Microparasitic Diseases Research Articles

The economic value of R0 for selective breeding against microparasitic diseases

BackgroundMicroparasitic diseases are caused by bacteria and viruses. Genetic improvement of resistance to microparasitic diseases in breeding programs is desirable and should aim at reducing the basic reproduction ratio {text{R}}_{0}. Recently, we developed a method to derive the economic value of {text{R}}_{0} for macroparasitic diseases. In epidemiological models for microparasitic diseases, an animal’s disease status is treated as infected or not infected, resulting in a definition of {text{R}}_{0} that differs from that for macroparasitic diseases. Here, we extend the method for the derivation of the economic value of {text{R}}_{0} to microparasitic diseases.MethodsWhen {text{R}}_{0} le 1, the economic value of {text{R}}_{0} is zero because the disease is very rare. When {text{R}}_{0}. is higher than 1, genetic improvement of {text{R}}_{0} can reduce expenditures on vaccination if vaccination induces herd immunity, or it can reduce production losses due to disease. When vaccination is used to achieve herd immunity, expenditures are proportional to the critical vaccination coverage, which decreases with {text{R}}_{0}. The effect of {text{R}}_{0} on losses is considered separately for epidemic and endemic disease. Losses for epidemic diseases are proportional to the probability and size of major epidemics. Losses for endemic diseases are proportional to the infected fraction of the population at the endemic equilibrium.ResultsWhen genetic improvement reduces expenditures on vaccination, expenditures decrease with {text{R}}_{0} at an increasing rate. When genetic improvement reduces losses in epidemic or endemic diseases, losses decrease with {text{R}}_{0} at an increasing rate. Hence, in all cases, the economic value of {text{R}}_{0} increases as {text{R}}_{0} decreases towards 1.Discussion{text{R}}_{0} and its economic value are more informative for potential benefits of genetic improvement than heritability estimates for survival after a disease challenge. In livestock, the potential for genetic improvement is small for epidemic microparasitic diseases, where disease control measures limit possibilities for phenotyping. This is not an issue in aquaculture, where controlled challenge tests are performed in dedicated facilities. If genetic evaluations include infectivity, genetic gain in {text{R}}_{0} can be accelerated but this would require different testing designs.ConclusionsWhen {text{R}}_{0} le 1, its economic value is zero. The economic value of {text{R}}_{0} is highest at low values of {text{R}}_{0} and approaches zero at high values of {text{R}}_{0}.

Microparasitic disease dynamics in benthic suspension feeders: Infective dose, non-focal hosts, and particle diffusion

Benthic suspension-feeders can accumulate substantial numbers of microparasitic pathogens by contacting or filtering particles while feeding, thus making them highly vulnerable to infectious diseases. The study of disease dynamics in these marine organisms requires an innovative approach to modeling. To do so, we developed a single-population deterministic compartmental model adapted from the mathematical theory of epidemics. The model is a continuous-time model, unstructured in spatial or age terms, and configured to simulate the dynamics of diverse dose (body burden)-dependent infectious disease transmission processes in suspension feeders caused by susceptible individuals contacting or absorbing (filtering) infectious waterborne pathogens. Different scenarios were simulated to explore the effect of recruitment, filtration rate, particle loss, diffusion-like processes in the water column and non-focal hosts (i.e. non-susceptible in terms of disease) on disease incidence. An increase in recruitment (i.e. new disease free susceptibles) can reduce the prevalence of infection due to the dilution effect of adding more susceptibles, but the disease can spread faster for the same reason. Lower infective particle accumulation rates or increasing particle loss rates in the environment reduce the prevalence of infection. This effect is trivial when the water is saturated with infective particles released by infected and/or dead animals. Diffusion of particles from the local pool available to suspension feeders to the adjacent remote pool, prompted by a large remote volume and high particle exchange, limits epizootic development. Similarly, the likelihood of an epizootic can be constrained in a large susceptible population when competition for pathogens, more ‘active’ in active filter feeders than in passive suspension feeders, reduces the per capita infective particle accumulation rate. In passive suspension feeders, decreasing the area of the feeding surface has the same effect in constraining disease development. The effect of competition for infective particles in essence diluting the infective particle concentration in the water column is magnified when the susceptible population is part of a community with non-focal filter feeders, and is particularly effective in limiting disease development in high infective dose systems. At the same time, this active foraging strategy makes filter feeders more vulnerable to epizootics. The model is a suitable framework for studying the disease dynamics and determinants of disease outbreaks in benthic suspension feeders.

Endemicity of chytridiomycosis features pathogen overdispersion.

Pathogens can be critical drivers of the abundance and distribution of wild animal populations. The presence of an overdispersed pathogen load distribution between hosts (where few hosts harbour heavy parasite burdens and light infections are common) can have an important stabilizing effect on host-pathogen dynamics where infection intensity determines pathogenicity. This may potentially lead to endemicity of an introduced pathogen rather than extirpation of the host and/or pathogen. Overdispersed pathogen load distributions have rarely been considered in wild animal populations as an important component of the infection dynamics of microparasites such as bacteria, viruses, protozoa and fungi. Here we examined the abundance, distribution and transmission of the model fungal pathogen Batrachochytrium dendrobatidis (Bd, cause of amphibian chytridiomycosis) between wild-caught Litoria rheocola (common mist frogs) to investigate the effects of an overdispersed pathogen load distribution on the host population in the wild. We quantified host survival, infection incidence and recovery probabilities relative to infectious burden, and compared the results of models where pathogen overdispersion either was or was not considered an important feature of host-pathogen dynamics. We found the distribution of Bd load between hosts to be highly overdispersed. We found that host survival was related to infection burden and that accounting for pathogen overdispersion allowed us to better understand infection dynamics and their implications for disease control. In addition, we found that the pattern of host infections and recoveries varied markedly with season whereby (i) infections established more in winter, consistent with temperature-dependent effects on fungal growth, and (ii) recoveries (loss of infection) occurred frequently in the field throughout the year but were less likely in winter. Our results suggest that pathogen overdispersion is an important feature of endemic chytridiomycosis and that intensity of infection determines disease impact. These findings have important implications for our understanding of chytridiomycosis dynamics and the application of management strategies for disease mitigation. We recommend quantifying individual infectious burdens rather than infection state where possible in microparasitic diseases.

Experimental evidence for costs due to chewing lice in the European bee-eater (Merops apiaster)

Animals frequently host organisms on their surface which can be beneficial, have no effect or a negative effect on their host. Ectoparasites, by definition, are those which incur costs to their host, but these costs may vary. Examples of avian ectoparasites are chewing lice which feed exclusively on dead feather or skin material; therefore, costs to their bird hosts are generally considered small. Theoretically, many possible proximate effects exist, like loss of tissue or food, infected bites, transmission of microparasitic diseases or reduced body insulation due to loss of feathers, which may ultimately also have fitness consequences. Here, we experimentally examined a possible negative impact of 2 feather-eating louse species (Meropoecus meropis and Brueelia apiastri) on male and female European bee-eaters (Merops apiaster) by removing or increasing louse loads and comparing their impact to a control group (lice removed and immediately returned) after 1 month. A negative effect of chewing lice was found on body mass and sedimentation rate and to a lesser extent on haematocrit levels. Males and females lost more weight when bearing heavy louse loads, and were more susceptible to infestations as indicated by the higher sedimentation rate. Our results further suggest differences in sex-specific susceptibility.

From Host Immunity to Pathogen Invasion: The Effects of Helminth Coinfection on the Dynamics of Microparasites

Concurrent infections with multiple parasites are ubiquitous in nature. Coinfecting parasites can interact with one another in a variety of ways, including through the host's immune system via mechanisms such as immune trade-offs and immunosuppression. These within-host immune processes mediating interactions among parasites have been described in detail, but how they scale up to determine disease dynamic patterns at the population level is only beginning to be explored. In this review, we use helminth-microparasite coinfection as a model for examining how within-host immunological effects may influence the ecological outcome of microparasitic diseases, with a specific focus on disease invasion. The current literature on coinfection between helminths and major microparasitic diseases includes many studies documenting the effects of helminths on individual host responses to microparasites. In many cases, the observed host responses map directly onto parameters relevant for quantifying disease dynamics; however, there have been few attempts at integrating data on individual-level effects into theoretical models to extrapolate from the individual to the population level. Moreover, there is considerable variability in the particular combination of disease parameters affected by helminths across different microparasite systems. We develop a conceptual framework identifying some potential sources of such variability: Pathogen persistence and severity, and resource availability to hosts. We also generate testable hypotheses regarding diseases and the environmental contexts when the effects of helminths on microparasite dynamics should be most pronounced. Finally, we use a case study of helminth and mycobacterial coinfection in the African buffalo to illustrate both progress and challenges in understanding the population-level consequences of within-host immunological interactions, and conclude with suggestions for future research that will help improve our understanding of the effects of coinfection on dynamics of infectious diseases.

Research Article: The Effect of Infectiousness, Duration of Sickness, and Chance of Recovery on a Population: A Simulation Study

Abstract. Mathematical modeling has become a mainstream approach in scientific research when it is not feasible to design adequate experimentation. Agent based modeling provides rapid assessments of possible scenarios, especially in epidemiological studies where the goal is to carry out quick and effective preventive steps when an infection breaks out. In this paper, the relationships between infectiousness, chance of recovery, duration of a micro-parasitic disease, and the population dynamics of the host via parameter sweeps in a simple model system were analyzed. A disease with a very low infection rate is unable to spread in the population, unless the population density is high and the duration of the sickness is long. In cases of low recovery rates the number of sick and immune individuals showed a maximum value at 30% infectiousness. As the size of the population decreases, the population density decreases, and therefore, the transmission rate decreases as well. This effect leads to a new equilibrium...

The Ecological Interactions between a Microsporidian Parasite and its Host Daphnia magna

1. Freshwater plankton populations suffer frequent epidemics of microparasitic diseases. The mechanisms which lead to outbreak and spread of these parasites are poorly understood. A set of experiments was carried out to distinguish between hypotheses explaining the introduction, spread and persistence of a microparasite in Daphnia magna. 2. Transmission of the microsporidian parasite Pleistophora intestinzlis is horizontal through ingestion of free-floating parasite spores, or from spores taken up from pond sediments by the host. At 4 o C parasite spores remained infectious after 3 months, explaining how the parasite persists through periods of host diapause. 3. Parasite transmission probability was inversely related to the water volume in which infected and uninfected hosts were kept. The same density effect was found for the intensity of infections. 4. Host nutritional conditions did not influence parasite multiplication inside the host. However, well-fed hosts became infected more often than poorly fed daphnids of the same age, which can best be explained by their larger size, and consequently their higher filtering rates. 5. Both sexes and all life stages tested of the host were susceptible to infection. Growth and transmission of the parasite was greatly impaired at 6 o C, but no differences in parasite growth were found between 12, 16, 20 and 23 o C. 6. The impact of P. intestinalis on host fecundity was inversely correlated with initial spore dose. 7. Long spore survival outside the host, reduced transmission at low temperatures and density-dependent transmission were the main factors in the interaction of P. intestinalis and its host D. magnia. The results are consistent with field studies of other horizontally transmitted microsporidian parasites in cladoceran and rotifer populations

Virulence and Local Adaptation of a Horizontally Transmitted Parasite

Parasites are thought to maximize the number of successfully transmitted offspring by trading off propagule production against host survival. In a horizontally transmitted microparasitic disease in Daphnia, a planktonic crustacean, increasing geographic distance between host and parasite origin was found to be correlated with a decrease in spore production and virulence. This finding indicates local adaptation of the parasite, but contradicts the hypothesis that long-standing coevolved parasites are less virulent than novel parasites. Virulence can be explained as the consequence of balancing the positive genetic correlation between host mortality and strain-specific spore production.

Quantifying the impact of disease on threatened species

Determining whether a disease or parasite is having a substantial impact on a population of a threatened species is not straightforward. Highly pathogenic parasites are not those which have the greatest influence on hosts, and diseases present at high prevalence are not likely to have a major effect on the host population. I develop simple mathematical models which show that a microparasitic disease such as a viral or bacterial disease will have the greatest impact on its host if it prevents host reproduction, but does not affect host mortality. If infected hosts can still reproduce, intermediate levels of pathogenicity have the greatest impact on hosts. Macroparasites such as helminths likewise have maximum impact on hosts at intermediate pathogenicity. The impact of a helminth on its host population is, however, determined by a complex interplay between pathogenicity per parasite and the nature of the host response to infection. For example, in the absence of density-dependent constraints on parasites within individual hosts, the smaller the impact per parasite on the host, the greater the impact of the parasitic infection on the overall population. Several recommendations can be made to wildlife managers who detect a disease or parasite and wish to determine its impact on a population of a threatened species. There is no entirely satisfactory alternative to experimental manipulation. Treating part of a population and comparing suvivorship or fecundity with controls is the only way to confirm the impact of a disease on a free-ranging population. Such an approach is impractical with every potential pathogen in a population. Some idea as to which pathogens may be of significance to the population can be gained from comparison of disease prevalence or parasite burden between dead and dying hosts and the overall population. Overall high prevalence or high pathogenicity are not good indicators on their own.