Alteration of intestinal dysbiosis by fecal microbiota transplantation does not induce remission in patients with chronic active ulcerative colitis.

BACKGROUND: In patients with ulcerative colitis (UC), alterations of the intestinal microbiota, termed dysbiosis, have been postulated to contribute to intestinal inflammation. Fecal microbiota transplantation (FMT) has been used as effective therapy for recurrent Clostridium difficile colitis also caused by dysbiosis. The aims of the present study were to investigate if patients with UC benefit from FMT and if dysbiosis can be reversed. METHODS: Six patients with chronic active UC nonresponsive to standard medical therapy were treated with FMT by colonoscopic administration. Changes in the colonic microbiota were assessed by 16S rDNA-based microbial community profiling using high-throughput pyrosequencing from mucosal and stool samples. RESULTS: All patients experienced short-term clinical improvement within the first 2 weeks after FMT. However, none of the patients achieved clinical remission. Microbiota profiling showed differences in the modification of the intestinal microbiota between individual patients after FMT. In 3 patients, the colonic microbiota changed toward the donor microbiota; however, this did not correlate with clinical response. On phylum level, there was a significant reduction of Proteobacteria and an increase in Bacteroidetes after FMT. CONCLUSIONS: FMT by a single colonoscopic donor stool application is not effective in inducing remission in chronic active therapy-refractory UC. Changes in the composition of the intestinal microbiota were significant and resulted in a partial improvement of UC-associated dysbiosis. The results suggest that dysbiosis in UC is at least in part a secondary phenomenon induced by inflammation and diarrhea rather than being causative for inflammation in this disease.

The ignored diversity: complex bacterial communities in intensive care units revealed by 16S pyrosequencing.

Indoor microbial communities play an important role in everyday human health, especially in the intensive care units (ICUs) of hospitals. We used amplicon pyrosequencing to study the ICU microbiome and were able to detect diverse sequences, in comparison to the currently used standard cultivation technique that only detected 2.5% of the total bacterial diversity. The phylogenetic spectrum combined species associated with the outside environment, taxa closely related to potential human pathogens, and beneficials as well as included 7 phyla and 76 genera. In addition, Propionibacterium spp., Pseudomonas spp., and Burkholderia spp. were identified as important sources of infections. Despite significantly different bacterial area profiles for floors, medical devices, and workplaces, similarities by network analyses and strains with identical molecular fingerprints were detected. This information will allow for new assessment of public health risks in ICUs, help create new sanitation protocols, and further our understanding of the development of hospital-acquired infections.

Alterations in the colonic microbiota in response to osmotic diarrhea.

BACKGROUND & AIMS: Diseases of the human gastrointestinal (GI) tract are often accompanied by diarrhea with profound alterations in the GI microbiota termed dysbiosis. Whether dysbiosis is due to the disease itself or to the accompanying diarrhea remains elusive. With this study we characterized the net effects of osmotic diarrhea on the composition of the GI microbiota in the absence of disease. METHODS: We induced osmotic diarrhea in four healthy adults by oral administration of polyethylene glycol 4000 (PEG). Stool as well as mucosa specimens were collected before, during and after diarrhea and 16S rDNA-based microbial community profiling was used to assess the microbial community structure. RESULTS: Stool and mucosal microbiotas were strikingly different, with Firmicutes dominating the mucosa and Bacteroidetes the stools. Osmotic diarrhea decreased phylotype richness and showed a strong tendency to equalize the otherwise individualized microbiotas on the mucosa. Moreover, diarrhea led to significant relative shifts in the phyla Bacteroidetes and Firmicutes and to a relative increase in the abundance of Proteobacteria on the mucosa, a phenomenon also noted in several inflammatory and diarrheal GI diseases. CONCLUSIONS: Changes in microbial community structure induced by osmotic diarrhea are profound and show similarities to changes observed in other GI diseases including IBD. These effects so must be considered when specimens from diarrheal diseases (i.e. obtained by stratification of samples according to diarrheal status) or conditions wherein bowel preparations like PEG (i.e. specimens obtained during endoscopy) are used.

Host-parasite interaction and microbiome response: effects of fungal infections on the bacterial community of the Alpine lichen Solorina crocea.

The lichen symbiosis allows a self-sustained life under harsh environmental conditions, yet symbiotic integrity can be affected by fungal parasites. Nothing is known about the impact of these biologically diverse and often specific infections on the recently detected bacterial community in lichens. To address this question, we studied the arctic-alpine 'chocolate chip lichen' Solorina crocea, which is frequently infected by Rhagadostoma lichenicola. We sampled healthy and infected lichens at two different sites in the Eastern Alps. High abundances of Acidobacteria, Planctomycetes, and Proteobacteria were identified analyzing 16S rRNA gene regions obtained by barcoded pyrosequencing. At the phylum and genus level, no significant alterations were present among infected and healthy individuals. Yet, evidence for a differentiation of communities emerged, when data were analyzed at the strain level by detrended correspondence analysis. Further, a profile clustering network revealed strain-specific abundance shifts among Acidobacteria and other bacteria. Study of stability and change in host-associated bacterial communities requires a fine-grained analysis at strain level. No correlation with the infection was found by analysis of nifH genes responsible for nitrogen fixation.