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Streptococcus pneumoniae can be found in the normal flora of the throat and upper respiratory tract of humans. However, it can commonly become pathogenic causing diseases such as pneumonia and meningitis. S. pneumoniae is unique in that a large percentage of its genome encodes for proteins involved in carbohydrate metabolism. A number of these pathways are essential for full virulence of the bacterium, including a putative fucose utilization pathway. There are two strain-dependent varieties of fucose operons in S. pneumoniae. The type 1 operon consists of a putative extracellular galactosidase (Sp4GH98), intra-cellular fucosidase (GH95A), PTS relay system (EIIA, EIIB, EIIC, EIID), fucose mutarotase (FcsU), fucose isomerase (FcsI), fuculose kinase (FcsK), and fuculose 1-phosphate aldolase (FcsA). Alternatively, the type 2 operon consists of a putative extracellular galactosidase (Sp3GH98), intra-cellular fucosidase (GH29), two intra-cellular galactosidases (GH36A and B), ABC transporter system, and fucose processing enzymes (FcsI, FcsK, and FcsA). The objective of this research is to characterize individual components from both fucose operons ultimately to generate both pneumococcal fucose utilization pathways. Specific focus on the extracellular GH98 enzymes provided evidence that these fucose pathways are initiated by the depolymerization of specific histo-blood group antigens presented on host cells. It is then proposed that the products liberated from the complex carbohydrate degradation are transported into the bacterium for further cleavage by intracellular GH enzymes releasing fucose for processing. This process is critical for S. pneumoniae virulence and may be involved in bacterial internalization by host cells suggesting a novel role for this pathway in pneumococcal pathogenesis. / Graduate

Recently, there has been growing awareness that many animals and plants harbour bacterial symbionts that help protect them against natural enemies. The mushroom-breeding fly Drosophila neotestacea is commonly infected with a virulent parasitic nematode, Howardula aoronymphium. Infections are severe, reducing adult survival and mating success, and until recently virtually all females were rendered sterile. We have discovered that D. neotestacea harbours a strain of the bacterial symbiont Spiroplasma that restores fertility to nematode-parasitized female flies. Spiroplasma appears to be both increasing in frequency and spreading westward across N. America. My thesis examines associations between flies, nematodes and Spiroplasma in British Columbia, which appears to lie at the edge of the range of advancing Spiroplasma infections. I identified Spiroplasma-infected flies in British Columbia for the first time. Sequencing a number of Spiroplasma genes, as well as fly mitochondrial DNA, strongly suggests that the defensive symbiont is spreading westward. Furthermore, high nematode infection rates in BC, as well as laboratory experiments demonstrating the ability of Spiroplasma to restore fertility to nematode-parasitized BC flies, suggest that there is a strong selective pressure for Spiroplasma to continue to spread in BC. I also examined the generality of Spiroplasma-mediated defense by exposing flies to a gram-negative bacterial pathogen, Pectobacterium carotovorum. Exposure dramatically reduced survival regardless of Spiroplasma infection, suggesting that Spiroplasma does not defend against gram-negative bacteria. / Graduate / 0718

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No description available.