Dataset Information

SPop: Age-structured discrete-time population dynamics model in C, Python, and R.

ABSTRACT: This article describes the sPop packages implementing the deterministic and stochastic versions of an age-structured discrete-time population dynamics model. The packages enable mechanistic modelling of a population by monitoring the age and development stage of each individual. Survival and development are included as the main effectors and they progress at a user-defined pace: follow a fixed-rate, delay for a given time, or progress at an age-dependent manner. The model is implemented in C, Python, and R with a uniform design to ease usage and facilitate adoption. Early versions of the model were previously employed for investigating climate-driven population dynamics of the tiger mosquito and the chikungunya disease spread by this vector. The sPop packages presented in this article enable the use of the model in a range of applications extending from vector-borne diseases towards any age-structured population including plant and animal populations, microbial dynamics, host-pathogen interactions, infectious diseases, and other time-dependent epidemiological processes.

SUBMITTER: Erguler K

PROVIDER: S-EPMC6198259 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

sPop: Age-structured discrete-time population dynamics model in C, Python, and R.

Erguler Kamil K

F1000Research 20180808

This article describes the sPop packages implementing the deterministic and stochastic versions of an age-structured discrete-time population dynamics model. The packages enable mechanistic modelling of a population by monitoring the age and development stage of each individual. Survival and development are included as the main effectors and they progress at a user-defined pace: follow a fixed rate, delay for a given time, or progress at an age-dependent manner. The model is implemented in C, Py ...[more]

PMID: 30410730

Similar Datasets

Project description:BackgroundTrachoma, the worldwide leading infectious cause of blindness, is due to repeated conjunctival infection with Chlamydia trachomatis. The effects of control interventions on population levels of infection and active disease can be promptly measured, but the effects on severe ocular sequelae require long-term monitoring. We present an age-structured mathematical model of trachoma transmission and disease to predict the impact of interventions on the prevalence of blinding trachoma.Methodology/principal findingsThe model is based on the concept of multiple reinfections leading to progressive conjunctival scarring, trichiasis, corneal opacity and blindness. It also includes aspects of trachoma natural history, such as an increasing rate of recovery from infection and a decreasing chlamydial load with subsequent infections that depend upon a (presumed) acquired immunity that clears infection with age more rapidly. Parameters were estimated using maximum likelihood by fitting the model to pre-control infection prevalence data from hypo-, meso- and hyperendemic communities from The Gambia and Tanzania. The model reproduces key features of trachoma epidemiology: 1) the age-profile of infection prevalence, which increases to a peak at very young ages and declines at older ages; 2) a shift in this prevalence peak, toward younger ages in higher force of infection environments; 3) a raised overall profile of infection prevalence with higher force of infection; and 4) a rising profile, with age, of the prevalence of the ensuing severe sequelae (trachomatous scarring, trichiasis), as well as estimates of the number of infections that need to occur before these sequelae appear.Conclusions/significanceWe present a framework that is sufficiently comprehensive to examine the outcomes of the A (antibiotic) component of the SAFE strategy on disease. The suitability of the model for representing population-level patterns of infection and disease sequelae is discussed in view of the individual processes leading to these patterns.

Project description:BACKGROUND: Culicoides imicola KIEFFER, 1913 (Diptera: Ceratopogonidae) is the principal vector of Bluetongue disease in the Mediterranean basin, Africa and Asia. Previous studies have identified a range of eco-climatic variables associated with the distribution of C. imicola, and these relationships have been used to predict the large-scale distribution of the vector. However, these studies are not temporally-explicit and can not be used to predict the seasonality in C. imicola abundances. Between 2001 and 2006, longitudinal entomological surveillance was carried out throughout Italy, and provided a comprehensive spatio-temporal dataset of C. imicola catches in Onderstepoort-type black-light traps, in particular in Sardinia where the species is considered endemic. METHODS: We built a dynamic model that allows describing the effect of eco-climatic indicators on the monthly abundances of C. imicola in Sardinia. Model precision and accuracy were evaluated according to the influence of process and observation errors. RESULTS: A first-order autoregressive cofactor, a digital elevation model and MODIS Land Surface Temperature (LST)/or temperatures acquired from weather stations explained ~77% of the variability encountered in the samplings carried out in 9 sites during 6?years. Incorporating Normalized Difference Vegetation Index (NDVI) or rainfall did not increase the model's predictive capacity. On average, dynamics simulations showed good accuracy (predicted vs. observed r corr?=?0.9). Although the model did not always reproduce the absolute levels of monthly abundances peaks, it succeeded in reproducing the seasonality in population level and allowed identifying the periods of low abundances and with no apparent activity. On that basis, we mapped C. imicola monthly distribution over the entire Sardinian region. CONCLUSIONS: This study demonstrated prospects for modelling data arising from Culicoides longitudinal entomological surveillance. The framework explicitly incorporates the influence of eco-climatic factors on population growth rates and accounts for observation and process errors. Upon validation, such a model could be used to predict monthly population abundances on the basis of environmental conditions, and hence can potentially reduce the amount of entomological surveillance.

Project description:Vectorial capacity and the basic reproductive number (R(0)) have been instrumental in structuring thinking about vector-borne pathogen transmission and how best to prevent the diseases they cause. One of the more important simplifying assumptions of these models is age-independent vector mortality. A growing body of evidence indicates that insect vectors exhibit age-dependent mortality, which can have strong and varied affects on pathogen transmission dynamics and strategies for disease prevention.Based on survival analysis we derived new equations for vectorial capacity and R(0) that are valid for any pattern of age-dependent (or age-independent) vector mortality and explore the behavior of the models across various mortality patterns. The framework we present (1) lays the groundwork for an extension and refinement of the vectorial capacity paradigm by introducing an age-structured extension to the model, (2) encourages further research on the actuarial dynamics of vectors in particular and the relationship of vector mortality to pathogen transmission in general, and (3) provides a detailed quantitative basis for understanding the relative impact of reductions in vector longevity compared to other vector-borne disease prevention strategies.Accounting for age-dependent vector mortality in estimates of vectorial capacity and R(0) was most important when (1) vector densities are relatively low and the pattern of mortality can determine whether pathogen transmission will persist; i.e., determines whether R(0) is above or below 1, (2) vector population growth rate is relatively low and there are complex interactions between birth and death that differ fundamentally from birth-death relationships with age-independent mortality, and (3) the vector exhibits complex patterns of age-dependent mortality and R(0) ? 1. A limiting factor in the construction and evaluation of new age-dependent mortality models is the paucity of data characterizing vector mortality patterns, particularly for free ranging vectors in the field.

Project description:BACKGROUND:Tuberculosis (TB) is the leading cause of death in South Africa. The burden of disease varies by age, with peaks in TB notification rates in the HIV-negative population at ages 0-5, 20-24, and 45-49 years. There is little variation between age groups in the rates in the HIV-positive population. The drivers of this age pattern remain unknown. METHODS:We developed an age-structured simulation model of Mycobacterium tuberculosis (Mtb) transmission in Cape Town, South Africa. We considered five states of TB progression: susceptible, infected (latent TB), active TB, treated TB, and treatment default. Latently infected individuals could be re-infected; a previous Mtb infection slowed progression to active disease. We further considered three states of HIV progression: HIV negative, HIV positive, on antiretroviral therapy. To parameterize the model, we analysed treatment outcomes from the Cape Town electronic TB register, social mixing patterns from a Cape Town community and used literature estimates for other parameters. To investigate the main drivers behind the age patterns, we conducted sensitivity analyses on all parameters related to the age structure. RESULTS:The model replicated the age patterns in HIV-negative TB notification rates of Cape Town in 2009. Simulated TB notification rate in HIV-negative patients was 1000/100,000 person-years (pyrs) in children aged <5 years and decreased to 51/100,000 in children 5-15 years. The peak in early adulthood occurred at 25-29 years (463/100,000 pyrs). After a subsequent decline, simulated TB notification rates gradually increased from the age of 30 years. Sensitivity analyses showed that the dip after the early adult peak was due to the protective effect of latent TB and that retreatment TB was mainly responsible for the rise in TB notification rates from the age of 30 years. CONCLUSION:The protective effect of a first latent infection on subsequent infections and the faster progression in previously treated patients are the key determinants of the age-structure of TB notification rates in Cape Town.

Dataset Information

SPop: Age-structured discrete-time population dynamics model in C, Python, and R.

Publications

sPop: Age-structured discrete-time population dynamics model in C, Python, and R.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets