Background: Clostridium difficile is a natural resident of the intestinal microbiota; however, it becomes harmful when the normal intestinal microbiota is disrupted, and overgrowth and toxin production occurs. The toxins can cause bloating and diarrhoea, which may cause severe disease and have the potential to cause outbreaks in hospitals and other healthcare settings. Normally, antibiotic agents are used for treatment, although for some of the patients, these treatments provide only a temporary relief with a recurrence of C. difficile-associated diarrhoea.
Objective: The effects of polydextrose (PDX), Lactobacillus acidophilus NCFM, and L. paracasei Lpc-37 on the growth of C. difficile were investigated in an in vitro model of infected human large intestine.
Design: The semi-continuous colonic model is composed of four connected vessels inoculated with human faecal microbes and spiked with pathogenic C. difficile (DSM 1296). PDX in two concentrations (2 and 4%), NCFM, and Lpc-37 were fed to the system during the 2-day simulation, and the growth of C. difficile and several other microbial groups were monitored using quantitative polymerase chain reaction (qPCR) and 16S rDNA sequencing.
Results: The microbial community structure of the simulation samples was closely grouped according to treatment, and the largest shifts in the microbial composition were seen with PDX. The microbial diversity decreased significantly with 4% PDX, and the OTU containing C. difficile was significantly (p<0.01) decreased when compared to control and lactobacilli treatments. The mean numbers of C. difficile also decreased as detected by qPCR, although the reduction did not reach statistical significance.
Conclusions: The treatments influenced the colonic microbiota, and a trend for reduced numbers of C. difficile as well as alterations of several microbial groups could be detected. This suggests that PDX may be able to modulate the composition and/or function of the colonic microbiota in such manner that it affects the pathogenic C. difficile.
Background: The composition of the vaginal microbiota is known to be important for health. When infections occur, antimicrobial therapy is often poorly efficacious.
Objective and design: We used 16S rRNA gene sequencing to characterize changes in the bacterial microbiota following oral antimicrobial and probiotic interventions.
Results: While the bacterial vaginal profiles of women with vulvovaginal candidiasis were dominated by lactobacilli as in healthy women, and unchanged by therapy, Gardnerella vaginalis, Prevotella, Atopobium, Sneathia, and Megasphaera dominated the vagina of women with bacterial vaginosis (BV), and treatment with tinidazole plus Lactobacillus reuteri RC-14+L. rhamnosus GR-1 resulted in an increased relative abundance of indigenous L. iners or L. crispatus.
Conclusions: The ability to restore homeostasis provides a rationale for conjoint use of probiotics with antibiotic treatment of BV.
Background: It is well known that nutrient availability can alter the gut microbiota composition, while the effect on diversity and temporal stability remains largely unknown.
Methods: Here we address the equine caecal microbiota temporal stability, diversity, and functionality in response to diets with different levels of nutrient availability. Hay (low and slower nutrient availability) versus a mixture of hay and whole oats (high and more rapid nutrient availability) were used as experimental diets.
Results: We found major effects on the microbiota despite that the caecal pH was far from sub-clinical acidosis. We found that the low nutrient availability diet was associated with a higher level of both diversity and temporal stability of the caecal microbiota than the high nutrient availability diet. These observations concur with general ecological theories, suggesting a stabilising effect of biological diversity and that high nutrient availability has a destabilising effect through reduced diversity.
Conclusion: Nutrient availability does not only change the composition but also the ecology of the caecal microbiota.