Dataset Information

Estimating infectious disease transmission distances using the overall distribution of cases.

ABSTRACT: The average spatial distance between transmission-linked cases is a fundamental property of infectious disease dispersal. However, the distance between a case and their infector is rarely measurable. Contact-tracing investigations are resource intensive or even impossible, particularly when only a subset of cases are detected. Here, we developed an approach that uses onset dates, the generation time distribution and location information to estimate the mean transmission distance. We tested our method using outbreak simulations. We then applied it to the 2001 foot-and-mouth outbreak in Cumbria, UK, and compared our results to contact-tracing activities. In simulations with a true mean distance of 106m, the average mean distance estimated was 109m when cases were fully observed (95% range of 71-142). Estimates remained consistent with the true mean distance when only five percent of cases were observed, (average estimate of 128m, 95% range 87-165). Estimates were robust to spatial heterogeneity in the underlying population. We estimated that both the mean and the standard deviation of the transmission distance during the 2001 foot-and-mouth outbreak was 8.9km (95% CI: 8.4km-9.7km). Contact-tracing activities found similar values of 6.3km (5.2km-7.4km) and 11.2km (9.5km-12.8km), respectively. We were also able to capture the drop in mean transmission distance over the course of the outbreak. Our approach is applicable across diseases, robust to under-reporting and can inform interventions and surveillance.

SUBMITTER: Salje H

PROVIDER: S-EPMC5159225 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Estimating infectious disease transmission distances using the overall distribution of cases.

Salje Henrik H Cummings Derek A T DAT Lessler Justin J

Epidemics 20161007

The average spatial distance between transmission-linked cases is a fundamental property of infectious disease dispersal. However, the distance between a case and their infector is rarely measurable. Contact-tracing investigations are resource intensive or even impossible, particularly when only a subset of cases are detected. Here, we developed an approach that uses onset dates, the generation time distribution and location information to estimate the mean transmission distance. We tested our m ...[more]

PMID: 27744095

Similar Datasets

Project description:BackgroundThe spread of infectious diseases in populations is controlled by the susceptibility (propensity to acquire infection), infectivity (propensity to transmit infection), and recoverability (propensity to recover/die) of individuals. Estimating genetic risk factors for these three underlying host epidemiological traits can help reduce disease spread through genetic control strategies. Previous studies have identified important 'disease resistance single nucleotide polymorphisms (SNPs)', but how these affect the underlying traits is an unresolved question. Recent advances in computational statistics make it now possible to estimate the effects of SNPs on host traits from epidemic data (e.g. infection and/or recovery times of individuals or diagnostic test results). However, little is known about how to effectively design disease transmission experiments or field studies to maximise the precision with which these effects can be estimated.ResultsIn this paper, we develop and validate analytical expressions for the precision of the estimates of SNP effects on the three above host traits for a disease transmission experiment with one or more non-interacting contact groups. Maximising these expressions leads to three distinct 'experimental' designs, each specifying a different set of ideal SNP genotype compositions across groups: (a) appropriate for a single contact-group, (b) a multi-group design termed "pure", and (c) a multi-group design termed "mixed", where 'pure' and 'mixed' refer to groupings that consist of individuals with uniformly the same or different SNP genotypes, respectively. Precision estimates for susceptibility and recoverability were found to be less sensitive to the experimental design than estimates for infectivity. Whereas the analytical expressions suggest that the multi-group pure and mixed designs estimate SNP effects with similar precision, the mixed design is preferred because it uses information from naturally-occurring rather than artificial infections. The same design principles apply to estimates of the epidemiological impact of other categorical fixed effects, such as breed, line, family, sex, or vaccination status. Estimation of SNP effect precisions from a given experimental setup is implemented in an online software tool SIRE-PC.ConclusionsMethodology was developed to aid the design of disease transmission experiments for estimating the effect of individual SNPs and other categorical variables that underlie host susceptibility, infectivity and recoverability. Designs that maximize the precision of estimates were derived.

Project description:Individuals differ widely in their contribution to the spread of infection within and across populations. Three key epidemiological host traits affect infectious disease spread: susceptibility (propensity to acquire infection), infectivity (propensity to transmit infection to others) and recoverability (propensity to recover quickly). Interventions aiming to reduce disease spread may target improvement in any one of these traits, but the necessary statistical methods for obtaining risk estimates are lacking. In this paper we introduce a novel software tool called SIRE (standing for "Susceptibility, Infectivity and Recoverability Estimation"), which allows for the first time simultaneous estimation of the genetic effect of a single nucleotide polymorphism (SNP), as well as non-genetic influences on these three unobservable host traits. SIRE implements a flexible Bayesian algorithm which accommodates a wide range of disease surveillance data comprising any combination of recorded individual infection and/or recovery times, or disease diagnostic test results. Different genetic and non-genetic regulations and data scenarios (representing realistic recording schemes) were simulated to validate SIRE and to assess their impact on the precision, accuracy and bias of parameter estimates. This analysis revealed that with few exceptions, SIRE provides unbiased, accurate parameter estimates associated with all three host traits. For most scenarios, SNP effects associated with recoverability can be estimated with highest precision, followed by susceptibility. For infectivity, many epidemics with few individuals give substantially more statistical power to identify SNP effects than the reverse. Importantly, precise estimates of SNP and other effects could be obtained even in the case of incomplete, censored and relatively infrequent measurements of individuals' infection or survival status, albeit requiring more individuals to yield equivalent precision. SIRE represents a new tool for analysing a wide range of experimental and field disease data with the aim of discovering and validating SNPs and other factors controlling infectious disease transmission.

Project description: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.

Dataset Information

Estimating infectious disease transmission distances using the overall distribution of cases.

Publications

Estimating infectious disease transmission distances using the overall distribution of cases.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets