Vector Mortality Rate Research Articles

A Numerical Study of the Dynamics of Vector-Born Viral Plant Disorders Using a Hybrid Artificial Neural Network Approach.

Most plant viral infections are vector-borne. There is a latent period of disease inside the vector after obtaining the virus from the infected plant. Thus, after interacting with an infected vector, the plant demonstrates an incubation time before becoming diseased. This paper analyzes a mathematical model for persistent vector-borne viral plant disease dynamics. The backpropagated neural network based on the Levenberg-Marquardt algorithm (NN-BLMA) is used to study approximate solutions for fluctuations in natural plant mortality and vector mortality rates. A state-of-the-art numerical technique is utilized to generate reference data for obtaining surrogate solutions for multiple cases through NN-BLMA. Curve fitting, regression analysis, error histograms, and convergence analysis are used to assess accuracy of the calculated solutions. It is evident from our simulations that NN-BLMA is accurate and reliable.

Robustness of the reproductive number estimates in vector-borne disease systems.

BackgroundThe required efforts, feasibility and predicted success of an intervention strategy against an infectious disease are partially determined by its basic reproduction number, R0. In its simplest form R0 can be understood as the product of the infectious period, the number of infectious contacts and the per-contact transmission probability, which in the case of vector-transmitted diseases necessarily extend to the vector stages. As vectors do not usually recover from infection, they remain infectious for life, which places high significance on the vector’s life expectancy. Current methods for estimating the R0 for a vector-borne disease are mostly derived from compartmental modelling frameworks assuming constant vector mortality rates. We hypothesised that some of the assumptions underlying these models can lead to unrealistic high vector life expectancies with important repercussions for R0 estimates.Methodology and principal findingsHere we used a stochastic, individual-based model which allowed us to directly measure the number of secondary infections arising from one index case under different assumptions about vector mortality. Our results confirm that formulas based on age-independent mortality rates can overestimate R0 by nearly 100% compared to our own estimate derived from first principles. We further provide a correction factor that can be used with a standard R0 formula and adjusts for the discrepancies due to erroneous vector age distributions.ConclusionVector mortality rates play a crucial role for the success and general epidemiology of vector-transmitted diseases. Many modelling efforts intrinsically assume these to be age-independent, which, as clearly demonstrated here, can lead to severe over-estimation of the disease’s reproduction number. Our results thus re-emphasise the importance of obtaining field-relevant and species-dependent vector mortality rates, which in turn would facilitate more realistic intervention impact predictions.

Epidemiological significance of dengue virus genetic variation in mosquito infection dynamics.

The kinetics of arthropod-borne virus (arbovirus) transmission by their vectors have long been recognized as a powerful determinant of arbovirus epidemiology. The time interval between virus acquisition and transmission by the vector, termed extrinsic incubation period (EIP), combines with vector mortality rate and vector competence to determine the proportion of infected vectors that eventually become infectious. However, the dynamic nature of this process, and the amount of natural variation in transmission kinetics among arbovirus strains, are poorly documented empirically and are rarely considered in epidemiological models. Here, we combine newly generated empirical measurements in vivo and outbreak simulations in silico to assess the epidemiological significance of genetic variation in dengue virus (DENV) transmission kinetics by Aedes aegypti mosquitoes. We found significant variation in the dynamics of systemic mosquito infection, a proxy for EIP, among eight field-derived DENV isolates representing the worldwide diversity of recently circulating type 1 strains. Using a stochastic agent-based model to compute time-dependent individual transmission probabilities, we predict that the observed variation in systemic mosquito infection kinetics may drive significant differences in the probability of dengue outbreak and the number of human infections. Our results demonstrate that infection dynamics in mosquitoes vary among wild-type DENV isolates and that this variation potentially affects the risk and magnitude of dengue outbreaks. Our quantitative assessment of DENV genetic variation in transmission kinetics contributes to improve our understanding of heterogeneities in arbovirus epidemiological dynamics.

Wash-resistance of pirimiphos-methyl insecticide treatments of window screens and eave baffles for killing indoor-feeding malaria vector mosquitoes: an experimental hut trial, South East of Zambia

BackgroundThe effectiveness of long-lasting insecticidal-treated nets (LLINs) and indoor residual spraying (IRS) for malaria control is threatened by resistance to commonly used pyrethroid insecticides. Rotations, mosaics, combinations, or mixtures of insecticides from different complementary classes are recommended by the World Health Organization (WHO) for mitigating against resistance, but many of the alternatives to pyrethroids are prohibitively expensive to apply in large national IRS campaigns. Recent evaluations of window screens and eave baffles (WSEBs) treated with pirimiphos-methyl (PM), to selectively target insecticides inside houses, demonstrated malaria vector mortality rates equivalent or superior to IRS. However, the durability of efficacy when co-applied with polyacrylate-binding agents (BA) remains to be established. This study evaluated whether WSEBs, co-treated with PM and BA have comparable wash resistance to LLINs and might therefore remain insecticidal for years rather than months.MethodsWHO-recommended wire ball assays of insecticidal efficacy were applied to polyester netting treated with or without BA plus 1 or 2 g/sq m PM. They were then tested for insecticidal efficacy using fully susceptible insectary-reared Anopheles gambiae mosquitoes, following 0, 5, 10, 15, then 20 washes as per WHO-recommended protocols for accelerated ageing of LLINs. This was followed by a small-scale field trial in experimental huts to measure malaria vector mortality achieved by polyester netting WSEBs treated with BA and 2 g/sq m PM after 0, 10 and then 20 standardized washes, alongside recently applied IRS using PM.ResultsCo-treatment with BA and either dosage of PM remained insecticidal over 20 washes in the laboratory. In experimental huts, WSEBs treated with PM plus BA consistently killed similar proportions of Anopheles arabiensis mosquitoes to PM-IRS (both consistently ≥ 94%), even after 20 washes.ConclusionCo-treating WSEBs with both PM and BA results in wash-resistant insecticidal activity comparable with LLINs. Insecticide treatments for WSEBs may potentially last for years rather than months, therefore, reducing insecticide consumption by an order of magnitude relative to IRS. However, durability of WSEBs will still have to be assessed in real houses under representative field conditions of exposure to wear and tear, sunlight and rain.

Epidemiological consequences of immune sensitisation by pre-exposure to vector saliva.

Blood-feeding arthropods—like mosquitoes, sand flies, and ticks—transmit many diseases that impose serious public health and economic burdens. When a blood-feeding arthropod bites a mammal, it injects saliva containing immunogenic compounds that facilitate feeding. Evidence from Leishmania, Plasmodium and arboviral infections suggests that the immune responses elicited by pre-exposure to arthropod saliva can alter disease progression if the host later becomes infected. Such pre-sensitisation of host immunity has been reported to both exacerbate and limit infection symptoms, depending on the system in question, with potential implications for recovery. To explore if and how immune pre-sensitisation alters the effects of vector control, we develop a general model of vector-borne disease. We show that the abundance of pre-sensitised infected hosts should increase when control efforts moderately increase vector mortality rates. If immune pre-sensitisation leads to more rapid clearance of infection, increasing vector mortality rates may achieve greater than expected disease control. However, when immune pre-sensitisation prolongs the duration of infection, e.g., through mildly symptomatic cases for which treatment is unlikely to be sought, vector control can actually increase the total number of infected hosts. The rising infections may go unnoticed unless active surveillance methods are used to detect such sub-clinical individuals, who could provide long-lasting reservoirs for transmission and suffer long-term health consequences of those sub-clinical infections. Sensitivity analysis suggests that these negative consequences could be mitigated through integrated vector management. While the effect of saliva pre-exposure on acute symptoms is well-studied for leishmaniasis, the immunological and clinical consequences are largely uncharted for other vector-parasite-host combinations. We find a large range of plausible epidemiological outcomes, positive and negative for public health, underscoring the need to quantify how immune pre-sensitisation modulates recovery and transmission rates in vector-borne diseases.

A dynamic model for estimating adult female mortality from ovarian dissection data for the tsetse fly Glossina pallidipes Austen sampled in Zimbabwe.

Human and animal trypanosomiasis, spread by tsetse flies (Glossina spp), is a major public health concern in much of sub-Saharan Africa. The basic reproduction number of vector-borne diseases, such as trypanosomiasis, is a function of vector mortality rate. Robust methods for estimating tsetse mortality are thus of interest for understanding population and disease dynamics and for optimal control. Existing methods for estimating mortality in adult tsetse, from ovarian dissection data, often use invalid assumptions of the existence of a stable age distribution, and age-invariant mortality and capture probability. We develop a dynamic model to estimate tsetse mortality from ovarian dissection data in populations where the age distribution is not necessarily stable. The models correspond to several hypotheses about how temperature affects mortality: no temperature dependence (model 1), identical temperature dependence for mature adults and immature stages, i.e., pupae and newly emerged adults (model 2), and differential temperature dependence for mature adults and immature stages (model 3). We fit our models to ovarian dissection data for G. pallidipes collected at Rekomitjie Research Station in the Zambezi Valley in Zimbabwe. We compare model fits to determine the most probable model, given the data, by calculating the Akaike Information Criterion (AIC) for each model. The model that allows for a differential dependence of temperature on mortality for immature stages and mature adults (model 3) performs significantly better than models 1 and 2. All models produce mortality estimates, for mature adults, of approximately 3% per day for mean daily temperatures below 25°C, consistent with those of mark-recapture studies performed in other settings. For temperatures greater than 25°C, mortality among immature classes of tsetse increases substantially, whereas mortality remains roughly constant for mature adults. As a sensitivity analysis, model 3 was simultaneously fit to both the ovarian dissection and trap data; while this fit also produces comparable mortality at temperatures below 25°C, it is not possible to obtain good fits to both data sources simultaneously, highlighting the uncertain correspondence between trap catches and population levels and/or the need for further improvements to our model. The modelling approach employed here could be applied to any substantial time series of age distribution data.

Estimation of reproduction number and non stationary spectral analysis of dengue epidemic

In this work we analyze the post monsoon Dengue outbreaks by analyzing the transient and long term dynamics of Dengue incidences and its environmental correlates in Ahmedabad city in western India from 2005 to 2012. We calculate the reproduction number Rp using the growth rate of post monsoon Dengue outbreaks and biological parameters like host and vector incubation periods and vector mortality rate, and its uncertainties are estimated through Monte–Carlo simulations by sampling parameters from their respective probability distributions. Reduction in Female Aedes mosquito density required for an effective prevention of Dengue outbreaks is also calculated. The non stationary pattern of Dengue incidences and its climatic correlates like rainfall temperature is analyzed through Wavelet based methods. We find that the mean time lag between peak of monsoon and Dengue is 9 weeks. Monsoon and Dengue cases are phase locked from 2008 to 2012 in the 16 to maintain consistency make it “16 to 32” 32 weeks band. The duration of post monsoon outbreak has been increasing every year, especially post 2008, even though the intensity and duration of monsoon has been decreasing. Temperature and Dengue incidences show correlations in the same band, but phase lock is not stationary.

Malaria control and senescence: the importance of accounting for the pace and shape of aging in wild mosquitoes

The assumption that vector mortality remains constant with age is used widely to assess malaria transmission risk and predict the public health consequences of vector control strategies. However, laboratory studies commonly demonstrate clear evidence of senescence, or a decrease in physiological function and increase in vector mortality rate with age. Despite recognition of its importance, practical limitations have stifled definitive observations of mosquito senescence in the wild, where rates of extrinsic mortality are much higher than those observed under protected laboratory conditions. We developed methods to integrate available field data to understand mortality in wild Anopheles gambiae, the most import vector of malaria in sub‐Saharan Africa. We found evidence for an increase in rates of mortality with age. As expected, we also found that overall mortality is far greater in wild cohorts than commonly observed under protected laboratory conditions. The magnitude of senescence increases with An. gambiae lifespan, implying that most wild mosquitoes die long before cohorts can exhibit strong senescence. We reviewed available published mortality studies of Anopheles spp. to confirm this fundamental prediction of aging in wild populations. Senescence becomes most apparent in long‐living mosquito cohorts; cohorts with low extrinsic mortality, such as protected laboratory cohorts, suffer a relatively high proportion of senescent deaths. Imprecision in estimates of vector mortality and changes in mortality with age will severely bias models of vector borne disease transmission risk, such as malaria, and the sensitivity of transmission to bias increases as the extrinsic incubation period of the parasite decreases. While we focus here on malaria, we caution that future transmission models of anti‐vectorial interventions must incorporate both realistic mortality rates and age‐dependent changes in mortality.

Contrasting the consumptive and non‐consumptive cascading effects of natural enemies on vector‐borne pathogens

AbstractPredicting disease dynamics requires a community perspective, incorporating multi‐species interactions involving hosts, pathogens, vectors, and consumers. In systems where pathogens are dependent on a vector for transmission from one host to another, predators can indirectly influence disease risk through direct effects on vectors. These effects may be consumptive if predators reduce vector abundance by capturing and killing vectors, or non‐consumptive if predators induce anti‐predator behavioral responses by vectors. Studies are accumulating that document cascading effects of predators on vector‐borne disease risk, but the mechanisms underlying these effects are often uncertain. Using a previously developed epidemiological model as a framework, I outline several mechanistic pathways by which predators can have consumptive and non‐consumptive effects on vectors, and present theoretical predictions about the cascading influence of these pathways on pathogen prevalence. I then review selected examples from the literature of vector‐borne plant pathogen systems where particular mechanistic pathways have been implicated. Together, the model predictions and the literature review reveal that, depending on the particular mechanisms at work, predators may reduce, leave unaffected, or even increase pathogen prevalence. In general, the consumptive effects of predators on vectors result in consistent reductions in pathogen prevalence. However, the non‐consumptive effects of predators that arise as a result of changes in pathogen transmission rates, vector birth rates, and non‐predation vector mortality rates are more variable, with the potential for context‐dependency and counter‐intuitive outcomes. Interactions among pathways are also possible, such that the magnitude of consumptive effects can depend upon the strength of non‐consumptive effects and vice versa. I conclude by highlighting the importance of teasing apart the various mechanistic pathways by which predators may indirectly influence pathogen prevalence, and clarifying the relationships among them, to accurately predict the consequences of predation for disease risk and the usefulness of biological control of vectors for suppression of plant pathogens.

Zooprophylaxis or zoopotentiation: the outcome of introducing animals on vector transmission is highly dependent on the mosquito mortality while searching

BackgroundZooprophylaxis, the diversion of disease carrying insects from humans to animals, may reduce transmission of diseases such as malaria. However, as the number of animals increases, improved availability of blood meals may increase mosquito survival, thereby countering the impact of diverting feeds.MethodsComputer simulation was used to examine the effects of animals on the transmission of human diseases by mosquitoes. Three scenarios were modelled: (1) endemic transmission, where the animals cannot be infected, eg. malaria; (2) epidemic transmission, where the animals cannot be infected but humans remain susceptible, e.g. malaria; (3) epidemic disease, where both humans and animals can be infected, but develop sterile immunity, eg. Japanese encephalitis B. For each, the passive impact of animals as well as the use of animals as bait to attract mosquitoes to insecticide was examined. The computer programmes are available from the author. A teaching model accompanies this article.ResultsFor endemic and epidemic malaria with significant searching-associated vector mortality, changing animal numbers and accessibility had little impact. Changing the accessibility of the humans had a much greater effect. For diseases with an animal amplification cycle, the most critical factor was the proximity of the animals to the mosquito breeding sites.ConclusionEstimates of searching-associated vector mortality are essential before the effects of changing animal husbandry practices can be predicted. With realistic values of searching-associated vector mortality rates, zooprophylaxis may be ineffective. However, use of animals as bait to attract mosquitoes to insecticide is predicted to be a promising strategy.

Modelling the transmission dynamics of Ross River virus in Southwestern Australia

During the 1995-1996 Australian financial year, over 1300 notifications of Ross River (RR) virus disease were notified in humans from Southwestern Australia. Due to the mild symptoms of the disease, it is difficult to diagnose and subclinical infections are common. However, these subclinical infections do give rise to immunity. For planning and control, it is important for public health authorities to estimate the true number of people who have contracted the disease and to assess the impact of key epidemiological parameters. A mathematical model was developed to describe the transmission of RR virus between its hosts (humans and kangaroos) and its vectors (mosquitoes). For this model, the threshold conditions and relative removal rates were calculated and interpreted. Finally, a computer program was written to simulate the model in order to estimate the total number, both clinical and sub clinical human infections given known and hypothetical epidemiological parameter values. Within this simulation sensitivity of the results to changes in the parameters were examined. The analysis of the threshold conditions conformed well to established principles of arboviral transmission and control. It was observed that conditions which can prevent an outbreak occuring include reducing the number of susceptibles in host and vector populations, reducing the infection rates between hosts and vectors and shortening the duration of viraemia. Results on the sensitivity analysis showed that some parameters such as the extrinsic incubation period, mosquito mortality rate in winter and the proportion of Western Grey Kangaroos in the marsupial population have little effect on human incidence. However, the transmission rate between hosts and vectors, vector-mortality rate in summer and the proportion of infectious vectors among infected vectors have pronounced effects. The simulation results on the ratio of clinical to subclinical human infections predicted a minimum ratio of 1:2 and a maximum ratio of 1:65, which is consistent with data obtained during previous sero-epidemiological studies.

Bednet impregnation for Chagas disease control: a new perspective.

To determine the efficacy and acceptability of deltamethrin-impregnated bednets in controlling Chagas disease in South America. In three endemic departments of Colombia, a qualitative study on people's knowledge about Chagas disease, vectors, preventive measures and their willingness for collaboration in control operations was undertaken. Additionally, in an entomological study with 100 laboratory-bred Chagas vectors (Rhodnius prolixus), vectors were released for 5 nights (20 each night) in an experimental room, with the human bait protected for one night by an unimpregnated and for four nights by a deltamethrin-impregnated bednet (13 mg/m2). Vectors were stained with fluorescent powder for observation, collected after 10 h exposure in the experimental room and observed for a further 72 h. The study population did not know anything about Chagas disease, but believed the vector to transmit cutaneous leishmaniasis. Therefore willingness to take part in control operations was high. The experimental hut study showed a vector mortality rate of 95% in a room with impregnated nets and of 10% in a room with unimpregnated nets. This study opens a new perspective for Chagas disease control in integrated vector borne disease prevention programmes.

Satellite imagery, tsetse and trypanosomiasis in Africa

This paper describes the application of remote sensing to studies on the African trypanosomiases causing sleeping sickness in man and ‘nagana’ in domestic animals. After giving some biological background to the problem, an important relationship between the risk of infection of domestic animals, tsetse fly numbers and fly infection rates is presented. An understanding of the latter leads to a prediction of risk in cattle. The problems of analysing and interpreting the distribution and abundance patterns of flies are explored, and a mortality climogram approach is described in which the important meteorological variables appear to be temperature and saturation deficit. This approach, which can be applied to data collected at only very few sites, leads to extensive predictions of the distributional limits of the tsetse Glossina morsitans Westwood. These predictions are supported by the known distribution of this species throughout Africa. A similarity noted between published whole-Africa normalised difference vegetation indices (NDVI) and tsetse distribution leads to an exploration of the usefulness of NDVI for such vector studies. The likely information content of the images is identified through principal component analysis, and correlations are shown between NDVI values and annual temperature, saturation deficit and rainfall figures for more than 300 sites throughout the sub-Saharan region of the continent. NDVI values are highly correlated with both saturation deficit and rainfall figures. Significant correlations are shown between vector mortality rates and mean monthly NDVI values, and between the physical size of the vectors (known to reflect the mortality rates affecting the parental population) and NDVI along an approximately 700 km transect across a whole range of eco-climate conditions in West Africa. Reasons are suggested for the localisation of human sleeping sickness to just one of several regions sampled by the transect. Finally, seasonal changes in case numbers of human sleeping sickness in both Uganda and Kenya are correlated with mean monthly NDVI from the areas concerned. The first of these correlations is negative, the second positive. Explanations for this difference are given in terms of the different vector species and epidemiological situations in these long-standing foci in East Africa. It is concluded that the rather limited amount of information available in NDVI has already proved enormously useful, and a plea is made for a more complete exploration of National Oceanic and Atmospheric Administration (NOAA) data, especially at the highest available resolution, whilst not neglecting the vitally important ground-based studies that made possible the results presented in this paper.