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Background In 2015, Singapore had the first and only reported foodborne outbreak of invasive disease caused by the group B Streptococcus (GBS; Streptococcus agalactiae ). Disease, predominantly septic arthritis and meningitis, was associated with sequence type (ST)283, acquired from eating raw farmed freshwater fish. Although GBS sepsis is well-described in neonates and older adults with co-morbidities, this outbreak affected non-pregnant and younger adults with fewer co-morbidities, suggesting greater virulence. Before 2015 ST283 had only been reported from twenty humans in Hong Kong and two in France, and from one fish in Thailand. We hypothesised that ST283 was causing region-wide infection in Southeast Asia. Methodology/Principal findings We performed a literature review, whole genome sequencing on 145 GBS isolates collected from six Southeast Asian countries, and phylogenetic analysis on 7,468 GBS sequences including 227 variants of ST283 from humans and animals. Although almost absent outside Asia, ST283 was found in all invasive Asian collections analysed, from 1995 to 2017. It accounted for 29/38 (76%) human isolates in Lao PDR, 102/139 (73%) in Thailand, 4/13 (31%) in Vietnam, and 167/739 (23%) in Singapore. ST283 and its variants were found in 62/62 (100%) tilapia from 14 outbreak sites in Malaysia and Vietnam, in seven fish species in Singapore markets, and a diseased frog in China. Conclusions GBS ST283 is widespread in Southeast Asia, where it accounts for a large proportion of bacteraemic GBS, and causes disease and economic loss in aquaculture. If human ST283 is fishborne, as in the Singapore outbreak, then GBS sepsis in Thailand and Lao PDR is predominantly a foodborne disease. However, whether transmission is from aquaculture to humans, or vice versa , or involves an unidentified reservoir remains unknown. Creation of cross-border collaborations in human and animal health are needed to complete the epidemiological picture.

Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis (Mtb). The interaction between Mtb and macrophages, which is regulated by microRNAs, determines the development of TB. However, the function of microRNA‐20b‐5p (miR‐20b‐5p) in RAW 264.7 macrophages against Mtb remains unknown. In this study, we analyzed the expression level of miR‐20b‐5p in macrophage responses to Mtb infection and exosomes derived from macrophages after Mtb infection. MiR‐20b‐5p mimics and inhibitor were, respectively, transfected to evaluate the effect of miR‐20b‐5p on Mtb and macrophages. In addition, the targets of miR‐20b‐5p were predicted by a bioinformatics analysis. The macrophages were respectively transfected with miR‐20b‐5p mimics and inhibitor to determine the messenger RNA expression levels of the targets by reverse transcription‐polymerase chain reaction assay. The results revealed that the miR‐20b‐5p expression level was decreased in the infected macrophages at different times. MiR‐20b‐5p was shown in the exosomes released from macrophages infected with Mtb. Upregulation of the miR‐20b‐5p level suppressed the survival of Mtb in macrophages, while downregulation of the miR‐20b‐5p level enhanced the survival of Mtb in macrophages. Overexpression of miR‐20b‐5p decreased the cell viability and induced apoptosis in Mtb‐infected macrophages, while underexpression of miR‐20b‐5p increased the cell vitality and attenuated apoptosis in Mtb‐infected macrophages. The bioinformatics analysis revealed that Mcl‐1 was a target of miR‐20b‐5p. MiR‐20b‐5p negatively regulated the expression of Mcl‐1. Overall, this study is the first to demonstrate the effect of miR‐20b‐5p on Mtb infection and present miR‐20b‐5p and exosomes as the potential therapeutic targets of TB.

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