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This narrative review critically explores the role of the gut microbiota in functional bowel disorders of IBS-type. Starting with changes in the microbiota composition and diversity, as they have been often found in correlative IBS studies, it raises the question of cause and consequence, of sensitivity and specificity of findings in comparison to other diseases, and of the scientific and clinical options to manipulate the microbiota. This includes a discussion of pre- and probiotics and antibiotics as well as the role of nutrition and the microbiota exchange with fecal microbiota transfer (FMT). For IBS, most of these strategies have not been found to be successful therapies. This may be due to the heterogeneity of the disease itself, but eventually also due to the concepts of microbiological research, e. g., the term dysbiosis, or in methodological differences of the molecular-genetic research that are not visible in the published papers. Future studies should aim to identify those factors that may explain and predict the response to such therapies., Competing Interests: NM does not report any conflict of interests; PE is the consultant of a number of companies producing probiotics: SymbioPharm, Germany; Alimentary Health, Ireland; 4 D Phaarma, U.K., and has received honoraria and travel support from these companies and from many others., (© Georg Thieme Verlag KG Stuttgart · New York.)

The Role of the Exposome in the Emergence of Chronic Inflammatory Bowel Diseases Abstract. Inflammatory Bowel Disease (IBD) including Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory conditions of the gut related to a combination of genetic and environmental factors that impact on normal host-microbe interactions. The gastrointestinal tract is exposed to an overwhelming load of foreign antigens arising from commensal microorganisms, dietary products and occasional pathogens. But these factors explain only a small fraction of disease risk. During the last two decades advances in genomics, epigenomics and understanding of the intestinal microbiota have improved our knowledge in IBD pathogenesis. Although our ability to predict relapses and response to treatment remains limited, the importance of the external environment to modify the risk of IBD and to precipitate relapses in patients with established disease rises. The term 'exposome' is proposed to reflect a life-course of environmental influences beginning in-utero and proceeding right through childhood to adulthood. While the exposome is still a concept which needs practical perspective to enable better patient care, this review highlights important components of environmental contributors to improve our understanding on pathophysiologic mechanisms in IBD.

Background:  Chronic granulomatous disease is a rare disease with a prevalence of approximately 150 cases in Germany. An intestinal manifestation that mimics chronic inflammatory bowel disease (IBD) has only been described in a few cases. As a result of a deficient superoxide-synthesis, frequent and recurrent infections caused by rare pathogens have been described. We present the case of a 28-year old patient who has been diagnosed with IBD at the age of 2 years. He showed recurrent liver abscesses and the picture of a chronic IBD., Methods:  Clinical and laboratory data was obtained and endoscopic, radiologic and histologic examinations, tests for granulocytic functions as well as a genetic analysis were performed. Literature of the PubMed database and recent literature were analyzed., Case:  Under immunosuppressive therapy, with TNF -blocker Adalimumab followed by therapy with integrin-receptor antagonist Vedolizumab, the patient developed recurrent abscesses of the liver. Those were the result of infection with a sensitive Staphylococcus aureus strain. Colonoscopy showed stenosis of the rectum and some inflammatory activity. Intestinal symptoms were unresponsive to all therapies for IBD. Furthermore, there was a presence of active acne and recurrent liver abscesses due to bacteria not typical for intestinal infections. Consequently, we considered a granulocyte dysfunction as the underlying cause. Diagnosis of a chronic granulomatous disease was confirmed by flow cytometry and oxidative burst test. Genetic analysis showed a homozygote mutation of the p47phox (NCF1) gene located on chromosome 7, which represents the most common autosomal recessive form with 20 - 25 % of cases., Results:  In light of recent literature, this case report shows that chronic granulomatous disease should be considered as a differential diagnosis to therapy refractory IBD. This is the case, especially in young patients, when recurrent bacterial lesions caused by intestine-atypical pathogens appear., Competing Interests: Disclosure The authors report no conflicts of interest in this work., (© Georg Thieme Verlag KG Stuttgart · New York.)

Background: Liver and intestine are in close contact with each other. The risk of damage to the liver increases, when the intestinal barrier is damaged ("leaky gut") ., Method: The review article describes how intestinal bacteria influence the pathogenesis of chronic liver diseases and what treatment options are available., Results and Conclusions: Intestinal dysbiosis plays an important role in the development of chronic liver diseases such as alcoholic liver disease, nonalcoholic fatty liver disease, primary biliary cholangitis, primary sclerosing cholangitis, and cirrhosis. Intestinal microbial modulating therapy with probiotics, prebiotics or synbiotics shows positive effects. The more precise meaning of this therapeutic approach needs to be clarified in further studies.

Epidemiological data indicate a disproportional increase in the incidence of multiple sclerosis (MS) over the last decades, particularly in industrialized countries. Although this increase is also associated with altered diagnostic criteria and improved sensitivity of imaging procedures, current data suggest that particularly alterations in our way of life play an important role. In recent years the importance of the gut and intestinal microbiome for some neurological diseases and in particular for MS was recognized. Because nutritional habits have a substantial influence on the composition of the microbiome and our nutrition has changed considerably in the last decades, nutritional components can play an important role in the pathogenesis of MS. In this further education article we summarize the currently available evidence on the role of the gut and on the effects of dietary components on the microbiome in the pathogenesis of MS.

In the past decade the gut microbiome has received scientific attention like few other topics. It has become increasingly apparent that the commensal microbiota plays an important role in maintaining the health of the host. Changes of the microbiota composition or function coincide with different disorders such as infectious (i. e. Clostridium difficile infection) or inflammatory bowel diseases like Crohn's disease or ulcerative colitis. Although the significance of this observation has not yet been fully elucidated and understood, several of attempts aimed at modulating the microbiota composition have been made. This article gives an update on current advances and clinical implications of the gut microbiome in infectious and inflammatory bowel diseases., (© Georg Thieme Verlag KG Stuttgart · New York.)

The tendency to increased body fat storage depends on microbiota. Their composition follows a natural annual rhythm, as apparent by hibernating animals and humans living close to nature. Life shaped by "western industrialization", including microbiome shocks such as antibiotics, low-fiber and low-bacteria diets combined with the consumption of industrialized food leads to the loss of bacterial species in the body. This induces deficiency symptoms, diseases and results in lower energy yields from food. It might also result in the loss of intestinal mucous and "leaky gut". Inflammation then contributes to dyslipidemia and obesity. The diversity of microbial species is transmitted to the offspring. Humans living in close touch with nature have a significantly higher bacterial diversity than people in the "developed world". Microbiome therapy including thorough chewing, established meal rhythms, healthy high-fiber diet and strategic intake of bacteria can regenerate this effects., (© Georg Thieme Verlag KG Stuttgart · New York.)

Background: The complexity and diversity of the human intestinal microbiome has only recently been characterized. The multiple metabolic and immunologic effects of the bacterial flora have demonstrated the symbiosis between the microbiome and its host. This symbiosis is disturbed in a multitude of diseases, especially in critically ill patients., Objectives: A review of the changes in the intestinal microbiome of critically ill patients and the use of probiotics., Material and Methods: Nonsystematic literature search in PubMed on the topics: (1) changes in the intestinal microbiome in critically ill patients, (2) interventions using probiotics in critically ill patients, and (3) use of fecal transplantation in Clostridium difficile colitis., Results: Trauma, sepsis, systemic inflammatory response syndrome, and other conditions lead to shifts in the composition of the intestinal microbiome, which are correlated with clinical outcome. The most obvious change is a profound loss of obligate anaerobe bacteria, leading also to metabolic changes. Probiotics have been used in several studies and show efficacy in the reduction of infectious complication but not in overall mortality. C. difficile colitis as the model disease for a disturbed microbiome can be treated effectively by transfer of donor feces, which also restores the diversity of the microbiome., Conclusion: Taking into account the successful intervention of fecal transplantation on the intestinal microbiome, new products developed using the current knowledge of the intestinal microbiome could be more effective.

Recent scientific results underline the importance of the intestinal microbiome, the totality of all intestinal microbes and their genes, for the health of the host organism. The intestinal microbiome can therefore be considered as a kind of "external organ". It has been shown that the intestinal microbiota is a complex and dynamic ecosystem that influences host immunity and metabolism beyond the intestine. The composition and functionality of the intestinal microbiota is of major importance for the development and maintenance of intestinal functions. Inflammatory bowel diseases (IBD) are characterized by dysregulated interactions between the host and its microbiota.The present contribution summarizes current knowledge of the composition and development of the intestinal microbiome and gives an overview of the bidirectional interaction between host and microbiota. The contribution informs about insights regarding the role of the intestinal microbiota in IBD and finally discusses the protective potential of microbial therapies in the context of IBD.

The intestinal microbiota contributes to the regulation of the intestinal immune system and protection against intestinal infections. Recent studies revealed that the locally restricted intestinal microbiota affects systemic immunity and influences the induction of autoimmunity.

Intra-abdominal infections are generally the result of invasion and multiplication of enteric bacteria in the wall of a hollow viscus within the abdomen to produce peritonitis or abscess. When the infection extends into the peritoneal cavity or another normally sterile region of the abdominal cavity, the infection is described as a "complicated" intra-abdominal infection. Treatment of patients with complicated intra-abdominal infections involves antimicrobial therapy, generally in conjunction with an appropriate and timely surgical source control. Nearly all intra-abdominal infections are caused by multiple microorganisms that constitute the intestinal flora (aerobes and facultative and obligate anaerobes, with Enterobacteriaceae, enterococci and Bacteroides fragilis isolated most frequently). The emergence of drug resistance (e.g. ESBL-producing Enterobacteriaceae or resistant enterococci and staphylococci) poses a substantial threat to patients with surgical infections. Especially in patients with nosocomially acquired infections inadequate empiric antibiotic treatment is associated with treatment failure and death. In patients at risk broader spectrum antibiotic regimens with coverage of resistant Gram-negative bacilli and anaerobes and Gram-positive bacteria such as enterococci (including VRE) and staphylococci should be considered.

Introduction: Gastrointestinal infections are a significant cause of diarrhea and a worldwide problem with annually one billion illnesses and 3 to 4 million deaths. Gram negative bacteria like Enteropathogenic E. coli (EPEC) in developing countries and Enterohemorrhagic E. coli (EHEC) in the developed world are responsible for the majority of acute diarrheal episodes, especially among children less than three years of age. Pathogenic E. coli are supplied with an arsenal of effector proteins to modify and neutralize specific cellular functions of the host organism., Methods: Based on personal and extensively published results we provide a selected overview of Gram negative virulence functions with a focus on lymphostatin., Results: Lymphostatin is an effector protein encoded by lifA/efa-1 (lymphocyte inhibitory factor A/ EHEC factor for adherence). lifA/efa-1 and homologous genes have been identified in EPEC, EHEC, and mouse pathogen Citrobacter rodentium, as well as various Chlamydia strains. Multiple groups have shown that in various EHEC strains lifA/efa-1 is part of a larger pathogenicity island responsible for increased virulence. Statistically, DNA Microarray analysis associated lifA/efa-1 as the single most imortant gene with diarrhea caused by EPEC. Interestingly, lifA/efa-1 encodes for two critical enzymatic activities that have been identified in other pathogenic bacteria: glucosyltransferase- in Clostridium- and protease activity in Yersinia strains. In vitro studies identified lymphostatin as an effector protein with an immunosuppressive effect on peripheral blood and gastrointestinal mucosa T lymphocytes. Further, lymphostatin regulates the barrier function of epithelial monolayer cultures: activation of small GTPase RhoA and inhibition of Cdc42 lead to disassembly of adherens junctions and tight junctions, respectively. Besides an effect on immune and epithelial barrier function, lymphostatin also functions as an adhesion factor for EPEC and EHEC, is essential for colonization of mouse and calf intestine, and regulates bacterial effector proteins., Summary: Lymphostatin is a common toxin in Gram negative bacteria with multiple functions: cell adhesion, immunosuppression, disruption of epithelial barrier function, and intestinal colonization.

Genetic predisposition, nutritional and environmental influences, intestinal pathogens, psychological stress, and disturbed intestinal barrier function have been accepted as important factors in the pathogenesis of chronic inflammatory bowel diseases. Uncontrolled reactions of T-cells and proinflammatoric cytokines are the common denominator of all factors contributing to pathogenesis. The detection of NOD2 gene mutation in about 25% of patients with Crohn's disease was an important step towards an understanding of the molecular background of the disease. The NOD2 proteins functions as an intracellular sensor of bacterial cell membrane constituents and is a crucial part of the innate immune system. In Crohn's disease, the secretion of defensins, naturally occurring antimicrobial peptides, is disturbed. There is evidence that several pathways involved in the reaction of the innate immune system may be disturbed in CED, ultimately leading to an uncontrolled activity of the adaptive immune system.

Polysaccharides are widespread biopolymers, which quantitatively represent the most important group of nutrients in botanical feed. In animal nutrition polysaccharides, which cannot be degraded by endogeneous enzymes and therfore reach the colon almost indigested, are summarized as "non-starch-polysaccharides (NSP)". Individual NSP groups have different chemical and physical characteristics, that result in various effects on physiology of intestine and on organism in general. They affect e.g. digesta passage, nutrient resorption, microbial growth and activity, lipid metabolism and immune systeme. The physiological effects lead to conclusion that some polysaccharides are suitable tools in health management of farm animals. However, limitations result from antinutritive effects and from little scientific knowledge about modes of action in vivo.

Defensins are endogenous antimicrobial peptides with a broad activity spectrum. Even at micromolar concentrations gramnegative and grampositive bacteria, but also mycobacteria, as well as fungi (candida), viruses (herpes) and protozoa (giardia lamblia) are destroyed. As part of the innate immune system defensins are expressed by the intestinal epithelium and contribute to the maintenance of the mucosal barrier. This barrier appears to be defective in inflammatory bowel diseases since on one hand, the immune response is directed against the "normal" luminal bacterial flora and on the other hand, mucosal adherent and invasive bacteria have been observed in these diseases. A defective defensin expression may well explain these phenomena. Indeed, Crohn's disease of the terminal ileum, especially if associated with a NOD2 mutation, is characterised by a diminished alpha-defensin (human defensin 5 and 6) expression, and in inflamed Crohn's colitis, in contrast to ulcerative colitis, the beta-defensin (human beta-defensins 2 and 3) response is reduced. Through a deficient chemical mucosal barrier this defect could lead to increased bacterial invasion into the intestinal mucosa and might well explain an adequate inflammatory response. Although the final proof that this deficient defensin response leads to a reduced antibacterial activity of the intestinal mucosa is still lacking, the most plausible concept of pathogenesis of Crohn's disease is a defensin deficiency syndrome.

Infant botulism represents a distinct entity of botulism. Ingestion of the ubiquitously present spores of Clostridium botulinum leads to germination of the organism and neurotoxin production in the infant intestine. Symptoms typically develop gradually in contrast to classical food botulism in which an acute onset of symptoms shortly after the ingestion of preformed toxin in a food is characteristic. Microbiologically, the diagnosis is established by identification of Clostridium botulinum organism and toxin in stool specimen. However, positive results in these tests provide only indirect evidence for the clinical relevance of the neurotoxin since asymptomatic carriers have been found. The toxin irreversibly blocks the release of acetylcholin from the motoric end plate which results in muscle weakness and paralysis. Depending on the amount of toxin produced, infant botulism exhibits a broad clinical spectrum ranging from oligosymptomatic forms to a fulminant course with acute respiratory failure within hours leading to sudden death. Unrecognized mild forms or beginning muscle weakness can be a co-factor for other risk factors of sudden infant death (SIDS). In studies analyzing infants who died from SIDS, botulism bacteria or toxin were found in up to 20 % of cases. Infant botulism therefore represents an important differential diagnosis of unexplained and inconclusive muscular hypotonia in the first year of life.

The identification of lactic acid bacteria in a complex microbiota using bacteriological culture in combination with phenotypic and genotypic identification techniques is laborious and time-consuming. New molecular methods permit a fast and culture-independent characterisation of such microbiota. Denaturing gradient gel electrophoresis (DGGE) of PCR fragments of the 16S rRNA gene has been proven to be a suitable tool. Here the use of PCR-DGGE with group specific primers is described to investigate the dynamic of sourdough microbiota from addition of the starter until the microbiota remained stable. Species were identified by applying an identification ladder obtained from reference strains or by sequence analysis of the PCR fragments. Furthermore, a method for detection of strains in complex microbiota is described. A strain specific chromosomal DNA fragment of Lactobacillus paracasei LTH 2579 was isolated applying the subtraction hybridisation. Based on the acquired target sequence a specific PCR system was established and combined with a PCR system specific for the species L. paracasei. Use of this detection system permitted to identify and quantitatively detect L. paracasei LTH 2579 in fermented sausages and upon consumption in faecal samples.

Aim of this study is to clinically, microbiologically and histopathologically characterize inflammatory bowel disease (IBD) in the cat. Nine cats with chronic persistent or intermitent vomitus and diarrhea were examined between 1998 and 2001. All cats had a thuorough diagnostic workup performed. Full thickness biopsies from stomach, duodenum, jejunum, ileum and colon were surgically obtained for histopathological examination. Duodenal juice was obtained by direct aspiration for microbiologic qualitative and semiquantitative examination. Seven cats euthanized for other medical reasons were used as controls. Six cats had a lymphoplasmacytic IBD and three an eosinophilic IBD. Four cats with IBD had additional diseases diagnosed. Three cats with IBD had elevated bacterial counts. Retrospectively no correlation could be found between clinical symptoms and histopathological results. Serum TLI was not able to differentiate chronic pancreatitis and IBD. Serum folic acid and cobalamin did not correlate with the distribution of lesions in the gastrointestinal tract. Finally, no correlation was found between bacterial counts in the proximal duodenum and IBD.

On the basis of association-experiments with gnotobiotic rats, we described the immunogenicity of two selected bacterial species (Bifidobacterium adolescentis and Bacteroides thetaiotaomicron). B. adolescentis is a gram-positive lactic acid producing bacterium, strains of which are claimed to have probiotic properties. B. thetaiotaomicron is a gram-negative rod, autochthonous to the human as well as to the rats' intestinal tract. Colonization of the gut was monitored by determination of bacterial cell counts in the animals' feces. In order to investigate the systemic immune reaction, the amounts of specific serum-IgG and -IgA against both bacterial species were measured in the serum. The intestinal immune reaction was examined by measuring the specific IgA in the rats' feces. Knowing about the antibody levels in gnotobiotic rats induced by monoassociation we subsequently disassociated two groups of rats in order to investigate the impact of B. adolescentis on the immune reaction against B. thetaiotaomicron. One group was disassociated simultaneously with B. adolescentis and B. thetaiotaomicron, the second group was disassociated with these bacteria in sequence. B. adolescentis was merely able to induce a mucosal immune reaction, while B. thetaiotaomicron challenged the mucosal as well as the systemic immune system. Furthermore B. adolescentis obviously suppressed the systemic and mucosal immune reaction against the autochthonous B. thetaiotaomicron.

Introduction: Surgical therapy of carcinoma of the esophagus or cardia by transthoracic esophageal resection is associated with a high morbidity in which nosocomial infections have a great importance. This study investigates the influence of prophylactic selective bowel decontamination on the course and results of transthoracic resection of the esophagus., Methods: Seventy patients with carcinoma of the esophagus and cardia were included in this prospective and partially randomized study at the University of Heidelberg. Twenty-five patients received prophylactically selective bowel decontamination with tobramycin, polymyxin B and amphotericin B. The treatment course was documented uniformly. In addition, microbiological screening was performed by swab examinations of nose, throat and anus, by urine and blood cultures, and the documentation of results of additional microbiological diagnostic studies., Results: Bacteriological screening confirmed a reduction in infectious agents and a change of their spectrum in the respiratory and digestive tract without an increase in multiresistant bacteria. Patients who received selective bowel decontamination had a lower infection rate, a shorter artificial respiration period and a shorter intensive care stay without statistically significant differences. The mortality rate was 4% vs 9% in the control group (95% confidence interval -0.172-0.116)., Conclusion: This study confirms the feasibility and microbiological effectiveness of selective bowel decontamination in the context of surgical therapy which is associated with a high nosocomial infection rate. The result of the clinical treatment seems slightly more favorable in the treatment group. Decisive are complications caused by surgery which fundamentally determine the clinical course and frequently cause infectious complications. The prophylactic use of selective bowel decontamination may be useful in patients with an increased risk of prolonged ventilation support or colon interposition but it is not to be generally recommended.

Administration of autochthonous intestinal microflora to chicks during the early period after hatching (Competitive Exclusion) is a widely accepted prophylactic method to control Salmonella infections in poultry. The method of competitive exclusion consists in an administration of intestinal flora from healthy adult birds to chicks during the first hours or days of their life. Use of competitive exclusion cultures will considerably enhance resistance to all Salmonella serovars colonising the chicken intestine and reduce shedding of salmonellas by infected animals. However, sole use of this method does not completely prevent Salmonella colonisation of the animals nor elimination of the agents from poultry flocks. At present, only complex competitive exclusion cultures whose composition has not been defined are capable of inducing an adequately high and reproducible efficacy. Effective preparations with a defined composition have not yet been developed because knowledge of the mechanisms of action of the competitive exclusion cultures as well as the effective species of the various bacterial genera is still inadequate. Since in approval procedures, the competitive exclusion cultures with a non-defined composition can neither be classified as medicines nor feed additives nor vaccines, WHO has proposed to establish the product category "Normal Gut Flora" (WHO, 1994). Basic prerequisites for an effective reduction of non-host-adapted Salmonella serovars in, or their elimination from poultry flocks are the performance and assurance of effective hygienic measures. Like the methods of immunisation using live or inactivated Salmonella vaccines in poultry, the method of competitive exclusion constitutes an additional prophylactic method that may be applied directly in the animal to enhance its resistance to Salmonella infection.

The polymerase chain reaction and cultural method was applied to detect Mycobacterium avium subspecies paratuberculosis (M. p.) in fecal samples of 165 suspected and of 35 diseased cattle, 18 intestinal tissues and 14 lymph nodes of diseased ruminants as well as organ material (n = 10) were also tested. An agreement (+/+, -/-) in the results between both methods was found in 89.7% of all cases examined. 12.7% of samples of suspected and 9.1% of diseased animals were only positive by PCR. In cases of intestinal lymph node and tissue as well as udder tissue of diseased cattle a total agreement between PCR and culture was observed. Lymph node of lung of one diseased cow was positive only in PCR.

In immunocompetent persons, Candida species are members of the normal flora of the gastrointestinal tract. Budding yeasts, in particular Candida albicans, can, however, in patients with a corresponding disposition, spread topically and systemically, that is, they may become pathogenic. In hematological/oncological patients with severe immunodeficiency, for example, the mycelium may infiltrate the muscularis mucosae, with involvement also of the vascular system. The relationships between recurrent diarrhea and Candida are still discussed controversial; various data do, however, suggest that massive colonization with Candida might well represent a(n additional) diarrhea-provoking factor. Similar considerations may also be assumed to apply to diarrhea induced by antibiotic therapy. For immunocompetent persons, guidelines exist for the yeast cell count in the stools. The interpretation of quantitative findings must, however, always be made on an individual basis and against the background of clinical symptoms and/or any particular predisposition of the patient. Reliable treatment of superficial candidasis can be achieved with oral polyene antifungal antibiotics (nystatin, amphotericin B).

Sexual partners harbour often identical yeast strains in the vagina, orointestinal tract and sperm in cases of recurrent vulvovaginal candidoses. Mycologic cultures from the vagina, mouth and stool of the patient and from the mouth and sperm of her partner were cultured on Sabouraud-Glucose-Agar and, if positive, specified by Candida ID-Agar (Biomerieux), rice agar and the system Walk away (Dade). Equal species were compared by DNR-fingerprinting using PCR. The vagina of 22 women was in 21 cases infected by Candida albicans and in one case by Candida glabrata. The culture of mouth or stool of 18 women was in 11 cases identical with those of the vagina. In 13 cases of 18 sexual male partners Candida albicans was found being identical with the strain of the female partner in 8 cases. 4 of the identical strains were grown from the sperm. Future prospective investigations shall prove whether a consequent treatment of both partners to eradicate all identical yeasts is able to improve the treatment results in such women.

The intestinal tract is the motor of sepsis in the "gut-MOF hypothesis". Acute pancreatitis causes an early severe reduction of intestinal microcirculation with consequent production of radicals and cytokines damaging intestinal integrity. The intestinal organ dysfunction syndrome results in a breakdown of barrier function and a loss of propulsive activity. This leads to microbial overgrowth and bacterial translocation. This liberates cytokines and causes secondary pancreatic infection after lymphatic and systemic bacterial dissemination. Infected pancreatic necrosis by enteric microorganisms is the main cause of pancreatic sepsis.

Bilophila wadsworthia is an obligately anaerobic, gram-negative rod, which was first described in 1989. The natural habitat of this species seems to be the lower intestinal tract where it was recovered from about 60% of the persons investigated. Bilophila wadsworthia is mainly associated with intra-abdominal infections, but the species was also isolated as part of aerobic-anaerobic mixed infections at various extra-abdominal sites. Otological infections due to Bilophila wadsworthia have as yet not been described. In the present paper, we report a case of a patient with postoperative otitis externa following stapedectomy, probably caused by the anaerobes Bacteroides fragilis and Bilophila wadsworthia.