Pathogenicity of streptococcus agalactiae in oreochromis niloticus

// Yang He 1, 6, * , Jin-Lu Huang 5, * , Kai-Yu Wang 1, 2 , De-Fang Chen 2 , Yi Geng 1 , Xiao-Li Huang 2 , Ping Ou-Yang 1 , Yi Zhou 3 , Jun Wang 6 , Jie Min 4 and Wei-Min Lai 1 1 Department 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 2 Department of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, Wenjiang, Sichuan, 611130, P. R. China 3 College of Life Science, Sichuan Agricultural University, Ya’an, Sichuan, 625000, P. R. China 4 College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Sichuan, 611130, P. R. China 5 Veterinary Research Institution of Haida, Guangdong, Guangzhou, 511490, P.R. China 6 College 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: kywang1955@126.com 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 × 10 7 cfu/mL and that of GBS resuspended in bacterial culture medium was 7.7 × 10 6 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.