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Background: Tubercolosis (EPTB) is an infectious disease that affects tissue outside the lungs. EPTB patients cannot be source of infection, therefore the findings in the community indicate that there are still active pul- monary TB patients acting as a source of infection. Understanding distributions of EPTB can be used as indicator to individu- ate the unmonitored source of TB transmission in the community. Objectives: The aim of this study is to analyze EPTB using spatial modeling based on patients’ location. Methods: This study is an observational research with spatial analysis approach using SatScanv.9.4.4 and ArcGis v.10.4. Involving 46 samples of EPTB patients in Anatomy Pathology Laboratory of RSUD Abdul Wahab Sjahranie in 2017 and 7 pul- monary TB patients who were contacts of EPTB patients. The distribution of EPTB patients is mostly located in areas with high population density. Results: The results showed that the dis- tribution pattern of EPTB patients was mostly in areas with high population densi- ties. Space-time permutation model shows there are 3 clusters of EPTB with a 2.91, 0.97, 1.13 km radius centered on -0.504177 S/117.092132 E, -0.476895 S /117.141700 E, -0.517031 S/117.092132 E. Conclusion: The distribution of patients with EPTB and pulmonary TB indicates there is an interaction between EPTB and pulmonary TB in the cluster area. Bernoulli model shows that there is 1 cluster of EPTB and pulmonary TB with relative risk 5.29, radius of 3.19 km, and centered on - 0.458159 S / 117.149945 E.

Reefs at Ko Samae San (S), Khao Ma Cho (K), and Ko Tao Mo (T), in the Gulf of Thailand (GoT) represent a biodiversity hotspot, and bacteria play significant roles in maintaining the health of these coral reefs and their biogeochemical cycles. Therefore, this study analyzed bacterial communities (microbiota) from healthy corals and nearby seawater and sediment, using B-RISA and 16S rRNA gene sequencing. Sampling was done in one dry and one wet season to provide an initial assessment of variation with environmental conditions. The most prevalent coral species were Porites lutea, Platygyra sinensis, Acropora humilis, and Acropora millepora. The B-RISA and the sequencing results were correlated, which increased confidence the results. The microbiota varied among corals, seawater, and sediment and between the wet and dry seasons. Percentages of bacteria with known functions varied among sample types and seasons, and their relative abundances supported previously reported essential functions, such as prevention of disease (e.g., Pseudoalteromonas, Psychrobacter, and Cobetia were more abundant on corals in the dry season). Pearson's correlations and multiple factor regressions identified dissolved oxygen (DO), temperature, salinity, and density as significant influences on the microbiota. The equations estimated the relative abundance of a community comprising 147 bacterial genera, as well as the relative abundance of Pseudomonas, Clostridium, Verrucomicrobium, and Epulopiscium (R2 ≥ 0.721). These results represent the first descriptions of microbiota from corals, and surrounding seawater and sediments in the upper GoT.

Reef sites of Ko Samae San (S), Khao Ma Cho (K) and Ko Tao Mo (T) in the upper Gulf of Thailand have abundant corals and represent a hotspot of marine biodiversity. Coral reefs serve as major networks of food and energy, where bacteria, microbial eukaryotes (fungi) and small eukaryotes play significant roles as primary producers that convert inorganic compounds to organic compounds, degraders of toxic substances, and recyclers. These functions sustain food and energy supplies. Advances in metagenomics and next-generation sequencing can provide knowledge of diversity without limitations imposed by media and other conditions associated with laboratory cultures. Scientists have researched bacterial diversity of coral sites; however, a database for fungi and small eukaryotes from Thailand’s sites with abundant corals is lacking. The present study combined fungal ribosomal intergenic spacer analysis (F-RISA) and 18S rRNA gene sequencing to unveil the first culture-independent microbial and small eukaryotes from these sites at two times and across four species of coral (Porites lutea, Platygyra sinensis, Acropora humilis, and Acropora millepora), seawater and sediment. Results showed that the small eukaryotic communities on corals were distinct from communities in the surrounding seawater and sediment. The communities were relatively similar at the three sites and during the two periods of time. Pearson’s correlations indicated the community diversity were associated with water quality (e.g., dissolved oxygen concentrations and density of water).

Candida albicans is the most common fungus in the human intestinal microbiota but not in mice. To make a murine sepsis model more closely resemble human sepsis and to explore the role of intestinal C. albicans, in the absence of candidemia, in bacterial sepsis, live- or heat-killed C. albicans was orally administered to mice at 3h prior to cecal ligation and puncture (CLP). A higher mortality rate of CLP was demonstrated with Candida-administration (live- or heat-killed) prior to CLP. Fecal Candida presented only in experiments with live-Candida administration. Despite the absence of candidemia, serum (1→3)-β-D-glucan (BG) was higher in CLP with Candida-administration than CLP-controls (normal saline administration) at 6h and/or 18h post-CLP. Interestingly, fluconazole attenuated the fecal Candida burden and improved survival in mice with live-Candida administration, but not CLP-control. Microbiota analysis revealed increased Bacteroides spp. and reduced Lactobacillus spp. in feces after Candida administration. Additionally, synergy in the elicitation of cytokine production from bone marrow-derived macrophages, in vitro, was demonstrated by co-exposure to heat-killed E. coli and BG. In conclusion, intestinal abundance of fungi and/or fungal-molecules was associated with increased bacterial sepsis-severity, perhaps through enhanced cytokine elicitation induced by synergistic responses to molecules from gut-derived bacteria and fungi. Conversely, reducing intestinal fungal burdens decreased serum BG and attenuated sepsis in our model.