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Most pathogens are generalists capable of infecting multiple host species or strains. Trade‐offs in performance among different hosts are expected to limit the evolution of generalism. Despite the commonness of generalism, the variation in infectivity, transmission, and trade‐offs in performance among host species have rarely been studied in the wild. To understand the ecological and evolutionary drivers of multi‐host pathogen infectivity and transmission potential, I studied disease severity, transmission dynamics, and infectivity variation of downy mildew pathogen Peronospora sparsa on its three host plants Rubus arcticus, R. chamaemorus, and R. saxatilis. In a survey of 20 wild and cultivated sites of the three host species, disease severity varied by host species and by host population size but not among wild and cultivated sites. To understand how alternative host presence and plant diversity affect transmission of the pathogen, I conducted a transmission experiment. In this experiment, alternative host abundance and plant diversity together modified P. sparsa transmission to trap plants. To understand how resistance to P. sparsa varies among host species and genotypes, I conducted an inoculation experiment using 10 P. sparsa strains from different locations and 20 genotypes of the three host species. Significant variation in infectivity was found among host genotypes but not among host species. When trade‐offs for infectivity were tested, high infectivity in one host species correlated with high infectivity in another host species. However, when pathogen transmission‐related life‐history correlations were tested, a positive correlation was found in R. arcticus but not in R. saxatilis. The results suggest that host resistance may shape pathogen life‐history evolution with epidemiological consequences in a multi‐host pathogen. [ABSTRACT FROM AUTHOR]

Abstract: More is not automatically better. Generation and accumulation of information reflecting the complexity of zoonotic diseases as ecological systems do not necessarily lead to improved interpretation of the obtained information and understanding of these complex systems. The traditional conceptual framework for analysis of diseases ecology is neither designed for, nor adaptable enough, to absorb the mass of diverse sources of relevant information. The multidirectional and multidimensional approaches to analyses form an inevitable part in defining a role of zoonotic pathogens and animal hosts considering the complexity of their inter‐relations. And the more data we have, the more involved the interpretation needs to be. The keyword for defining the roles of microbes as pathogens, animals as hosts, and environmental parameters as infection drivers is “functional importance.” Microbes can act as pathogens toward their host only if/when they recognize the animal organism as the target. The same is true when the host recognizes the microbe as a pathogen rather than harmless symbiont based on the context of its occurrence in that host. Here, we propose conceptual tools developed in the realm of the interdisciplinary sciences of complexity and biosemiotics for extending beyond the currently dominant mindset in ecology and evolution of infectious diseases. We also consider four distinct hierarchical levels of perception guiding how investigators can approach zoonotic agents, as a subject of their research, representing differences in emphasizing particular elements and their relations versus more unified systemic approaches. [ABSTRACT FROM AUTHOR]

Background and purpose: Deep brain stimulation (DBS) for severe Parkinson's disease (PD) outperforms the best medical treatment in controlling motor symptoms and improving quality of life. Nevertheless disease progression cannot be controlled, and the development of dementia over time is nearly inevitable, often resulting in nursing home placement. Ten-year survival, development of hallucinations, dementia and nursing home placement were examined and adverse events were assessed. Method: Patient files were scrutinized from baseline up to 10 years of treatment or death on all 79 PD patients treated with DBS of the subthalamic nucleus from 1998 to 2003 at Aarhus University Hospital. Results: Twenty-four patients died during the follow-up period of 10 years. Age above 60 years at surgery increased mortality 2.3-fold (P = 0.04). Of the 55 surviving patients 29 (53%) were demented and 19 (35%) were in nursing homes. Average time from operation to dementia was 5.6 ± 2.9 years. Hallucinations and nursing home placement were associated with increased mortality. Conclusion: Survival of 70% after a mean of 25 years of PD including 10 years with DBS illustrates that this is a selected group of PD patients. The prevalence of dementia steadily increased after surgery as expected from disease progression and can be an early event. Compared with the few similar long-term studies, the present study presents a larger cohort followed at the same DBS center for a longer period of time and none was lost to follow-up, making conclusions more valid. The present findings are of significant prognostic help for the patient, caregiver and physician when treatment with DBS has to be decided. [ABSTRACT FROM AUTHOR]

Genetic data from field isolates of foot-and-mouth disease virus (FMDV) have been used to trace the source of recent outbreaks of FMD, to design better vaccines and diagnostic tests for FMDV, and to make conclusions regarding the general variability in the FMDV genome. Though epidemiologic data associated with FMDV isolates are available, these data have been used rarely to explore possible associations of epidemiologic factors with evolution or variation of the FMDV genome. In this study, factors associated with variation in the primary immunogenic peptide gene of FMDV (VP1), for a sample of 147 serotype O, Pan Asia strain sequences were explored using traditional analytical epidemiologic methods: logistic regression and multinomial-response logistic regression. Hypothesized factors included host type (bovine, ovine, buffalo, or porcine) and geographical region (Middle East, South Asia, East Asia, Southeast Asia, and Europe). Results of two regression analyses suggest that host type and region, considered to be possible surrogates for host management, may be associated with selection in the VP1 amino acid sequence in FMDV. For example, isolates from cattle and sheep in South Asia appear to converge with a proposed ancestor sequence, whereas isolates from the same species in the Middle East and Southeast Asia appear to diverge. The methods demonstrated here could be used on a more detailed dataset to explore the selective pressure of host immunity on the evolution of FMDV antigens in an endemic setting. More broadly, epidemiologic methods could be applied extensively to molecular data to explore the causes of genomic variation in disease-causing organisms. [ABSTRACT FROM AUTHOR]

Many significant diseases of human civilization are thought to have arisen concurrently with the advent of agriculture in human society. It has been hypothesised that the food produced by farming increased population sizes to allow the maintenance of virulent pathogens, i.e. civilization pathogens, while domestic animals provided sources of disease to humans. To determine the relationship between pathogens in humans and domestic animals, I examined phylogenetic data for several human pathogens that are commonly evolutionarily linked to domestic animals: measles, pertussis, smallpox, tuberculosis, taenid worms, and falciparal malaria. The majority arc civilization pathogens, although I have included others whose evolutionary origins have traditionally been ascribed to domestic animals. The strongest evidence for a domestic-animal origin exists for measles and pertussis, although the data do not exclude a non-domestic origin. As for the other pathogens, the evidence currently available makes it difficult to determine if the domestic-origin hypothesis is supported or refuted; in fact, intriguing data for tuberculosis and taenid worms suggests that transmission may occur as easily from humans to domestic animals. These findings do not abrogate the importance of agriculture in disease transmission; rather, if anything, they suggest an alternative, more complex series of effects than previously elucidated. Rather than domestication, the broader force for human pathogen evolution could be ecological change, namely anthropogenic modification of the environment. This is supported by evidence that many current emerging infectious diseases are associated with human modification of the environment. Agriculture may have changed the transmission ecology of pre-existing human pathogens, increased the success of pre-existing pathogen vectors, resulted in novel interactions between humans and wildlife, and, through the domestication of animals, provided a stable conduit for human infection by wildlife diseases. [ABSTRACT FROM AUTHOR]