For many organisms, embryonic development begins directly after an egg (ovum) has been fertilized by sperm; however, some organisms delay the onset of embryonic development until conditions are favorable for raising young. This delayed onset of development could occur by delaying implantation of fertilized ovum on the uterine wall, as seen in many mammals. Birds delay embryonic development by laying a set of fertilized ova over a period of consecutive days. These fertilized ova are protected from the ambient environment by an exterior shell, and it is in this shell outside of the female s body that embryonic development occurs, but only when females initiate incubation. The number of fertilized ova (eggs) that can be laid by a single female in a single clutch varies among and within bird species, and understanding this variation remains a vital, unanswered question in ornithology. A latitudinal gradient in clutch size is widely recognized, but the reason for this pattern is unclear. Some birds lay relatively large clutches over many days, thus we should expect that eggs could withstand fairly long exposure to ambient temperature and remain viable. However, recent evidence suggests that egg viability declines with increased exposure to ambient temperatures. The egg viability hypothesis predicts that eggs will fail to hatch if exposed to warm ambient temperatures for prolonged periods. I conducted a natural experiment to determine whether egg viability can explain site-specific variation in hatching failure. Hatching failure is higher in a suburban population of Florida Scrub-Jays than it is in a wildland population, possibly because suburban scrub-jays lay larger clutches. Scrub-jays, like many bird species, lay one egg per day and begin incubation with the last-laid egg, thus first-laid eggs in the larger suburban clutches should be exposed to the warm ambient temperatures of sub-tropical Florida longer than first-laid eggs in the smaller clutches typical of the wildland population. As predicted, I found hatching failure is higher in first-laid eggs in the suburbs, and these eggs experience increased exposure to warm ambient temperatures. At both sites, females appear to begin incubation earlier in the laying period as ambient temperatures increase seasonally, possibly to minimize exposure to warm ambient temperatures and minimize hatching failure in first-laid eggs. However, early onset of incubation causes eggs to hatch asynchronously ( > 24 hours between the first and last-hatched egg), and hatching asynchrony increases within-brood size-asymmetries, which leads to an increased frequency of brood reduction (the nonrandom loss of last-hatched young because of starvation). Thus, a tradeoff may exist between beginning incubation earlier in the laying period to minimize hatching failure in first-laid eggs and delaying the onset of incubation to minimize hatching asynchrony and brood reduction. This tradeoff can have profound effects on avian clutch sizes, and may potentially explain the widely known negative relationship between latitude and clutch size.

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.