Group B Streptococci pathogenesis

• colonization

  • lives in vaginal epithelium

  • can penetrate membranes, causing an inflammatory process that induces labor

• PGE₂ is what humans use to ripen membranes, and GBS can produce this

• spread along villus blood vessels to produce chrorioamnionitis
  

• lung injury when it is aspirated, mediated by β-hemolysin

• neonatal pneumonia
  

  • hemorrhagic pneumonitis

• through direct tissue damage or ability to invade epithelial/endothelial cells, GBS can enter the circulation
  

• organism has a capsule that impairs deposition of antibodies for phagocytosis and also produces some peptidases that degrade chemoattractants

• septicemia leading to release of IL-1, PG, TNFα, TXA₂ leads to septic shock

• late-onset infections
  

  • bone/joints

  • endocarditis

• necrotizing fasciitis
  

GBS hemolysin: gene discovery

• chopped up DNA to see which gene was required for hemolysis

• cylE mutants lacked hemolysin activity and this could be restored

DPPC inhibits GBS hemolysin injury

• one of the reason that preemies may be so susceptible to GBS is because they do not produce dipalmitoylphosphatidylcholine (DPPC) in adequate amounts to inhibit GBS hemolysin injury

GBS infections: meningitis

GBS penetrates blood-brain barrier endothelium

• neutrophils are sent to the site of infection, and a spinal tap tells us the neutrophil count, aiding in diagnosis

• GBS induces blood-brain barrier genes
  

Category: Microbiology Notes