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Journal Article

Capsular polysaccharide of Streptococcus agalactiae is an essential virulence factor for infection in Nile tilapia ( Oreochromis niloticus Linn.)

Defeng Zhang; Xiaoli Ke; Zhigang Liu; Jianmeng Cao; Youlu Su; Maixin Lu; Fengying Gao; Miao Wang; Mengmeng Yi; Fengling Qin
Journal of Fish Diseases · Vol. 42, Issue 2 · pp. 293-302 · 2019

Abstract

Streptococcus agalactiae (Group B Streptococcus , GBS) is associated with diverse diseases in aquatic animals. The capsule polysaccharide (CPS) encoded by the cps gene cluster is the major virulence factor of S. agalactiae ; however, limited information is available regarding the pathogenic role of the CPS of serotype Ia piscine GBS strains in fish. Here, a non‐encapsulated mutant (Δ cps ) was constructed by insertional mutagenesis of the cps gene cluster. Mutant pathogenicity was evaluated in vitro based on the killing of whole blood from tilapia, in vivo infections, measuring mutant survival in tilapia spleen tissues and pathological analysis. Compared to wild‐type (WT) GBS strain, the Δ cps mutant had lower resistance to fresh tilapia whole blood in vitro ( p 0.01), and more easily cleared in tilapia spleen tissue, and was highly attenuated in tilapia and zebrafish. Additionally, compared to the Δ cps mutant, numerous GBS strains and severe tissue necrosis were observed in the tilapia spleen tissue infected with WT strains. These results indicated that the CPS is essential for GBS pathogenicity and may serve as a target for attenuation in vaccine development. Gaining a better understanding of the role, the GBS pathogenicity in fish will provide insight into related pathogenesis and host–pathogen interactions.

Bibliographic Information

JournalJournal of Fish Diseases
PublisherWiley
Publication Date2019-02-01
Publication Year2019
Volume42
Issue2
Pages293-302
Document TypeJournal Article
Print ISSN0140-7775
eISSN1365-2761
DOI10.1111/jfd.12935
SubjectGeneral Aquaculture, Fisheries & Fish Science

Access Information

NARA Access Coverage1997-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/13652761
Publisher PageOpen Publisher Page
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