THE EFFECT OF PNEUMOCOCCUS AUTOLYSATES UPON PNEUMOCOCCUS DERMAL INFECTION IN THE RABBIT

K Goodner1

  • 1Hospital of The Rockefeller Institite for Medical Research.

Insights

Pneumococcus autolysate enhances bacterial invasiveness in skin infections but does not change virulence. This substance also causes purpura in mice and inhibits blood clotting, suggesting a role in natural infections.

Area of Science:

  • Microbiology and Immunology
  • Bacterial Pathogenesis
  • Dermal Infections

Background:

  • Streptococcus pneumoniae (pneumococcus) is a significant human pathogen.
  • Bacterial autolysates are released from bacteria during cell lysis.
  • The role of bacterial autolysis in modulating host-pathogen interactions is not fully understood.

Purpose of the Study:

  • To investigate the effect of pneumococcus autolysate on the invasiveness of pneumococcus in dermal infections.
  • To explore other properties of pneumococcus autolysate, including its effects on purpura induction and blood coagulation.
  • To discuss the potential implications of bacterial autolysis in natural pneumococcal infections.

Main Methods:

  • Pneumococcus dermal infection model in rabbits.
  • Addition of pneumococcus autolysate to infective inoculum.
  • Observation of bacterial invasiveness and virulence.
  • Induction of purpura in mice.
  • In vitro assessment of rabbit blood coagulation inhibition.

Main Results:

  • Pneumococcus autolysate addition significantly favored the invasiveness of the pneumococcus strain used in rabbit dermal infections.
  • The autolysate did not alter the inherent virulence characteristics of the pneumococcus strain.
  • The tested autolysates demonstrated the ability to induce purpura in mice and inhibit rabbit blood coagulation.

Conclusions:

  • Pneumococcus autolysate can enhance bacterial invasiveness in localized infections.
  • The observed effects on purpura and blood coagulation suggest potential mechanisms for pneumococcal pathogenesis.
  • Bacterial autolysis may play a crucial role in the progression of natural pneumococcal infections.

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