(R2032) Modeling the Effect of Sanitation Effort on the Spread of Carrier-dependent Infectious Diseases due to Environmental Degradation

In this present study, an SIS model is proposed and analyzed to study the effect of sanitation effort in controlling the spread of carrier-dependent infectious disease in a human habitat due to environmental degradation. The dynamics of the model consist of six dependent variables, the susceptible population density, infective population density, carrier population density, cumulative density of environmental degradation and the density of sanitation effort applied on carrier population and degraded environment. In the modeling process, the carrier population density and sanitation effort are modeled logistically and the degradation of the environment is assumed to be directly proportional to the population in the habitat. The analysis of the model is performed by using the stability theory of differential equations and numerical simulations. The study of model shows that as the degradation of environment increases, the density of the carrier population increases which ultimately increases the infective population. Further, the result shows that by applying suitable sanitation effort on the carrier population density and on the cumulative density of environmental degradation, the carrier population density decreases and hence the infective population. Thus, it is very important to keep our environment clean by applying proper sanitation to prevent the spread of carrier-dependent infectious diseases

Analysis of a Vaccination Model for Carrier Dependent Infectious Diseases with Environmental Effects

We have proposed and analyzed a nonlinear mathematical model for the spread of carrier dependent infectious diseases in a population with variable size structure including the role of vaccination. It is assumed that the susceptibles become infected by direct contact with infectives and/or by the carrier population present in the environment. The density of carrier population is assumed to be governed by a generalized logistic model and is dependent on environmental and human factors which are conducive to the growth of carrier population. The model is analyzed using stability theory of differential equations and numerical simulation. We have found a threshold condition, in terms of vaccine induced reproduction number R(φ) which is, if less than one, the disease dies out in the absence of carriers provided the vaccine efficacy is high enough, and otherwise the infection is maintained in the population. The model also exhibits backward bifurcation at R(φ) = 1. It is also shown that the spread of an infectious disease increases as the carrier population density increases. In addition, the constant immigration of susceptibles makes the disease more endemic

The effect of density dependent emigration on spread of infectious diseases: a modelling study

In this study, we proposed and analyzed an SIS mathematicalmodel by considering population densitydependent emigration. It is assumed that the diseaseis transmitted by direct contact of infective and susceptiblepopulations. We also assumed that the rate ofcontact is emigration dependent i.e. contact rate is variablewhich depends on the current population of habitatas well as on non-emigrating population density of habitat.The equilibria and their stability are studied by usingthe stability theory of differential equations and simulation.The model analysis shows that the spread of infectiousdisease in habitat decreases if the rate of emigrationincreases but it increases as the population density of nonemigratingpopulation increases. The simulation study ofthe model confirms these analytical results

Modeling and Analysis of the Spread of an Infectious Disease Cholera with Environmental Fluctuations

A nonlinear delayed mathematical model with immigration for the spread of an infectious disease cholera with carriers in the environment is proposed and analyzed. It is assumed that all susceptible are affected by carrier population density. The carrier population density is assumed to follow the logistic model and grows due to conducive human population density related factors. The model is analyzed by stability theory of differential equations and computer simulation. Both the disease-free (DFE), (CFE) and endemic equilibria are found and their stability investigated. Bifurcation analyses about endemic equilibrium are also carried out analytically using the theory of differential equations. The model study shows that the spread of the infectious disease cholera increases due to growth of carriers in the environment and disease becomes more endemic due to immigration. Numerical simulations are also carried out to investigate the influence of certain parameters on the spread of disease, to support the analytical results of the model

Modeling and Analysis of the Spread of Japanese Encephalitis with Environmental Effects

A nonlinear mathematical model for the spread of Japanese Encephalitis, caused by infected mosquito feeding on susceptible human population incorporating demographic and environmental factors is proposed and analyzed. In the modeling process, it is assumed that the growth rates of reservoir animal population and vector mosquito population are enhanced due to environmental discharges caused by human population related factors. The model is analyzed by stability theory of differential equations and computer simulation. Both the disease-free and the endemic equilibria are found and their stability is investigated. It is found that whenever the disease-free equilibrium is locally asymptotically stable, the endemic equilibrium does not exist. The analysis of the model shows that if the growth rates of reservoir animal population and vector mosquito population caused by environmental factors increase, the spread of Japanese Encephalitis increases and the disease becomes more endemic due to human immigration. Numerical simulations are also carried out to investigate the influence of certain parameters on the spread of disease, to support the analytical results and illustrate possible behavioral scenario of the model

The influence of predation on community resilience to disease

1. Outbreaks of generalist pathogens are influenced by host community structure, including population density and species diversity. Within host communities predation can influence pathogen transmission rates, prevalence and impacts. However, the influence of predation on community resilience to outbreaks of generalist pathogens are not fully understood. 2. The role of predation on host community resilience to disease was assessed using an epidemiological multi-host Susceptible-Exposed-Infectious-Recovered (SEIR) model. Sphaerothecum destruens, an emerging fungal-like generalist pathogen, was used as a model pathogen. Six cyprinid and salmonid fishes, including an asymptomatic carrier, were selected as model hosts that are known to be impacted by S. destruens, and they were used within a model host community. 3. Pathogen release into the host community was via introduction of the asymptomatic carrier. Mortality from infection, pathogen incubation rate, and host recovery rate were set to a range of evidence-based values in each species and were varied in secondary consumers to predict top-down effects of infection on the resilience of a host community. Predation pressure within the fish community was varied to test its effects on infection prevalence and host survival in the community. 4. Model predictions suggested that predation of the asymptomatic hosts by fishes in the host community was insufficient to eliminate S. destruens. S. destruens persisted in the community due to its rapid transmission from the asymptomatic host to susceptible host fishes. Following transmission, pathogen prevalence in the community was driven by transmission within and between susceptible host fishes, indicating low host community resilience. However, introducing low densities of a highly specific piscivorous fish into the community to predate asymptomatic hosts could limit pathogen prevalence in the host community, thus increasing resilience. 5. The model predictions indicate that whilst resilience to this generalist pathogen in the host community was low, this could be increased using management interventions. The results suggest that this model has high utility for predicting community resilience to disease and thus can be applied to other generalist parasites to determine risks of disease emergence

Modeling the Effect of Environmental Factors on the Spread of Bacterial Disease in an Economically Structured Population

We have proposed and analyzed a nonlinear mathematical model for the spread of bacterial disease in an economically structured population (rich and poor) including the role of vaccination. It is assumed that rich susceptible get infected through direct contact with infectives in the same class and with infectives from the poor class who work as service providers in the houses of rich people, living in much cleaner environment. The susceptible in the poor class are assumed to become infected through direct contact with infectives in the same class as well as by bacteria present in their own environment, degraded due to unhygienic environmental conditions. It is further assumed that the bacteria population affects only the population in the degraded environment of the poor class but does not survive in the clean environment of rich people. The density of bacteria population is assumed to be governed by a logistic model and is dependent on environmental discharges conducive to the growth of bacteria population. The cumulative density of environmental discharges depends upon the human population related factors of the poor class. The model analysis shows that the increased growth rate of environmental discharges increases the bacteria population density in the poor class due to unhygienic environmental conditions leading to increase the infectives in the poor class i.e., service providers. As a consequence, due to interaction with these service providers the spread of disease increases in the rich class. The improved environmental conditions of the region inhabited by service providers along with suitable vaccination strategy can be helpful in reducing the spread of the disease

ASF Exit Strategy: Providing cumulative evidence of the absence of African swine fever virus circulation in wild boar populations using standard surveillance measures

EFSA assessed the role of seropositive wild boar in African swine fever (ASF) persistence. Surveillance data from Estonia and Latvia investigated with a generalised equation method demonstrated a significantly slower decline in seroprevalence in adult animals compared with subadults. The seroprevalence in adults, taking more than 24 months to approach zero after the last detection of ASFV circulation, would be a poor indicator to demonstrate the absence of virus circulation. A narrative literature review updated the knowledge on the mortality rate, the duration of protective immunity and maternal antibodies and transmission parameters. In addition, parameters potentially leading to prolonged virus circulation (persistence) in wild boar populations were reviewed. A stochastic explicit model was used to evaluate the dynamics of virus prevalence, seroprevalence and the number of carcasses attributed to ASF. Secondly, the impact of four scenarios on the duration of ASF virus (ASFV) persistence was evaluated with the model, namely a: (1) prolonged, lifelong infectious period, (2) reduction in the case‐fatality rate and prolonged transient infectiousness; (3) change in duration of protective immunity and (4) change in the duration of protection from maternal antibodies. Only the lifelong infectious period scenario had an important prolonging effect on the persistence of ASF. Finally, the model tested the performance of different proposed surveillance strategies to provide evidence of the absence of virus circulation (Exit Strategy). A two‐phase approach (Screening Phase, Confirmation Phase) was suggested for the Exit Strategy. The accuracy of the Exit Strategy increases with increasing numbers of carcasses collected and tested. The inclusion of active surveillance based on hunting has limited impact on the performance of the Exit Strategy compared with lengthening of the monitoring period. This performance improvement should be reasonably balanced against an unnecessary prolonged ‘time free’ with only a marginal gain in performance. Recommendations are provided for minimum monitoring periods leading to minimal failure rates of the Exit Strategy. The proposed Exit Strategy would fail with the presence of lifelong infectious wild boar. That said, it should be emphasised that the existence of such animals is speculative, based on current knowledge.info:eu-repo/semantics/publishedVersio

Who acquires infection from whom and how? Disentangling multi-host and multi-mode transmission dynamics in the 'elimination' era

Multi-host infectious agents challenge our abilities to understand, predict and manage disease dynamics. Within this, many infectious agents are also able to use, simultaneously or sequentially, multiple modes of transmission. Furthermore, the relative importance of different host species and modes can itself be dynamic, with potential for switches and shifts in host range and/ or transmission mode in response to changing selective pressures, such as those imposed by disease control interventions. The epidemiology of such multi-host, multi-mode infectious agents thereby can involve a multi-faceted community of definitive and intermediate/secondary hosts or vectors, often together with infectious stages in the environment, all of which may represent potential targets, as well as specific challenges, particularly where disease elimination is proposed. Here, we explore, focusing on examples fromboth human and animal pathogen systems, why and how we should aim to disentangle and quantify the relative importance of multi-host multi-mode infectious agent transmission dynamics under contrasting conditions, and ultimately, how this can be used to help achieve efficient and effective disease control. This article is part of the themed issue 'Opening the black box: re-examining the ecology and evolution of parasite transmission'