Probiotic usage has become popular with both medical practitioners and the community in general; patients commonly seek advice regarding what, if any, such preparation would be useful for their own diseases. Since such advice should be evidence-based, identified randomized clinical trials (RCTs) for a number of gastrointestinal conditions were reviewed; the data were organized by individual probiotic genera/species. Only trials in adults were considered. Most of the identified RCTs were small and low-quality, so any conclusions to be drawn will be limited at least by methodologic problems. Using the GRADE system to consider the reliability of the evidence generated from these RCTs, it did appear that the use of fecal microbial transplantation to treat recurrent Clostridium difficile infection is well justified. Given the methodologic issues, there was moderately good evidence for preventing antibiotic-associated diarrhea with Lactobacillus, Bifidobacterium, Streptococcus, or Saccharomyces boulardii and for using Lactobacillus, Bifidobacterium, or Saccharomyces as adjunct therapy in the treatment of Helicobacter pylori. There were other conditions for which some supportive evidence was available. These conditions include VSL#3 for maintaining remissions in patients with pouchitis or treating active ulcerative colitis (UC), fecal microbial transplantation for treating active UC, Bifidobacterium for treating patients with UC in remission, Lactobacillus in patients with painful diverticulosis, a variety of probiotics (Lactobacillus, Bifidobacterium, Streptococcus, or VSL#3) in patients with minimal hepatic encephalopathy, and providing synbiotics to patients postoperatively after liver transplantation. Unfortunately, other limitations in the evidence made it very likely that future research will have an effect on the estimated benefit; these interventions cannot yet be recommended for routine use.

Several enteric clostridial diseases can affect humans and animals. Of these, the enteric infections caused by Clostridium perfringens and Clostridium difficile are amongst the most prevalent and they are reviewed here. C. perfringens type A strains encoding alpha toxin (CPA) are frequently associated with enteric disease of many animal mammalian species, but their role in these diseased mammals remains to be clarified. C. perfringens type B encoding CPA, beta (CPB) and epsilon (ETX) toxins causes necro-hemorrhagic enteritis, mostly in sheep, and these strains have been recently suggested to be involved in multiple sclerosis in humans, although evidence of this involvement is lacking. C. perfringens type C strains encode CPA and CPB and cause necrotizing enteritis in humans and animals, while CPA and ETX producing type D strains of C. perfringens produce enterotoxemia in sheep, goats and cattle, but are not known to cause spontaneous disease in humans. The role of C. perfringens type E in animal or human disease remains poorly defined. The newly revised toxinotype F encodes CPA and enterotoxin (CPE), the latter being responsible for food poisoning in humans, and the less prevalent antibiotic associated and sporadic diarrhea. The role of these strains in animal disease has not been fully described and remains controversial. Another newly created toxinotype, G, encodes CPA and necrotic enteritis toxin B-like (NetB), and is responsible for avian necrotic enteritis, but has not been associated with human disease. C. difficile produces colitis and/or enterocolitis in humans and multiple animal species. The main virulence factors of this microorganism are toxins A, B and an ADP-ribosyltransferase (CDT). Other clostridia causing enteric diseases in humans and/or animals are Clostridium spiroforme, Clostridium piliforme, Clostridium colinum, Clostridium sordellii, Clostridium chauvoei, Clostridium septicum, Clostridium botulinum, Clostridium butyricum and Clostridium neonatale. The zoonotic transmission of some, but not all these clostridsial species, has been demonstrated.

Antibiotic-associated diarrhoea is among the most common adverse events related to antibiotic use. Most cases are mild, but Clostridium difficile infection causes a spectrum of disease, ranging from occasional diarrhoea to colitis, toxic megacolon, and potentially death. Recent developments in our understanding of the biology of the gut microbiota have provided new insights into the pathogenesis of these conditions, and have revealed a role for manipulation of the gut microbiota as a novel therapeutic approach. This review will give an overview of the assessment of these conditions, before focusing on the rapidly developing area of their treatment.

Dysbiosis of intestinal microflora has been postulated in ulcerative colitis (UC), which is characterized by imbalance of mucosal tissue associated bacterial communities. However, the specific changes in mucosal microflora during different stages of UC are still unknown. The aim of the current study was to investigate the changes in mucosal tissue associated microbiota during acute exacerbations and remission stages of UC. The mucosal microbiota associated with colon biopsy of 12 patients suffering from UC (exacerbated stage) and the follow-up samples from the same patients (remission stage) as well as non-IBD subjects was studied using 16S rRNA gene-based sequencing and quantitative PCR. The total bacterial count in patients suffering from exacerbated phase of UC was observed to be two fold lower compared to that of the non-IBD subjects (p = 0.0049, Wilcox on matched-pairs signed rank tests). Bacterial genera including Stenotrophomonas, Parabacteroides, Elizabethkingia, Pseudomonas, Micrococcus, Ochrobactrum and Achromobacter were significantly higher in abundance during exacerbated phase of UC as compared to remission phase. The alterations in bacterial diversity with an increase in the abnormal microbial communities signify the extent of dysbiosis in mucosal microbiota in patients suffering from UC. Our study helps in identifying the specific genera dominating the microbiota during the disease and thus lays a basis for further investigation of the possible role of these bacteria in pathogenesis of UC.

IL-36α (gene symbol Il1f6), a member of the IL-36 family, is closely associated with inflammatory diseases, including colitis and psoriasis. In this study, we found that Il1f6-/- mice developed milder psoriasiform dermatitis upon treatment with imiquimod, a ligand for TLR ligand 7 (TLR7) and TLR8, whereas Il1f6-/- mice showed similar susceptibility to dextran sodium sulfate-induced colitis to wild-type mice. These effects were observed in both cohoused and separately housed conditions, and antibiotic treatment did not cancel the resistance of Il1f6-/- mice to imiquimod-induced dermatitis. Bone marrow (BM) cell transfer revealed that IL-36α expression in skin-resident cells is important for the pathogenesis of dermatitis in these mice. Following stimulation with IL-36α, the expression of Il1f6 and Il1f9 (IL-36γ), but not Il1f8 (IL-36β), was enhanced in murine BM-derived Langerhans cells (BMLCs) and murine primary keratinocytes but not in fibroblasts from mice. Upon stimulation with agonistic ligands of TLRs and C-type lectin receptors (CLRs), Il1f6 expression was induced in BMLCs and BM-derived dendritic cells. Furthermore, IL-36α stimulation resulted in significantly increased gene expression of psoriasis-associated Th17-related cytokines and chemokines such as IL-1α, IL-1β, IL-23, CXCL1, and CXCL2 in BMLCs and fibroblasts, and IL-1α, IL-1β, IL-17C, and CXCL2 in keratinocytes. Collectively, these results suggest that TLR/CLR signaling-induced IL-36α plays an important role for the development of psoriasiform dermatitis by enhancing Th17-related cytokine/chemokine production in skin-resident cells via a local autoamplification loop.

Background: Clostridium difficile has been shown to be a nosocomial infection associated with diarrhoea and pseudomembranous colitis in hospitalized patients especially old patients. In my previous studies, it was shown the occurrence of C. difficile in animals feces and vegetables which may act as a source of infection to humans. The aim of the study was to determine the prevalence of C. difficile in retail raw cow, sheep, and goat, meat in Jazan, Saudi Arabia. Method: A total of 600 raw meat samples from cow, sheep, and goat were collected during June-December 2015, and tested for the presence of C. difficile. The method used to check for the presence of C. difficile was by choosing selective enrichment media in C. difficile broth, followed by alcohol shock-treatment and plating onto C. difficile selective medium. C. difficile isolates were typed using PCR ribotyping and also analyzed for antibiotic susceptibility. Results: It was shown that, 9 of 600 meat samples (1.5%) were contaminated with C. difficile. The prevalence of C. difficile was as follow: 7 out of 600 (1.17%) were found in cow, 2 out of 600 (0.3%) were found in sheep, while was no C. difficile was isolated from goat. Eleven out of 18 C. difficile isolates were positive for tcdA, tcdB and cdtB toxin genes and were classified as ribotype 078. Three strains were positive tcdA, and tcdB, and two strains possessed only tcdB. C. difficile strains showed high resistance to ampicillin, gentamycin, erythromycin and nalidixic acid. Conclusions: The present work shows the potential risk of raw meet in transmitting C. difficile to humans.

Despite compelling evidence pointing to a critical role of gut microflora in inflammatory bowel disease (IBD) pathogenesis, the role of antibiotics in clinical practice remains limited, largely due to heterogeneous trials with often conflicting evidence. In this review, we revisit previous randomized controlled trials and high-quality uncontrolled studies in an effort to better elucidate the role of antibiotics in contemporary treatment algorithms. The most established role of antibiotics is in perianal Crohn's disease (CD), utilizing ciprofloxacin with or without metronidazole often as an adjunct to biological therapy. Evidence also points to a likely modest role of various antibiotic classes in mild to moderate luminal CD, including ciprofloxacin, metronidazole, azithromycin, and rifaximin. The benefit of metronidazole in preventing postoperative recurrence in CD is well reported; however, the long-term benefit of this intervention remains uncertain. The use of antibiotics in ulcerative colitis (UC) is even more controversial, but studies using broad-spectrum oral antibiotic cocktails have reported a possible role in acute severe colitis and chronic persistent UC. Similarly, the role of oral vancomycin and gentamicin in very early-onset IBD has interesting preliminary results. Adverse events of antibiotics, the resulting alterations in the microbiome with its associated unknown long-term sequela, and the emergence of antibiotic-resistant strains must be carefully balanced. Therefore, although antibiotics may be underused in the treatment of IBD, their integration into clinical practice must be approached judiciously and individually.