2021 Student Symposium Research and Creative Activity Book of Abstracts

The UMaine Student Symposium (UMSS) is an annual event that celebrates undergraduate and graduate student research and creative work. Students from a variety of disciplines present their achievements with video presentations. It’s the ideal occasion for the community to see how UMaine students’ work impacts locally – and beyond. The 2021 Student Symposium Research and Creative Activity Book of Abstracts includes a complete list of student presenters as well as abstracts related to their works

Modelling vector-borne and other parasitic diseases. Proceedings of a workshop

Session one of this report highlights ILRAD's research programs and the modelling needs of ILRAD and FAO. Session two deals with vector and helminth population dynamics with particular reference to ticks, tsetse and helminth. Parasite transmission and host parasite interaction are discussed in sessions three and four respectively. These two sessions deal with theileria, trypanosomes and leishmania. Parasite variations and polymorphism is the topic of session five. Session six discusses the effect of disease control programs and session seven reviews modelling systems. The last two sessions deal with the application of modelling, and collection, collation, analysis and dissemination of data on vector-borne and other parasitic diseases

2020 Student Symposium Research and Creative Activity Book of Abstracts

The UMaine Student Symposium (UMSS) is an annual event that celebrates undergraduate and graduate student research and creative work. Students from a variety of disciplines present their achievements with video presentations. It’s the ideal occasion for the community to see how UMaine students’ work impacts locally – and beyond. The 2020 Student Symposium Research and Creative Activity Book of Abstracts includes a complete list of student presenters as well as abstracts related to their works

Peromyscus leucopus – a reservoir of zoonotic agents and a model for understanding infection tolerance

Infection tolerance is the ability to minimize damage caused by pathogens or the host's response to them. A prime example of such resilience is the white-footed deermouse, or P. leucopus, a reservoir of agents of zoonoses like Lyme disease, anaplasmosis, or Powassan virus encephalitis. Despite being persistently infected with pathogens, deermice can strike a delicate balance, keeping the pathogens in check while avoiding maladaptive host response that could lead to inflammation-induced damage. This unique resilience makes deermice an excellent animal model for understanding infection tolerance: they don't get sick and remain fit for their populations' proliferation. As a result, they live longer than most other rodents of the same size. A deeper understanding of how deermice moderate inflammation and other damaging host responses, including sepsis, could explain why some patients with certain infections experience more prolonged or severe disease courses. These individuals may lack the capacity that deermice possess to avoid sickness. Identifying and characterizing factors of infection tolerance in deermice that reduce inflammation elicited by microbes or their toxins may thus lead to more effective therapies. In this dissertation, I describe the microbiome of P. leucopus from a closed colony using metagenomics and compare it to that of M. musculus and a natural population of P. leucopus. Our findings reveal that deermice have a higher number of lactobacilli in their gastrointestinal microbiota. We also discovered new species of lactobacilli that are specific to deermice. As the microbiome influences the immune system, I employ sequencing and immunology techniques to examine tolerance in immune-related tissues of P. leucopus. Immunity evolved to protect the host from pathogens, but inflammatory molecules can cause pathology, chronic conditions, and accelerated aging. The second part of the study explains some of the mechanisms for striking tolerance without developing pathology through inflammation in P. leucopus while infected with Borrelia hermsii or SARS-CoV-2. This study suggests that P. leucopus responds to pathogens by recruiting and activating leucocytes during the initial stage of infection while regulating the activity of these cells with anti-inflammatory cytokines. This model of infection tolerance was evaluated and characterized compared to M. musculus by the early response to endotoxins and bacterial infection. Each rodent species responded by activating a different immune response route. While P. leucopus displayed an alternatively activated macrophage profile and reduced transcription of endogenous retroviruses, as well as consistently moderate pathogenesis, M. musculus displayed classically activated macrophages and higher expression of endogenous retroviral proteins. We are the first to report infection of P. leucopus with SARS-CoV-2 and describe the host response in the brain

Modeling ecological disturbances in the Southeastern United States

Society requires better insights into how disturbances will alter the global carbon cycle. Ecosystem models help us understand the carbon cycle and make predictions about how the terrestrial land sink will change under future climate regimes. Disturbances drive ecosystem cycling, but modeling disturbances has unique challenges, particularly in incorporating heterogeneity and parameter uncertainty. In this dissertation, I explore two questions. 1) How can we capture disturbance ecology in models?, which I explore in my first and second chapters, and 2) How can we use those models to make projections for the Southeastern US?, which I explore in my third and fourth chapters. Both my first and second chapters point to the practical trade-offs in model structure and realism. In my first chapter, I found that representing spatially implicit contagious disturbances in terms of shape and frequency accurately captured structural changes over time and separated the disturbance regimes of different regions. Representing spatially implicit disturbances in terms of shape and frequency sacrificed the specificity of a space-based approach but may be more computationally efficient. In my second chapter, I developed a framework for calibrating models based on an iterative cycle between uncertainty analysis and literature synthesis, targeted field campaigns, and statistical constraint. I found that targeted field work and statistical constraint reduced parameter uncertainty until structural uncertainty began to dominate. Models that capture disturbance dynamics can help us anticipate effects of global change factors like climate change and invasive species. In my third chapter, I found that elevated temperatures reduce cogongrass biomass, and that cogongrass facilitates pine dominance over oaks in a mixed pine-oak stand. This suggests that cogongrass mediates inter-species competition at an ecosystem scale. Prescribed burns are a management technique used to suppress cogongrass and has an add-on benefit of reducing tick populations. However, climate change may threaten how frequently prescribed fires can be safely deployed. In my fourth chapter, I found that tick populations are most sensitive to leaf litter and humidity, which allows for management strategies as an alternative to prescribed burns

Environmental Aspects of Zoonotic Diseases

Environmental Aspects of Zoonotic Diseases provides a definitive description, commentary and research needs of environmental aspects related to zoonotic diseases. There are many interrelated connections between the environment and zoonotic diseases such as: water, soil, air and agriculture. The book presents investigations of these connections, with specific reference to environmental processes such as: deforestation, floods, draughts, irrigation practices, soil transfer and their impact on bacterial, viral, fungal, and parasitological spread. Environmental aspects such as climate (tropical, sub-tropical, temperate, arid and semi-arid), developed and undeveloped countries, animal traffic animal border crossing, commercial animal trade, transportation, as well geography and weather on zoonosis, are also discussed and relevant scientific data is condensed and organized in order to give a better picture of interrelationship between the environment and current spread of zoonotic diseases

Ultrasensitive detection of toxocara canis excretory-secretory antigens by a nanobody electrochemical magnetosensor assay.

peer reviewedHuman Toxocariasis (HT) is a zoonotic disease caused by the migration of the larval stage of the roundworm Toxocara canis in the human host. Despite of being the most cosmopolitan helminthiasis worldwide, its diagnosis is elusive. Currently, the detection of specific immunoglobulins IgG against the Toxocara Excretory-Secretory Antigens (TES), combined with clinical and epidemiological criteria is the only strategy to diagnose HT. Cross-reactivity with other parasites and the inability to distinguish between past and active infections are the main limitations of this approach. Here, we present a sensitive and specific novel strategy to detect and quantify TES, aiming to identify active cases of HT. High specificity is achieved by making use of nanobodies (Nbs), recombinant single variable domain antibodies obtained from camelids, that due to their small molecular size (15kDa) can recognize hidden epitopes not accessible to conventional antibodies. High sensitivity is attained by the design of an electrochemical magnetosensor with an amperometric readout with all components of the assay mixed in one single step. Through this strategy, 10-fold higher sensitivity than a conventional sandwich ELISA was achieved. The assay reached a limit of detection of 2 and15 pg/ml in PBST20 0.05% or serum, spiked with TES, respectively. These limits of detection are sufficient to detect clinically relevant toxocaral infections. Furthermore, our nanobodies showed no cross-reactivity with antigens from Ascaris lumbricoides or Ascaris suum. This is to our knowledge, the most sensitive method to detect and quantify TES so far, and has great potential to significantly improve diagnosis of HT. Moreover, the characteristics of our electrochemical assay are promising for the development of point of care diagnostic systems using nanobodies as a versatile and innovative alternative to antibodies. The next step will be the validation of the assay in clinical and epidemiological contexts

Director\u27s report of research in Kansas 2008

The 2008 Director\u27s Report of Research in Kansas provides a list of journal articles, station publications, and other published manuscripts from scientists in our departments, centers, fields, and associated programs. On cover: July 1, 2003 to June 30, 200

To V, R0 to V ?

Outbreaks of infectious disease can be caused by only a few highly infectious individuals. These individuals are produced by variation in traits affecting contact between infected and susceptible individuals, the likelihood that contact results in infection and the duration of infection. High-risk individuals are difficult to predict because traditional assessments of disease transmission, such as R0, rely on population averages that conceal the variation that produces high transmission-risk phenotypes. Contact rate between infected and susceptible individuals, is primarily determined by behaviour whereas physiological immunity is the main determinant of the likelihood that contact causes infection and infection duration. I characterise variation in traits affecting the determinants of disease transmission and use this to predict individual variation in disease transmission, V. Using the fruit fly, Drosophila melanogaster, and its viral pathogen Drosophila C Virus, I have found pervasive and complex effects of genetic and sex-specific variation, mating, and infection on suites of behaviours, physiological traits and outcomes of infection. Many of my results point to an individual’s disease transmission potential being determined by genetic background and sex. Males, for example, typically survive DCV infection longer than females, however the amount of virus they shed is also determined by their genetic background. To predict how this variation could affect disease transmission dynamics, I simulated outbreaks of DCV in theoretical populations. These populations exhibited genetic and sex-specific variation based on my experiments and significantly affected population-level outbreak dynamics. Differences in these dynamics highlight potentially high-risk transmission classes of individuals, defined by their genetic background and sex