Research Papers:
Pathogenicity of streptococcus agalactiae in oreochromis niloticus
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Abstract
Yang He1,6,*, Jin-Lu Huang5,*, Kai-Yu Wang1,2, De-Fang Chen2, Yi Geng1, Xiao-Li Huang2, Ping Ou-Yang1, Yi Zhou3, Jun Wang6, Jie Min4 and Wei-Min Lai1
1Department of Basic Veterinary, College of Veterinary Medicine, Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Wenjiang, Sichuan, 611130, P. R. China
2Department of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, Wenjiang, Sichuan, 611130, P. R. China
3College of Life Science, Sichuan Agricultural University, Ya’an, Sichuan, 625000, P. R. China
4College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Sichuan, 611130, P. R. China
5Veterinary Research Institution of Haida, Guangdong, Guangzhou, 511490, P.R. China
6College of Life Science, Neijiang Normal University, Neijiang, Sichuan, 641100, P. R. China
*These authors contributed equally to this work
Correspondence to:
Kai-Yu Wang, email: [email protected]
Keywords: oreochromis niloticus; group B streptococcus; histopathology; ultrapathology; ISH–PCR
Received: April 25, 2017 Accepted: October 28, 2017 Published: January 02, 2018
ABSTRACT
To extend our understanding of the pathogenesis of group B streptococcus (GBS), an infection model was established in the Nile tilapia, and the 50% lethal dose (LD50), the toxicity of the extracellular products, the histopathology, ultrapathology, and dynamic distribution of the bacterium were evaluated. After experimental intraperitoneal (i.p.) infection of the Nile tilapia, the LD50 of GBS resuspended in normal saline was 2.3 × 107 cfu/mL and that of GBS resuspended in bacterial culture medium was 7.7 × 106 cfu/mL. Enzymatic analysis of the extracellular products detected lipase and urease activities. The affected fish showed gross symptoms similar to those of naturally infected fish, including external signs (lethargy, abdominal distension, and abnormal swimming) and internal signs (hemorrhagic liver, enlarged and reddened spleen, hyperemic brain and kidney, empty stomach, and hemorrhagic enteritis). Histologically, hemorrhage, congestion, edema, and necrosis were apparent in the liver, kidney, spleen, heart, and brain. Bacterial colonization was first observed at 2 h postinfection (hpi) in the spleen, 4 hpi in the liver, and 12 hpi in the kidney, brain, and heart. Ultrastructurally, the cells showed nuclear shrinkage, hydropic mitochondrial damage, and increased secondary lysosomes. The bacteria were freely disseminated in the cytoplasm of phagocytes, brain microvascular endothelial cells, neurons, and blood vessels. These results indicate that GBS and their extracellular products are pathogenic to the Nile tilapia, damaging its splenic phagocytes, vascular and renal endothelial cells, liver hepatocytes, and brain neurocytes.
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