The F-strain of Mycoplasma gallisepticum (FMG) is commonly used in vaccination programs to displace infections by more virulent natural or wild type Mycoplasma gallisepticum strains. However, a better understanding of the mechanisms responsible for altered egg production (EP) and egg quality in commercial layers infected with FMG is important, as these alterations can cause economic loss to the United States layer industry. This study was designed to examine potential mechanism(s) responsible for alterations in EP and egg quality by FMG-inoculation. The effects of FMG on production parameters and physiological characteristics of commercial laying hens were evaluated. In isolation units, 12 wk FMG inoculation delayed onset of lay approximately one wk, decreased overall EP, and decreased EP 34 wk post-inoculation. A 12 wk FMG inoculation also resulted in a higher incidence of fatty liver hemorrhagic syndrome, ovarian follicular regression, and decreased isthmal and vaginal proportions of the reproductive tract. Ovarian regression may be related to retarded production (liver), transport (blood), and/or uptake (ovary) of yolk particles. Changes in blood characteristics (i.e. lipid composition) with FMG colonization of the liver may become manifest through changes in egg constituents. As evidenced through changes in the relative weights of various reproductive organs, colonization of these organs by FMG, in addition to the liver, may also be a cause of the effects observed on EP. Increases in hematocrit, serum triglycerides, and plasma protein between 8 and 10 wk post FMG-inoculation, suggest that the initial weeks of EP are stressful. Post-peak decreases in these same variables suggest a more chronic inhibition on lipid and protein synthesis in the liver. Decreased blood lipid concentration may be directly responsible for the reductions in yolk lipid, cholesterol, and fatty acid deposition in 12 wk FMG-inoculated hens. Dual adverse effects in the caged layer facility on feed conversion and egg mass were realized in 22 wk FMG-inoculated birds. In contrast, a 12 wk FMG inoculation delayed onset of lay without a loss in total EP or egg mass. Therefore, inoculation with FMG at 12 wk is more practical and cost effective. Higher degrees of physiological stress experienced by hens in a caged layer facility may exacerbate the effects of FMG inoculation seen in the isolation units. These data demonstrate that alterations in performance and egg characteristics of commercial layers inoculated with FMG at either 12 or 22 wk of age and housed in either isolation units or caged layer facilities are related to mutual functional disturbances in the blood, liver, ovary, and oviduct without concomitant intestinal changes.

No description available.

Anthropogenic resource provisioning of wildlife has increasingly been hypothesized to alter pathogen spread. Although bird feeding is the most widespread form of intentional wildlife provisioning, we know relatively little about how the degree of anthropogenic feeding at a site impacts wild birds in ways relevant to disease transmission. We manipulated the density of bird feeders (low versus high) available at otherwise similar sites and tracked the local abundance, body condition (scaled-mass index), feeding behavior, and movement across the landscape in wild house finches (Haemorhous mexicanus), a feeder-dependent species subject to outbreaks of a contagious pathogen commonly spread at feeders. The local abundance of house finches was significantly higher at sites with high feeder density but, surprisingly, finches at high-density feeder sites had poorer body condition than those at low-density sites. Behaviorally, birds at high-density feeder sites had longer average feeding bouts and spent more time per day on feeders than birds at low-density feeder sites. Further, birds first recorded at low-density feeder sites were more likely to move to a neighboring high-density feeder site than vice versa. Overall, because local abundance and time spent on feeders have been linked with the risk of disease outbreaks in this species, effects of bird feeder density on both traits may, in turn, influence disease dynamics in house finches. Our results suggest that heterogeneity in the density of bird feeders can have diverse effects on wild birds, with potential consequences for disease transmission. / Master of Science / Feeding wildlife has increasingly been thought to change the spread of disease. Although bird feeding is the most widespread form of intentional wildlife feeding, we know relatively little about how much human feeding impacts wild birds in ways that affect disease transmission. We changed the density of bird feeders (low versus high) available at otherwise similar areas and tracked the local abundance, body condition, feeding behavior, and movement across the landscape in wild house finches (Haemorhous mexicanus), a feeder-dependent species subject to outbreaks of a infectious disease commonly spread at feeders. The local abundance of house finches was significantly higher at sites with high feeder density but, surprisingly, finches at high-density feeder sites had poorer body condition than those at low-density sites. Behaviorally, birds at high-density feeder sites had longer average bouts on feeders and spent more time per day on feeders than birds at low-density feeder sites. Further, birds first recorded at low-density feeder sites were more likely to move to a neighboring high-density feeder site than vice versa. Overall, because local abundance and time spent on feeders have been linked with the risk of disease outbreaks in this species, effects of bird feeder density on both traits may, in turn, increase disease spread in house finches. Our results suggest that variation in the density of bird feeders can have diverse effects on wild birds, with potential consequences for disease transmission.

Infectious disease is a ubiquitous aspect of life on earth; however, parasites and pathogens are not distributed equally among individual hosts. Due to its ability to shape the way that individuals interact with other potential hosts and the environment, behavior is one of the most salient ways through which host biology varies in the context of disease. Variation in animal behavior can impact both transmission and the extent of a host's pathogen acquisition, and thus can have important consequences for infectious disease dynamics. Additionally, in this world of rapid urbanization where landscapes and wildlife resources are being altered, it is important to understand the ways in which human activity impact wildlife behavior, and in turn, disease dynamics. Here, we used both observational and experimental studies in field and laboratory settings to investigate the relationships among host behavior and physiology, anthropogenic food sources, and disease transmission in a natural host-pathogen system. First, we examined the relationship between house finch (Haemorhous mexicanus) stress physiology, exploratory behaviors, and social behaviors in the wild. We provided evidence that more exploratory house finches interact with more individuals in the wild, and have higher baseline concentrations of circulating stress hormones. Next, we found evidence that the amount of time spent on bird feeders drives both the acquisition and transmission of the bacterial pathogen Mycoplasma gallisepticum (Mg), indicating that variation in host foraging behavior has important transmission consequences in this system. Lastly, we found that the density of bird feeders available to house finches predicts the extent of Mg transmission in captivity. Taken together, these results highlight the important role that behavioral heterogeneity can play in the acquisition and spread of pathogens, as well as the potential impacts of human behavior on wildlife disease dynamics. Future work should seek to identify specific physiological mechanisms driving Mg acquisition and transmission as they relate to variation in host behavior, and the ways in which bird feeders impact disease-relevant behaviors in the wild. / Ph. D. / Infectious disease impacts almost every living creature on earth; however, some individuals are more likely to become sick and spread disease than others. Animal behavior can strongly influence disease dynamics due to its ability to shape the way that individuals interact with one another and the environment. Behavior can impact an individual’s likelihood of both acquiring and spreading disease, and thus can have important consequences for disease outbreaks. Additionally, as urban areas are expanding, it is important to understand the ways in which human activity impact wildlife behavior, and in turn, disease dynamics. Through both laboratory and field studies, we investigate the relationships among host behavior and physiology, human-related food sources, and disease transmission in a natural wildlife disease system. First, we examined the relationships between stress hormones, exploratory behaviors, and social behaviors of house finches, a common songbird. We provided evidence that more exploratory house finches interact with more individuals in the wild, and have higher concentrations of stress hormones. Next, we found evidence that the amount of time that house finches spend on bird feeders drives both the likelihood of acquiring and spreading conjunctivitis (=pink eye). This means that certain individuals are more likely to get sick and pass the disease on to others than other individuals are. Lastly, we found that when the density of bird feeders available to house finches is high, we see more disease transmission. Taken together, these 5 results highlight the important role that variation in behavior can play in acquiring and spreading disease, as well as the potential impacts of human behavior on wildlife health.

Immunological heterogeneity is the norm in most free-living vertebrate populations, creating a diverse and challenging landscape for pathogens to replicate and transmit. This dissertation work sought to determine sources of immunological heterogeneity, as well as the consequences of this heterogeneity on pathogen fitness and evolution. A major source of heterogeneity in free-living host populations is the degree of exposure to a pathogen, as well as a host's history of exposure to a pathogen, which can create variation in standing immunity. We sought to determine the role of exposure heterogeneity on host susceptibility and immunity to secondary infection, and the influence of this heterogeneity on pathogen fitness and virulence evolution in a wild bird-bacterium system. We first determined that exposure level has a significant effect on host susceptibility to infection, severity of disease and infection, as well as immunity produced to secondary infection. Subsequently, we tested whether exposure history, and the immunity formed from this previous exposure, altered the within-host fitness advantage to virulent pathogens. We determined that previous low-level repeat exposure, which wild hosts likely encounter while foraging, produces a within-host environment which greatly favors more virulent pathogens. While within-host processes are vital for understanding and interpreting the evolutionary pressures on a pathogen, the ultimate metric of pathogen fitness is transmission. We therefore tested whether exposure history altered the transmission potential of a host and whether prior host exposure selected for more virulent pathogens. The transmission potential of a host significantly decreased with previous exposure, and high levels of previous exposure selected for more virulent pathogens. While we anticipated selection to be strongest at low-levels of exposure based on our previous results, we found here that high doses of prior exposure resulted in the strongest transmission advantage to virulence. This study also provided insight into the nuanced nature of transmission, which our results indicate is determined both by the degree of within-host pathogen replication as well as host disease severity. Together, our findings underscore the importance of exposure level and exposure history in natural populations in determining susceptibility, immunity and pathogen virulence evolution. / Doctor of Philosophy / Infectious diseases disrupt and threaten all life on this planet. To better anticipate and understand why some diseases are more harmful than others, it is vital that we consider the natural variability that exists in animal populations. A major source of variation in populations that experience disease is exposure level to a pathogen, as well as the history of exposure to a pathogen, which can alter an individual’s protection against future exposures. We sought to determine the role of exposure level on the likelihood of an individual contracting an infection, their protection from future infections, and the influence this has on pathogen evolution in a wild bird-bacterium system. We determined that exposure level has a significant effect on the likelihood an individual has of becoming infected, how severe the infection became, as well as how protected they were from future infections. Subsequently, we tested whether exposure history, and the immunity formed from previous exposure, altered the ability of pathogen strains that cause different levels of harm to replicate. We determined that previous low-level exposure, which hosts likely encounter in the wild, creates a level of immunity that favors more harmful strains of the pathogen. While understanding what happens within a host is important, the ultimate metric for predicting whether more or less harmful types of pathogens will persist is the ability of each pathogen type to spread from one host to another. We therefore tested whether exposure history altered the spread potential of a host and whether previous exposure preferentially favored the spread of more harmful pathogens. The spread potential of a host was much lower if that host had previously been exposed to the pathogen, and high levels of previous exposure in hosts only allowed the more harmful pathogen types to spread. We also found that a host’s spread potential was the result of both how much pathogen they had in their body, as well as how inflamed their affected tissues were. Together, our results indicate that natural variation in prior exposure to pathogens, which is common in all animal populations, including humans, can favor more harmful pathogen types.

Los alojamientos ganaderos son una fuente importante de material particulado (“particulate matter”, PM) y bioaerosoles. Estas sustancias tienen un efecto perjudicial tanto para la salud humana y animal como para el medio ambiente. Para reducir los niveles de PM y bioaerosoles en alojamientos ganaderos es necesario conocer el origen de los mismos y los factores que afectan a su generación y suspensión en el aire. Esta Tesis Doctoral aborda aspectos relacionados con la concentración, origen y propiedades físicas, químicas y biológicas del PM en el aire de granjas de conejos y aves, su relación con los bioaerosoles patógenos y técnicas para reducirlos. Este trabajo pretende contribuir a paliar los efectos negativos de estas sustancias tanto en el interior de los alojamientos ganaderos como en el exterior. Los objetivos específicos planteados en la presente Tesis Doctoral fueron: i). caracterizar la morfología y la composición química del PM de distintos tamaños así como la concentración de bacterias en el aire de granjas de conejos, ii). cuantificar la concentración y emisión del PM de distintos tamaños en el aire e identificar las principales actividades que contribuyen a la generación del PM en granjas de conejos, iii). evaluar la distribución espacial de bacterias aerobias mesófilas en el aire durante un ciclo de producción de broilers y examinar su relación con la concentración y evolución del PM, iv). evaluar y comparar diferentes técnicas para muestrear y detectar el patógeno Salmonella spp. en el aire de granjas de broilers y v). evaluar la aplicación de desinfectantes en el aire como medida de reducción de los bioaerosoles en granjas de gallinas ponedoras con especial atención al patógeno Mycoplasma gallisepticum. Los resultados de esta Tesis indican que en los alojamientos avícolas y cunícolas se generan y emiten cantidades importantes de PM y bioaerosoles, por encima de los valores límite de exposición que marca la Directiva 2008/50/CE relativa a la calidad del aire ambiente y a una atmósfera más limpia en Europa, sobre todo en granjas de aves. Estas sustancias deben ser controladas y reducidas para proteger el medio ambiente, la salud y bienestar de las personas y animales. En alojamientos cunícolas, el PM mostró una morfología y composición química compleja, siendo las partículas irregulares y angulosas, ricas en S, Ca, Mg, Na y Cl, las más abundantes. La concentración de bacterias aerobias mesófilas en el aire por metro cúbico varió entre 3,1x103 y 1,6x106 unidades formadoras de colonia (UFC). Las principales fuentes generadoras de PM fueron la piel, el pienso y las heces provenientes de las actividades de limpieza de la nave, sobre todo de barrer y de los propios animales. La concentración media de PM10 (partículas de 10 μm de diámetro o inferior) fue 0,08±0,06 mg/m3 para conejos de cebo y 0,05±0,06 mg/m3 para conejas y la concentración media de PM2,5 (partículas de 2,5 μm de diámetro o inferior) fue 0,01±0,02 mg/m3 para conejos de cebo y 0,01±0,04 mg/m3 para conejas. Las emisiones variaron entre 6 y 15 mg/plaza/día para PM10 y entre 0,2 y 3,0 mg/plaza/día para PM2,5. En alojamientos de broilers, la concentración de bacterias varió entre 3,0 y 6,5 log UFC/m3. La mayoría de bacterias se asociaron con partículas entre 3,3 y más de 7,0 μm de diámetro obteniéndose una correlación positiva entre las concentraciones de PM10 y PM2,5 y las de bacterias. Respecto a la detección de patógenos en el aire, no se detectó Salmonella spp. cultivable en una explotación de broilers infectados experimentalmente mediante el uso de borboteadores de aire y técnicas de cultivo tradicional. No obstante, se detectó este patógeno en el aire mediante impactación y técnicas moleculares. Por lo tanto, no se recomienda el uso de borboteadores y técnicas de cultivo para la detección y/o cuantificación de Salmonella spp. cultivable en el aire. En alojamientos de gallinas, la concentración media de PM10 fue 0,55±0,38 mg/m3 y 0,02±0,03 mg/m3 para PM2,5. La concentración de bacterias varió entre 4,1 y 5,7 log UFC/m3. La aplicación de un desinfectante químico de amplio espectro en el aire no fue efectiva ni para reducir los niveles de bacterias aerobias mesófilas en el aire ni de Mycoplasma spp. Es necesario estudiar diferentes productos, dosis o técnicas de aplicación. En su conjunto, los resultados presentados en esta Tesis Doctoral proporcionan una información útil sobre el PM y los bioaerosoles en el aire de alojamientos ganaderos, que permitirá diseñar e implementar medidas de reducción prácticas y eficaces que mejoren la calidad del aire en los alojamientos ganaderos y reduzcan su emisión al exterior. / Adell Sales, E. (2014). Material particulado y bioaerosoles en el aire de granjas de aves y conejos: cuantificación, caracterización y medidas de reducción [Tesis doctoral]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/44231

Throughout their lives, animals are faced with numerous ecological challenges stemming from abiotic and biotic conditions of their environment. Phenotypic shifts in response to one challenge can have cascading effects on other organismal systems, with downstream implications for individual fitness. Infectious disease presents a significant ecological challenge for most organisms on earth. Additionally, how an animal responds to disease can be shifted by exposure to other ecological challenges. Thus, infectious disease can both present an ecological challenge itself or shift as a consequence of another challenge. In this work, I used experimental captive studies on wild-caught house finches (Haemorhous mexicanus) to elucidate how an animal might shift its phenotypes when presented with an ecological challenge. In the first experiment, I examined how nutritional stress during nestling development impacted the magnitude of house finch responses to the bacterial pathogen Mycoplasma gallisepticum (MG). Although nutritional stress limited mass gain in nestlings, individual responses to MG did not vary with nutritional stress, possibly indicating that the development of immune responses is resilient even in the face of suboptimal nutritional conditions. Next, I investigated infectious disease as a challenge in itself and asked how individual social preferences were shifted by MG infection. I demonstrated that MG-infected house finches showed augmented sociality relative to control birds, choosing to spend more time with a group of conspecifics than alone. Because this increased social preference was no longer present once birds recovered, this phenotypic change in sociality may have specific benefits for actively infected birds. Finally, my last experiment expands upon these results, exploring whether group-living particularly benefits infected birds by offsetting two common fitness costs of infection: reduced foraging abilities and decreased anti-predator responses. Here we found that group-living provides all individuals with improved foraging and anti-predator behaviors, with the strongest benefits of group-living apparent for infected finches. This suggests that augmented sociality in infected house finches has important implications for surviving infection, and potentially, for the spread of MG within populations. As animals continue to face increasing and novel ecological challenges, it is vitally important to understand individual responses to environmental challenges, which can have long-term effects for all levels of biological organization. In particular, my work highlights the role of social behavior as a potentially adaptive phenotypic response to infectious disease in wild animals. Taken together, my results demonstrate the importance of continuing to study infectious disease from multiple perspectives to better understand how animals will respond to a shifting world. / Doctor of Philosophy / All animals must respond to challenges in their environment, which can impact their lives in a variety of ways. Infectious disease is a significant challenge for most organisms on earth. Infection with a disease-causing pathogen must be met by the individual with behavioral, physiological, and immunological responses to increase the animal's likelihood of survival. Additionally, an animal's response to disease can be shifted by exposure to other adverse environmental conditions, such as reduced access to food. On the one hand, infectious disease can present a challenge in itself. Alternatively, how an animal responds to disease may shift as a consequence of another challenge. In this work, I brought wild-caught birds into a captive setting and performed three experiments to determine how an animal might respond to common ecological challenges. First, I studied how food shortages during early life impacted how strongly birds responded to infection with a disease-causing bacteria. In this study I found that host responses to disease did not shift, even when birds were given less food and experienced reduced mass growth during early life. Although young animals are developing rapidly and are particularly vulnerable to challenges in their environment, my results indicate that the development of responses to disease is resilient even in the face of suboptimal conditions. Next, I investigated how social behaviors were shifted due to disease. Here I demonstrated that diseased birds were more social than healthy birds, preferring to spend more time with a group of other birds than alone. In contrast, once these same birds had recovered from infection and were again healthy they became less social, which suggests that diseased birds in particular may benefit from being part of a group. My final experiment expanded upon these results, exploring whether group-living can help increase an individual's survival by compensating for two consequences of disease: reduced ability to acquire food and evade predators. Here I found that group-living provides individual benefits in terms of both acquiring food and evading predators, both of which have important implications for an individual's survival, especially while experiencing disease. As animals continue to face increasing and new challenges due to global change, it becomes vitally important to understand individual responses to environmental changes. While the work highlighted here presents an important step in understanding individual responses, future work should use observational studies in the wild to determine how the social preferences and behaviors I demonstrated here are actually occurring in a natural habitat. Taken together, my results highlight the importance of continuing to study infectious disease from multiple perspectives to better understand how animals will respond to a shifting world.

No description available.