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Group A Streptococcus (GAS): its surface phosphoglycerate kinase (PGK) and recent epidemiology in Alberta Open Access


Other title
Group A Streptococcus (GAS)
Invasive GAS epidemiology
emm pattern
M protein-based vaccines
Surface phosphoglycerate kinase (PGK)
Type of item
Degree grantor
University of Alberta
Author or creator
Hirji, Faisal H
Supervisor and department
Tyrrell, Gregory (Laboratory Medicine and Pathology)
Examining committee member and department
Tyrrell, Gregory (Laboratory Medicine and Pathology)
Charlton, Carmen (Laboratory Medicine and Pathology)
Rennie, Robert (Laboratory Medicine and Pathology)
Li, Xing-Fang (Laboratory Medicine and Pathology)
Laboratory Medicine and Pathology
Molecular Pathology
Date accepted
Graduation date
2017-11:Fall 2017
Master of Science
Degree level
Streptococcus pyogenes, also known as Group A Streptococcus (GAS) is a bacterium that causes diseases such as pharyngitis, acute rheumatic fever and invasive disease. In Alberta, the invasive GAS incidence rate has increased from 4.77/100 000 (2010) to 7.69/100 000 (2016). GAS emm 1 and 59 were the most common emm types associated with invasive disease in 2004-2011. However, a more in-depth insight into recent emm types and epidemiological trends correlated with invasive GAS has not been conducted. In addition, the theoretical coverage of invasive GAS with the 26-valent and 30-valent vaccines, two GAS vaccine candidates, in Alberta has not been assessed. With regards to the 26-valent and 30-valent vaccines, an issue that arises may be their limited coverage. To improve the coverage, GAS phosphoglycerate kinase (PGK) could be added to the candidates or be an alternative to them. GAS PGK is a glycolytic enzyme that is present on the bacterial surface and reacts with human immunoglobulin. Although PGK has been demonstrated on the surface of a few GAS emm types, an extensive assessment of its surface presence has not been conducted. In addition, the mechanisms behind PGK surface expression on GAS have not been explored either. The objectives of this research project are to investigate epidemiological trends associated with invasive GAS in Alberta in 2013- 2016, provide an assessment of the theoretical coverage of the 26-valent and 30-valent vaccines in Alberta for invasive GAS and determine the extent of surface PGK presence in GAS emm types tested using enzyme linked immunosorbent assay. Between 2013- 2016, a total of 1 085 invasive GAS cases were selected for analysis. The top five invasive GAS emm types in Alberta during this period, in order of prevalence, were emm 1 (204 cases), 82 (71 cases), 28 (70 cases), 101 (66 cases) and 41 (62 cases). Other interesting features were that invasive GAS emm 74 was first detected in Alberta (fifteen cases in 2016) and GAS emm 59 invasive cases increased from five cases (2013) to 20 (2016), possibly indicating its reemergence in the province. Invasive GAS in Alberta also shows seasonality, affects males (incidence rate of 9.9/100 000 population in 2016) more than females (6.1/100 000 population) and seems to mainly target 51->80 year olds based on specific laboratory-acquired data. According to the theoretical coverage assessment for the 26-valent and 30-valent vaccines, the 30-valent vaccine had better coverage than the 26-valent vaccine in combating recent invasive GAS in Alberta. However, the non-coverage of both vaccine candidates seems to be gradually worsening in Alberta over the years assessed. Therefore, the GAS PGK antigen may help to increase the coverage for the 30-valent vaccine in Alberta. Twenty-one GAS strains were tested for surface PGK. Out of these 21, 19 demonstrated the surface protein. These 19 strains consisted of 17 different M/emm types, of which 14 had previously not been known to possess surface PGK. In addition, the surface expression of PGK on GAS was not apparently affected by the tissue microenvironment. Rather, surface PGK expression was GAS strain-specific. The comparison of GAS strains with detectable and non-detectable surface PGK may lead to a better understanding as to how this protein is surface expressed, as well as its additional roles in GAS pathogenesis.
This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for the purpose of private, scholarly or scientific research. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.
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