Preparation and characterization of monoclonal antibodies to group-specific antigenic determinant of group a streptococcus polysaccharide

1999 ◽  
Vol 128 (4) ◽  
pp. 1032-1034
Author(s):  
E. A. Bazanova ◽  
N. A. Borodiyuk ◽  
O. S. Grigor'eva ◽  
E. N. Semenova ◽  
N. Yu. Brineva ◽  
...  
1994 ◽  
Vol 118 (5) ◽  
pp. 1189-1192
Author(s):  
T. A. Danilova ◽  
T. K. Asoskova ◽  
N. A. Borodiyuk ◽  
L. V. Beletskaya ◽  
V. G. Nesterenko

2003 ◽  
Vol 41 (10) ◽  
pp. 4888-4891 ◽  
Author(s):  
S. K. P. Lau ◽  
P. C. Y. Woo ◽  
T.-c. Yim ◽  
A. P. C. To ◽  
K.-y. Yuen

2005 ◽  
Vol 49 (5) ◽  
pp. 2130-2132 ◽  
Author(s):  
Jeff Powis ◽  
Allison McGeer ◽  
Carla Duncan ◽  
Ryan Goren ◽  
Joyce C. S. de Azavedo ◽  
...  

ABSTRACT Fluoroquinolone susceptibility testing was performed on invasive group A streptococcus isolates from 1992-1993 and 2003 from Ontario, Canada. None were nonsusceptible to levofloxacin. Two of 153 (1.3%) from 1992-1993 and 7 of 160 (4.4%) from 2003 had a levofloxacin MIC of 2 μg/ml; all nine had parC mutations, and eight were serotype M6.


2017 ◽  
Vol 55 (6) ◽  
pp. 1837-1846 ◽  
Author(s):  
Jennifer E. Cornick ◽  
Anmol M. Kiran ◽  
Roberto Vivancos ◽  
Jon Van Aartsen ◽  
Jenny Clarke ◽  
...  

ABSTRACTAnemm32.2 invasive group A streptococcus (iGAS) outbreak occurred in Liverpool from January 2010 to September 2012. This genotype had not previously been identified in Liverpool, but was responsible for 32% (14/44) of all iGAS cases reported during this time period. We performed a case-case comparison ofemm32.2 iGAS cases with non-emm32.2 control iGAS cases identified in the Liverpool population over the same time period to assess patient risk factors foremm32.2 iGAS infection. Theemm32.2 iGAS cases were confined to the adult population. We show that homelessness, intravenous drug use, and alcohol abuse predisposed patients toemm32.2 iGAS disease; however, no obvious epidemiological linkage between the patients withemm32.2 iGAS could be identified. Comparative whole-genome sequencing analysis ofemm32.2 iGAS and non-emm32.2 control isolates was also performed to identify pathogen factors which might have driven the outbreak. We identified 19 genes, five of which had previously been implicated in virulence, which were present in all of theemm32.2 iGAS isolates but not present in any of the non-emm32.2 control isolates. We report that a novelemm32.2 genotype emerged in Liverpool in 2010 and identified a specific subset of genes, which could have allowed this novelemm32.2 genotype to persist in a disadvantaged population in the region over a 3-year period.


Virology ◽  
1992 ◽  
Vol 191 (1) ◽  
pp. 272-281 ◽  
Author(s):  
Hiroshi Tsunemitsu ◽  
Clem K. Ojeh ◽  
Baoming Jiang ◽  
Ron A. Simkins ◽  
Peggy A. Weilnau ◽  
...  

2000 ◽  
Vol 182 (6) ◽  
pp. 1702-1711 ◽  
Author(s):  
Miriam Ravins ◽  
Joseph Jaffe ◽  
Emanuel Hanski ◽  
Ilanit Shetzigovski ◽  
Shira Natanson‐Yaron ◽  
...  

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