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|Title:||The role of neuraminidase in the development of pneumococcal pneumonia|
|Presented at:||University of Leicester|
|Abstract:||Streptococcus pneumoniae causes the diseases pneumonia, bacteraemia and meningitis. Among the putative virulence factors of S. pneumoniae is the enzyme neuraminidase. Neuraminidase cleaves terminal sialic acid residues from glycolipids, glycoproteins and oligosaccharides. The pneumococcus has two neuraminidase genes, nanA and nanB. This project was to study their role in pneumococcal disease.;A NanA-deficient mutant (NanA) and a NanB-deficient mutant (NanB) were obtained in the serotype 2 strain, D39. These mutants were used to identify roles for NanA and NanB in the development of pneumonia and bacteraemia. The mean survival times of mice infected with each strain were; D39 2 days, NanA>10days and NanB 4.4. days. The mutants had significantly reduced virulence compared to the wild type.;After intranasal infection NanA cells were rapidly lost from the nasopharynx, trachea and lung. The rate at which NanA cells were removed could suggest a role for NanA in the secure adhesion of pneumococcal cells to the mucosa, to facilitate colonisation.;In the nasopharynx, trachea and lung NanB behaved in a similar way to the wild type early in infection, however, later when D39 multiplied, NanB cells did not. The reason for this behaviour is unknown but two possibilities are; greater susceptibility of NanB to killing by neutrophils or NanB has a nutritional role in vivo. By cleaving sialic acids from cells of the epithelium NanB may expose sugars which could be hydrolysed by the other enzymes.;Neither NanA nor NanB cells were recovered from the blood after intranasal infection. Whether this represents a defect in invasion or an inability to replicate in the blood remains to be seen.|
|Rights:||Copyright © the author. All rights reserved.|
|Appears in Collections:||Theses, Dept. of Biology|
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