable; if R0 > 1
 thenE0 is unstable[10].
0



S = Λ − (θ + µ)S + ωV + ψ(R 1 + R2 ) Now we want to calculate the basic reproduc-

 − βS I
tion number; by use the technique of Next

 N

 V 0 = θS − (ω + µ)V − β(1 − γ)V NI Generation Matrix defined as G = FV−1 . Then
0 I
C = β(1 − τ )S N − (µ +  + δ)C  

 0 I I
S

 I = βτ S N + β(1 − γ)V N + δC − (χ + µ + α)I  0 βτ 

 0 F= N 

 R 1 = C + χρI − (µ + σ + ψ)R1 S V
 R0 = χ(1 − ρ)I + σR − (µ + ψ)R 0 β(1 − τ ) + β(1 − γ)
2 1 2 N N
(1) ,
 
The Table (1) bellow describes the parameters µ++δ 0
that we used in the equations and note that all V =
−δ χ+µ+α
parameters are assumed to be non-negative
and the inverse of the matrix V it’s
TABLE 1: Description of model parameters  
1 0
δ++µ
parameter parameter description V−1 =  δ 1

Λ Recruitment rate
(δ +  + µ)(α + µ + χ) α + µ + χ
θ Vaccine uptake rate
µ Natural death rate
ω vaccine wanes rate Then the basic reproduction number is the
β transmission rate spectral radius of the matrix FV−1 and given
γ Vaccine efficacy by
δ rate of transformed
from carrier to infected
R0 =
α rate of death due the disease
χ recovered rate βδΛτ (µ + ω)[β(1 − γ)θΛ + βΛ(1 − τ )(µ + ω)(δ +  + µ)]
ρ Proportion moving to R1 without N µ(δ +  + µ)(α + µ + χ)(θ + µ + ω)
first passing through R2
 recover rate of carriers
rate of loss of immunity
ψ
3.2 Global stability of the disease-free
τ Proportion moving to I without
first passing through C equilibrium
σ rate of occurred disability after
a period of time
To study the global stability of the disease-
free equilibrium we use the theorem by
Castillo-Chavez

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Red Sea University Journal of Basic and Applied Science ISSN: 1858-7658 (Online)
Vol(2) Special Issue (2) April-2017 ISSN: 1858-7690 (Print)
Theorem 2:(Castillo-Chavez). For the system: A|DF E =
βτ Λ(µ+ω)
!
dX −(µ +  + δ) N µ(θ+µ+ω)
= F (X, Z) δ β(1−τ )Λ(µ+ω)+β(1−γ)θΛ
− (χ + µ + α)
dt N µ(θ+µ+ω)
dZ
= G(X, Z), G(X, 0) = 0 Then we find the column-vector Ĝ(X, Z) is
dt
where the components of the column-vector given by Ĝ(X, Z) = AZ − G(X, Z) =
X ∈ Rm denotes the number of the unin- βτ Λ(µ+ω)I
!
βτ SI
−
fected individuals and the components of vec- N µ(θ+µ+ω)
[βΛ(1−τ )(µ+ω)+βθΛ(1−γ)]I
N
β(1−τ )SI+β(1−γ)V I
tor Z ∈ Rn denotes the number of infected N µ(θ+µ+ω)
− N
individuals. U0 = (X ∗ , 0) denotes the disease-
free equilibrium of this system. The fixed point so Ĝ(X, Z) is greater than zero, and hence con-
U0 = (X ∗ , 0) is a globally asymptotically sta- dition (H2) of the theorem 2 (Castillo-Chavez)
ble equilibrium for this system provided that is satisfied. Hence the disease-free equilibrium
R0 < 1(locally asymptotically stable) and the (DFE) point is globally stable.
following two conditions satisfied:
(H1) For dX dt
= F (X ∗ , 0), X ∗ is a globally 3.3 Existence of the endemic equilibrium
asymptotically stable We looking for the existence of the endemic
(H2) G(X, Z) = AZ − Ĝ(X, Z), Ĝ(X, Z) ≥ 0 equilibrium, then by set all equations to zero
for (X, Z) ∈ Ω, where A = DZ G(X ∗ , 0) is and solve the system we got the following:
an M-matrix (the off-diagonal elements of A
are nonnegtive) and Ω is the region where the θS ∗ N
V∗ =
model makes biological meaning. N (ω + µ) + β(1 − γ)I
we rewrite the system (1) in the form
C ∗ + χρI
dX R1∗ =
= F (X, Z) (2) µ+σ+ψ
dt
dZ σ(ψC ∗ + χρI)
= G(X, Z), G(X, 0) = 0 (3) χ(1 − ρ)I +
µ+σ+ψ
dt R2∗ =
ψ+µ
where
τ βI 2 N (χ + µ + α)(µ + ψ + δ)N (ω + µ) + β(1 − γ)I
X = (S, V, R1 , R2 ) C∗ = 
N (µ + ψ + δ) (βI(1 − τ )(µ + ψ + δ) + δβτ I)(N (
Z = (C, I) 
ω + µ) + β(1 − γ)I) + θβN (1 − γ)(µ + ψ + δ)I
Now for the system (1) and from equation(2)
we fine IN (χ + µ + α)(µ + ψ + δ)[N (ω + µ) + β(1 − γ)I]
 Λ(µ + ω) T S∗ =
Λθ (βI(1 − τ )(µ + ψ + δ) + δβτ I)(N (ω + µ) + β
F (X, 0) = , , 0, 0
µ(θ + µ + ω) µ(θ + µ + ω) (1 − γ)I) + θβN (1 − γ)(µ + ψ + δ)I
Now for the system (1) and from equation(3) Now by substitute all these results in the first
we find equation of the system we got the cubic equa-
dZ tion
= G(X, Z) =
dt AI 3 + BI 2 + CI = 0

  Then I = 0 is the disease free equilibrium and

βτ SI
N
− (µ +  + δ)C we have to solve the quadratic equation AI 2 +
β(1−τ )SI+β(1−γ)V I
N
+ δC − (χ + µ + α)I BI + C = 0, where 
A = ψχβ

2
δτ + (1 − τ )(µ + δ + ) + β 2 (1 − γ)(χ +
and
µ + α) τ ψ − N (ψ + µ)(µ +  + δ) 
 
C B = Λβ 2 (1 − γ)(ψ + µ) δτ + (1 − τ )(µ + δ + ) −
Z= βN (ψ + µ)(χ + µ + α)(µ +  + δ) (θ + µ)(1 − γ) +
I

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Vol(2) Special Issue (2) April-2017 ISSN: 1858-7690 (Print)
 TABLE 2: Estimated Values of Parameters
N (ω + µ) + ψβτ N (ω + µ)((χ + µ + α) + χδ) +
ψχβN (µ +  + δ)((1 −τ )(ω + µ) + θ(1 − γ))  parameter Estimated Value
C = Λβ(ω + µ)(ψ + µ) δτ + (1 −  τ )(µ + δ + ) + Λ 0.2
θ 0.01
N 2(ψ + µ)(χ + µ + α)(µ +  + δ) ωθ + (θ + µ)(ω + µ 0.00004
µ) + ΛN θβ(1 − γ)(ψ + µ)(µ +  + δ) ω 0.5
When

β 0.4
γ 0.5
β 2ψ χ(δτ + (1 − τ )(µ + δ + )) + τ (1 − γ)(χ + α + δ 0.2
µ) < β 2 N (1 − γ)(ψ + µ)(χ + µ + α)(µ +  + δ) α 0.5
then A < 0 χ 0.3
ρ 0.85
B C  0.3
∴I + I+ =0
2
(4) ψ 0.5
A A
τ 0.3
σ 0.15
since C > 0 then the last term CA has a
negative sign.
Then equation (4) has two roots have different
signs, and we will except the positive one. This
leads to I ∗ > 0.
250

∴ The endemic equilibrium is exist and unique.

200

4 N UMERICAL SIMULATION AND DIS -

Susceptible(S)
150

Vaccinated(V)

CUSSION
Compartments

Carriers(C)

4.1 Estimation of Parameters

100

Infected(I)

In the SV CIR1 R2 S Meningitis model

Recov.W.out Disab.(R1)

discussed in previous section, we fix

50

Recov.W Disab.(R2)

parameters as follows (1) the transfer out

of the carrier class is to infected class δC, (2)
0

the recovery rate is χ, (3) the mean infectious 0 5 10 15

Time/Month
20 25 30

period is χ1 and (4) the main latent period is

(a) Interaction between Compartments
1
δ
. The rest of parameters some of them are
estimated and some form references.
350

The initial conditions were [S = 1000, V = S

5, C = 0, I = 1, R1 = 0, R2 = 0].
300

all rates per month are summarized in

V
250

Table (2). To simulate the result we C

used an custom R script in the Rstudio I

200
Compartments

(http://www.rstudio.com/). R1
150

R2
100

4.2 Result
In the figure (2a) below we show that in a time
50

span of 30 month, during the initial months

0

the number of susceptible individuals drops, 0 10 20

Time/Month
30 40 50

while other classes increase, and remain con-

stant for the rest of the time. The number of
other compartments reached their peaks and
drop to remain stable in some point near to
Disease Free Equilibrium.
(b) Interaction between Compartments when θ =
0.1, ω = 0.003 and γ = 0.7
In the figure (2b), when we increased the

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Red Sea University Journal of Basic and Applied Science
Vol(2) Special Issue (2) April-2017
vaccine uptake rate to become (θ = 0.1) and
take vaccine wanes rate very small (ω = 0.003)
then we got that the number of vaccinated
individuals increased and remain stable and
the behaviour of the other compartment stay
the same as the figure (2a). So we conclude
that if people continue to receive vaccination,
infection is controlled.
5 C ONCLUSION
The Meningitis disease, is a major problem
facing Africa, especially in Sub-Saharan Africa
(Meningitis belt). This disease can kill in a
few hours (even with treatment) a percentage
of 10% of infected individuals, and 20% of
survivors will have disabilities.
There are many different types of vaccines, the
last one introduced in 2010, but even that the
infection still exist.
Our main aim in this study was to investi-
gate the effect of vaccination in the spread of
Meningitis disease with present of survivors
with disabilities.
We have extended and implemented the
SV CIRS deterministic model to model the
Meningitis disease. The analysis of this model
showed that the disease-free equilibrium is
globally asymptotically stable. Also the en-
demic equilibrium exists and unique if A < 0.
Our simulation has showed that the disease
can be controlled if the vaccine uptake rate is
high. Our current results have some limitations
as they depend on the assumptions about the
natural history of Meningitis disease, its epi-
demiology, and the values of the parameters
we have used.
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ISSN: 1858-7658 (Online)
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