Most outbreaks of foodborne illness in the United States occur as a result of improper food-handling and preparation practices in homes or food establishments. Some food-safety recommendations that are difficult to incorporate into handling and cooking procedures have contributed to a gap between food-safety knowledge and the actual behavior. The first part (Chapter 3, 4) of this study sought to ensure microbial safety by establishing alternative processing of meat products that can be easily practiced by food-operators and consumers. In Chapter 3, a novel method was developed to thaw frozen chicken-breast by submersion in hot water at 60 °C, an appropriate temperature setting for foodservice hot-holding equipment. This method is rapid (compared to either refrigerator or cold-water thawing that also uses a significant amount of water), safe, and the final cooked-product sensory-quality was not different from refrigerator-thawed and cooked product (microwave thawing results in localized overheating). Chapter 4 developed marinade-cooking (91 °C) and holding (60 °C) procedures for hamburger-patties. Frozen patties were partially grilled and finished cooking in marinade. The moderate temperature of marinade cooking overcomes the chances of thick-patties being surface-overcooked while innermost portions remain undercooked as seen in high-temperature cooking methods (grilling and pan-frying). Consumers liked the marinade-finished cooked and held patties (up to 4 h) equally or more (holding-time dependent) compared to patties grilled and held in a hot-steam cabinet. Reducing salt in perishable foods including cheese is microbial-safety concern especially in their distribution and storage. The second part (Chapter 5, 6) of this study sought to evaluate microbial safety of low-salt hard-type cheese. Aged Cheddar cheeses were inoculated with either Listeria monocytogenes (3.5 log CFU/g) or Salmonella spp. (4.0 log CFU/g) and their survival or growth was monitored at 4, 10, and 21°C for up to 90, 90, and 30 d, respectively. Low-salt (0.7% NaCl) Cheddar formulated at pH 5.1 or 5.7 exhibited no-growth or gradual reduction in L. monocytogenes and Salmonella counts. The results suggest that low-salt Cheddar is as safe as its full-salt counterparts (1.8% NaCl) and that salt may only be a minor food-safety hurdle regarding the post-aging contamination and growth of L. monocytogenes and Salmonella.

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Ambient temperature is an important abiotic factor shaping the process of pathogen transmission because of its effects on hosts, pathogens, and interactions between them. However, most experimental studies demonstrating the effects of temperature on transmission remain correlative and often exclude endothermic taxa, which modify behavior and energy allocation strategies in colder environments in ways that could increase pathogen spread. Additionally, because many endotherms serve as important reservoirs for zoonotic diseases and are facing conservation threats due to disease, understanding how temperature influences transmission in these systems has downstream relevance to human and wildlife health. In this dissertation, I use three laboratory experiments to determine how temperature affects several mechanisms of transmission in a naturally occurring songbird-pathogen system. House finches (Haemorhous mexicanus) are small songbirds that rely on bird feeders to meet thermoregulatory demands during winter. However, interactions with other birds at the feeder and contact with contaminated feeder surfaces are important sources of transmission of the bacterial pathogen Mycoplasma gallisepticum (MG). These interactions likely contribute to the fall and winter outbreaks of mycoplasmal conjunctivitis, a disease characterized by severe conjunctival swelling and changes in behavior in house finches. In my first experiment, I simulated infection in house finches to determine how temperature (warm versus cold) affected contact-relevant sickness behaviors, and in turn, the potential for transmission. I found that ambient temperature had a complex effect on some but not all contact-relevant sickness behaviors in this system, which could have key implications for downstream pathogen spread. Next, I investigated how ambient temperatures influenced another mechanism of transmission, the viability and pathogenicity of MG harbored on bird feeder surfaces. I found that MG remained viable and pathogenic to birds significantly longer when incubated on feeder surfaces at colder versus warmer temperatures. In my final chapter, I determined how temperature influenced the pairwise-transmission of MG from an experimentally-inoculated "donor" bird to its susceptible "receiver" bird cagemate. Here I examined how temperature influenced host infectiousness and estimated exposure dose, as well as the behaviors of both sick and healthy birds. I found that donor birds in colder temperatures were slower to recover from infection, and thus remained infectious for longer, compared to donor birds in warmer temperatures. I also found that receiver birds had more contacts with bird feeders and higher estimated doses of MG in colder temperatures. Despite evidence suggesting that MG transmission could be more successful in colder versus warmer temperatures, overall transmission success did not differ by temperature treatment. My work highlights the complex and non-uniform effects of temperature on aspects of the MG transmission process and suggests ways that temperature could have major implications for seasonal disease dynamics in this system. More broadly, my dissertation provides a framework for testing how different abiotic factors could influence the spread of other directly-transmitted diseases, which will be needed now more than ever in the face of global climate change. / Doctor of Philosophy / Temperature can alter disease spread by changing how organisms interact with each other and their environment. Most scientific studies on this topic have focused on diseases in plants and cold-blooded animals, even though temperature can influence disease spread in warm-blooded animals as well. Warm-blooded animals must use large amounts of energy to stay warm in colder temperatures and will often change their behavior or how they spend their energy to save on energetic costs. In some cases, the way that warm-blooded animals respond to colder temperatures can also increase the risk of disease spread. Understanding how warm-blooded animals spread disease is important because many warm-blooded animals carry human diseases, and because climate change brings both conservation and disease threats. In this dissertation, I test how temperature influences factors that cause disease spread in a wild songbird. House finches (Haemorhous mexicanus) are social backyard birds that eat from bird feeders, particularly in winter months when ample food is needed to keep their bodies warm. However, busy bird feeders can cause sick and healthy birds to interact more frequently, and bird feeders themselves often carry the bacterium Mycoplasma gallisepticum (MG), which causes contagious pink-eye like symptoms in birds. Like many animals, house finches that are sick with MG save energy during infection by spending less time being active. Colder temperatures can be problematic for sick birds because they must spend energy to stay warm but save enough energy for fighting infection. In my first experiment, I examined this conflict between temperature and infection in birds, and in turn, how this conflict could shape disease spread. I found that temperature affected some but not all sickness-related behaviors in house finches, which could mean more disease spread at some temperatures, and less at others. My next experiment studied the bacterium itself, and how well it can survive outside of birds in winter versus summer temperatures. I found that not only was MG better at surviving on a bird feeder in colder temperatures, but it also caused worse disease symptoms in birds over time. In my last experiment, I infected one bird with MG and determined if disease was more likely to spread to its healthy cagemate in warmer or colder temperatures. This was important for studying the effects of temperature on two other factors related to disease spread: the ability of sick hosts to remain contagious to others and the approximate number of pathogens eventually picked up by healthy individuals. I found that in colder temperatures, sick hosts had a harder time recovering, remaining contagious for longer. I also found that healthy bird partners were more likely to spend time at bird feeders in colder temperatures, where they encountered more pathogens on feeder surfaces. Despite these findings, overall MG spread was not higher in colder temperatures. This study provided some of the first evidence showing the complicated relationship between temperature and MG spread in house finches and suggests how temperature could play a role in the seasonal outbreaks of MG seen in nature. My study also provides a blueprint for studying how other environmental factors, such as humidity and rainfall, could shape the spread of other infectious diseases, which will be more important now than ever in a rapidly changing climate.