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Nutrition3 papers

Infection caused by Streptococcus iniae

Last edited: 4/16/2026

Overview

Streptococcus iniae infection is a significant pathogen affecting farmed tilapia, particularly impacting growth, immune function, and survival rates in juvenile fish 1.

Diagnosis

  • Clinical signs include lethargy, loss of appetite, skin ulcers, and hemorrhagic septicemia 1.
  • Laboratory tests reveal decreased white blood cell count, elevated hematocrit, hemoglobin, and liver enzymes (AST, ALT) in deficient conditions 1.
  • Histopathological examination may show signs of liver stress and inflammatory response 1.
  • Management

  • Supplementation with vitamin E can mitigate the severity of infection by enhancing immune response and antioxidant capacity 1.
  • No specific drug treatments for S. iniae infection in tilapia are mentioned in the provided abstracts.
  • Special Populations

  • Juvenile Fish (Fingerlings): Vitamin E deficiency significantly impacts the health and susceptibility to S. iniae infection in juvenile tilapia, highlighting the importance of proper nutrition 1.
  • Key Recommendations

  • Ensure adequate dietary vitamin E supplementation in juvenile tilapia diets to enhance immune function and reduce susceptibility to Streptococcus iniae infection (Evidence: Moderate 1).
  • Monitor hematological parameters (white blood cell count, hematocrit, hemoglobin, liver enzymes) in infected populations to assess disease severity and response to nutritional interventions (Evidence: Moderate 1).
  • Implement regular health checks and early detection strategies for clinical signs of S. iniae infection in farmed tilapia populations (Evidence: Expert opinion 1).
  • References

    1 Qiang J, Wasipe A, He J, Tao YF, Xu P, Bao JW et al.. Dietary vitamin E deficiency inhibits fat metabolism, antioxidant capacity, and immune regulation of inflammatory response in genetically improved farmed tilapia (GIFT, Oreochromis niloticus) fingerlings following Streptococcus iniae infection. Fish & shellfish immunology 2019. link

    Original source

    1. [1]

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