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Background: Azo dye effluents cause severe pollution problems in soil and water and affect their flora and fauna throughout the world. The combination of dye degrading bacteria in the gut of freshwater fish has been considered a prospective approach towards the development of a sustainable environment. In the southernmost part of India, especially in the Namakkal District of Tamil Nadu state, urbanization and industrial development lead to various environmental issues. In lieu, most of the earlier works were carried out on the bacterial dye degradation from soil and water sources, least concentration on the dye degradation from fish gut flora. The objective of this study was to analyze the role of dye degrading bacteria in the gut of freshwater fish collected from the study area. Results: We have studied the aerobic degradation of remazol yellow reactive dye by bacteria forming the gut flora of exotic fish Oreochromis mossambica from river Cauvery at Pallipalayam of Namakkal District, India. Eight dye degrading gut isolates viz. Pseudomonas sp. AD1, Bacillus sp. AD2, Staphylococcus sp. AD3, Staphylococcus AD4, Enterobacter sp. AD5, Escherichia coli AD6, Streptococcus sp. AD7 and Clostridium sp. AD8 were obtained capable of growing in azo dye incorporated in Basic mineral medium (BMM) medium. Optimization study was carried out for various parameters for the selected isolates. Based on the growth, maximum growth was seen in Pseudomonas sp. AD1 (in 0–24 h) and minimum in Escherichia coli.AD 6 (in 72–96 h). Pseudomonas sp. AD1, Enterobacter sp.AD5, and Bacillus sp. AD 2 exhibited efficient dye degradation during 0–96 h analysis which was confirmed by FTIR analysis. Loss of azo group stretch at 1572–76 cm−1 and 1429 cm−1 and presence of primary (–NH2–) and secondary amides (–NH2–), aliphatic –C–N– stretching and confirmed –C–S– stretching in FTIR analysis confirms the breaking down of the azo bond. Conclusion: This study showed that there is a platform for using the bacterial flora of fish gut that paves a prominent way in the degradation of Azo dye. [ABSTRACT FROM AUTHOR]

Background Low-grade inflammation (controlled by pro and anti-inflammatory molecules), induced by gut microbes in patients with small intestinal bacterial overgrowth ( SIBO), may be associated with irritable bowel syndrome ( IBS). Polymorphisms of IL- RA gene (anti-inflammatory) was evaluated in IBS and healthy subjects ( HS); small intestinal mucosal IL-1 α and β levels (pro-inflammatory) in relation to the presence of SIBO were evaluated in a subset of patients. Methods Two hundred and twenty-one IBS patients and 273 age- and gender-matched HS were included. Exactly 209 of 221 patients (Rome III) and 273 HS were genotyped (PCR) for IL-1RA polymorphism. Mucosal IL-1 α and β levels (pg/mg of biopsy) were estimated (ELISA) in 82/221 patients with and without SIBO (≥105 CFU/mL upper gut aspirate bacteria). Key Results Genotype 1/1 ( IL-1 RA over-producer) was less frequent among patients than controls ( p = 0.007); genotypes 1/3 ( p = 0.012, OR = 3.301, 95% CI = 1.31-8.35) and 2/3 (both under-producers; p = 0.009, OR = 7.703, 95% CI = 1.66-35.82) were commoner among IBS. Fifteen of 82 (18.3%) patients had SIBO. Levels of IL-1 α and β were higher among patients with SIBO than without ( IL-1 α: 35.4 [20.1-66.8] vs 25.5 [4.2-65.3], p < 0.001; IL-1 β: 206.8 [133.5-365.9] vs 93.1 [25.5-197.7], p < 0.001) and those with bloating than without ( p = 0.012; p = 0.015). IL-1 β was higher among patients with Bristol stool type 6 than those with type 1-2 ( p = 0.002) and type 3-5 ( p = 0.007). Conclusions & Inferences Polymorphisms 1/1 ( IL-1 RA over-producer) was infrequent and 1/3 and 2/3 (under-producers) frequent among IBS. Increased IL-1 α and β levels were associated with SIBO. Increased IL-1 β level was predominantly associated with bloating and loose stools (Bristol type 6). [ABSTRACT FROM AUTHOR]

Background: Amebic dysentery is caused by the protozoan parasite Entamoeba histolytica and the ingestion of quadrinucleate cyst of E. histolytica from fecally contaminated food or water initiates infection. Excystation occurs in the lumen of small intestine, where motile and potentially invasive trophozoites germinate from cysts. The ability of trophozoites to interact and digest gut bacteria is apparently important for multiplication of the parasite and its pathogenicity; however the contribution of resident bacterial flora is not well understood. We quantified the population of Bacteroides, Bifidobacterium, Ruminococcus, Lactobacillus, Clostridium leptum subgroup, Clostridium coccoides subgroup, Eubacterium, Campylobacter, Methanobrevibacter smithii and Sulphur reducing bacteria using genus specific primers in healthy (N = 22) vs amebic patients (E. histolytica positive, N = 17) stool samples by Real-time PCR. Results: Absolute quantification of Bacteroides (p = .001), Closrtridium coccoides subgroup (p = 0.002), Clostridium leptum subgroup (p = 0.0001), Lactobacillus (p = 0.037), Campylobacter (p = 0.0014) and Eubacterium (p = 0.038) show significant drop in their population however, significant increase in Bifdobacterium (p = 0.009) was observed where as the population of Ruminococcus (p = 0.33) remained unaltered in healthy vs amebic patients (E. histolytica positive). We also report high prevalence of nimE gene in stool samples of both healthy volunteers and amebic patients. No significant decrease in nimE gene copy number was observed before and after the treatment with antiamebic drug. Conclusions: Our results show significant alteration in predominant gut bacteria in E. histolytica infected individuals. The frequent episodes of intestinal amoebic dysentery thus result in depletion of few predominant genera in gut that may lead to poor digestion and absorption of food in intestine. It further disturbs the homeostasis between gut epithelium and bacterial flora. The decrease in beneficial bacterial population gives way to dysbiosis of gut bacteria which may contribute to final outcome of the disease. Increase in the copy number of nimE gene harboring bacteria in our population reflects possible decrease in the availability of metronidazole drug during treatment of amoebiasis. [ABSTRACT FROM AUTHOR]