Research in Mathematics

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Mathematical model for prevention and control of

cholera transmission in a variable population

Martins O. Onuorah, F. A. Atiku & H. Juuko |

To cite this article: Martins O. Onuorah, F. A. Atiku & H. Juuko | (2022) Mathematical model for
prevention and control of cholera transmission in a variable population, Research in Mathematics,
9:1, 2018779, DOI: 10.1080/27658449.2021.2018779

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RESEARCH IN MATHEMATICS
2022, VOL. 9, NO. 1, 1–13
https://doi.org/10.1080/27658449.2021.2018779

APPLIED & INTERDISCIPLINARY MATHEMATICS | RESEARCH ARTICLE

Mathematical model for prevention and control of cholera transmission in

a variable population
a
Martins O. Onuorah , F. A. Atikub and H. Juukoc
a
School of Mathematics and Computing, Department of Mathematics, Main Campus, Kampala International University, Kansanga, Uganda;
b
School of Engineering and Applied Sciences, Department of Mechanical Engineering, Western Campus, Kampala International University,
Isaak, Uganda; cCollege of Education Open and Distance Learning, Main Campus, Kampala International University, Kansanga, Uganda

ABSTRACT ARTICLE HISTORY

In this paper, an extended SIRB deterministic epidemiological model for Cholera was developed Received 19 January 2021
and strictly analysed to ascertain the impact of immigration in cholera transmission and to assess Accepted 12 December 2021
the suitability of the various control measures. The model was found to have two equilibria, KEYWORDS
namely, disease-free equilibrium (DFE) and a unique endemic equilibrium (EE). The local stability Stability; equilibrium;
of the DFE and EE were found to be dependent on a certain epidemiological threshold known as simulation; epidemiology;
the basic reproductive number, R0 (number of secondary infections resulting from the introduction uniformly persistence
of a single infected individual into a population), in that DFE is stable when R0 < 1, whereas the EE is
stable when R0 > 1. Furthermore, we used the Lyapunov function and geometric approach respec­
tively to show that the DFE and EE are globally asymptotically stable and that Cholera will persist in
the population when R0 > 1. Our model was fitted to Uganda Cholera cases (1999–2015). The best
fit parameters were then used to carry out numerical simulation of the model. Specifically, the
impact of the control over the long and short cycle transmission routes were found to be more
effective than vaccination in combating the menace of Cholera in Uganda. Finally, the effects of
immigration in the transmission of cholera were validated via numerical simulation using esti­
mated and base line parameter values.

1. Introduction
Cholera is a severe diarrheal infection contacted upon
consumption of food or water that is tainted with the
bacterium Vibrio cholera (Elimian et al., 2019). It is an
extremely noxious disease that can cause severe acute
watery diarrhea, which can be symptomatic or asympto­
matic (Chayu, 2020). The incubation period is between
12 hours and 5 days after which an exposed individual
begin to manifest symptoms (Kahn et al., 2020). If con­
taminated individuals do not get treatment, the acid
level of their body becomes excessive which can multi­
ply the probability of cholera related death within
24 hours (Elimian et al., 2020; Monje et al., 2020).
Recent publications show that sufferers can recover
with immunity which can be long lasting depending
on many factors (Harris, 2018). Cholera has a record
of seven known pandemic, (Fatlawi et al., 2018; Pande
et al., 2018), the most fatal among all the pandemics is
the third that occurred between 1852 and 1859, and cuts
across all continents of the world excluding the
Antarctica and claimed about 23,000 in great Britain
(Fatlawi et al., 2018; Piret & Boivin, 2021). The seventh
and the current cholera pandemic began in Indonesia in
1961 (Boucher et al., 2015; Pande et al., 2018; Piret &
Boivin, 2021). It spread across Asia and the Middle East,
reaching Africa in 1997 (J. Deen et al., 2020;
Ramamurthy et al., 2019). Researchers recently
hypothesised between 1.3 million and 4 million cases
of cholera and 28,000–243,000 cholera deaths annually
throughout the world (Awofeso & Aldabk, 2018).
Cholera is still endemic to sub-Saharan African mostly
among countries with poor infrastructure (Legros,
2018). In 2019 the world cholera cases, deaths and case
fatality rate was put as 499,477, 2990 and 0.6% respec­
tively (World Health Organization, 2019).
Mathematics modeling has been and will always
remain a vital tool in the fight against diseases, mathe­
matical modeling analysis has provided information for
various countries in making public health policies in the
ongoing COVID-19 pandemic (Enserink &
Kupferschmidt, 2020). Over the years, rigorous analyti­
cal and numerical analysis of models has contributed to
the fight against Cholera. Edward and Nkuba (2015)
showed in their work that the use of multiple control

CONTACT Martins O. Onuorah martins.onuorah@kiu.ac.ug School of Mathematics and Computing, Department of Mathematics, Main Campus,
Kansanga, Kampala International University, Uganda
Reviewing editor: Yuriy Rogovchenko Universitetet i Agder, NORWAY
© 2022 The Author(s). This open access article is distributed under a Creative Commons Attribution (CC-BY) 4.0 license.
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2 M. O. ONUORAH ET AL.
measures is far more effective than the application of
single control. Chen et al. (2016) proposed and analysed
a partial differential equation model to ascertain the
effect of human diffusion, and bacteria convection in
Cholera transmission, they also investigated the various
factors that determine the spatial spread of cholera. Sun
et al. (2017) developed a mathematical model to char­
acterize the transmission process of Cholera in China,
the result of their analysis shows that improved envir­
onmental sanitation and provision of clean water is
a better strategy than vaccination. Yang et al. (2017)
proposed two sets of models to ascertain the impact of
awareness/unawareness, their results highlight the
importance of model validation as a prerequisite for
adoption as the two closely related models have different
dynamical behaviours.
More recently, Ayoade et al. (2018), in their work,
showed the possibility of human to human transmission
of cholera and that vaccination and treatment with drug
remains are sufficient to eliminate cholera. Lemos-Paião
et al. (2019) proposed and analysed a mathematical
model for cholera considering vaccination, their analy­
sis and simulation suggest that vaccination has the abil­
ity to stem down cases if started in good time earlier.
Mokati et al. (2019), in their paper, proposed a model to
control cholera via quarantine. Chayu (2020), in his
work, introduced the multi-scale modelling where he
considered the between and within host characteristics.
Yang and Wang (2019), in their model, studied the
effects of medical resources in cholera transmission,
they fitted their model to the Yemen cholera outbreak
during 2017–2018. Meszaros et al. (2020) studied the
transmission of cholera between and within households,
they voted for vaccination far and above water treat­
ment and the use of drugs. Hailemariam Hntsa and
Nerea Kahsay (2020) proposed a model for eradication
of cholera and validated their assumptions using
numerical simulation. Kolaye et al. (2020) proposed
the control of cholera via sensitization and sanitization.
Bakare and Hoskova-
Mayerova (2021), in their paper, developed an optimal
control model for cholera, their analysis shows that the
four control measures considered have the capacity to
control and eradicate cholera in asymptomatic popula­
tions. Phan et al. (2021) developed a stochastic model of
cholera incorporating environmental fluctuation in the
transmission dynamics. Hezam et al. (2021) proposed
an optimal mathematical model that integrates COVID-
19 and cholera, their model aimed at minimizing
infected persons and other costs associated with the
two diseases. Sharma and Singh (2021), in their
research, established the backward bifurcation of
a cholera model with some treatment functions.
The novelty in our work includes the incorporation
of (i) the effects of immigration on the spread of cholera
in a variable population; (ii) short and long cycle trans­
mission route; (iii) model validation using data from
cholera endemic country; and (iv) vaccinated
individuals
The rest of the paper is organised as follows, Section 2
contains the model formulation and assumptions. In
Section 3, we obtained the basic reproductive number
and analysed rigorously, the local and global dynamics
of the model. In Section 4, we fit our model to cholera
reported cases in Uganda from 1999 to 2015, and per­
form some numerical simulation. Finally, in Section 5,
we presented the conclusion, discussion, limitations and
further research.
2. Model formulation
The model assumes a heterogeneous mixing of the
human population and the Vibrio cholera (concentra­
tion). The human population is divided into the suscep­
tible SðtÞ, infected human IðtÞ, and the recovered human
RðtÞ, such that the total human population NðtÞ ¼
SðtÞ þ IðtÞ þ RðtÞ while the Vibrio concentration is
represented by BðtÞ. The susceptible human is generated
by immigration, and the natural birth rate of the human
population β. It is diminished by infection resulting from
interaction with the Vibrio cholera in the environment
(long cycle) at the rate α1 and in the household (short
cycle) at the rate α2 . These two transmission rates are
controlled by ω and φ respectively. The population is
further depleted by the proportion of susceptible indivi­
duals ν who received the oral cholera vaccine. The flow as
shown in Figure 1 can be represented using differential
equation
dS B
¼ ð1 σÞA þ βS ωα1 S φα2 SI
dt K þB
ðν þ μÞS: (1)
The infected human population is generated by infected
immigrants σA, and infection resulting from the contact
of susceptible human with Vibrio cholera in the environ­
B
ment and house hold. ωα1 S KþB is the proportion of
infected resulting from long route and φα2 SI is the pro­
portion from the short route. It is diminished by death
due to infection at the rate δ, natural death at the rate μ
and recovery from the infection at the rate λ. Thus,
dI B
¼ σA þ ωα1 S þ φα2 SI
dt KþB
ðγ þ ε þ μ þ δÞI: (2)
The recovered human is generated as infected indivi­
duals recover at the rate λ and by vaccination of
 RMS: RESEARCH IN MATHEMATICS & STATISTICS 3

susceptible individuals at the rate ν. It is diminished by 3. Local and global analysis of the model
the natural death rate μ. This gives;
In this section, we obtain the effective reproductive
dR number and explore the local and global dynamics of
¼ γI þ νS μR: (3)
dt the model.
The concentration of the Vibrio cholera is generated by
the activities of infected human ε and is decreased by the 3.1 The equilibrium point
decay rate τ Thus,
At the equilibrium points, the rate of change of the
dB
¼ εI τB ηB: (4) model equations are assumed to be zero, that
dt
is dS dI dR dB
dt ¼ dt ¼ dt ¼ dt ¼ 0.
Let N ¼ S þ I þ R þ B: Then dNdt ¼ σA μN δI Equating Equations (1)–(4) to zero, we have:
ðτ þ ηÞB þ βS: It follows that Lim sup NðtÞ � σA
μ :
t!1 B
Thus the region σA þ βS ωα1 S φα2 SI νS μS
n o KþB
D ¼ ðS; I; R; BÞ 2 Rþ : S þ I þ R þ B � σA
4 ¼ 0; (5)
μ , is
a positive invariant set for the system Equations (1)–
B
(4) and that; ð1 σÞA þ ωα1 S þ φα2 SI ðγ þ ε þ μ þ δÞI
K þB
ðH1 Þ There exists a compact absorbing set K � D. ¼ 0;
ðH2 Þ Equations (1)–(4) has a unique equili­
brium �x in D (6)

Figure 1. The schematic diagram for cholera transmission.

4 M. O. ONUORAH ET AL.

Figure 2. Yearly reported cases of cholera in Uganda from 1999 to 2015. Source: The data was extracted from Bwire et al. (2013 and
Health (2017).

Figure 3. The fit of the SIBR model Equations (1)–(4) with the data (Cumulative cases of reported cholera in Uganda from 1999 to 2015).

γI þ νS μR ¼ 0; (7) 3.1.1 Disease free equilibrium (DFE)

At disease free equilibrium, the infective compartments
εI τB ηB ¼ 0 ; (8) are zero, i.e. I ¼ B ¼ 0. Then substituting I ¼ B ¼ 0
 RMS: RESEARCH IN MATHEMATICS & STATISTICS 5

Figure 4. (a) Simulation of the infected human population with vaccination, long and short cycle control in place. All parameter values
are as presented in Tables 1 and 2. (b) Simulation of the infected human population with long and short cycle control in place. All
parameter values are as presented in Tables 1 and 2 except for ν ¼ 0. (c) Simulation of the infected human population with
vaccination. All parameter values are as presented in Tables 1 and 2 except for ω ¼ 0; φ ¼ 0.

into Equations (5)–(8) and simplifying we have that the Substituting Equations (10) and (11) into Equation (5),
DFE of the model Equations (1)–(4) is given by and simplifying we have,

E� ¼ ðS � � � � � �
� ;I ;R ;B Þ � S ��
¼
φα2 ðμ þ δÞ
þ
ωα1
þνþμ β
1
:
σA νσA A Aðτ þ ηÞ σA
¼ ; 0; ;0 : (9)
ðν þ μ βÞ μðν þ μ βÞ
(12)

3.1.2 Endemic equilibrium (EE) Substituting Equations (10) and (12) into Equation (7)
Endemic equilibrium refers to an equilibrium state and simplifying, we have,
where all the compartments of the model are non- � �
zero. To obtain the EE, we solve Equations (5)–(8) γðμ þ δÞ ν φα2 ðμ þ δÞ ωα1
R�� ¼ þ þ
simultaneously and let the EE be represented A σA A Aðτ þ ηÞ
by E�� ¼ ðS�� ; I �� ; R�� ; B�� Þ. 1
þν þ μ βÞ� (13)
Adding Equations (5)–(9), and solving for I we μ
have,
ðμ þ δÞ 3.2 Basic reproductive number
I �� ¼ : (10)
A
The basic reproductive number, ðR0 Þ is a very important
Substituting Equation (10) into Equation (8) and sol­ threshold in disease control. It is defined as the number of
ving, we have, secondary infections resulting from the introduction of an
infective individual into a population where everyone is
εðμ þ δÞ susceptible. The basic reproductive number is however
B�� ¼ : (11) referred to as the effective reproductive number ðRC Þ
Aðτ þ ηÞ
6 M. O. ONUORAH ET AL.

Figure 5. Simulation of the infected human population with variable values of σ; all other parameter values are as presented in
Tables 1 and 2.

when a proportion of the population is immune to the RC ¼ ρðFV 0 Þ

disease as is applicable in this paper. Most public health φα2 S�
¼
policy is targeted at reducing this threshold to the barest ðγ þ ε þ μ þ δÞ
minimum for every disease that poses a public health ωα1 S� ε
þ : (14)
challenge. It is used by modellers to analyse both the ðτ þ ηÞðγ þ ε þ μ þ δÞ
local and global dynamics of epidemic models.
Equation (14) is the spectral radius (largest absolute value)
Following Driessche and Watmough (2002), we
of the eigenvalues of the product matrix FV 0 and thus the
establish the effective reproductive number of our
effective reproductive number.
model by using the next generation operator method.
The matrices F; (for the new infective terms) and V;
Theorem 1. The disease free equilibrium Equation (9) is
(for the transition terms) are respectively given by
locally asymptotically stable when RC < 1
� � Proof
φα2 S� ωα1 S�
F¼ ,
0 0 System (1) to (4) has Jacobian matrix given by;
� � 2 3
ðγ þ ε þ μ þ δÞ 0 ðνþμ βÞ φα2 S� 0 ωα1 S�
V¼ .
ε ðτ þ ηÞ � 6 0 φα2 S� ðγþεþμþδÞ 0 ωα1 S� 7
I ðτ þ ηÞ0 JE� 6
4
7:
5
V0 ¼ ν γ μ 0
ðτ þ ηÞðγ þ ε þ μ þ δÞ ε 0 ε 0 ðτ þηÞ
ðγ þ ε þ μ þ δÞ�; (15)
�
I Where the characteristic equation, ðλI JE Þ ¼ 0 of
FV 0 ¼ ½ φα2 S� ðτ þ ηÞ þ ωα1 εS� Equation (12) is given by;
ðτ þ ηÞðγ þ ε þ μ þ δÞ
ωα1 S� ðγ þ ε þ μ þ δÞ00�; ðλ þ μÞðλ þ ðτ þ ηÞðλ þ ðν þ μ βÞÞ
� φα S� ðτþηÞþωα S� ε � ðλ φα2 S� þ ðγ þ ε þ μ þ δÞÞ ¼ 0 (16)
2 1 ωα1 S�
¼ ðτþηÞðγþεþμþδÞ ðτþηÞ ; Clearly, the first two real negative eigenvalues of
0 0 Equation (16)
 RMS: RESEARCH IN MATHEMATICS & STATISTICS 7

Table 1. Parameters used in the model

Parameters Meaning Value Unit
A Number of immigrants 749; 471 1
year
σ Proportion of infected immigrants 0:394 year 1
ν vaccination rate 0 1 year 1
α1 The probability of contracting cholera from the environment, Estimated year 1
α2 The probability of contracting cholera from the household Estimated year 1
ω The rate at which environmental contract is controlled Estimated year 1
ρ The rate at which household contract controlled Estimated year 1
K Concentration of cholera vibrio in the environment 500 cell/day
γ Recovery rate 0:2 year 1
ε Rate of human contribution to cholera concentration 10 cell:mL 1 :day 1

δ Death due to cholera 0:02 year 1

τ Decay rate of vibrio 0:033 day 1
η Disinfectant rate 4 year 1
β Crude birth rate 0:43 year 1
μ Crude birth rate 0:005 year 1

Table 2. Estimated parameter values

Parameters Before optimization After optimization
α1 0.000015 0.000020269952498
α2 0.000966 0.000612728330244
ω 0.00162 0.002521360315476
φ 0.0073 0.000286356020343
SSE 8.762022988426222e+15 3.199487798191693e+07

are λ1 ¼ μ, λ2 ¼ ðτ þ ηÞ. Theorem 2. The disease free equilibrium Equation (9) is

For the last two eigenvalues, we consider globally asymptotically stable when RC < 1:
ðλ ðν þ μ βÞÞðλ φα2 S� þ ðγ þ ε þ μ þ δÞÞ ¼ 0. Proof
Simplifying, we have; We approach the proof of theorem 2 by the applica­
tion of Lyapunov function. We define the Lyapunov
λ2 λ½ðν þ μ βÞ ðγ þ ε þ μ þ δÞ þ φα2 S� �
candidate;
ðν þ μ βÞððν þ μ βÞðγ þ ε þ μ þ δÞÞ
þ φα2 S� ;aλ2 þ bλ þ c V ¼ ðγ þ ε þ μ þ δÞI;
¼ 0: (17) � �
dV B
Equation (17) is a quadratic equation, if we let λ3 and ¼ ðγ þ ε þ μ þ δÞ ð1 σÞA þ S ωα1
dt KþB
λ4 be the roots of the equation, then the sum and þφα2 Þ ðγ þ ε þ μ þ δÞ�I;
product of the roots will obviously be
since S < S� ;
b ¼ λ3 þ λ4 ; c ¼ λ3 λ4 ; � �
dV � B�
where � ðγ þ ε þ μ þ δÞ ð1 σÞA þ S ωα1
dt K þ B�
b ¼ ðν þ μÞ βÞ þ ððγ þ ε þ μ þ δÞ φα2 S� Þ; þφα2 Þ ðγ þ ε þ μ þ δÞ�I
� ðγ þ ε þ μ
c ¼ ðν þ μÞ βÞððγ þ ε þ μ þ δÞ φα2 S� ÞÞ:
þ δÞ½ð1 σÞA þ S� φα2 ðγ þ ε þ μ þ δÞ�I;
(18) � ðγ þ�ε þ μ �
such that when σAφα2
þ δÞ ð1 σÞA þ ðγ þ ε þ μ þ δÞ I;
ðν þ μ βÞ
RC < 1; φα2 S� < ðγ þ ε þ μ þ δÞ; β < ðν þ μÞ; we
have b > 0; c > 0.
dV
� ðγ þ ε þ μ
Hence λ3 < 0; λ4 < 0: So all roots of are real and dt � �
negative therefore E� is local asymptotically stable in þ δÞ ð1 σÞA2 σðR0 1Þ I:
D.x (19)
8 M. O. ONUORAH ET AL.

Hence from Equation (19), RC � 1 which implies dS B

¼ σA ωα1 S φα2 SI ðν þ μ βÞS;
that dV
dt � 0: We conclude that dt K þB
dI B
¼ ð1 σÞA þ ωα1 S þ φα2 SI ðγ þ ε þ μ þ δÞI;
VðS; I; R; BÞ is negative definite and this proves the dt K þB
global stability of the disease free equilibrium. dB
¼ εI τB ηB:
dt
Theorem 3. The endemic equilibrium of the model (22)
Equations (1) to (4) is locally asymptotically stable
For Equation 16, we use the geometric method
when RC > 1:
credited to Mchael Y. and Muldowney (1996) to obtain
Proof
the asymptotic stability condition for its endemic equi­
The endemic equilibrium (10) has Jacobian matrix
" librium in the case that RC > 1: further, we show the
��
ðνþμ βÞ ωα 1B
KþB�� φα2 I
�
φα2 S� 0 ωα1 S� existence of a compact set in the interior of D that is
JE ��
ωα1 B�� � absorbing for Equation (22) which is equivalent to
KþB�� φα2 I φα2 S� ðγ
showing that Equation (22) is uniformly persistent,
þεþμþδÞ0ωα1 S� νγ μ00ε0 ðτþηÞ�: (20)
hence there exists a constant κ > 0; such that every
�� solution ðSðtÞ; IðtÞ; BðtÞÞ of Equation (16) with initial
The characteristic equation, ðλI JE Þ ¼ 0, of
Equation (20) is given by, data ðSð0Þ; Ið0Þ; Bð0ÞÞ in the interior of D satisfies;
� lim inf SðtÞ � κ; lim inf IðtÞ � κ; lim inf BðtÞ � κ:
ðλ þ μÞðλ þ ðτ þ ηÞ λ2 þ bλ þ c ¼ 0 (21) t!1 t!1 t!1
h ��
i Therefore κ is independent of the initial data D accord­
where b ¼ ðν þ μ βÞ þ ωα 1B
KþB �� þ φα2 I ��
þ ing to Sun et al. (2017), we prove the following result.
ððγ þ ε þ μ þ δÞ φα2 S�� Þ; Preposition 2. The system Equation (22) is uniformly
� persistent if and only if RC > 1
ωα1 B��
c ¼ ðν þ μ βÞ þ Proof
K þ B��
�� �� Combining the local stability analysis of the disease
þφα2�I �ððγ þ ε þ μ þ δÞ � φα2 S Þ
�� free equilibrium, theorems 4.1 and 4.3 in (=Freedman
ωα1 B
φα2 I �� φα2 S�� ; et al. (1994), we know that the system Equation (22) is
K þ B�� �
uniformly persistent if and only RC > 1; the proof of
I ��
¼ ð1 φÞα2 S�� �� ðγ þ ε proposition 2 is completed.
S
� ��
�
ωα1 B
þμ þ δÞ 2 ðν þ μ βÞ� Theorem 4. Assume that RC > 1; then the endemic equi­
K þ B��
� � librium of Equation (22) is globally asymptotically stable.
ωα1 B��
þ ðγ þ ε þ μ þ δÞ ðν þ μ βÞ þ :
K þ B�� Proof
Clearly, λ1 ; λ2 are negative, Consider Equation (23) being the Jacobia of
Then b ¼ λ3 þ λ4 ; c ¼ λ3 λ4 , such that when Equation (22).
� ��
� �
I ��
R0 < 1; 2 ωα 1B
KþB �� þ ðν þ μ βÞ < S�� ðγ þ ε þ μ þ δÞ; B
ωα1 KþB φα2 I ðν þ μ βÞ φα2 S 0
J¼ B
β < ν þ μ we have b > 0; c > 0. Hence λ3 < 0; λ4 < 0: So all ωα1 KþB
roots of Equation (21) are real and negative therefore þφα2 Iφα2 S ðγ þ ε þ μ þ δÞ00ε ðτ þ ηÞ� ; (23)
E�� is local asymptotically stable and that completes the with second additive compound matrix given by
proof of theorem 3. 2 3
b11 þ b22 b23 b13
J ð2Þ ¼ 4 b32 b11 þ b33 b12 5 ;
3.3 Global stability of endemic equilibrium b31 b21 b22 þ b33
Since Equations (1), (2), and (4) are without R we con­ (24)
sider the subsystem where
 RMS: RESEARCH IN MATHEMATICS & STATISTICS 9

B B
b11 ¼ ωα1 φα2 I ðν þ μ βÞ; Dþ jYðtÞj � εjXðtÞj þ ωα1
K þB
b12 ¼ φα2 S; KþB φα2 I ðν þ μ βÞ ðτ þ ηÞjYðtÞj
h i
B
B þφα2 SjZðtÞj; Dþ jQðtÞj � ωα1 KþB φα2 I jYðtÞj
b21 ¼ ωα1 φα2 I;
K þB þ½φα2 S ðγ þ ε þ μ þ δÞ ðτ þ ηÞjZðtÞj�:
b22 ¼ φα2 S ðγ þ ε þ μ þ δÞ; Hence,
b13 ¼ a23 ¼ a31 ¼ 0; �0 �
I I B0 I
b32 ¼ ε; Dþ ðjYðtÞj þ jZðtÞjÞ ¼ ðjYðtÞj þ jZðtÞjÞ
B I B B
�0
b33 ¼ ðτ þ ηÞ: I εI I B0
þ Dþ ðjYðtÞj þ jZðtÞjÞ; � þ
B B I B
From Equation (24), the periodic solutions of the system
I
Equation (22) is as follows ν μ þ β τ ηÞ ðjYðtÞj þ jZðtÞjÞ: (28)
� B
dX B
¼ ωα1 φα2 ðI SÞ ðν þ μ βÞ It follows from Equations (27) and (28) that
dt KþB
dY Dþ QðtÞ � maxfg1 ðtÞ; g2 ðtÞgQðtÞ;
ðγ þ ε þ μ þ δÞ�X;
dt (29)
B
¼ εX þ ωα1 φα2 I ðν þ μ βÞ where
KþB � �
dZ B B
ðτ þ ηÞY þ φα2 SZ; ¼ ωα1 φα2 I Y g1 ðtÞ ¼ ωα1 φα2 I ν μ þ βÞ γ ε μ δÞ;
dt KþB K þB
þ½φα2 S ðγ þ ε þ μ þ δÞ ðτ þ ηÞZ:� (25)
To show the global asymptomatic stability of Equation (30)
(25), we define Lyapunov function Q given as;
� � εI I 0 B0 B
I g2 ðtÞ ¼ þ ωα1 φα2 I ν μþβ
QðX; Y; Z : S; I; BÞ ¼ sup ðXÞ; ðjY j þ jZ jÞ B I B K þB
B τ η:
Assume that ςðtÞ ¼ ðSðtÞ; IðtÞ; BðtÞÞ is the D-periodic (31)
solution of Equation (22). Then from the preposi­
Rewriting the second and third equations of
tion 2, the orbit ςðtÞ remains at a positive distance
Equation (23) we have
from the boundary of D so there exist κ > 0 such
that; ð1 σÞA B
þ ωα1 S þ φα2 S
QðX; Y; Z : S; I; BÞ � κ supfðXÞ; jY j; jZjg: I ðK þ BÞI
I0
(26) ¼ þ ðγ þ ε þ μ þ δÞ; (32)
I
For all ðX; Y; ZÞ 2 R3 and ðS; I; BÞ 2 ςðtÞ. Let and
ðXðtÞ; YðtÞ; ZðtÞÞ be a solution of Equation (25) and
the right hand derivative of QðtÞ exists and calculated εI B0
¼ þ ðτ þ ηÞ:
thus; B B

� Thus
B
Dþ jXðtÞj � ωα1 φα2 ðI SÞ I 0 ðtÞ
KþB maxfg ðtÞ; g2 ðtÞg � ε;
IðtÞ
μ βÞ ðγ þ ε þ μ þ δÞ�jXðtÞj;
ðν þ �
B and
� ωα1 φα2 ðI SÞ ðν þ μ βÞ ðγ þ ε ð#
KþB
þμ þ�δÞ�jXðtÞj þ εðjYðtÞj þ jZðtÞjÞ maxfg1 ðtÞ; g2 ðtÞgdt � log IðtÞj#0 ε# ¼ ε#:
0
B
� ωα1 φα2 ðI SÞ ðν þ μ βÞ ðγ þ ε þ μ It follows from Equation (29) that lim QðtÞ ¼ 0; that
KþB t!1
BI is, lim XðtÞ ¼ lim YðtÞ ¼ lim ZðtÞ ¼ 0 by Equation
þδÞ�jXðtÞj þ ðjYðtÞj þ jZðtÞjÞ; (27) t!1 t!1 t!1
IB (24) and the second compound matrix Equation (26)
10 M. O. ONUORAH ET AL.
is asymptotically stable, which implies that periodic
solution ςðtÞ is asymptotically orbitally stable.
Furthermore, it follows that the Jacobia of Equation
!��
(22) at endemic equilibrium E ¼ ðS�� ; I �� ; B�� Þ is
� B��
ωα1 KþB �� φα2 I �� ðνþμ βÞφα2 S�� 0
J!�� ¼ ��
E ωα1 B
KþB�� þφα2 I �� φα2 S�� ðγþεþμþδÞ00ε ðτþηÞ�:
(34)
And since
� �
B��
φα2 I �� þ ðν þ μ βÞ
ωα1 KþB �� ðφα2 S
��
ðγ
� �
� �
þε þ μ þ δÞÞ < 0, then ð 1Þ�J!�� � > 0:
E
!��
Hence the unique endemic equilibrium E ¼
ðS�� ; I �� ; B�� Þ of Equation (22) is globally asymptotically
stable according to theorem 2.5 of Li and Wang (2002).
4 Data fitting
Cholera remains a major cause of morbidity and mor­
tality in Uganda and the country reports an average of
1,850 cholera cases and 45 deaths annually (Health,
2017). The most affected communities are slums in
Kampala, and other boundary communities located
in the northern region of the country (Bwire et al.,
2013), this underscores the role of immigration to the
spread of cholera. Similarly, between 2011 and 2015,
58% cholera was reported in about 5–10 % of the
population; and this was in the fishing communities
in the country (Bwire et al., 2016). This is a pointer to
the role of poor sanitation and poorly developed infra­
structure as it is the case with these communities.
Prevention is by enhanced hygiene, availability of por­
table water that is safe for drinking/ domestic use, good
environmental/sewerage infrastructures and the use of
oral Cholera vaccines which provide limited protection
for a period of less than or equal to 5 years (Health,
2017).
To evaluate the effectiveness of the control strategies
of cholera in Uganda, we first need reasonable para­
meter values. In line with the aim of this paper, we
target the contract probability at both long and short
cycle route as well as their control parameters, namely
α1 ; α2 ; ω and φ.
To accomplish this, we generated a Matlab code to fit
the data (Figure 2) to the model Equations (1)–(4), as
shown in Figure 3. The estimated parameter values, and
the SSE before and after optimization (in the least
square sense) are show in Table 2.
4. 1 Numerical simulation
We use the values of the model parameters provided in
Tables 1 and 2 to simulate the model as presented in
Figures 4 and 5.
5. Conclusion and recommendation
In this paper, we extended and analysed an SIRB model
to underscore the importance of immigration in cholera
transmission and to assess some control strategies of this
public health challenge. The SIRB deterministic model
was validated by fitting the infected compartment of the
SIRB model with the data (cumulative reported cases of
cholera between 1999 and 2015 in Uganda), as shown in
Figure 3. Our model simulation, Figure 4(b) shows that
control at the short and long cycle transmission routes is
a better strategy than vaccination (Figure 4(c)), in the
control of cholera in Uganda, which is in line with
Edward and Nkuba (2015). However, as shown in
Figure 4(a) ,the simulation of the infected population
with vaccination, long cycle and short cycle control is
the best strategy to the fight against Cholera in Uganda.
The contribution of immigration to the spread of Cholera
in Uganda is affirmed by the simulation of the infected
population with different values of σ; see, Figure 5.
Further, the elimination of cholera will be achieved
longer than expected, as shown by Figure 4; this is also
supported by the persistence characteristics of our model
shown in preposition 2. For a holistic approach to con­
trol, prevention, and possible elimination of cholera in
Uganda, the government should increase access to safe
water, environmental/sewerage infrastructures and vac­
cination in high risk communities. Also, awareness on
the need for sanitation and personal hygiene should be
taken to the high risk communities.
In the feature, we intend to improve the model via
the following:
(i) The data used for the parameter estimation is the
cumulated reported cases for years 1999 through
2015, extracted from Bwire et al. (2013) and
Health (2017), which may be under/over
reported. The model therefore can be improved
by the use of up to date data which will make
cholera characterization in Uganda more reliable.
(ii) Cholera epidemics are believed to be positively
correlated with temperature (Asadgol et al.,
2019). The incorporation of temperature depen­
dent parameter in the long cycle transmission
route of the susceptible equation will also
improve the model.
 RMS: RESEARCH IN MATHEMATICS & STATISTICS 11

(iii) Cholera incidence is found to vary with age
groups (Deen, 2008); therefore, the quality of
the model could be improved by introduction
of age structure.
(iv) Whereas our model is deterministic and we live in
a spatial world, the transmission velocity of the
cholera can be tracked by spatial model (Sun
et al., 2017) for more informed and timely policy
intervention.
Acknowledgements
The authors acknowledges Kampala International University
for the internet facilities made available in the cause of this
research.
PUBLIC INTEREST STATEMENT
In this paper, we represented the transmission dynamics of
chorea with four ordinary differential equations (the model).
The novelty in the model includes the incorporation of (i) short
cycle transmission route example from contaminated food
within the house and long cycle route example through drink­
ing water from the public source. (ii) The effects of immigration
on the spread of cholera in a population (iii) model validation
using data from a cholera endemic country and (iv) vaccinated
individuals. The analysis of the model shows that if the number
of person(s) infected by an infected individual is less than one
person, cholera will be controlled in that population. Secondly,
the analysis implies that cholera burden in a population is
impacted by the number of immigrants who are infected and
calls for proper surveillance within border communities.
Finally, the analysis indicates that control at the short and
long transmission routes is more effective than vaccination.

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