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Feeding strategies for growing monogastric livestock (particularly pigs) must focus on maximising animal performance, while attempting to reduce environmental P load. Achieving these goals requires a comprehensive understanding of how different P feeding strategies affect animal responses and an ability to predict P retention. Although along with Ca, P is the most researched macromineral in pig nutrition, knowledge gaps still exist in relation to: (1) the effects of P feed content on feed intake (FI); (2) the impact of P intake on body composition; (3) the distribution of absorbed P to pools within the body. Here, we address these knowledge gaps by gathering empirical evidence on the effects of P-deficient feeds and by developing a predictive, mechanistic model of P utilisation and retention incorporating this evidence. Based on our statistical analyses of published literature data, we found: (1) no change in FI response in pigs given lower P feed contents; (2) the body ash-protein relationship to be dependent upon feed composition, with the isometric relationship only holding for pigs given balanced feeds and (3) the priority to be given towards P retention in soft tissue over P retention in bones. Subsequent results of the mechanistic model of P retention indicated that a potential reduction in P feeding recommendations could be possible without compromising average daily gain; however, such a reduction would impact P deposition in bones. Our study enhances our current knowledge of P utilisation and by extension excretion and could contribute towards developing more accurate P feeding guidelines.
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Alimentación Animal/análisis , Fenómenos Fisiológicos Nutricionales de los Animales/efectos de los fármacos , Dieta/veterinaria , Fósforo Dietético/farmacología , Fósforo/deficiencia , Animales , Composición Corporal/efectos de los fármacos , PorcinosRESUMEN
Ca digestibility and utilisation in growing pigs are not well understood, and are usually neglected in diet formulation. This has implications not only for the accurate determination of its requirements but also for its interactions with other nutrients. A systematic review and meta-analysis (meta-regression) of published trials was carried out to quantify factors affecting Ca absorption and utilisation, and to derive an estimate of Ca endogenous excretion. The analysis was carried out on the data from forty studies, corresponding to 201 treatments performed on 1204 pigs. The results indicated that although Ca absorption and retention (g/kg of body weight per d) increased with increasing Ca intake (P<0·001), non-phytate-P intake (P<0·001) and exogenous phytase supplementation (P<0·001), these values decreased with increasing phytate-P intake (P<0·05). Interactions between exogenous phytase and Ca intake, indicating reduced efficacy of this enzyme (P<0·001), and between phytate-P intake and exogenous phytase, counteracting the direct negative effect of phytate-P (P<0·05) on Ca absorption and retention, were also detected. There were no effects of animal-related characteristics, such as pig genotype in Ca absorption and retention. The large amount of variance explained in Ca absorption (90 %) and retention (91 %) supported our choice of independent variables. Endogenous Ca losses obtained via linear regression were 239 mg/kg of DM intake (95 % CI 114, 364). These outcomes advance the current understanding of Ca digestibility and utilisation, and should contribute towards establishing requirements for digestible Ca. Consequently, pig diets will be more correctly formulated if digestible Ca values are used in estimating requirements for Ca.
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Alimentación Animal/análisis , Calcio de la Dieta/administración & dosificación , Calcio/metabolismo , Dieta/veterinaria , Porcinos/crecimiento & desarrollo , Animales , DigestiónRESUMEN
Market trade-routes can support infectious-disease transmission, impacting biological populations and even disrupting trade that conduces the disease. Epidemiological models increasingly account for reductions in infectious contact, such as risk-aversion behaviour in response to pathogen outbreaks. However, responses in market dynamics clearly differ from simple risk aversion, as are driven by other motivation and conditioned by "friction" constraints (a term we borrow from labour economics). Consequently, the propagation of epidemics in markets of, for example livestock, is frictional due to time and cost limitations in the production and exchange of potentially infectious goods. Here we develop a coupled economic-epidemiological model where transient and long-term market dynamics are determined by trade friction and agent adaptation, and can influence disease transmission. The market model is parameterised from datasets on French cattle and pig exchange networks. We show that, when trade is the dominant route of transmission, market friction can be a significantly stronger determinant of epidemics than risk-aversion behaviour. In particular, there is a critical level of friction above which epidemics do not occur, which suggests some epidemics may not be sustained in highly frictional markets. In addition, friction may allow for greater delay in removal of infected agents that still mitigates the epidemic and its impacts. We suggest that policy for minimising contagion in markets could be adjusted to the level of market friction, by adjusting the urgency of intervention or by increasing friction through incentivisation of larger-volume less-frequent transactions that would have limited effect on overall trade flow. Our results are robust to model specificities and can hold in the presence of non-trade disease-transmission routes.
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Comercio , Enfermedades Transmisibles/epidemiología , Epidemias , Modelos Biológicos , Modelos Económicos , Animales , Bovinos , Francia , Humanos , Ganado , Probabilidad , Porcinos , Factores de TiempoRESUMEN
Exotic pathogens and pests threaten ecosystem service, biodiversity, and crop security globally. If an invasive agent can disperse asymptomatically over long distances, multiple spatial and temporal scales interplay, making identification of effective strategies to regulate, monitor, and control disease extremely difficult. The management of outbreaks is also challenged by limited data on the actual area infested and the dynamics of spatial spread, due to financial, technological, or social constraints. We examine principles of landscape epidemiology important in designing policy to prevent or slow invasion by such organisms, and use Phytophthora ramorum, the cause of sudden oak death, to illustrate how shortfalls in their understanding can render management applications inappropriate. This pathogen has invaded forests in coastal California, USA, and an isolated but fast-growing epidemic focus in northern California (Humboldt County) has the potential for extensive spread. The risk of spread is enhanced by the pathogen's generalist nature and survival. Additionally, the extent of cryptic infection is unknown due to limited surveying resources and access to private land. Here, we use an epidemiological model for transmission in heterogeneous landscapes and Bayesian Markov-chain-Monte-Carlo inference to estimate dispersal and life-cycle parameters of P. ramorum and forecast the distribution of infection and speed of the epidemic front in Humboldt County. We assess the viability of management options for containing the pathogen's northern spread and local impacts. Implementing a stand-alone host-free "barrier" had limited efficacy due to long-distance dispersal, but combining curative with preventive treatments ahead of the front reduced local damage and contained spread. While the large size of this focus makes effective control expensive, early synchronous treatment in newly-identified disease foci should be more cost-effective. We show how the successful management of forest ecosystems depends on estimating the spatial scales of invasion and treatment of pathogens and pests with cryptic long-distance dispersal.
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Ecosistema , Modelos Biológicos , Enfermedades de las Plantas/prevención & control , Enfermedades de las Plantas/parasitología , Árboles/parasitología , California , Simulación por ComputadorRESUMEN
Small grain cereals are frequently infected with mycotoxigenic Fusarium fungi. Oats have a particularly high risk of contamination with type A trichothecene mycotoxins; their glucoside conjugates have also been reported. Agronomy practices, cereal variety and weather conditions have been suggested to play a role in Fusarium infection in oats. The current study investigates concentrations of free and conjugated Fusarium mycotoxins in organic and conventional oats grown in Scotland. In 2019, 33 milling oat samples (12 organic, 21 conventional) were collected from farmers across Scotland, together with sample questionnaires. Samples were analysed for 12 mycotoxins (type A trichothecenes T-2-toxin, HT-2-toxin, diacetoxyscirpenol; type B trichothecenes deoxynivalenol, nivalenol; zearalenone and their respective glucosides) using LC-MS/MS. The prevalence of type A trichothecenes T-2/HT-2 was very high (100% of conventional oats, 83% of organic oats), whereas type B trichothecenes were less prevalent, and zearalenone was rarely found. T-2-glucoside and deoxynivalenol-glucoside were the most prevalent conjugated mycotoxins (36 and 33%), and co-occurrence between type A and B trichothecenes were frequently observed (66% of samples). Organic oats were contaminated at significantly lower average concentrations than conventional oats, whereas the effect of weather parameters were not statistically significant. Our results clearly indicate that free and conjugated T-2- and HT-2-toxins pose a major risk to Scottish oat production and that organic production and crop rotation offer potential mitigation strategies.
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Fusarium , Micotoxinas , Toxina T-2 , Tricotecenos Tipo B , Zearalenona , Micotoxinas/análisis , Avena/microbiología , Grano Comestible/química , Zearalenona/análisis , Cromatografía Liquida , Contaminación de Alimentos/análisis , Espectrometría de Masas en Tándem , Toxina T-2/análisis , Escocia , GlucósidosRESUMEN
Morning loaded calorie intake in humans has been advocated as a dietary strategy to improve weight loss. This is also supported by animal studies suggesting time of eating can prevent weight gain. However, the underlying mechanisms through which timing of eating could promote weight loss in humans are unclear. In a randomized crossover trial (NCT03305237), 30 subjects with obesity/overweight underwent two 4-week calorie-restricted but isoenergetic weight loss diets, with morning loaded or evening loaded calories (45%:35%:20% versus 20%:35%:45% calories at breakfast, lunch, and dinner, respectively). We demonstrate no differences in total daily energy expenditure or resting metabolic rate related to the timing of calorie distribution, and no difference in weight loss. Participants consuming the morning loaded diet reported significantly lower hunger. Thus, morning loaded intake (big breakfast) may assist with compliance to weight loss regime through a greater suppression of appetite.
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Apetito , Hambre , Animales , Dieta Reductora , Ingestión de Energía/fisiología , Metabolismo Energético , Voluntarios Sanos , Humanos , Obesidad/metabolismo , Pérdida de PesoRESUMEN
Recent technological advances make it possible to deliver feeding strategies that can be tailored to the needs of individual pigs in order to optimise the allocation of nutrient resources and contribute toward reducing excess nutrient excretion. However, these efforts are currently hampered by the challenges associated with: (1) estimation of unobserved traits from the available data on bodyweight and feed consumption; and (2) characterisation of the distributions and correlations of these unobserved traits to generate accurate estimates of individual level variation among pigs. Here, alternative quantitative approaches to these challenges, based on the principles of inverse modelling and separately inferring individual level distributions within a Bayesian context were developed and incorporated in a proposed precision feeding modelling framework. The objectives were to: (i) determine the average and distribution of individual traits characterising growth potential and body composition in an empirical population of growing-finishing barrows and gilts; (ii) simulate the growth and excretion of nitrogen and phosphorus of the average pig offered either a commercial two-phase feeding plan, or a precision feeding plan with daily adjustments; and (iii) simulate the growth and excretion of nitrogen and phosphorus across the pig population under two scenarios: a two-phase feeding plan formulated to meet the nutrient requirements of the average pig or a precision feeding plan with daily adjustments for each and every animal in the population. The distributions of mature bodyweight and ratio of lipid to protein weights at maturity had median (IQR) values of 203 (47.8) kg and 2.23 (0.814) kg/kg, respectively; these estimates were obtained without any prior assumptions concerning correlations between the traits. Overall, it was found that a proposed precision feeding strategy could result in considerable reductions in excretion of nitrogen and phosphorus (average pig: 8.07 and 9.17% reduction, respectively; heterogenous pig population: 22.5 and 22.9% reduction, respectively) during the growing-finishing period from 35 to 120 kg bodyweight. This precision feeding modelling framework is anticipated to be a starting point toward more accurate estimation of individual level nutrient requirements, with the general aim of improving the economic and environmental sustainability of future pig production systems.
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There is a paradigm shift from the traditional focus on the "average" individual towards the definition and analysis of trait variation within individual life-history and among individuals in populations. This is a result of increasing availability of individual phenotypic data. The shift allows the use of genetic and environment-driven variations to assess robustness to challenge, gain greater understanding of organismal biological processes, or deliver individual-targeted treatments or genetic selection. These consequences apply, in particular, to variation in ontogenetic growth. We propose an approach to parameterise mathematical models of individual traits (e.g., reaction norms, growth curves) that address two challenges: 1) Estimation of individual traits while making minimal assumptions about data distribution and correlation, addressed via Approximate Bayesian Computation (a form of nonparametric inference). We are motivated by the fact that available information on distribution of biological data is often less precise than assumed by conventional likelihood functions. 2) Scaling-up to population phenotype distributions while facilitating unbiased use of individual data; this is addressed via a probabilistic framework where population distributions build on separately-inferred individual distributions and individual-trait interpretability is preserved. The approach is tested against Bayesian likelihood-based inference, by fitting weight and energy intake growth models to animal data and normal- and skewed-distributed simulated data. i) Individual inferences were accurate and robust to changes in data distribution and sample size; in particular, median-based predictions were more robust than maximum- likelihood-based curves. These results suggest that the approach gives reliable inferences using few observations and monitoring resources. ii) At the population level, each individual contributed via a specific data distribution, and population phenotype estimates were not disproportionally influenced by outlier individuals. Indices measuring population phenotype variation can be derived for study comparisons. The approach offers an alternative for estimating trait variability in biological systems that may be reliable for various applications, for example, in genetics, health, and individualised nutrition, while using fewer assumptions and fewer empirical observations. In livestock breeding, the potentially greater accuracy of trait estimation (without specification of multitrait variance-covariance parameters) could lead to improved selection and to more decisive estimates of trait heritability.
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The broad-spectrum antiparasitic drug ivermectin was licensed for use against onchocerciasis in 1987, yet the mechanisms by which it exerts a fast decrease and long-lasting suppression of Onchocerca volvulus microfilaridermia, and inhibition of microfilarial release by female worms remain largely unknown. A better understanding of the effects of ivermectin on O volvulus microfilariae and macrofilariae is crucial to improve our ability to predict the long-term effect of treatment. We did a systematic review of individual and population-based ivermectin trials to investigate the temporal dynamics of the drug's microfilaricidal and embryostatic efficacy after administration of a single, standard dose (150 microg/kg). Meta-analyses on data from 26 microfilarial and 15 macrofilarial studies were linked by a mathematical model describing the dynamics of potentially fertile female parasites to skin microfilariae. The model predicts that after treatment, microfilaridermia would be reduced by half after 24 h, by 85% after 72 h, by 94% after 1 week, and by 98-99% after 1-2 months, the latter also corresponding to the time when the fraction of females harbouring live microfilariae is at its lowest (reduced by around 70% from its original value). Our results provide a baseline microfilarial skin repopulation curve against which to compare studies done after long-term treatment.
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Filaricidas/uso terapéutico , Ivermectina/uso terapéutico , Onchocerca volvulus/efectos de los fármacos , Oncocercosis/tratamiento farmacológico , Piel/parasitología , Adolescente , Adulto , Animales , Niño , Preescolar , Ensayos Clínicos como Asunto , Relación Dosis-Respuesta a Droga , Femenino , Humanos , Masculino , Matemática , Persona de Mediana Edad , Oncocercosis/parasitología , Ensayos Clínicos Controlados Aleatorios como Asunto , Resultado del TratamientoRESUMEN
Acquisition of partially protective immunity is a dominant feature of the epidemiology of malaria among exposed individuals. The processes that determine the acquisition of immunity to clinical disease and to asymptomatic carriage of malaria parasites are poorly understood, in part because of a lack of validated immunological markers of protection. Using mathematical models, we seek to better understand the processes that determine observed epidemiological patterns. We have developed an age-structured mathematical model of malaria transmission in which acquired immunity can act in three ways ("immunity functions"): reducing the probability of clinical disease, speeding the clearance of parasites, and increasing tolerance to subpatent infections. Each immunity function was allowed to vary in efficacy depending on both age and malaria transmission intensity. The results were compared to age patterns of parasite prevalence and clinical disease in endemic settings in northeastern Tanzania and The Gambia. Two types of immune function were required to reproduce the epidemiological age-prevalence curves seen in the empirical data; a form of clinical immunity that reduces susceptibility to clinical disease and develops with age and exposure (with half-life of the order of five years or more) and a form of anti-parasite immunity which results in more rapid clearance of parasitaemia, is acquired later in life and is longer lasting (half-life of >20 y). The development of anti-parasite immunity better reproduced observed epidemiological patterns if it was dominated by age-dependent physiological processes rather than by the magnitude of exposure (provided some exposure occurs). Tolerance to subpatent infections was not required to explain the empirical data. The model comprising immunity to clinical disease which develops early in life and is exposure-dependent, and anti-parasite immunity which develops later in life and is not dependent on the magnitude of exposure, appears to best reproduce the pattern of parasite prevalence and clinical disease by age in different malaria transmission settings. Understanding the effector mechanisms underlying these two immune functions will assist in the design of transmission-reducing interventions against malaria.
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Envejecimiento/inmunología , Brotes de Enfermedades/estadística & datos numéricos , Susceptibilidad a Enfermedades/inmunología , Inmunidad Innata/inmunología , Malaria/inmunología , Malaria/transmisión , Modelos Inmunológicos , Distribución por Edad , Simulación por Computador , Susceptibilidad a Enfermedades/epidemiología , Gambia/epidemiología , Humanos , Malaria/epidemiología , Malaria/parasitología , Tanzanía/epidemiologíaRESUMEN
BACKGROUND: The durations of untreated stage 1 (early stage, haemo-lymphatic) and stage 2 (late stage, meningo-encephalitic) human African trypanosomiasis (sleeping sickness) due to Trypanosoma brucei gambiense are poorly quantified, but key to predicting the impact of screening on transmission. Here, we outline a method to estimate these parameters. METHODS: We first model the duration of stage 1 through survival analysis of untreated serological suspects detected during Médecins Sans Frontières interventions in Uganda and Sudan. We then deduce the duration of stage 2 based on the stage 1 to stage 2 ratio observed during active case detection in villages within the same sites. RESULTS: Survival in stage 1 appears to decay exponentially (daily rate = 0.0019; mean stage 1 duration = 526 days [95%CI 357 to 833]), possibly explaining past reports of abnormally long duration. Assuming epidemiological equilibrium, we estimate a similar duration of stage 2 (500 days [95%CI 345 to 769]), for a total of nearly three years in the absence of treatment. CONCLUSION: Robust estimates of these basic epidemiological parameters are essential to formulating a quantitative understanding of sleeping sickness dynamics, and will facilitate the evaluation of different possible control strategies.
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Trypanosoma brucei gambiense , Tripanosomiasis Africana/epidemiología , Adolescente , Adulto , Animales , Niño , Progresión de la Enfermedad , Femenino , Estudios de Seguimiento , Humanos , Masculino , Prevalencia , Sudán/epidemiología , Tripanosomiasis Africana/diagnóstico , Uganda/epidemiologíaRESUMEN
Conventional epidemiological studies of infections spreading through trade networks, e.g., via livestock movements, generally show that central large-size holdings (hubs) should be preferentially surveyed and controlled in order to reduce epidemic spread. However, epidemiological strategies alone may not be economically optimal when costs of control are factored in together with risks of market disruption from targeting core holdings in a supply chain. Using extensive data on animal movements in supply chains for cattle and swine in France, we introduce a method to identify effective strategies for preventing outbreaks with limited budgets while minimizing the risk of market disruptions. Our method involves the categorization of holdings based on position along the supply chain and degree of market share. Our analyses suggest that trade has a higher risk of propagating epidemics through cattle networks, which are dominated by exchanges involving wholesalers, than for swine. We assess the effectiveness of contrasting interventions from the perspectives of regulators and the market, using percolation analysis. We show that preferentially targeting minor, non-central agents can outperform targeting of hubs when the costs to stakeholders and the risks of market disturbance are considered. Our study highlights the importance of assessing joint economic-epidemiological risks in networks underlying pathogen propagation and trade.
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Enfermedades de los Animales/economía , Enfermedades de los Animales/epidemiología , Ganado , Modelos Biológicos , Modelos Económicos , Animales , BovinosRESUMEN
Knowledge of the incubation period of infectious diseases (time between host infection and expression of disease symptoms) is crucial to our epidemiological understanding and the design of appropriate prevention and control policies. Plant diseases cause substantial damage to agricultural and arboricultural systems, but there is still very little information about how the incubation period varies within host populations. In this paper, we focus on the incubation period of soilborne plant pathogens, which are difficult to detect as they spread and infect the hosts underground and above-ground symptoms occur considerably later. We conducted experiments on Rhizoctonia solani in sugar beet, as an example patho-system, and used modelling approaches to estimate the incubation period distribution and demonstrate the impact of differing estimations on our epidemiological understanding of plant diseases. We present measurements of the incubation period obtained in field conditions, fit alternative probability models to the data, and show that the incubation period distribution changes with host age. By simulating spatially-explicit epidemiological models with different incubation-period distributions, we study the conditions for a significant time lag between epidemics of cryptic infection and the associated epidemics of symptomatic disease. We examine the sensitivity of this lag to differing distributional assumptions about the incubation period (i.e. exponential versus Gamma). We demonstrate that accurate information about the incubation period distribution of a pathosystem can be critical in assessing the true scale of pathogen invasion behind early disease symptoms in the field; likewise, it can be central to model-based prediction of epidemic risk and evaluation of disease management strategies. Our results highlight that reliance on observation of disease symptoms can cause significant delay in detection of soil-borne pathogen epidemics and mislead practitioners and epidemiologists about the timing, extent, and viability of disease control measures for limiting economic loss.
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Epidemias , Interacciones Huésped-Patógeno , Periodo de Incubación de Enfermedades Infecciosas , Modelos Teóricos , Enfermedades de las Plantas , AlgoritmosRESUMEN
Invasive soilborne plant pathogens cause substantial damage to crops and natural populations, but our understanding of how to prevent their epidemics or reduce their damage is limited. A key and experimentally-tested concept in the epidemiology of soilborne plant diseases is that of a threshold spacing between hosts below which epidemics (invasive spread) can occur. We extend this paradigm by examining how plant-root growth may alter the conditions for occurrence of soilborne pathogen epidemics in plant populations. We hypothesise that host-root growth can 1) increase the probability of pathogen transmission between neighbouring plants and, consequently, 2) decrease the threshold spacing for epidemics to occur. We predict that, in systems initially below their threshold conditions, root growth can trigger soilborne pathogen epidemics through a switch from non-invasive to invasive behaviour, while in systems above threshold conditions root growth can enhance epidemic development. As an example pathosystem, we studied the fungus Rhizoctonia solani on sugar beet in field experiments. To address hypothesis 1, we recorded infections within inoculum-donor and host-recipient pairs of plants with differing spacing. We translated these observations into the individual-level concept of pathozone, a host-centred form of dispersal kernel. To test hypothesis 2 and our prediction, we used the pathozone to parameterise a stochastic model of pathogen spread in a host population, contrasting scenarios of spread with and without host growth. Our results support our hypotheses and prediction. We suggest that practitioners of agriculture and arboriculture account for root system expansion in order to reduce the risk of soilborne-disease epidemics. We discuss changes in crop design, including increasing plant spacing and using crop mixtures, for boosting crop resilience to invasion and damage by soilborne pathogens. We speculate that the disease-induced root growth observed in some pathosystems could be a pathogen strategy to increase its population through host manipulation.
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Productos Agrícolas/microbiología , Interacciones Huésped-Patógeno/fisiología , Modelos Biológicos , Enfermedades de las Plantas/microbiología , Raíces de Plantas/microbiología , Rhizoctonia/fisiología , Microbiología del Suelo , Simulación por Computador , Enfermedades de las Plantas/prevención & control , Raíces de Plantas/crecimiento & desarrollo , Dinámica Poblacional , Rhizoctonia/patogenicidadRESUMEN
BACKGROUND: The persistence of malaria as an endemic infection and one of the major causes of childhood death in most parts of Africa has lead to a radical new call for a global effort towards eradication. With the deployment of a highly effective vaccine still some years away, there has been an increased focus on interventions which reduce exposure to infection in the individual and -by reducing onward transmission-at the population level. The development of appropriate monitoring of these interventions requires an understanding of the timescales of their effect. METHODS & FINDINGS: Using a mathematical model for malaria transmission which incorporates the acquisition and loss of both clinical and parasite immunity, we explore the impact of the trade-off between reduction in exposure and decreased development of immunity on the dynamics of disease following a transmission-reducing intervention such as insecticide-treated nets. Our model predicts that initially rapid reductions in clinical disease incidence will be observed as transmission is reduced in a highly immune population. However, these benefits in the first 5-10 years after the intervention may be offset by a greater burden of disease decades later as immunity at the population level is gradually lost. The negative impact of having fewer immune individuals in the population can be counterbalanced either by the implementation of highly-effective transmission-reducing interventions (such as the combined use of insecticide-treated nets and insecticide residual sprays) for an indefinite period or the concurrent use of a pre-erythrocytic stage vaccine or prophylactic therapy in children to protect those at risk from disease as immunity is lost in the population. CONCLUSIONS: Effective interventions will result in rapid decreases in clinical disease across all transmission settings while population-level immunity is maintained but may subsequently result in increases in clinical disease many years later as population-level immunity is lost. A dynamic, evolving intervention programme will therefore be necessary to secure substantial, stable reductions in malaria transmission.
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Malaria/inmunología , Malaria/prevención & control , Modelos Biológicos , África/epidemiología , Humanos , Malaria/transmisión , Vacunas contra la Malaria/inmunología , Grupos de Población , Vigilancia de la Población/métodosRESUMEN
Gambiense human African trypanosomiasis (HAT, sleeping sickness) is widely assumed to be 100% pathogenic and fatal. However, reports to the contrary exist, and human trypano-tolerance has been postulated. Furthermore, there is uncertainty about the actual duration of both stage 1 and stage 2 infection, particularly with respect to how long a patient remains infectious. Understanding such basic parameters of HAT infection is essential for optimising control strategies based on case detection. We considered the potential existence and relevance of human trypano-tolerance, and explored the duration of infectiousness, through a review of published evidence on the natural progression of gambiense HAT in the absence of treatment, and biological considerations. Published reports indicate that most gambiense HAT cases are fatal if untreated. Self-resolving and asymptomatic chronic infections probably constitute a minority if they do indeed exist. Chronic carriage, however, deserves further study, as it could seed renewed epidemics after control programmes cease.
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Tripanosomiasis Africana/fisiopatología , Animales , Camerún/epidemiología , Côte d'Ivoire/epidemiología , Progresión de la Enfermedad , Reservorios de Enfermedades , Humanos , Prevalencia , Remisión Espontánea , Trypanosoma brucei gambiense , Tripanosomiasis Africana/epidemiología , Tripanosomiasis Africana/transmisiónRESUMEN
1. The transient dynamics and stability of a population are determined by the interplay between species density, its spatial distribution and the positive and negative density-dependent processes regulating population growth. 2. Using the human-helminth parasite system as an example, we propose that the life-stage upon which negative density dependence operates will influence the rate of host reinfection following anthelmintic chemotherapy, and the likely success of control programmes. 3. Simple deterministic models are developed which highlight how a parasite species whose population size is down-regulated by density-dependent establishment will reinfect a host population at a faster rate than a species with density-dependent parasite fecundity. 4. Different forms of density dependence can produce the same equilibrium behaviour but different transient dynamics. Under-representing the nature and magnitude of density-dependent mechanisms, and in particular those operating upon establishing life-stages, may cause the resilience of the parasite population to a control perturbation to be underestimated.
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Helmintos/fisiología , Modelos Biológicos , Animales , Interacciones Huésped-Parásitos , Humanos , Densidad de Población , Reproducción/fisiología , Factores de TiempoRESUMEN
Here we analyze patterns of human infection with Onchocerca volvulus (the cause of river blindness) in different continents and ecologies. In contrast with some geohelminths and schistosome parasites whose worm burdens typically exhibit a humped pattern with host age, patterns of O. volvulus infection vary markedly with locality. To test the hypothesis that such differences are partly due to heterogeneity in exposure to vector bites, we develop an age- and sex-structured model for intensity of infection, with parasite regulation within humans and vectors. The model is fitted to microfilarial data from savannah villages of northern Cameroon, coffee fincas of central Guatemala, and forest-dwelling communities of southern Venezuela that were recorded before introducing ivermectin treatment. Estimates of transmission and infection loads are compared with entomological and epidemiological field data. Host age- and sex-heterogeneous exposure largely explains locale-specific infection patterns in onchocerciasis (whereas acquired protective immunity has been invoked for other helminth infections). The basic reproductive number, R0, ranges from 5 to 8, which is slightly above estimates for other helminth parasites but well below previously presented values.