The reemergence of tuberculosis (TB) from the 1980s to the early 1990s instigated extensive researches on the mechanisms behind the transmission dynamics of TB epidemics. This article provides a detailed review of the work on the dynamics and control of TB. The earliest mathematical models describing the TB dynamics appeared in the 1960s and focused on the prediction and control strategies using simulation approaches. Most recently developed models not only pay attention to simulations but also take care of dynamical analysis using modern knowledge of dynamical systems. Questions addressed by these models mainly concentrate on TB control strategies, optimal vaccination policies, approaches toward the elimination of TB in the U.S.A., TB co-infection with HIV/AIDS, drug-resistant TB, responses of the immune system, impacts of demography, the role of public transportation systems, and the impact of contact patterns. Model formulations involve a variety of mathematical areas, such as ODEs (Ordinary Differential Equations) (both autonomous and non-autonomous systems), PDEs (Partial Differential Equations), system of difference equations, system of integro-differential equations, Markov chain model, and simulation models.

Library of Congress Cataloging-in-Publication Data Brauer, Fred.Mathematical models in population biology and epidemiology /Fred Brauer, Carlos Castillo-Chavez.p. cm.-(Texts in applied mathematics; 40) Includes bibliographical references (p.).

Despite improved control measures, Ebola remains a serious public health risk in African regions where recurrent outbreaks have been observed since the initial epidemic in 1976. Using epidemic modeling and data from two well-documented Ebola outbreaks (Congo 1995 and Uganda 2000), we estimate the number of secondary cases generated by an index case in the absence of control interventions R0. Our estimate of R0 is 1.83 (SD 0.06) for Congo (1995) and 1.34 (SD 0.03) for Uganda (2000). We model the course of the outbreaks via an SEIR (susceptible-exposed-infectious-removed) epidemic model that includes a smooth transition in the transmission rate after control interventions are put in place. We perform an uncertainty analysis of the basic reproductive number R0 to quantify its sensitivity to other disease-related parameters. We also analyse the sensitivity of the final epidemic size to the time interventions begin and provide a distribution for the final epidemic size. The control measures implemented during these two outbreaks (including education and contact tracing followed by quarantine) reduce the final epidemic size by a factor of 2 relative the final size with a 2-week delay in their implementation.

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The science and management of infectious disease are entering a new stage. Increasingly public policy to manage epidemics focuses on motivating people, through social distancing policies, to alter their behavior to reduce contacts and reduce public disease risk. Person-to-person contacts drive human disease dynamics. People value such contacts and are willing to accept some disease risk to gain contact-related benefits. The cost-benefit trade-offs that shape contact behavior, and hence the course of epidemics, are often only implicitly incorporated in epidemiological models. This approach creates difficulty in parsing out the effects of adaptive behavior. We use an epidemiological-economic model of disease dynamics to explicitly model the trade-offs that drive person-toperson contact decisions. Results indicate that including adaptive human behavior significantly changes the predicted course of epidemics and that this inclusion has implications for parameter estimation and interpretation and for the development of social distancing policies. Acknowledging adaptive behavior requires a shift in thinking about epidemiological processes and parameters.susceptible-infected-recovered model | R 0 | reproductive number | bioeconomics T he science and management of infectious disease is entering a new stage. The increasing focus on incentive structures to motivate people to engage in social distancing-reducing interpersonal contacts and hence public disease risk (1)-changes what health authorities need from epidemiological models. Social distancing is not new-for centuries humans quarantined infected individuals and shunned the obviously ill, but new approaches are being used to deal with modern social interactions. Scientific development of social distancing public policies requires that epidemiological models explicitly address behavioral responses to disease risk and other incentives affecting contact behavior. This paper models the role of adaptive behavior in an epidemiological system. Recognizing adaptive behavior means explicitly incorporating behavioral responses to disease risk and other incentives into epidemiological models (2, 3). The workhorse of modern epidemiology, the compartmental epidemiological model (4, 5), does not explicitly include behavioral responses to disease risk. The transmission factors in these models combine and confound human behavior and biological processes. We develop a simple compartmental model that explicitly incorporates adaptive behavior and show that this modification alters understanding of standard epidemiological metrics. For example, the basic reproductive number, R 0 , is a function of biological processes and human behavior, but R 0 lacks a behavioral interpretation in the existing literature. Biological and behavioral feedbacks muddle R 0 's biological interpretation and confound its estimation.Prior approaches that incorporate behavior into epidemiological models generally fall into three categories: specification of nonlinear contact rate functions, expanded epidemiologi...

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In this article we use global and regional data from the SARS epidemic in conjunction with a model of susceptible, exposed, infective, diagnosed, and recovered classes of people ("SEIJR") to extract average properties and rate constants for those populations. The model is fitted to data from the Ontario (Toronto) in Canada, Hong Kong in China and Singapore outbreaks and predictions are made based on various assumptions and observations, including the current effect of isolating individuals diagnosed with SARS. The epidemic dynamics for Hong Kong and Singapore appear to be different from the dynamics in Toronto, Ontario. Toronto shows a very rapid increase in the number of cases between March 31st and April 6th, followed by a significant slowing in the number of new cases. We explain this as the result of an increase in the diagnostic rate and in the effectiveness of patient isolation after March 26th. Our best estimates are consistent with SARS eventually being contained in Toronto, although the time of containment is sensitive to the parameters in our model. It is shown that despite the empirically modeled heterogeneity in transmission, SARS' average reproductive number is 1.2, a value quite similar to that computed for some strains of influenza (J. Math. Biol. 27 (1989) 233). Although it would not be surprising to see levels of SARS infection higher than 10% in some regions of the world (if unchecked), lack of data and the observed heterogeneity and sensitivity of parameters prevent us from predicting the long-term impact of SARS. The possibility that 10 or more percent of the world population at risk could eventually be infected with the virus in conjunction with a mortality rate of 3-7% or more, and indications of significant improvement in Toronto support the stringent measures that have been taken to isolate diagnosed cases.