The objective of this study was to determine the causative agent of an outbreak with clinical signs similar to those of piscine streptococcosis in farmed snakeskin gourami ( Trichopodus pectoralis). Initial microscopic examination revealed the predominance of a Gram-positive, cocci bacteria in the brain and kidney of the diseased fish. This bacterium was successfully isolated and identified as Streptococcus suis based on nucleotide homology of 16S rDNA and species-specific PCR. This isolate tested negative for serotype 2, one of the major zoonotic serotypes. Experimental infection was then performed to investigate the pathogenicity of the bacterium and its histopathological manifestation. Naïve juvenile and adult snakeskin gourami were injected intraperitoneally with a low dose (1.2×10 5 CFU/fish) and a high dose (1.2×10 7 CFU/fish) of S. suis. Cumulative mortality appeared to be dose- and size-dependent. Experimentally diseased fish exhibited clinical signs consistent with naturally diseased fish. Severe histopathological changes in multiple organs were observed in both juvenile and adult fish, including meningitis, severe congestion in the brain and eyes, thickened stromal layers of the retina, severe hepatic lipidosis and tissue degeneration. Notably, numerous granulomas containing massive bacterial cells in the necrotic core were observed in the infected fish. Relatively pure colonies of S. suis were recovered from tissues of experimentally diseased fish. Taken together, this study fulfilled Koch’s postulates, indicating that S. suis is a new piscine pathogen. Although this is a case report, public awareness and biosecurity measures should be considered to prevent the spread of the disease. Further surveillance of the pathogen’s distribution and research into the underlying causes of fish-host adaptation will provide insights into the genuine impact and appropriate disease control strategies.

Tilapia lake virus (TiLV) is an emerging virus that is rapidly spreading across the world. Over the past 6 years (2014–2020), TiLV outbreaks had been reported in at least 16 countries, spanning three continents, including Asia, Africa, and America. Despite its enormous economic impact, its origin, evolution, and epidemiology are still largely poorly characterised. Here, we report eight TiLV whole genome sequences from Thailand sampled between 2014–2019. Together with publicly available sequences from various regions of the world, we estimated the origin of TiLV to be between 2003–2009, 5–10 years before the first report of the virus in Israel in 2014. Our analyses consistently showed that TiLV started to spread in 2000s, and reached its peak in 2014–2016, matching well with the timing of its first report. From 2016 onwards, the TiLV population declined steadily. This could be a result of herd immunity building up in the fish population, and / or a reflection of a better awareness of the virus coupled with a better and more cautious protocol of Tilapia importation. Despite the fact that we included all publicly available sequences, our analyses revealed long unsampled histories of TiLVs in many countries, especially towards its basal diversification. This result highlights the lack and the need for systematic surveillance of TiLV in fish.