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- Creators: Barrett, The Honors College
- Creators: School of Life Sciences
colony collapse. This paper aims to understand how these different factors contribute to the decline of honeybee populations by using two separate approaches: data analysis and mathematical modeling. The data analysis examines the relative impacts of mites, pollen, mites, and viruses on honeybee populations and colony collapse. From the data, low initial bee populations lead to collapse in September while mites and viruses can lead to collapse in December. Feeding bee colonies also has a mixed effect, where it increases both bee and mite populations. For the model, we focus on the population dynamics of the honeybee-mite interaction. Using a system of delay differential equations with five population components, we find that bee colonies can collapse from mites, coexist with mites, and survive without them. As long as bees produce more pupa than the death rate of pupa and mites produce enough phoretic mites compared to their death rates, bees and mites can coexist. Thus, it is possible for honeybee colonies to withstand mites, but if the parasitism is too large, the colony will collapse. Provided
this equilibrium exists, the addition of mites leads to the colony moving to the interior equilibrium. Additionally, population oscillations are persistent if they occur and are connected to the interior equilibrium. Certain parameter values destabilize bee populations, leading to large
oscillations and even collapse. From these parameters, we can develop approaches that can help us prevent honeybee colony collapse before it occurs.
This study highlights the significance of zoonotic diseases, which make up almost 60% of infectious diseases in humans, and their origin from animals. Among mammalian viruses, primates, bats, and rodents have been identified as high-risk carriers. Within the rodent family Cricetidae, the species complex of Peromyscus eremicus, Peromyscus californicus, Peromyscus fraterculus, and Osgoodomys banderanus have been found to play a crucial role in disease transmission. These four species are phylogenetically related and share similar physical appearances and ecological niches. They have been identified as carriers of several zoonotic diseases, including Hantavirus, Arenavirus, Yersinia pestis, and Flavivirus, with a history of spread to humans. Despite their implications for public health, many of these species remain understudied. Thus, this study aims to provide a systematic review of the existing literature on these four species to summarize the findings on virus prevalence and distribution. The review shows that sampling efforts have been uneven and recent efforts have been lacking, with potential undiscovered zoonotic diseases. The concentration of sampling efforts in California and gaps in the literature are concerning, especially with changing agriculture and climate change potentially affecting rodent communities.
In completing this thesis project, I attempted to hypothesize the trigger in my own personal diagnosis of type 1 diabetes through literature research as well as further research on viruses and their contribution to autoimmune disorders. I had previously hypothesized that, based on my own family life, type 1 diabetes could possibly be a non-heritable disease despite its consistent inheritance pattern discovered by researchers; however, the research presented in this thesis project rejects this idea and supports the theory that I may have been previously susceptible to this disorder and would have developed type 1 diabetes naturally. There were multiple viruses discovered during the literature research conducted that could possibly have been triggers in the acceleration of my disease. The major link between enteroviruses and autoimmune disorders was discovered, as well as influenza A and SARS-COV-2 and this is explained further in this project.