Deterministic and stochastic epidemics with several kinds of susceptibles

1985 ◽  
Vol 17 (01) ◽  
pp. 1-22 ◽  
Author(s):  
Frank Ball

We consider the spread of a general epidemic amongst a population consisting of invididuals with differing susceptibilities to the disease. Deterministic and stochastic versions of the basic model are described and analysed. For both versions of the model we show that assuming a uniform susceptible population, with average susceptibility, leads to an increased spread of infection. We also show how our results can be extended to the carrier-borne epidemic model of Weiss (1965).

1985 ◽  
Vol 17 (1) ◽  
pp. 1-22 ◽  
Author(s):  
Frank Ball

We consider the spread of a general epidemic amongst a population consisting of invididuals with differing susceptibilities to the disease. Deterministic and stochastic versions of the basic model are described and analysed. For both versions of the model we show that assuming a uniform susceptible population, with average susceptibility, leads to an increased spread of infection. We also show how our results can be extended to the carrier-borne epidemic model of Weiss (1965).


Complexity ◽  
2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Zun-Guang Guo ◽  
Jing Li ◽  
Can Li ◽  
Juan Liang ◽  
Yiwei Yan

In this paper, we investigate pattern dynamics of a nonlocal delay SI epidemic model with the growth of susceptible population following logistic mode. Applying the linear stability theory, the condition that the model generates Turing instability at the endemic steady state is analyzed; then, the exact Turing domain is found in the parameter space. Additionally, numerical results show that the time delay has key effect on the spatial distribution of the infected, that is, time delay induces the system to generate stripe patterns with different spatial structures and affects the average density of the infected. The numerical simulation is consistent with the theoretical results, which provides a reference for disease prevention and control.


2018 ◽  
Vol 23 (4) ◽  
pp. 457-474 ◽  
Author(s):  
Guruprasad Samantaa ◽  
Shyam Pada Bera

In this paper, we have considered a dynamical model of Chlamydia disease with varying total population size, bilinear incidence rate, and pulse vaccination strategy in a random environment. It has been shown that the Chlamydia epidemic model has global positive solutions and, under some conditions, it admits a unique positive periodic disease-free solution, which is globally exponentially stable in mean square. We have defined two positive numbers R1 and R2 (< R1). It is proved that the susceptible population will be persistent in the mean and the disease will be going to extinct if R1 < 1 and the susceptible population as well as the disease will be weakly persistent in the mean if R2 > 1. Our analytical findings are explained through numerical simulation, which show the reliability of our model from the epidemiological point of view.


1967 ◽  
Vol 4 (01) ◽  
pp. 19-33 ◽  
Author(s):  
C. J. Ridler-Rowe

The epidemic model considered here, first given by Bartlett (see for example [2]), provides for the immigration of new susceptibles and infectives, as well as describing the spread of infection to susceptibles already present and the removal of infectives. The epidemic curve, relating the numbers of susceptibles and infectives, has been studied for certain cases by Bartlett [1], Kendall [6] and others, and provides a motivation for the results given here. With the aid of criteria given by Reuter [8], [9], the main question considered is the asymptotic behaviour of the mean duration of the epidemic. The behaviour of the limits of the transition probabilities pij (t) as t → ∞ is also investigated.


2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Wenjuan Wang ◽  
Jingqi Xin ◽  
Fengqin Zhang

We incorporate the immigration of susceptible individuals into an SEIR epidemic model, assuming that the immigration rate decreases as the spread of infection increases. For this model, the basic reproduction number,R0, is found, which determines that the disease is either extinct or persistent ultimately. The obtained results show that the disease becomes extinct asR0<1and persists in the population asR0>1.


2016 ◽  
Vol 26 (09) ◽  
pp. 1630024 ◽  
Author(s):  
Ranjit Kumar Upadhyay ◽  
Parimita Roy

Recently, the 2014 Ebola virus (EBOV) outbreak in West Africa was the largest outbreak to date. In this paper, an attempt has been made for modeling the virus dynamics using an SEIR model to better understand and characterize the transmission trajectories of the Ebola outbreak. We compare the simulated results with the most recent reported data of Ebola infected cases in the three most affected countries Guinea, Liberia and Sierra Leone. The epidemic model exhibits two equilibria, namely, the disease-free and unique endemic equilibria. Existence and local stability of these equilibria are explored. Using central manifold theory, it is established that the transcritical bifurcation occurs when basic reproduction number passes through unity. The proposed Ebola epidemic model provides an estimate to the potential number of future cases. The model indicates that the disease will decline after peaking if multisectorial and multinational efforts to control the spread of infection are maintained. Possible implication of the results for disease eradication and its control are discussed which suggests that proper control strategies like: (i) transmission precautions, (ii) isolation and care of infectious Ebola patients, (iii) safe burial, (iv) contact tracing with follow-up and quarantine, and (v) early diagnosis are needed to stop the recurrent outbreak.


2019 ◽  
Vol 8 (2) ◽  
pp. 3071-3077

In this paper an SIR (Susceptible-infectious-recovered) epidemic model consisting of saturated incidence rate with vaccination to the susceptible individual in presence of infected immigrants is studied. Stabilities of disease free and endemic equilibrium are also analyzed. The impact of the infected immigrants in the spread of the illness in a populace is examined. A mathematical model has been used to investigate the inflow of the infected immigrants in a population who rapidly transmit the disease. By using appropriate vaccine level to the susceptible population, disease can be reduced. The main purpose of this work is minimizing the invectives and maximizes the recovered individuals. To attain this, apply optimal vaccination strategies by utilizing the pontryagin’s maximum principle (PMP). Speculative results are demonstrated through the numerical simulations


2014 ◽  
Vol 2014 ◽  
pp. 1-6
Author(s):  
Changhyuck Oh

The initial size of a completely susceptible population in a group of individuals plays a key role in drawing inferences for epidemic models. However, this can be difficult to obtain in practice because, in any population, there might be individuals who may not transmit the disease during the epidemic. This short note describes how to improve the maximum likelihood estimators of the infection rate and the initial number of susceptible individuals and provides their approximate Hessian matrix for the general stochastic epidemic model by using the concept of the penalized likelihood function. The simulations of major epidemics show significant improvements in performance in averages and coverage ratios for the suggested estimator of the initial number in comparison to existing methods. We applied the proposed method to the Abakaliki smallpox data.


1921 ◽  
Vol 19 (4) ◽  
pp. 350-379 ◽  
Author(s):  
W. W. C. Topley

The results so far obtained have raised many questions and answered few of them. The important rôle played in the spread of epidemic disease by the re-accumulation of a susceptible population is clearly indicated. It seems not unreasonable to hope that valuable information as to the effect produced by variations in the rate of such re-accumulation, and on other matters, may be obtained by the satisfying method of direct experiment. The bearing of such information on the well-known fluctuations in the incidence of epidemic diseases, and especially perhaps of those which fall most heavily on children, are too obvious to need emphasising.The following conclusions seem permissible at the present stage:(1) If susceptible mice be continuously added to an infected population the spread of infection will continue over a long period of time. There is no evidence that this period has a limit.(2) When susceptible mice are added continuously and at a constant rate to an infected population, the spread of infection, as judged by a mortality curve, is propagated in regularly recurring waves. These waves are most easily observed by noting the fluctutations in the total cage-population. It seems probable that the period of these fluctuations will be found to depend on the rate of addition of susceptible individuals, but this point has still to be determined.(3) The actual deaths may occur in large groups, with intervals during which deaths are few and far between, or they may fall in a succession of smaller groups, increasing and diminishing in size to form the larger waves. In all cases there is this tendency for the occurrence of such small groups of deaths with definite maximal points. There would seem to be two fluctuating processes, the one superimposed upon the other.(4) The average survival-time of mice added to the cage, and their chance of ultimate survival if no more susceptible mice are introduced, vary according to the phase at which they are added. If they gain entrance to the cage during the rise of a wave they are unlikely to live for long. If they are introduced during the fall of a wave their chances of survival are greatly increased, and they will usually outlive mice which are added at a later date but at a time before the commencement of the next wave.(5) The rate of extinction of a population, among which infection is actively spreading, will be far less rapid if they are kept isolated, than if further susceptible individuals continuously gain access to them. A proportion of the infected population, which would have survived indefinitely under the former circumstances, will die under the latter.(6) The ultimate survivors among such a population have not escaped infection, but have successfully resisted it. A considerable proportion of them are harbouring the causative parasite in their tissues.My sincere thanks are due to my colleagues, Dr H. B. Weir and Dr G. S. Wilson, for their constant help, and to Mrs Phyllis Worthington whose assistance in this work I have been able to obtain by the aid of the Medical Research Council.


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