The objective of this study was to field-test the "microenvironment concept" of avian botulism epizootiology. The "microenvironment concept" hypothesizes that aquatic invertebrate carcasses may serve both as a substrate for toxin production by Clostridium botulinum type C in nature and as a vehicle for toxin transmission to waterbirds. This concept has become the generally accepted, but inadequately tested, working hypothesis of type C botulism epizootiology. This study attempted to experimentally induce type C botulism in sentinel flocks of mallard ducks (Anas platyrhynchos) and American coots (Fulica americana) on sewage oxidation ponds in northern Utah. The three experimental oxidation ponds were inoculated with Cl. botulinum type C (strain X220B2) endospores in June,l974. Aquatic invertebrate populations were monitored throughout the summer. Rotenone was used in August in two of the experimental ponds (one pond served as a control) to kill aquatic invertebrates and thereby provide a large amount of substrate for clostridial growth and toxin production. No botulism was detected among the sentinel birds even though they routinely ingested invertebrate carcasses. None of the samples of dead invertebrates collected from the experimental ponds contained detectable (in white mice) botulinum toxin. It was concluded that the "microenvironment concept," as it now stands, cannot always be a sufficient explanation of how type C botulism epizootics are initiated in nature. Microbiological experiments designed to determine why the invertebrate carcasses collected from the study ponds contained no botulinum toxin were started and are now ongoing. Early results indicate that Cl. botulinum (X220B2) cells may not normally be able to effectively compete (at least in terms of toxin production) with other microorganisms present in the sewage ponds. It is suggested that the initiation of a type C botulism epizootic in nature may require the alleviation of the inhibitory effects of other putrefactive microorganisms upon clostridial metabolism and/ or toxin. This hypothesis is highly speculative and requires much further experimentation.

Master of Science / Department of Horticulture, Forestry, and Recreation Resources / David A. Haukos / There is a wide variety of diseases that affect wild migratory birds. Occurrence, causes, and impacts of disease outbreaks in wild bird populations are rarely studied beyond documentation of large epizootic events. The relationships between the wildlife-livestock-human interface is rapidly blurring together. Global interests in avian diseases increased around 1990 as a result of the prevalence of zoonosis and potential threat to domestic livestock. A central disease reporting protocol does not exist in many states, which has led to a lack of available historical knowledge of disease occurrence that could be used to predict and manage future outbreaks. Due to changes of abundance and distribution of the migrant populations of Ross’s goose (Chen rossii) and Snow goose (C. caerulescens), geese are increasing their stopover duration in Kansas potentially increasing risk of disease outbreaks. We compiled historic records of wild waterfowl disease events in Kansas from 1967-2014 and related the frequency of events with indices of light geese abundance from 1970-2014. We found 32 reports spanning 16 counties consisting of the diseases avian cholera, avian botulism, aspergillosis, renal coccidiosis, west Nile, aflatoxicosis, and mycotoxicosis. Using a retrospective survey, we found there was a significant relationship between population densities of light geese in Kansas during the Mid-Winter Waterfowl Inventory and occurrence of avian cholera. Efforts to increase the understanding of relationships between disease outbreaks and host species will improve management of future disease outbreaks. Understanding factors known to facilitate wild waterfowl disease events (e.g., environmental, species, and individual), may assist in disease identification and determine a disease management course of action. This course of action is predetermined in a disease management plan. Disease management plans should be developed at the state and station level; incorporating planning, response, disease control, and surveillance and monitoring schemes to build upon the centralized disease database and to promote future disease understanding.

This thesis investigates how the Bear River marsh’s protection became a national interest and a cause for conservation in the Progressive Era. The thesis documents how the marsh declined because of irrigation development culminating with an outbreak of avian botulism in 1910, and traces the long process to protect the marshland. The research focused on examining local water development patterns of the nineteenth and early twentieth centuries, ornithological research in the 1910s, and the national sportsmen’s conservation movement of the 1920s. Upon examination of these events, it becomes clear that a coalition of ornithologists, sportsmen, and policy makers worked together to institute change that affected the marsh. Through showing how groups came together in the past to work for conservation, this research highlights the important role that a coalition of groups can have in reshaping how a landscape is viewed and managed.

Purpose and scope Each year thousands of western waterfowl succumb to disease, predators, mechanical injury and other decimating factors . Based on a review of records it is conservatively estimated that an average of 25,000 ducks have succumbed to botulism on western marsh areas annually. In a recent study, the United States Fish and Wildlife Service valued each duck and goose at $8.00 (McLeod, 1950). Applying this value to the estimated annual numerical loss, a total of $200,000 has been lost each season in mortality of western waterfowl from botulism. Control of this malady would reduce annual waterfowl and monetary losses. Prevention and cure are the only means of controlling botulism in wild ducks. At present, no economical preventative measure exists and control is based on curing stricken birds. The purpose of this study was to evaluate the cost of treatment and rate of recovery of birds stricken with botulism when treated by selected methods . The 4 treatments selected for evaluation were: (1) hospital inoculation, (2) fresh water, (3) field inoculation, and (4) no treatment or control . Research included a comprehensive evaluation of factors such as age, sex, species, body condition, degree of affliction, reaction to various amounts of antitoxin, and reaction t o selected treatment methods, thought to be pertinent in botulism control. This study was conducted during botulism outbreaks of 1953 and 1954, and was confined to state-owned marshlands of Utah. Study areas Three major areas provided sick birds used in this research: (1) Ogden Bay Refuge, (2) Farmington Bay Refuge, and (3) the Public Shooting Grounds . These man-made marsh areas are located on the saline flat lands adjacent to Great Salt Lake. The majority, 1,979 or 89.3 percent, of sick birds were taken from Ogden Bay Refuge on the Weber River Delta. This state-owned waterfowl refuge contains approximately 13,700 acres of diversified habitat . Excellent conditions for the production and existence of Clostridium botulinum, type c, the causative agent of botulism, were apparently present throughout the area. Farmington Bay Refuge, approximately 20 miles south of Ogden Bay Refuge in Davis County, Utah, was dried for improvements in 1953, but was traversed regularly during the 1954 season. In preparation for the hunting season, water was diverted into the north lake of Farmington Bay on October 1, 1953. A two-man crew picked up and disposed of approximately 2,000 dead ducks from approximately 20 acres of the reflooded marsh on October 6, 1953. This was the most serious outbreak of the study and indicated the rapidity with which sickness advanced. Few sick birds were noted, which indicated that the crisis had passed. Farmington Bay Refuge provided 121 of the 2,214 ducks treated during 1953 and 1954. Not more than 12 sick or dead birds were seen on the Public Shooting Grounds, 8 miles west of Corinne, Utah, in 1953. During the 1953 season, 3 sick birds were transported from the area to Ogden Bay Refuge for treatment. In 1954 this state-owned shooting area supplied lll sick birds for treatment. Other areas were observed during the study but did not provide sick birds for treatment. These areas consisted of : (1) State -owned lands beyond Bear River Migratory Bird Refuge, and (2) Smith and Utah Lakes west of Provo, Utah.

Each year thousands of western waterfowl succumb to disease, predators, mechanical injury and other decimating factors. Based on a review of records it is conservatively estimated that an average of 25,000 ducks have succumbed to botulism on western marsh areas annually. In a recent study, the United States Fish and Wildlife Services valued each duck and goose at $8.00 (McLeod, 1950). Applying this value to the estimated annual numerical loss, a total of $200,000 has been lost each season in mortality of western waterfowl from botulism. Control of this malady would reduce annual waterfowl and monetary losses. Prevention and cure are the only means of controlling botulism in wild ducks. At present, no economical preventative measure exists and control is based on curing stricken birds. The purpose of this study was to evaluate the cost of treatment and rate of recovery of birds stricken with botulism when treated by selected methods. The 4 treatments selected for evaluation were: (1) hospital inoculation, (2) fresh water, (3) field inoculation, and (4) no treatment or control. Research included a comprehensive evaluation of factors such as age, sex, species, body condition, degrees of affliction, reaction to various amounts of antitoxin, and reaction to selected treatment methods, thought to be pertinent in botulism control. This study was conducted during botulism outbreaks of 1953 and 1954, and was confined to state-owned marshlands of Utah.

This study investigated factors associated with two mortality events: avian botulism in waterfowl and mortality associated with hatching asynchrony in prefledgling Franklins gulls (Larus pipixcan). The initial focus of my research was on the spatiotemporal relationship between mortality of Franklins gulls and the onset of botulism outbreaks in waterfowl, and the suitability of gull carcasses for proliferation and toxigenesis of Clostridium botulinum. From 1999 to 2001, dead hatch-year Franklins gulls were by far the most abundant carcasses, and the only source of toxin-laden maggots found on transects prior to the occurrence of avian botulism in waterfowl. Nest density was a significant predictor of hatch-year gull carcass density. High density of toxic material from gull carcasses prior to the onset of botulism in waterfowl coincided with high densities of susceptible birds; hence, mortality of Franklins gulls has the potential to be a major initiating factor for botulism outbreaks at Eyebrow Lake, Saskatchewan. The causes of gull mortality were conditions or diseases associated with starvation, stress, or immunosuppression, and most mortality occurred in third-hatched chicks. To separate effects of laying order from effects of hatching asynchrony on prefledgling survival, a cross-fostering experiment was conducted to create clutches containing asynchronously hatching eggs of the same laying order, and of similar egg mass, egg volume, and female quality. Hatching order, independent of laying order, significantly affected survival to fledging, whereas laying order had no observable effect, indicating that intraclutch variation in egg quality does not predetermine the fate of prefledglings, and may be less important than hatching asynchrony for survival of prefledgling Franklins gulls. Relationships among hatching asynchrony, laying order, mass, corticosterone, immune function, growth, and survival at two stages of development were complex. Hatching asynchrony significantly affected early and late prefledgling survival, and was directly or indirectly associated with mass, corticosterone level, and cell-mediated immune responses at early and later stages of development. Both hatching asynchrony and mass appeared to play key roles in mediating life history trade-offs among cell-mediated immune function, growth, and survival. In contrast to cell-mediated immune responses, primary humoral immune response was not directly affected by hatching order or mass, nor was it associated with survival to fledging. Rather, it was associated with laying order, neonatal testosterone, corticosterone at 2 weeks, growth of leg length, and clutch initiation date, illustrating the importance of examining more than one branch of the immune system in studies of life history trade-offs. This study is a step toward using a multipronged and multidisciplinary approach to demonstrate interactions and trade-offs among life history traits, the physiological mechanisms that produce these relationships, and how these relationships may change depending on stage of development.

This study investigated factors associated with two mortality events: avian botulism in waterfowl and mortality associated with hatching asynchrony in prefledgling Franklins gulls (Larus pipixcan). The initial focus of my research was on the spatiotemporal relationship between mortality of Franklins gulls and the onset of botulism outbreaks in waterfowl, and the suitability of gull carcasses for proliferation and toxigenesis of Clostridium botulinum. From 1999 to 2001, dead hatch-year Franklins gulls were by far the most abundant carcasses, and the only source of toxin-laden maggots found on transects prior to the occurrence of avian botulism in waterfowl. Nest density was a significant predictor of hatch-year gull carcass density. High density of toxic material from gull carcasses prior to the onset of botulism in waterfowl coincided with high densities of susceptible birds; hence, mortality of Franklins gulls has the potential to be a major initiating factor for botulism outbreaks at Eyebrow Lake, Saskatchewan. The causes of gull mortality were conditions or diseases associated with starvation, stress, or immunosuppression, and most mortality occurred in third-hatched chicks. To separate effects of laying order from effects of hatching asynchrony on prefledgling survival, a cross-fostering experiment was conducted to create clutches containing asynchronously hatching eggs of the same laying order, and of similar egg mass, egg volume, and female quality. Hatching order, independent of laying order, significantly affected survival to fledging, whereas laying order had no observable effect, indicating that intraclutch variation in egg quality does not predetermine the fate of prefledglings, and may be less important than hatching asynchrony for survival of prefledgling Franklins gulls. Relationships among hatching asynchrony, laying order, mass, corticosterone, immune function, growth, and survival at two stages of development were complex. Hatching asynchrony significantly affected early and late prefledgling survival, and was directly or indirectly associated with mass, corticosterone level, and cell-mediated immune responses at early and later stages of development. Both hatching asynchrony and mass appeared to play key roles in mediating life history trade-offs among cell-mediated immune function, growth, and survival. In contrast to cell-mediated immune responses, primary humoral immune response was not directly affected by hatching order or mass, nor was it associated with survival to fledging. Rather, it was associated with laying order, neonatal testosterone, corticosterone at 2 weeks, growth of leg length, and clutch initiation date, illustrating the importance of examining more than one branch of the immune system in studies of life history trade-offs. This study is a step toward using a multipronged and multidisciplinary approach to demonstrate interactions and trade-offs among life history traits, the physiological mechanisms that produce these relationships, and how these relationships may change depending on stage of development.