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Antibody-mediated bacterial killing of Ichthyobacterium seriolicida in Japanese amberjack.

Authors
  • Matsuyama, Tomomasa1
  • Fukuda, Yutaka2
  • Takano, Tomokazu3
  • Sakai, Takamitsu3
  • Nakayasu, Chihaya3
  • 1 National Research Institute of Aquaculture, Japan Fisheries Research and Education Agency, Mie, 516-0193, Japan. Electronic address: [email protected] , (Japan)
  • 2 Fisheries Research Division, Oita Prefectural Agriculture, Forestry and Fisheries Research Center, Kamiura, Oita, 879-2602, Japan. , (Japan)
  • 3 National Research Institute of Aquaculture, Japan Fisheries Research and Education Agency, Mie, 516-0193, Japan. , (Japan)
Type
Published Article
Journal
Veterinary immunology and immunopathology
Publication Date
Sep 01, 2018
Volume
203
Pages
73–77
Identifiers
DOI: 10.1016/j.vetimm.2018.08.009
PMID: 30243378
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Ichthyobacterium seriolicida is the causative agent of bacterial hemolytic jaundice (BHJ) in Japanese amberjack, Seriola quinqueradiata. Fish recovering from BHJ acquire protective immunity against reinfection. In this study, fish were passively immunized to determine whether serum antibody is involved in protection against BHJ. The susceptibility of I. seriolicida to the bactericidal activity of Japanese amberjack serum was also investigated. In passive immunization tests, significantly lower mortality was noted in fish that received convalescent serum. Bacteria were killed when exposed to convalescent serum but not serum from naïve fish. Electron microscopic analyses showed that I. seriolicida cells were morphologically altered by reaction with convalescent serum. Naïve fish serum became bactericidal upon addition of purified IgM from convalescent serum. Involvement of the classical complement pathway in the bactericidal mechanism was confirmed because bactericidal activity was lost upon heating convalescent serum or chelation treatment using EDTA. Convalescent fish serum thus protects against reinfection by I. seriolicida via humoral immunity mediated by activation of the classical complement pathway. Copyright © 2018 Elsevier B.V. All rights reserved.

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