William O. Kermack

Bio: William O. Kermack is an academic researcher from Royal College of Physicians. The author has contributed to research in topics: Population & Quinoline. The author has an hindex of 14, co-authored 60 publications receiving 17389 citations. Previous affiliations of William O. Kermack include Royal College of Physicians of Edinburgh.

A contribution to the mathematical theory of epidemics

Abstract: (1) One of the most striking features in the study of epidemics is the difficulty of finding a causal factor which appears to be adequate to account for the magnitude of the frequent epidemics of disease which visit almost every population. It was with a view to obtaining more insight regarding the effects of the various factors which govern the spread of contagious epidemics that the present investigation was undertaken. Reference may here be made to the work of Ross and Hudson (1915-17) in which the same problem is attacked. The problem is here carried to a further stage, and it is considered from a point of view which is in one sense more general. The problem may be summarised as follows: One (or more) infected person is introduced into a community of individuals, more or less susceptible to the disease in question. The disease spreads from the affected to the unaffected by contact infection. Each infected person runs through the course of his sickness, and finally is removed from the number of those who are sick, by recovery or by death. The chances of recovery or death vary from day to day during the course of his illness. The chances that the affected may convey infection to the unaffected are likewise dependent upon the stage of the sickness. As the epidemic spreads, the number of unaffected members of the community becomes reduced. Since the course of an epidemic is short compared with the life of an individual, the population may be considered as remaining constant, except in as far as it is modified by deaths due to the epidemic disease itself. In the course of time the epidemic may come to an end. One of the most important probems in epidemiology is to ascertain whether this termination occurs only when no susceptible individuals are left, or whether the interplay of the various factors of infectivity, recovery and mortality, may result in termination, whilst many susceptible individuals are still present in the unaffected population. It is difficult to treat this problem in its most general aspect. In the present communication discussion will be limited to the case in which all members of the community are initially equally susceptible to the disease, and it will be further assumed that complete immunity is conferred by a single infection.

A Contribution to the Mathematical Theory of Epidemics.

Abstract: (1) One of the most striking features in the study of epidemics is the difficulty of finding a causal factor which appears to be adequate to account for the magnitude of the frequent epidemics of disease which visit almost every population. It was with a view to obtaining more insight regarding the effects of the various factors which govern the spread of contagious epidemics that the present investigation was undertaken. Reference may here be made to the work of Ross and Hudson (1915-17) in which the same problem is attacked. The problem is here carried to a further stage, and it is considered from a point of view which is in one sense more general. The problem may be summarised as follows: One (or more) infected person is introduced into a community of individuals, more or less susceptible to the disease in question. The disease spreads from the affected to the unaffected by contact infection. Each infected person runs through the course of his sickness, and finally is removed from the number of those who are sick, by recovery or by death. The chances of recovery or death vary from day to day during the course of his illness. The chances that the affected may convey infection to the unaffected are likewise dependent upon the stage of the sickness. As the epidemic spreads, the number of unaffected members of the community becomes reduced. Since the course of an epidemic is short compared with the life of an individual, the population may be considered as remaining constant, except in as far as it is modified by deaths due to the epidemic disease itself. In the course of time the epidemic may come to an end. One of the most important probems in epidemiology is to ascertain whether this termination occurs only when no susceptible individuals are left, or whether the interplay of the various factors of infectivity, recovery and mortality, may result in termination, whilst many susceptible individuals are still present in the unaffected population. It is difficult to treat this problem in its most general aspect. In the present communication discussion will be limited to the case in which all members of the community are initially equally susceptible to the disease, and it will be further assumed that complete immunity is conferred by a single infection.

Contributions to the Mathematical Theory of Epidemics. II. The Problem of Endemicity

Abstract: In a previous communication an attempt was made to investigate mathe­matically the course of an epidemic in a closed population of susceptible individuals. In order to simplify the problem certain definite assumptions were made, namely, that all individuals were equally susceptible, and that death resulted, or complete immunity was conferred, as the result of an attack. The infectivity of the individual and his chances of death or recovery were represented by arbitrary functions, and the chance of a new infection occurring was assumed to be proportional to the product of the infected and susceptible members of the population. In spite of the introduction of the arbitrary functions, it was shown that in general a critical density of population existed, such that if the actual density was less than this, no epidemic could occur, but if it exceeded this by n an epidemic would appear on the introduction of a focus of infection, and further that if n was small relative to the population density, the size of the epidemic would be 2 n per unit area. It was shown that these conclusions could be readily extended to the case of a metaxenous disease, that is, one in which transmission takes place through an intermediate host. It is the purpose of the present paper to consider the effect of the continuous introduction of fresh susceptible individuals into the population. It appeared desirable to investigate this point, since it might make it possible to interpret certain aspects of the incidence of disease not only in human communities where there is usually an influx of fresh susceptible individuals either by immigration or by birth, but also in the animal experiments carried out by Topley and others—where fresh animals were introduced at a constant rate into the cages in which cases of disease were already present—from which certain definite results were obtained.

The Mathematics of Infectious Diseases

Abstract: Many models for the spread of infectious diseases in populations have been analyzed mathematically and applied to specific diseases. Threshold theorems involving the basic reproduction number $R_{0}$, the contact number $\sigma$, and the replacement number $R$ are reviewed for the classic SIR epidemic and endemic models. Similar results with new expressions for $R_{0}$ are obtained for MSEIR and SEIR endemic models with either continuous age or age groups. Values of $R_{0}$ and $\sigma$ are estimated for various diseases including measles in Niger and pertussis in the United States. Previous models with age structure, heterogeneity, and spatial structure are surveyed.

Epidemic processes in complex networks

Abstract: Complex networks arise in a wide range of biological and sociotechnical systems. Epidemic spreading is central to our understanding of dynamical processes in complex networks, and is of interest to physicists, mathematicians, epidemiologists, and computer and social scientists. This review presents the main results and paradigmatic models in infectious disease modeling and generalized social contagion processes.

Population biology of infectious diseases: Part II

Abstract: If the host population is taken to be a dynamic variable (rather than constant, as conventionally assumed), a wider understanding of the population biology of infectious diseases emerges. In this first part of a two-part article, mathematical models are developed, shown to fit data from laboratory experiments, and used to explore the evolutionary relations among transmission parameters. In the second part of the article, to be published in next week's issue, the models are extended to include indirectly transmitted infections, and the general implications for infectious diseases are considered.

BEAST 2.5: An advanced software platform for Bayesian evolutionary analysis.

Abstract: Elaboration of Bayesian phylogenetic inference methods has continued at pace in recent years with major new advances in nearly all aspects of the joint modelling of evolutionary data. It is increasingly appreciated that some evolutionary questions can only be adequately answered by combining evidence from multiple independent sources of data, including genome sequences, sampling dates, phenotypic data, radiocarbon dates, fossil occurrences, and biogeographic range information among others. Including all relevant data into a single joint model is very challenging both conceptually and computationally. Advanced computational software packages that allow robust development of compatible (sub-)models which can be composed into a full model hierarchy have played a key role in these developments. Developing such software frameworks is increasingly a major scientific activity in its own right, and comes with specific challenges, from practical software design, development and engineering challenges to statistical and conceptual modelling challenges. BEAST 2 is one such computational software platform, and was first announced over 4 years ago. Here we describe a series of major new developments in the BEAST 2 core platform and model hierarchy that have occurred since the first release of the software, culminating in the recent 2.5 release.