Invited Talk on Group B Streptococcal Pathogenesis by Asst. Professor at IIT Bombay

Dr. ­Anirban Banerjee, Department of Bioscience and Bioengineering, IIT Bombay addressed the students and faculty of Amrita School of Biotechnology on March 2, 2015. His seminar was titled “Molecular Basis of Group B Streptococcal Pathogenesis: The Hidden Facts”.

Group B Streptococcus (GBS) is a human pathogen that is responsible for pneumonia and meningitis in neonates, preterm birth, still birth, amnionitis and sepsis in pregnant women.   GBS is divided into different serotypes based upon the polysaccharides in the capsule layer on the outer membrane. The different stages of its pathogenesis are colonization, intra-amniotic infection, pneumonia and lung injury, leading to bacteremia and sepsis.   GBS which exhibits beta hemolytic activity, crosses the blood brain barrier (BBB), and causes meningitis.   In pregnant women, the Preterm Premature Rupture of Membrane (PPROM) leads to preterm birth.

Further studies revealed the interesting fact that the physical presence of bacteria is not necessary for PPROM.   AFM studies have shown that GBS produces membrane vesicles which travel from the genitourinary tract up to feto-maternal membrane barrier where they colonize.   The vesicles, which are produced by the serotypes 1A, 3 and 5, bud off from the membranes of the pathogen, and are found to be loaded with toxins and other virulence factors. Cell based studies of these vesicles have demonstrated the toxic effect of these vesicles on different cell lines. The infection of HeLa cells with the vesicles caused death of HeLa cells.

The two component signaling system in GBS is the COV S\R which is involved in the control of virulence by regulating expression of 150 genes. COV R is the response regulator which binds to DNA and regulate the gene expression by repressing the transcription of β-H\C (β-hemolysin). Stk 1 positively regulates β-H\C activity in GBS. T65 and D53 are mutually exclusive with regard to phosphorylation. T65 phosphorylation prevents D53 from phosphorylation. So COV R cannot bind to DNA and  β-H\C is expressed leading to invasion of host tissues. When D53 is phosphorylated, β-H\C is repressed leading to colonization on host tissues. COV R mutants can disrupt the BBB and cause inflammation in brain cells by the over expression of β-hemolysin. Evan’s blue permeability assay can be employed for the detection of COV R mutants showing the maximum invasion.

In summary, the talk by Dr. Anirban Banerjee provided interesting insight into a condition that has perhaps stayed hidden because of the complex and multi-factorial process involved in the pathogenesis of Streptococcal infections.

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