A beta-Poisson model for infectious disease transmission.

Abstract

Outbreaks of emerging and zoonotic infections represent a substantial threat to human health and well-being. These outbreaks tend to be characterised by highly stochastic transmission dynamics with intense variation in transmission potential between cases. The negative binomial distribution is commonly used as a model for transmission in the early stages of an epidemic as it has a natural interpretation as the convolution of a Poisson contact process and a gamma-distributed infectivity. In this study we expand upon the negative binomial model by introducing a beta-Poisson mixture model in which infectious individuals make contacts at the points of a Poisson process and then transmit infection along these contacts with a beta-distributed probability. We show that the negative binomial distribution is a limit case of this model, as is the zero-inflated Poisson distribution obtained by combining a Poisson-distributed contact process with an additional failure probability. We assess the beta-Poisson model's applicability by fitting it to secondary case distributions (the distribution of the number of subsequent cases generated by a single case) estimated from outbreaks covering a range of pathogens and geographical settings. We find that while the beta-Poisson mixture can achieve a closer to fit to data than the negative binomial distribution, it is consistently outperformed by the negative binomial in terms of Akaike Information Criterion, making it a suboptimal choice on parsimonious grounds. The beta-Poisson performs similarly to the negative binomial model in its ability to capture features of the secondary case distribution such as overdispersion, prevalence of superspreaders, and the probability of a case generating zero subsequent cases. Despite this possible shortcoming, the beta-Poisson distribution may still be of interest in the context of intervention modelling since its structure allows for the simulation of measures which change contact structures while leaving individual-level infectivity unchanged, and vice-versa.