Publication: Brain histopathology in red tilapia Oreochromis sp. experimentally infected with Streptococcus agalactiae serotype III
Issued Date
2020-01-01
Resource Type
ISSN
10970029
1059910X
1059910X
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2-s2.0-85082969655
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Mahidol University
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SCOPUS
Bibliographic Citation
Microscopy Research and Technique. (2020)
Suggested Citation
Iyapa Palang, Boonsirm Withyachumnarnkul, Saengchan Senapin, Wanna Sirimanapong, Rapeepun Vanichviriyakit Brain histopathology in red tilapia Oreochromis sp. experimentally infected with Streptococcus agalactiae serotype III. Microscopy Research and Technique. (2020). doi:10.1002/jemt.23481 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/54562
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Title
Brain histopathology in red tilapia Oreochromis sp. experimentally infected with Streptococcus agalactiae serotype III
Abstract
© 2020 Wiley Periodicals, Inc. One of the clinical manifestations of streptococcosis is swimming errors of the infected fish, which is likely caused by lesions in the brain. As most studies described brain histopathology in streptococcosis as meningitis, with a limited description of lesions in the whole brain, the aim of this study was therefore to explore histopathology of the whole brain of red tilapia experimentally infected with Streptococcus agalactiae serotype III. Transcripts relating to motoneuron functions and inflammatory responses were also investigated. In the S. agalactiae-infected fish, the parenchyma of the whole brain and its associated meninx primitiva were found to be markedly infiltrated by mononuclear cells and Gram-positive cocci. Hemorrhage, neuronal necrosis, and localized spongiform histopathology were observed, especially within the midbrain and the cerebellum. The lesion was observed in the medial longitudinal fasciculus and its nucleus. Expressions of the transcripts CD166, GAP43, SMN, and SV2B of the infected fish did not change, while those of IL-1β and TNF-α were significantly upregulated. It is likely that S. agalactiae cause extensive damage to the fish brain, especially in areas that control swimming activities, through both direct invasion of the bacteria and acute inflammatory responses of the brain resident macrophages, or microglia.