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1 Introduction
accounts to 3–5 million cholera cases and 100,000–120,000 deaths around the
globe.
Cholera is caused by the bacterium Vibrio cholera. The bacteria enter into the
human body through ingestion of contaminated water and food. Cholera can
transmit directly, from human to human, and also indirectly, from environment to
human. At primary stage, there may be no symptoms of the infection but in long
term, it may turn fatal and cause leg cramps, vomiting, and watery diarrhea (Mwasa
and Tchuenche 2011). In the absence of proper treatment, the infection results in
circulatory collapse, rapid dehydration, and death within 12–24 h (Sanchez et al.
1994). Despite several efforts, cholera is still an endemic in many parts of the world
(Safi et al. 2013). Accounts to this, a number of mathematical models are proposed
and analyzed to comprehend the dynamics of cholera. To study the spread of 1973
cholera in Mediterranean, a mathematical model was proposed and analyzed by
Capasso and Fontana (1979). In Codeço (2001), an extension of the general SIR
epidemic model is proposed by incorporating environmental component to under-
stand the dynamics of cholera. Hartley et al. (2005) extended the model proposed in
Codeço (2001) by introducing the concept of hyperinfectivity. The mathematical
model proposed in Mukandavire et al. (2011) considers both human-to-human and
environment-to-human transmission of cholera to study the patterns of disease
transmission in Zimbabwe. The model proposed in Mwasa and Tchuenche (2011),
and Posny et al. (2015) investigate the role of public health interventions to prevent
the spread of epidemics. As vaccination is a significant tool to reduce the size of the
epidemic, therefore a number of models pertaining to cholera address the role of
vaccination on the spread of cholera (Safi et al. 2013; Zhou et al. 2012; Zhou and
Cui 2011). The use of disinfectants is another potential method to prevent the
spread of cholera. Hence, mathematical models are also used to study the impact of
disinfectants on the dynamics of cholera (Misra and Singh 2012; Misra et al. 2012).
The manuscript is organized in four sections. A survey on possible causes of
backward bifurcation in epidemic models is performed in Sect. 2. The existence of
backward bifurcation is explored in Sect. 3. The manuscript ends with a conclusion
of our study in Sect. 4.
2 Backward Bifurcation
dS bSB
¼ ð1 qÞA /S þ hV l1 S
dt ðK þ BÞ
dV rbVB
¼ qA þ /S hV l1 V
dt ðK þ BÞ
ð1Þ
dI bSB rbVB
¼ þ ð d þ a þ l1 Þ
dt ðK þ BÞ ðK þ BÞ
dB
¼ gI l2 B
dt
The details of assumptions and parameters of the model can be find in Zhou et al.
(2012).
The model possesses two equilibrium points, namely disease free and endemic.
The disease-free equilibrium point is given as E0 ¼ ðS0 ; V 0 ; 0; 0Þ where,
A1 I 2 þ A2 I þ A3 ¼ 0
where,
A1 ¼ l2 ðl1 þ d þ aÞ l21 þ l1 h þ l1 / þ l1 b þ l1 br þ b2 r þ bh þ b/r
A2 ¼ Kl1 2l21 þ 2l1 h þ 2l1 / þ bl1 þ b/r þ bh þ l1 rb
Abrðrb þ l1 rq þ l1 þ h þ /r ql1 Þ
A3 ¼ Kl1 l2 ðl1 þ d þ aÞðl1 þ h þ /Þð1 Rv Þ
dS bSB cI
¼A l1 S þ rI þ
dt K þB bþI
dI bSB cI
¼ ðr þ l1 þ dÞI ð2Þ
dt K þ B bþI
dB
¼ gI l2 B
dt
P1 I 2 þ P2 I þ P3 ¼ 0
678 S. Sharma and N. Kumari
Here,
P1 ¼ g l1 r þ l21 þ bd þ bl1 þ l1 d
P2 ¼ Kl1 l2 r þ Kl1 l2 d þ Kl21 l2 þ gl1 bb þ gdbb þ bgrl1
þ l21 bg þ l1 dgb þ Abg
P3 ¼ Kl1 l2 ðbl1 þ c þ rb þ dbÞð1 R0 Þ
Motivated from this, we propose a new model with saturated removal rate b cIþ I as
follows
dS bSB
¼A dS
dt K þB
dI bSB cI
¼ ðr þ d þ dÞI
dt K þ B bþI ð3Þ
dR cI
¼ þ rI dR
dt bþI
dB
¼ gI lB
dt
In the model (3), A represents the total recruitment rate (including immigrants and
newborns). KbSBþ B is the disease transmission rate, where K is the concentration of the
bacteria that yields 50% chance of catching infection. The model also involves natural
recovery rate r. The natural death rate d is same for individuals of each compartment,
while the disease-related death rate is d. η is the rate at which infected population
contribute to the concentration of bacteria. The natural decay rate of the bacteria is µ.
The basic difference between models (2) and (3) is movement of the recovered
individuals. In model (2), the recovered individuals join the susceptible class and
may again get infected, while in model (3) recovered individuals join the removed
class and do not become infected, once recovered. Similar studies are available in
literature on generic compartmental models (Wang 2006, 2009).
Now, we obtain the disease-free equilibrium point as E 0 ¼ Ad ; 0; 0 : Next, we
calculate the basic reproduction number of the model using the next-generation
matrix method given by Van den Driessche and Watmough (2002) as
Agbb
R0 ¼
Kld ðrb þ bd þ db þ cÞ
AI 2 þ BI þ C ¼ 0
Possibility and Causes of Backward Bifurcation in a Cholera Model 679
where,
A ¼ g dr þ d 2 þ bd þ bd þ dd þ br
B ¼ gbbd þ gbbd þ gbbr þ gbc þ lKd 2 þ lKdd þ lKdr
þ gbd 2 þ gbdd þ gbdr þ gcd Abg
C ¼ Kld ðbd þ c þ rb þ dbÞð1 R0 Þ
Here, we state the following result for the existence of endemic equilibrium
Theorem 3.1 The proposed model system (3) has
(i) a unique endemic equilibrium whenever R0 [ 1;
(ii) a unique endemic equilibrium whenever R0 ¼ 1 and B < 0;
(iii) two endemic equilibriums if R0 \1, B < 0 and B2 4AC [ 0;
(iv) no endemic equilibrium otherwise.
Now, we discuss graphically the possibility of the backward bifurcation in
Fig. 3.
The infectious population at equilibria versus R0 shows a backward bifurcation
when Rc \R0 \1, leading to the existence of multiple endemic equilibria. The
saddle-node bifurcation occurs at R0 ¼ Rc , where the stable endemic equilibria
collide with other unstable endemic equilibria.
Although reinfection is not involved here, still the model shows the possibility of
the backward bifurcation.
4 Conclusion
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