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Background Bacteroides fragilis group (BFG) species are the most significant anaerobic pathogens and are also the most antibiotic-resistant anaerobic species. Therefore, surveying their antimicrobial resistance levels and investigating their antibiotic resistance mechanisms is recommended. Since their infections are endogenous and they are important constituents of the intestinal microbiota, the properties of the intestinal strains are also important to follow. The aim of this study was to investigate the main antibiotic gene content of microbiota isolates from healthy people and compare them with the gene carriage of strains isolated from infections. Results We detected 13, mainly antibiotic resistance determinants of 184 intestinal BFG strains that were isolated in 5 European countries (Belgium, Germany, Hungary, Slovenia and Turkey) and compared these with values obtained earlier for European clinical strains. Differences were found between the values of this study and an earlier one for antibiotic resistance genes that are considered to be mobile, with higher degrees for cfxA , erm (F) and tet (Q) and with lower degrees for msrSA , erm (B) and erm (G). In addition, a different gene prevalence was found depending on the taxonomical groups, e.g., B. fragilis and NBFB. Some strains with both the cepA and cfiA β-lactamase genes were also detected, which is thought to be exceptional since until now, the B. fragilis genetic divisions were defined by the mutual exclusion of these two genes. Conclusions Our study detected the prevalences of a series of antibiotic resistance genes in intestinal Bacteroides strains which is a novelty. In addition, based on the current and some previous data we hypothesized that prevalence of some antibiotic resistance genes detected in the clinical and intestinal BFG strains were different, which could be accounted with the differential composition of the Bacteroides microbiota and/or the MGE mobilities at the luminal vs. mucosal sites of the intestine.

The petroleum ether crude extracts of A. conyzoides (Pe-Ac) were used to treat three medically intimidating pests of Aedes aegypti , Anopheles stephensi , and Culex quinquefasciatus , to evaluate their non-target screening against the mosquito predator. The chemical scanning of Pe-Ac through GC-MS analysis revealed a total of nine compounds and the maximum peak area was observed in 1,5-Heptadien-3-yne (22.14%). At the maximum dosage of Pe-Ac (200 ppm), significant larvicidal activity was shown against the fourth instars of Ae. aegypti (96%), An. stephensi (93%), and Cx. quinquefasciatus (92%) respectively. The percentages of oviposition deterrence index (ODI) of all three mosquito vectors are maximum at the highest sub-lethal dosage of Pe-Ac (75 ppm) and minimum at the control dosage. The sub-lethal dosage blocked the activity of carboxylesterase activity and upregulated the detoxifying enzyme activity in a dose-dependent way. The adulticidal activity of Pe-Ac showed that the maximum adult mortality rate (100%) was recorded at the prominent dosage of Pe-Ac 600 ppm against the vectors of all three mosquitos at the maximum adulticidal time of 30 min. Histopathological investigation of fourth instar larvae of all three mosquitos treated with a sub-lethal dosage of Pe-Ac showed that the midgut cells (epithelium, lumen, and peritrophic matrix) are ruptured completely whereas they appear to be normal in control larvae. The non-toxicity evaluation of Pe-Ac compared with the chemical toxin Temephos in aquatic predator Toxorhynchites splendens revealed that the plant extracts are harmless even at the prominent dosage (1000 ppm) as compared to Temephos (1 and 2 ppm) and displayed a higher mortality rate against the mosquito predators. Thus the safety index recommends that the Pe-Ac is more explicit to targets and a suitable auxiliary to chemical pesticides. Graphical abstract

In a previous study, Exiguobacterium mexicanum strain 8N (DSM 16483T) and Microbacterium sp. strain 8L (DSM 16485) in gnotobiotic cultures of the brine shrimp, Artemia franciscana indicated beneficial effects on the development of Artemia larvae. In this study, Artemia larvae with and without autoclaved yeast as food, were challenged with strains 8N and 8L under monoxenic condition to determine ingestion, location and viability of bacterial cells in Artemia gut lumen. The results of light and scanning electron microscopy demonstrated that the bacterial cells of both strains were ingested by Artemia metanauplii. Furthermore, both strains were detected by fluorescence microscopy as live or dead cells along the Artemia gut lumen. However, the band profile in denaturing-gradient gel electrophoresis of the 16S rDNA sequence, retrieved from Artemia gut lumen exposed to both bacteria in monoxenic and dixenic conditions, showed only a band corresponding to strain 8N, suggesting that a differential bacterial ingestion or a differential generation of PCR products occurred. In all Artemia experiments, the cells of the strains 8N and 8L were confined within the chyme in the space limited by the perithrophic membrane. No evidence was found that the bacteria adhered or colonized the intestinal epithelium.

In line with Koch's postulates, studying virulence typically translates into identifying and characterizing the molecular determinants that underlie colonization of a host by a pathogen and the subsequent appearance of symptoms ( 1 ). In this conceptual framework, the presence of pathogens implies damage to the host whose intensity is proportional to the virulence of the pathogen. This approach is based on the observation that damage is often related to the expression of specific features of the pathogen, i.e., the virulence factors ( 2 ).

The liver is the largest gland in the body, representing 3–4% of total body weight in adult dogs and cats and up to 6% in puppies and kittens. Islet, acinar, and ductal cells of the pancreas all develop from dual outpouchings of the developing duodenum. The normal liver is uniformly dark red‐brown, smooth, and firm but friable. Careful inspection reveals a diffuse, finely mottled appearance due to the contrast in color between the darker hepatic parenchyma and the paler connective tissue that outlines the hepatic lobules, which are approximately 1 mm in diameter. The location, size, shape, color, consistency, and texture of the pancreas are assessed during gross inspection of the rest of the abdominal viscera. Pseudomelanosis, grey to black areas of discoloration, develops where the liver is in contact with the intestine. Iron released from degraded hemoglobin combines with hydrogen sulfide produced by bacteria in the gut lumen to produce iron sulfide (FeS).

This chapter contains section titled: Introduction Gastric Emptying References

An increasingly important role for gut microbiota in the initiation and progression of colorectal cancer (CRC) has been described. Even in the early stages of transformation, i.e., colorectal adenomas, changes in gut microbiota composition have been observed, and several bacterial species, such as pks+ Escherichia coli and enterotoxigenic Bacteroides fragilis, have been proposed to drive colon tumorigenesis. In recent years, several strategies have been developed to study mucosa-associated microbiota (MAM), which is more closely associated with CRC development than lumen-associated microbiota (LAM) derived from fecal samples. This review summarizes the state of the art about the oncogenic actions of gut bacteria and compares the different sampling strategies to collect intestinal microbiota (feces, biopsies, swabs, brushes, and washing aspirates). In particular, this article recapitulates the current knowledge on MAM in colorectal adenomas and serrated polyps, since studying the intestinal microbiota associated with early-stage tumors can elucidate the molecular mechanisms underpinning CRC carcinogenesis.

According to the driver–passenger model for colorectal cancer (CRC), the tumor-associated microbiota is a dynamic ecosystem of bacterial species where bacteria with carcinogenic features linked to CRC initiation are defined as “drivers”, while opportunistic bacteria colonizing more advanced tumor stages are known as “passengers”. We reasoned that also gut microbiota-associated metabolites may be differentially enriched according to tumor stage, and be potential determinants of CRC development. Thus, we characterized the mucosa- and lumen-associated microbiota (MAM and LAM, respectively) and mucosa-associated metabolites in low- vs. high-grade dysplastic colon polyps from 78 patients. We show that MAM, obtained with a new biopsy-preserving approach, and LAM differ in composition and α/β-diversity. By stratifying patients for polyp histology, we found that bacteria proposed as passengers by previous studies colonized high-grade dysplastic adenomas, whereas driver taxa were enriched in low-grade polyps. Furthermore, we report altered “mucosa-associated metabolite” levels in low- vs. high-grade groups. Integrated microbiota-metabolome analysis suggests the involvement of the gut microbiota in the production and consumption of these metabolites. Altogether, our findings support the involvement of bacterial species and associated metabolites in CRC mucosal homeostasis in a tumor-stage-specific manner. These distinct signatures may be used to distinguish low-grade from high-grade dysplastic polyps.

This study aims to investigate the effects of Huang Gan formula (HGF), a Chinese herbal prescription used for chronic kidney disease (CKD), on the regulation of the gut microbiota and colonic microenvironment of CKD. CKD rats were induced by 150 mg/kg adenine gavage for 4 weeks, then orally treated with or without 3.6 g/kg or 7.2 g/kg of HGF for 8 weeks. The renal function and structure were analyzed by biochemical detection, hematoxylin and eosin, Masson's trichrome, Sirius red and immunochemical staining. Average fecal weight and number in the colon were recorded to assess colonic motility. Further, the changes in the gut microbiota and colonic microenvironment were evaluated by 16S rRNA sequencing, RT-PCR or immunofluorescence. The levels of inflammatory cytokines, uremic toxins, and NF-κB signaling pathway were detected by RT-PCR, ELISA, chloramine-T method or Western blotting. Redundancy analysis biplot and Spearman's rank correlation coefficient were used for correlation analysis. HGF significantly improved renal function and pathological injuries of CKD. HGF could improve gut microbial dysbiosis, protect colonic barrier and promote motility of colonic lumens. Further, HGF inhibited systemic inflammation through a reduction of TNF-α, IL-6, IL-1β, TGF-β1, and a suppression of NF-κB signaling pathway. The serum levels of the selected uremic toxins were also reduced by HGF treatment. Spearman correlation analysis suggested that high-dose HGF inhibited the overgrowth of bacteria that were positively correlated with inflammatory factors (eg, TNF-α) and uremic toxins (eg, indoxyl sulfate), whereas it promoted the proliferation of bacteria belonging to beneficial microbial groups and was positively correlated with the level of IL-10. Our results suggest that HGF can improve adenine-induced CKD via suppressing systemic inflammation and uremia, which may associate with the regulations of the gut microbiota and colonic microenvironment.