• Blood organochlorines, immune function and health of free-ranging northern fur seal pups (Callorhinus ursinus)

      Beckmen, Kimberlee Beth; Blake, John E. (1999)
      This study examined organochlorine (OC) contaminant levels in blood and milk along with immune function and health of northern fur seals ( Callorhinus ursinus) from St. George Island, Alaska. This portion of the Pribilof Islands breeding stock has undergone a long-term decline between 4 and 6% per year for unknown reasons. To examine the possible role of neonatal OC exposure on health, two cohorts of pups (69 total) and 33 matched periparturient dams were captured for blood and milk sample collection. From the second cohort of 49 neonates, 43 were re-sampled 29 to 51 days later. OCs were extracted from whole blood and milk to identify 15 polychlorinated biphenyl (PCB) congeners and 4 metabolites of dichloro-diphenyl-trichloroethane by high performance liquid chromatography. Peripheral blood lymphocytes were isolated and cryopreserved for in vitro lymphoproliferative immunoassays. These cellular function assays, along with complete blood cell counts, growth rates and survival through the early developmental period, were used as indicators of health status. Humoral immune function was assessed by in vivo antibody responses to tetanus vaccination. Mean blood levels of PCBs were higher in neonate samples than in pups one to two months old. Seven of the eight congeners detected in blood were higher (lipid weight) in neonate blood than in dam blood or milk. First-born neonates were exposed to higher levels of OCs from ingested milk and had higher blood levels of OCs than neonates of older, multiparous dams. Higher OC exposure in neonates was correlated to higher blood OC levels and poorer lymphoproliferative responses as well as lowered serum. retinol and thyroxine. Higher proportions of pups born to old dams developed tetanus antibodies compared to the pups of young dams. Higher OC exposure and poor immune responses in first-born pups may indicate a higher risk of secondary morbidity and mortality than for pups born to multiparous dams but an affect on growth rate or survival to midway through the nursing period was not detected. Evidence of substantial OC contaminant exposure at a critical period of development for the immune system must be considered as a potential contributing factor to reduced post-weaning survival.
    • Brucella suis type 4 in foxes and their role as reservoirs/vectors among reindeer

      Morton, Jamie Kay; Williamson, Francis S. L. (1989)
      Field and laboratory studies were conducted to test the hypotheses that (1) the reindeer/caribou organism, Brucella suis type 4, is incidentally transmitted to reindeer predators such as foxes but does not cause reproductive disease in them, and (2) infected predators such as foxes are terminal hosts and do not serve as reservoirs of infection for reindeer. In field collections, serologic prevalence of brucellosis was similar for male and female foxes (Vulpes vulpes and Alopex lagopus). B. suis type 4 was isolated from female Vulpes and Alopex. No association between reproductive status of foxes and brucellosis infections was observed. Serologic titers in Vulpes experimentally infected by oral exposure to Brucella suis type 4 were detected first by the standard tube and plate agglutination tests which were followed by the buffered Brucella antigen, rivanol, and complement fixation tests. Brucella suis type 4 was isolated from the feces 4 to 6 days post-exposure (PE) and from the oral cavity for as long as 3 weeks PE in Vulpes challenged with 10$\sp9$ or 10$\sp{11}$ colony forming units. Brucella suis type 4 was isolated frequently from regional lymph nodes in the head up to 18 weeks PE, and from only more distant nodes at 22 and 66 weeks PE. Organisms did not localize in the reproductive tract. Clinical effects of brucellosis in Vulpes experimentally-infected were not observed. Pathologic lesions were not detected in the male and non-gravid female reproductive tract. Due to breeding failure, effects of Brucella suis type 4 on the pregnant fox reproductive tract were not determined in experimental infections. Gross and microscopic pathology was limited to lymph nodes. Fox to fox transmission attributed to aerosols from products shed by infected foxes occurred readily. Transmission from Vulpes to lemmings (Dicrostonyx rubricatus) that were exposed to urine from infected fox occurred frequently. Transmission from infected Vulpes to two reindeer (Rangifer tarandus) occurred under conditions of close confinement. Ingestion of organisms passed mechanically in the fox feces was considered the probable source of infection. Fox saliva containing Brucella was also implicated in transmitting the organism through bites or aerosols.
    • Central Nervous System Regulation Of Metabolic Suppression In Arctic Ground Squirrels

      Jinka, Tulasi Ram; Drew, Kelly L. (2010)
      The main focus of this dissertation is central nervous system regulation of metabolic suppression in hibernating mammals in general, and the Arctic ground squirrel (Urocitellus parryii) as a model for seasonal hibernation. Hibernation is a unique physiological, morphological, and behavioral adaptation to overcome the periods of resource limitation. Metabolic suppression seen in torpor during hibernation has several biomedical applications. A multitude of studies have revealed the role of the central nervous system in regulating hibernation, including a role for neurotransmitters and neuromodulators. Previous studies have shown that the neuromodulator adenosine mediates altered thermoregulation during induction of torpor in facultative hibernators, but it is not clear how adenosine influences torpor in seasonal hibernators. The main focus of the current project was to test the hypothesis that a seasonal change in purinergic signaling is necessary for the onset of spontaneous torpor in the Arctic ground squirrel. My dissertation reports that adenosine meets all of the necessary requirements for an endogenous mediator of torpor in the hibernating Arctic ground squirrel. A progressive increase in sensitivity to adenosine A 1 receptors mediated signaling defines the seasonal transition into the hibernation phenotype. I show that adenosine A1 receptor activation is necessary and sufficient to induce torpor in the Arctic ground squirrel. Glutamate is an excitatory neurotransmitter which is widely studied in hibernation research. My dissertation demonstrates that N-methyl-D-aspartate type glutamate receptors, located in the periphery or circumventricular organs, are involved in inducing arousal from torpor in the hibernating Arctic ground squirrel. This dissertation also presents evidence that dietary restriction sensitizes adenosine A1receptors in rats through an increase in surface expression in thermoregulatory regions of the brain (hypothalamus). This contributes to the decline in body temperature and respiratory rate in animals subjected to a restricted diet, which mimics a torpor-like effect.
    • Epizootic Of Beak Deformities In Alaska: Investigation Of An Emerging Avian Disease

      Van Hemert, Caroline; O'Hara, Todd; O'Brien, Diane; Handel, Colleen; Blake, John; Sharbaugh, Susan (2012)
      The sudden appearance of morphological abnormalities in a wild population is often associated with underlying ecological disturbances, including those related to introduction of new pathogens or pollutants. An epizootic of beak deformities recently documented among Black-capped Chickadees (Poecile atricapillus) and other resident bird species in Alaska has raised concern about underlying causes. This dissertation describes results from several recent studies of what we have termed "avian keratin disorder." The primary objectives of the research were to characterize the physiology and pathology of beak deformities and to address specific ecological questions related to this emerging avian disease. In a study of beak growth rates in captive chickadees, I determined that accelerated epidermal growth is the primary physical mechanism by which beak deformities develop and are maintained. Affected birds also exhibited high rates of mortality and skin lesions, suggesting that this disorder significantly compromises individual health. I used radiography, histopathology, and electron microscopy to describe the pathology of avian keratin disorder. As part of this effort, I established baseline information about normal passerine beak and claw structure and developed methods for processing hard-cornified tissues. The suite of lesions that I observed in affected chickadees does not correspond with any known avian diseases, suggesting the presentation of a novel disorder in wild birds. In addition, the detailed characterization of gross and microscopic changes has allowed me to eliminate a number of likely etiologies, including nutritional problems, microbial pathogens, and select toxicants. As a complement to diagnostic pathology, I conducted field studies to investigate possible causes and patterns of occurrence of beak deformities. I used stable isotope analysis to investigate the association between diet and beak deformities. I found that winter dietary patterns differed between chickadees with normal beaks and those with beak deformities, but that such differences are more likely a result than a cause of avian keratin disorder. My field research on Northwestern Crows in Alaska confirmed high prevalence of a nearly identical condition to that observed in chickadees. These findings indicate that avian keratin disorder affects multiple, ecologically-distinct species across a large geographic area. Together, the studies presented in this dissertation provide new insights and identify priority research areas for a rapidly emerging disease in wild birds.