Noseomsis of the European honeybee, Apis mellifera L., is caused by two species of Microsporidia: Nosema ceranae and N. apis. Both species infect primarily the midgut of adult honeybees and have been reported as the third major cause of honeybee losses in Canada. Despite their importance few studies have examined their epidemiology. The current study monitored both species using duplex quantitative Real-Time PCR to determine the seasonal patterns, and potential transmission sources (glands and hive debris) in naturally infected hives from June 2008 to July 2010. Seasonal patterns of both Nosema species differed throughout the years with N. ceranae displacing N. apis. Results also demonstrated the presence of both species in glands suggesting that gland secretions may transmit the parasites. Hive debris and frass also contained spores suggesting that it may transmit the parasites and that bees need not be killed to determine if a hive is infected. / La nosémose des abeilles domestiques, Apis mellifera L., est causée par deux espèces microsporidiennes: Nosema ceranae et N. apis. Elles infectent principalement l'intestin moyen des abeilles et sont la troisième cause de perte d'abeilles au Canada. Malgré ceci, très peu est connu de leurs épidémiologies. Cet étude a examiné les deux espèces en utilisant un duplex de PCR quantitatif pour examiner les variations saisonnières des espèces et divers manières de transmission (glandes et débris de ruche) en des ruches naturellement infectées entre juin 2008 et juillet 2010. Les résultats ont démontré différentes variations saisonnières et que N. ceranae déplace N. apis. Les deux espèces étaient présentes dans les glandes ce qui suggère que leurs sécrétions peuvent transmettre les parasites. Elles étaient aussi présentes dans les débris et les fèces ce qui suggère que ces matières peuvent servir de vecteurs d'infections. De plus, ces résultats proposent une méthode non invasive afin de combattre Ia nosémose des abeilles domestiques car il n'est pas nécessaire de sacrifier des abeilles afin de détecter Ia présence de parasites.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2008. / Source: Dissertation Abstracts International, Volume: 69-05, Section: B, page: 2683. Adviser: Tony L. Goldberg. Includes bibliographical references. Available on microfilm from Pro Quest Information and Learning.

The proposal that the biting attacks which occur during furious rabies infection are due to selective infection of CNS neurons was studied in skunks (a species important in naturally occurring disease). In this model, skunk street rabies virus infection generally produces furious rabies (characterized by increased activity and biting attacks) while Challenge virus standard (CVS) infection results in dumb rabies (absence of biting and marked depression). A detailed immunohistochemical study of brains of skunks experimentally infected with either CVS or skunk street rabies virus revealed only trace amounts of viral antigen in limbic system neurons and marked differences in viral distribution between skunk street rabies and CVS rabies viruses. These data were collected during early stage rabies when behavioral changes occur. Areas which contained heavy accumulation of street virus but low amounts of CVS rabies virus were the neuronal perikarya and processes of the dorsal motor nucleus of the vagus, dorsal raphe nucleus of the midbrain, hypoglossal and red nuclei. In contrast, large accumulations of CVS rabies virus were found in the Purkinje cells of the cerebellum, the habenular nuclei, and in the pyramidal cells throughout the cerebral cortex, while corresponding areas in all street virus-infected skunks contained minimal antigen. These findings were very consistent for animals of the same experimental group and between skunks inoculated both intramuscularly and intranasally with skunk street rabies virus. Skunks inoculated intramuscularly with CVS rabies virus failed to develop rabies. The correlation between virus infection of neurons and a possible pathogenesis of neural dysfunction was further studied using immunoperoxidase staining for the evaluation of CNS serotonin and met-enkephalin in skunks infected with either CVS rabies virus or skunk street rabies virus. There was no difference in the intensity of serotonin immunoperoxidase staining between uninfected control skunks or those infected with CVS or street rabies viruses. However, there was a reduction in the intensity of immuno-peroxidase staining for the neurotransmitter met-enkephalin, for rabid (both CVS and street rabies viruses) as compared to uninfected control skunks. These data showed that differences in the distribution of CVS rabies virus as compared to skunk street rabies virus in the CNS of experimentally infected rabid skunks, may account for the different clinical syndromes associated with these two viruses. The correlation of rabies virus accumulation within neurons to neurotransmitter imbalances during rabies disease requires further investigation to determine the mechanism by which this may occur.

The rabbit mixed leukocyte reaction (MLR) was systematically investigated in terms of the properties of the stimulator and responder cells. It was demonstrated that culturing the cells in medium RPMI-1640, supplemented with complement inactivated rabbit serum (final concentration 2.5%), for five days at 37°C, in a humidified atmosphere of air:CO2 (95:5) provided the optimal condition for the blastogenic response (3H-thymidine incorporation) of cells in the MLR. The cells of the Peyer's patches and the mesenteric lymph nodes responded to the greatest extent in the MLR. Thymus and bone marrow cells cultured individually or in combination did not respond. The cells of the Peyer's patches, spleen and mesenteric lymph nodes were the most potent stimulating cells. There was no correlation between stimulating capacity and the percentage of stimulator cells bearing surface immunoglobulins. Whole body irradiation of normal adult rabbits with doses of 600R or more resulted in the consistent elimination of the MLR responder cell activity in the immediate post irradiation period (1 to 2 days). There was no evidence of any preferential recovery of MLR responder activity by cells in any of the different lymphoid organs. The cells of skin allografted rabbits, following rejection of the allografts, showed accelerated one-way MLR responses specific to stimulator cells from the allograft donors.

Estrogens (estrone sulphate, estrone, estradiol-17beta sulphate and estradiol-17beta) were measured in the allantoic and amniotic fluids and the maternal peripheral, uterine venous and ovarian venous plasma of the ewe throughout gestation. Particular emphasis was placed on the interval day 20 to day 60 of gestation since the estrogen profile in the various fluid compartments of the pregnant ewe during the time of the implantation of the fetus into the uterus of the mother was of primary interest in this study. Estrone sulphate was the most important estrogen with respect to concentration present. It could first be measured in the allantoic and amniotic fluids at day 31 and peaked between days 45 and 50 of pregnancy. It was found that the changes in levels of estrone sulphate, estrone and estradiol-17beta sulphate in the allantoic fluid throughout gestation were very similar to what has been reported regarding estrone sulphate in the peripheral plasma of the pregnant pig, in the allantoic fluid of the cow and regarding total estrogens in the urine of the pregnant pig. A comparison of the estrogen levels in the uterine venous, ovarian venous and maternal peripheral plasma of the pregnant ewe implicated the conceptus, rather than the ovaries, as the source of these estrogens produced during gestation. The possible site or sites of production of these estrogens within the conceptus were discussed along with theories regarding where the conversion of the estrogens to active estradiol-17beta might take place. A functional relationship between estrogens and placental vascular development is postulated.

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