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Trojan horse effect: phagocyte-mediated Streptococcus iniae infection of fish

Amir Zlotkin1, Stefan Chilmonczyk, Marina Eyngor

  • 1Department of Clinical Microbiology, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel.

Infection and Immunity
|April 22, 2003
PubMed

Insights

Certain Streptococcus iniae strains survive and multiply within fish phagocytes, while others cause cell death. This intracellular lifestyle and apoptosis induction explain the varying virulence of S. iniae infections in salmonid fish.

Area of Science:

  • Immunology
  • Fish Pathology
  • Microbiology

Background:

  • Streptococcus iniae is a significant pathogen in salmonid aquaculture.
  • Understanding bacterial interactions with host immune cells is crucial for disease management.

Purpose of the Study:

  • To investigate the in vitro entry and survival mechanisms of different Streptococcus iniae serotypes within fish phagocytes.
  • To elucidate the role of phagocyte apoptosis in S. iniae pathogenesis.

Main Methods:

  • Utilized the salmonid macrophage-like cell line RTS-11 and primary trout pronephros phagocytes.
  • Performed in vitro invasion and survival assays for S. iniae serotypes.
  • Analyzed ex vivo opsonin-dependent phagocytosis and phagocyte apoptosis.

Main Results:

  • Both S. iniae serotypes efficiently invaded fish phagocytes.
  • Only the type II strain demonstrated prolonged survival (≥48 h) within pronephros phagocytes.
  • Approximately 70% of blood bacteria in diseased fish were intracellular, indicating an in vivo intracellular lifestyle.
  • S. iniae type II induced significant phagocyte apoptosis, correlating with higher virulence.

Conclusions:

  • Variations in intracellular lifestyle and apoptosis induction by S. iniae serotypes contribute to differential infection outcomes.
  • The ability of S. iniae type II to survive within phagocytes and induce apoptosis is key to its high virulence.
  • Intracellular survival and apoptosis may facilitate pathogen translocation to the central nervous system.

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