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WSN 170 (2022) 149-171 EISSN 2392-2192

Standard Incidence Model of Measles with two

Vaccination Strategies

David Nuwahereze1, Martins Onyekwelu Onuorah2,*,

Baba Mohammed Abdulahi2 and Innocent Kabandana3
1Department of Education Science, Faculty of Education Open and Distance E-Learning,
Kampala International University, Main Campus, Kampala, Uganda
2Departmentof Mathematics & Statistics, School of Mathematics and Computing,
Kampala International University, Main Campus, Kampala, Uganda
3Department of Computer Science, Kigali Independent University (ULK), Rwanda
*E-mail address: martins.onuorah@kiu.ac.ug

ABSTRACT
The essence of vaccination is to trigger the immune response to recognize and fight disease
causing-organisms. Vaccination has led to the elimination of some childhood diseases. The purpose of
this paper is to model the effects of two vaccination strategy in the control of measles. We accomplished
this using the popular SVEIR model, incorporating what we tagged recruitment and continuous
vaccination strategies. A critical threshold for disease control called the basic reproductive number was
obtained, and its sensitivity indexes indicates the parameters that will be targeted by health policy maker
to ensure control and elimination of measles. The disease-free equilibrium and endemic equilibrium
states were obtained and analyzed for stability. Our model was fitted to the measles outbreak data in
NunuKumba District, East Wollega Zone, Oromia Regional State, Western Ethiopia, for 17 weeks
between the 47th week of 2019 to the 11th week of 2020. We simulated some model variables using three
sets of data values, baseline parameter values from the literature, the estimated data from the mentioned
epidemic, and the fitted parameters.

Keywords: Standard Incidence, Measles, vaccination, reproductive number, stability, equilibrium,

simulation

( Received 03 June 2022; Accepted 26 June 2022; Date of Publication 27 June 2022 )
 World Scientific News 170 (2022) 149-171

1. INTRODUCTION

Measles is an airborne disease mainly affecting children between 9 months to 6 years,

although it can also affect adults. It spreads via droplets from infected persons' noses, mouths,
or throats. The symptoms usually begin with a high fever, hacking cough, red swelling eyelids,
muscle and body aches, irritability, running nose, watery eyes, and rashes. A certain percentage
of people with measles develop one or more complications associated with the disease, such as
blindness, encephalitis, and severe diarrhea (Mugoša et al., 2022). Measles is preventable by
vaccine and eliminated in some countries where vaccine coverage is high. Endemicity
worldwide occurs in settings with low vaccine coverage, poor nutrition, and inefficient health
care system. The resurgence of outbreaks has appeared in some countries where measles have
been eliminated due to imported cases and other factors (Dimala et al. 2021).
Mathematics modeling has always been a vital tool in the fight against diseases (Onuorah,
Atiku, and Juuko 2022). The analysis of such models has and will always provide valuable
information for public health policymakers.
(Bobashev et al. 2000) showed in their paper that reconstruction of the susceptible and
recruitment dynamics is beneficial for model fitting and forecasting a cholera outbreak. (Hove-
Musekwa et al., 2011) modeled the effect of malnutrition on the spread of cholera; the analysis
of their model suggests that good nutrition can address the burden. The findings of (Beay 2018)
showed that quarantine and treatment help eliminate measles from the system. (Huang et al.,
2018) used an SEIR model with periodic transmission rate to investigate the seasonal measles
epidemics and the effect of vaccination in China. (Gastañaduy et al., 2018) modeled the impact
of public health responses during a measles outbreak in an Amish community in Ohio, US.
The paper by (Akingbade, Adetona, and Ogundare 2018) showed a significant effect on
infective if at least 50% of the population possessed strong immunity against measles infection
at the initial stage. (Sowole et al. 2019) used measles data pertinent to Senegal to establish that
early treatment and therapy will eradicate measles faster in a population. (Nwafor et al. 2019)
demonstrated that the spread of measles depends on the interaction rate with infectious
individuals and that vaccination can stop the spread. (Aldila and Asrianti 2019) investigated the
impact of imperfect vaccines and quarantine on the control of measles. The paper by (Nudee,
Chinviriyasit, and Chinviriyasit 2019) showed that reducing the basic reproductive number of
measles less than unity is insufficient to eliminate measles in a community where a portion is
vaccinated.
(N Sinha, Klahn, and Pehlivan 2020) used different differential equations to analyze the
measles epidemic in the United States; their research shows that viral spread was suppressed in
the vaccinated compared to the unvaccinated. (Arsal, Aldila, and Handari 2020) presented a
short review of measles models. They suggested modeling the co-infection of measles with
other severe diseases, such as diarrhea, pneumonia, etc., and the effect of IgG antibodies, which
allow the immunity transferred from mothers. (Jaharuddin and Bakhtiar 2020) developed and
analyzed an optimal control model of measles incorporating vaccination therapy and treatment.
In (Kumar et al. 2020), a new numerical method was developed to solve the fractional SEIR
measles epidemic. (Abdelaziz et al. 2020) investigated a discrete-time SEIR measles epidemic
model with fractional-order. (Sowole et al. 2020), studied measles model with control at the
susceptible and exposed compartments. (Chin, Buckee, and Mahmud 2020) used a dynamic
mathematical model of measles transmission to evaluate the effectiveness of the reactive
vaccination campaigns in the Rohingya refugee camps.

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(Tilahun, Woldegerima, and Wondifraw 2020), developed a stochastic model of measles

transmission dynamics with double dose vaccination. (Siam and Nas 2020), developed a
measles model using five compartments without vaccination; their model was fitted to 2017
Malaysia measles data. (Enagi and Shehu 2020), they studied a measles model incorporating
vaccination and treatment and solved their model using the homotopy perturbation method.
(Madaki and Daya 2020), used the SIT model to study measles spread; they used the reported
cases at Yobe State Specialist Hospital, Damaturu, Nigeria, to fit their model. (Nazir et al.
2020), presented an analytical solution for the measles spread model with three doses of
vaccination using Caputo–Fabrizio fractional derivative (CFFD). (Qureshi 2020) investigated
measles dynamics using the conformable derivative of order alpha (α). (Memon, Qureshi, and
Memon 2020), used a nonlinear incidence model to study the use of a vaccine to control measles
in Pakistan. (Fakhruddin et al. 2020), investigated measles transmission in Jakarta via a SIHR
epidemic model involving vaccination from January to December 2017.
(Al-Darabsah 2021), studied the impact of the latent period on the epidemic in the
presence of an imperfect vaccine when the infection incidence rate is in a nonlinear general
form. (Menkir, Jbaily, and Verguet 2021) aimed to explore the influence of integrating income-
associated differences in parameters of the traditional dynamic of measles transmission.
(Amelia and Tasman 2021) studied the effect of vaccination on the coinfection of measles and
rubella. (Kusmawati and Chandra 2021), used an SEIR epidemic model incorporating
vaccination and immigration to study measles transmission in Indonesia. (Seydou and Tessa
2021) analyze a quasi-stationary distribution of the stochastic SVIR (Susceptible, Vaccinated,
Infected, and Recovered) model for the measles. (Paul et al. 2021), models measles dynamics
using treatment as a control. Developed a new epidemiological measles model while
considering integer and fractional order operators and presented a comparison. (Somma et al.
2021) formulated a mathematical model of measles incorporating Vitamin A supplement as
treatment.
More recently, (Liu et al. 2022) applied stochastic optimal control theory to the measles
epidemic model. (Abdul et al. 2022) developed a hyper infectious and less infectious bacteria,
so the model of SVIR-BhiBli type for measles dynamics. (El Hajji and Albargi 2022), studied a
generalized "SVEIR" epidemic model with general nonlinear incidence seconded with
nonlinear optimal control; both models were analyzed using the Gauss-Seidel method.
There are two strategies for incorporating vaccination into the epidemic model. The first is to
vaccinate individuals at entry into the system or skip vaccination. The second is to allow for
continuous vaccination of individuals while in the system. While most literature papers adopt
one of these two strategies, we adopt the two vaccination strategies in this paper. The
recruitment strategy aims to capture children between 12 to 15 months vaccinated as part of the
compulsory routine immunization. The second is to cater to adults who missed the first or are
not double sure they were vaccinated as a child.

2. MODEL FORMULATION AND ANALYSIS

This section presents a compartmental model to describe measles' transmission dynamics

and control. We assume that the population is homogeneously mixing and reflects increasing
dynamics such as birth and immigration, an individual can be infected through direct contact

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with an infectious individual. On recovery, the individual obtains permanent infection-acquired

immunity; that is, an individual cannot be infected again.
The total population (N) is divided into the following epidemiological classes:
Susceptible, S (Individuals who may get the disease); Exposed or Latent, E (Individuals who
are exposed to the disease); Infected, I (Individuals who have the disease and can transfer it to
others); Recovered, R (Individuals who have permanent infection-acquired immunity) and
Vaccinated, V (Individuals who have received the vaccine at birth plus individuals who receive
the vaccine as adults). Here we considered a perfect vaccine, meaning that vaccinated
individuals cannot be infected, unlike models where they considered imperfect vaccines
(Onuorah, Obi, and Babangida 2019) and others.
If there is an adequate contact of a Susceptible individual with an Infective individual,
then the transmission may occur; thus, the susceptible individuals may join the Exposed class,
E at the rate  . A proportion of the susceptible individual also leaves the compartment due to
vaccination at the point of recruitment at the rat  =  or while in the system at the rate 
When the Latent or incubation period ends; exposed individuals may progress to the Infectious
class I at the rate σ.
After some treatment, infectious individuals may recover and join the recovery class, R
at rate  . Since the disease is fatal, infected individuals may die due to the disease at the rate δ
or die naturally at the rate μ. The recovered class, R, consists of those with permanent infection-
acquired immunity. Our new model is a SVEIR model

Figure 1. Schematic diagram of measles transmission dynamics.

The model equation

From the model formulation and schematic diagram figure 1, we present the model
equations as follows:

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dS SI
= N (1 −  ) −  − S − S . (1)
dt N

dV
= N ( ) + S − V . (2)
dt

dE SI
= − ( +  ) E . (3)
dt N

dI
= E − ( +  +  ) I . (4)
dt

dR
= I − R . (5)
dt

The total population size is given by;

N = S + V + E + I + R. (6)

Adding equations (1) to (5) we have

dN
= N − N + I . (7)
dt

Table 1. Model state variables and parameters.

Variables Meaning

S (t) The population of susceptible individuals at time t.

V (t) The population of vaccinated individuals at time t.
E (t) The population of exposed individuals at time t.
I (t) The population of infected individuals at time t.
R (t) The population of reserved individuals at time t.
N Total population at time t.
Parameters
𝛽 The birth rate of the total population.
ᶓ Vaccine efficacy
 Vaccine coverage at birth

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 Transmission rate.
- Proportion of susceptible vaccinated at other time, not at
Ƞ
birth
 The natural death rate of humans in the district
 Progression rate from the exposed to the infectious class.
δ The death rate due to measles infection.
 The recovery rate of infected individuals.

Theorem:
The closed set

 
D = (S ,V , E, I , R )  5+ : S + V + E + I   . (8)
 

Is positively-invariant and attracting with respect to equations (1) to (5)

Proof.
From equations (6) and (7);

dN
  − N . (9)
dt

dN H 
It follows that  0 if N (t )  . Thus a standard comparison theorem, as in
dt 
(Derick and Onuorah 2019), can be used to show that,


N (t )  N (0)e  (t ) +

(1 − e − (t ) ) (10)

 
In particular, N (t )  if N ( 0) 
. Thus D is positively invariant. Further, if
 
 
N (0)  , then, either the solution enters D in finite time or N (t ) approaches , and the
 
infected variables E, I approaches 0. Hence D is attractive; that is, all solutions in  5
+
eventually enter D . Thus in D , the model equations (1) to (5) are well-posed
epidemiologically and mathematically (Hethcotet 2000). Hence it is sufficient to study the
dynamics of the model

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Disease Free Equilibrium (DFE)

There are three types of equilibrium states usually considered in epidemiological
modeling; the zero equilibrium, the disease-free equilibrium, and the endemic equilibrium
states. This work considers the disease-free equilibrium (DFE) and the endemic equilibrium
states. Generally, at the equilibrium states, the rate of change of the state variables with respect
to time is zero, i.e.

dS dV dE dI dR
= = = = = 0.
dt dt dt dt dt

For DFE, i.e., equilibrium points where there is no disease, we define disease
compartments as the exposed and Infectious human compartments E and I respectively. To
obtain the DFE of our model, we set the right hand side of the model (1) to (5) to zero as given
below;

SI
N (1 −  ) −  − S − S = 0 . (11)
N

N + S − V = 0 . (12)

SI
 − ( +  ) S . (13)
N

E − ( +  +  ) I = 0 . (14)

I − R = 0 . (15)

Solving (8) to (12) we have:

From (8)

SI
N (1 −  ) −  − S − S = 0,
N
N (1 −  ) − ( +  )S = 0,

N * (1 −  )
S* = . (16)
( +  )
From (9),

N * + S − V * = 0,
V * = N * + S ,

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N * + S *
V= ,. (17)


Substituting (16) into (17) and simplifying, we have

N * (( +  ) +  (1 −  ))
V* = . (18)
 (( +  )

We denote the disease-free equilibrium with E 0 such that;

 N * (1 −  ) N * (( +  ) +  (1 −  ) ) 
E0 = ( S * ,V * , E * , I * , R * ) =  , ,0,0,0  . (19)
 ( +  )  (( +  ) 

Endemic equilibrium state (EES)

The endemic equilibrium is an equilibrium state where at least one of the infected
compartments is non-zero. The following steps give the Endemic equilibrium for our model
equations (1) to (5).
We let

I
 = . (20)
N

Be the force of infection of susceptible human at steady state, further, we let

Ee = (S ** ,V ** , E ** , I ** , R** ) represent any arbitrary point of the endemic equilibrium of our
model substituting (20) into the right hand side of (1) to (5), and solving we have;

N ** (1 −  ) − S ** − S ** − S ** = 0 . (21)

N ** + S ** − V ** = 0 . (22)

S ** − ( +  ) S ** . (23)

E ** − ( +  +  ) I ** = 0 . (24)

I ** − R ** = 0 . (25)

Solving (18) to (22), we have;

N ** (1 −  ) − S **  − S ** − S ** = 0 ,

N ** (1 −  )
 S ** = . (26)
( +  +  )

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(1 −  )N ** (( +  +  ) +  )
V ** = . (27)
 ( +  +  )

S **
E ** = . (28)
 +

S **
I =
**
. (29)
( +  )( +  +  )

S **
R ** = .. (30)
 ( +  )( +  +  )

The basic effective reproductive number ( Rc )

The basic reproductive number R 0 is the number of secondary infections one infective
individual would create throughout the infectious period when the population is entirely
susceptible. On the other hand, the effective reproductive number R c is the number of secondary
infections that one infective individual would create throughout the infectious period when a
portion of the population is protected. When the DFE is locally asymptotically stable, the
disease cannot invade the population, but an invasion is always possible if the DFE is unstable
(Hethcotet 2000).
We use the following generation matrix approach as in (Emeka et al. 2018; Onuorah and
Nasasira 2021) to derive our effective Reproductive Number R c . Our model has two Infective
compartments, namely the Infective and Exposed. The matrices F and V for the new infective
and remaining transfer terms are below. Where the entries of F and V are partial derivatives of
f i (x ) and Vi (x ) . For our model, F and V are given below.

 S * 
0   +  0 
F = V =  . (31)
0
N* 
0   − ( +  +  ) 


 1 
 0 
 +
V −1 = . (32)
  1 
 ( +  )( +  +  ) ( +  +  ) 


Such that

 S * S * 
 * 
FV −1 =  N ( +  )( +  +  ) N ( +  +  )  .
* (33)
 
 0 0 

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where, the effective reproductive number R c is the spectral radius (dominant eigenvalue) of the
−I
product matrix FV , is calculated as follows;

FV −1 − I = 0 . (34)

That is;

S * S *
−
N * ( +  )( +  +  ) N * ( +  +  ) = 0 . (35)
0 −

S *
Therefore, 1 = 0 , and 2 = .
N * ( +  )( +  +  )

S *
R c =  ( FV − I ) = . (36)
N * ( +  )( +  +  )

Substituting equation (13) into (28); we have

 (1 −  )
Rc = (37)
( +  )( +  )( +  +  )

Local stability of the disease-free equilibrium

Theorem 1. The measles model (1) to (5) is local asymptotically if the effective reproductive
number Rc  1 .

Proof.
We prove Theorem 1 using the eigenvalues of the Jacobian matrix evaluated at DFE.

 − K1 0 0 K2 0 
 
 K3 − K4 0 0 0 
J0 =  0 0 − K5 K6 0  (38)
 
 0 0 K7 − K8 0 
 0 − K 10 
 0 0 K9

S * S *
where K1 = ( (1 −  ) +  ) , K 2 = , K 3 =  (1 −  ) , K 4 =  , K 5 = ( +  ) , K 6 = * ,
N* N
K 7 =  , K 8 = ( +  +  ) , K 9 =  , K 10 =  .

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We use the traditional characteristic equation method J 0 − I 5 = 0 as follows

− K1 −  0 0 K2 0
K3 − K4 −  0 0 0
J0 = 0 0 − K5 −  K6 0 =0 (39)
0 0 K7 − K8 −  0
0 0 0 K9 − K 10 − 

The stability of the disease-free equilibrium can be obtained by studying the eigenvalues
J 0 − I 5 = 0 . The equilibrium point is locally asymptotically stable if all the eigenvalues are
negative. The five eigenvalues are as follows. The determinant of the matrix J 0 − I = 0 is

( K 4 −  )( K1 −  )(( K10 −  )( K 5 −  )( K 8 −  ) − K 7 K 6 = 0 (40)

Simplifying, we have

1  S * 
1 =  − ( + 2 +  +  ) + ( + 2 +  +  ) 2 − 4( +  )(+ +  +  ) − *  ,
2  N 


S *
1  0 , if ( + 2 +  +  ) 2 − 4( +  )(+ +  +  ) −  ( + 2 +  +  ) .
N*

1  S * 
.
2 = − ( + 2 +  +  ) − ( + 2 +  +  ) − 4( +  )(+ +  +  ) − *
2

2  N 


3 = −  , and 5 = −  .

Since all the Eigen-values of the Jacobin are all negative, we conclude that the DFE of
the model is locally asymptotically stable whenever Rc  1 .

Global stability of the disease-free equilibrium

Theorem. If RC  1 , the DFE is globally asymptotically stable and unstable if RC  1

Proof. Applying the comparison theorem to the rate of change of equations (3) and (4) can be
rewritten as

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 dE 
     (1 −  ) S 
 dt  = (F − V ) E  −     +  − N  . (41)
 dI  I    
   
   0 
 dt 

where the matrices F and V are defined by equation (31). However, since we have that
S  (1 −  )
 for all t  0 in D . Thus
N +

 dE 
 
 dt   (F − V ) E  (42)
 dI  I 
 
 
 dt 

Given that all the eigenvalues of the matrix ( F − V ) have negative real parts, it follows
that the inequality (42) is stable for RC  1 from Lemma 1 (Driessche and Watmough 2002;).
It thus follows that (E, I) → (0, 0, 0) as t → ∞. The comparison theorem follows that (E, I) →
 (1 −  )
(0, 0). From equations (1) and (5), we have that S * → whenever (E = I = 0) Thus (E,
+
I) → E 0 as t →∞ for RC  1 , so E 0 is globally asymptotically stable.

Table 2. Parameters of the models, their interpretations, and numerical values

Parameters Meaning Value Reference

 (Adane et al.
The birth rate of susceptible human 0.0322
2021)
 Contact rate of susceptible human when b 0.005 Fitted
 Natural death of human 0.044
(Adane et al.
2021)
(Kuddus,
 Progression rate of exposed human 0.018 Mohiuddin, and
Rahman 2021)
The death rate of humans due to virus
 0.004 Estimated
infection
 The recovery rate of infectious human 0.14 Estimated
 Vaccine efficacy where (0    1) [0,1] Variable
 Vaccine coverage [0, 1] Variable
 The vaccination rate of susceptible adult [0,1] Variable

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Model fitting
To simulate our model variables with appropriate parameter values, we have to
parameterize our model. In doing this, we use three sets of parameter values: the baseline from
the literature, the estimated from the data, and the fitted parameters.
In this regard, our model is fitted to the measles weekly epidemic data displayed in Figure
2 above. We combine the ODE solver and the minimization routine embedded in Matlab. The
appropriate loss function for our minimization technique is the sum of squared error (SSE). The
graph of the data fitting is shown in Figure 3.

Numerical simulation
In this section, we use Matlab software to plot the graph of the numerical solution of our
model equations. Figures 4 to 10 are the numerical simulations of the measles model given by
equations (1) to (5), using the original system variables with parameter values as shown in Table
2. The numerical scheme used is the Runge-Kuta method (rkf45) embedded in Matlab software.
The rkf45 method is a fourth-order method, meaning that the local truncation error is on the
order of 0( h 5 ) , while the total accumulated error is of order 0( h 4 ) .

Figure 2. Measles outbreak data (Zalalem and Aklilu 2020) in Nunu Kumba District, East
Wollega Zone, Oromia Regional State, Western Ethiopia, for 17 weeks between the 47th week
of 2019 to the 11th week of 2020.

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Figure 3. Model fitting with the measles outbreak data in NunuKumba District, East Wollega
Zone, Oromia Regional State, Western Ethiopia, for 17 weeks between the 47th weeks of 2019
to the 11th week of 2020.

Figure 4. A 2D contour plot of basic reproductive number as a function of the recruitment rate
 and the continuous vaccination rate 

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Figure 5. A 2D contour plot of basic reproductive number as a function of the recruitment rate
 and the continuous vaccination rate  .

Figure 6. A 2D contour plot of basic reproductive number as a function of the recruitment rate
 and the continuous vaccination rate  .

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Figure 7. A 3D contour plot of basic reproductive number as a function of the recruitment rate
 and the continuous vaccination rate  .

Figure 8. A 2D contour plot of basic reproductive number as a function of the recruitment rate
 and the continuous vaccination rate  .

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Figure 9. A 3D contour plot of basic reproductive number as a function of the recruitment rate
 and the continuous vaccination rate  .

Figure 10. Simulation of the infected population with different values of the recovery rate  .

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Sensitivity of the basic reproductive number

Sensitivity Analysis is commonly used to determine the robustness of model prediction.
In this paper we used it to determine parameters that have high impact on the RC and should
be targeted by intervention strategies. The normalised forward sensitivity index of a variable
with respect to a parameter which is the ratio of relative changes in the parameter when the
variable is a differentiable function of the parameter. The normalised forward sensitivity index
R P
of RC that depends differentially on a parameter P is defined by PRC = C 
P RC

Table 3. The sensitivity index of the parameters of the basic reproductive numer.

Parameter Sensitivity index

𝛽 1
ᶓ – 0.3333
 – 0.3333
 +1
Ƞ – 0.8064
 – 0.9630
 +1
δ – 0.2564
 – 0.9740

3. CONCLUSIONS

This paper developed and analyzed a deterministic mathematical model for measles
transmission dynamics. The model incorporates both recruitment and continuous vaccination
strategies. The continuous strategy was introduced as a make-up for adults who missed the
vaccination opportunity at the point of recruitment. The disease-free and endemic equilibrium
of the model was obtained and analyzed for local stability using the basic reproductive number
as a threshold. We fitted the model to measles outbreak data in NunuKumba District, East
Wollega Zone, Oromia Regional State, Western Ethiopia, for 17 weeks between the 47th weeks
of 2019 to the 11th week of 2020.
Further, we carry out some simulations; Figure 4 is a 2D contour plot of the basic
reproductive number of the model with respect to the recruitment rate  , and the continuous
vaccination rate  , while Figure 5 is the 3D contour plot of the same variable. Figure 6 is the
2D contour plot of the recruitment rate  , and the recruitment vaccination coverage  , while

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Figure 7 is the 3D contour plot of the same variables. Figure 8 is a 2D contour plot of the
recruitment rate  , and the recruitment vaccination efficacy  , while Figure 9 is the 3D contour
plot of the same variables. Figure 10 is the simulation of the infected population with respect
to the recovery rate,  . The result of the simulations indicates that measles may not be
eliminated from the population by vaccination as the only control, but the outbreak can be
contained within weeks, as can be seen from Figure 10. Figures 4 to 9 show the values of the
basic reproductive number resulting from three critical parameters in 2D and 3D. The sensitivity
analysis of the basic reproductive number Table 3 shows that the birth rate  , progression of
the exposed  , and the contact rate are the most sensitive parameters.

Further research. We intend to consider country-wide data and incorporate other control
measures in the future.

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