Group B streptococcal beta-hemolysin induces mortality and liver injury in experimental sepsis

J Infect Dis. 2002 Jun 15;185(12):1745-53. doi: 10.1086/340818. Epub 2002 May 22.


New Zealand White rabbits were challenged with the wild-type (wt) group B streptococci (GBS) serotype III strain (COH1) and its isogenic nonhemolytic (NH) and hyperhemolytic (HH) mutants. Mortality differed significantly between rabbits infected with the HH mutant IN40 (67%), compared with rabbits infected with the wt COH1 strain (27%) and the NH strains COH1-20 and COH1:cylEDeltacat (13% and 0%, respectively; P<.05). Histopathologically, disseminated septic microabscesses surrounded by necrotic foci were found exclusively in the livers of HH mutant IN40-infected animals. Serum transaminase levels were 20-fold higher in the HH-infected group, compared with rabbits infected with the other strains. Positive TUNEL (in situ terminal deoxynucleotide transferase-mediated dUTP nick end labeling) staining and activation of caspase-3 in hepatocytes were more frequent in HH-infected than in wt-infected animals and absent in the NH mutant COH1-20-infected group, indicating that GBS beta-hemolysin triggers apoptotic pathways in hepatocytes. This work provides the first evidence that GBS beta-hemolysin plays a crucial role in the pathophysiology of GBS sepsis by inducing liver failure and high mortality.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Bacterial Proteins
  • Blood Pressure / drug effects
  • Caspase 3
  • Caspases / metabolism
  • Enzyme Activation
  • Hemolysin Proteins / toxicity*
  • In Situ Nick-End Labeling
  • Liver / drug effects*
  • Rabbits
  • Shock, Septic / mortality*
  • Streptococcus agalactiae
  • Transaminases / blood


  • Bacterial Proteins
  • Hemolysin Proteins
  • streptococcal group B hemolysin
  • Transaminases
  • Caspase 3
  • Caspases