ENTEROHEMORRHAGIC ESCHERICHIA COLI LEADING TO HAEMOLYTIC UREMIC SYNDROME - CASE STUDY AND REVIEW.

Escherichia coli is a gram-negative bacillus and considered to be the normal pathogen of intestinal and extraintestinal manifestations depending upon the strain. A variety of strains exist that are responsible for causing myriads of clinical presentation. E.coli O157: H7 being the most common and severe bacterial pathogen is the leading cause of bloody diarrhea. EHEC (Enterohemorrhagic E.coli) is responsible for causing severe complications like HC (Hemorrhagic colitis). Herein, we present the case of a young girl with E.coli O157:H7 infection and review the related literature. A previously healthy 37-year-old female presented with bloody diarrhea, fever, headache, and lower abdominal pain. As per history she had eaten a hamburger, denied any recent travel and absence of inflammatory bowel disease or bloody stools in family history. Physical examination revealed normal vital signs and the physical findings were unremarkable except for severe abdominal pain. Her stool was hem-occult positive. The complete blood count was within normal limits except neutrophilia and leukocytosis. An abdominal ultrasound showed thickened bowel loops consistent with colitis. First week of her hospital course, she continued to have bloody diarrhea and severe abdominal pain. Her final stool submitted to the laboratory on day 7 was consistent with a blood clot, following her developed low urine output and hematuria, with a serum creatinine of 2.1 mg/dl on day 5. Her renal symptoms were treated with fluids. She was given supportive treatment, and her platelet count and hemoglobin were stabilized. In early stages of bloody diarrhea, parental hydration plays a major role in accelerating volume expansion. Rapid stool analysis for these bacteria can alert specialists to deal with severe complications like HUS.

Fungal feelings in the irritable bowel syndrome: the intestinal mycobiome and abdominal pain.

Although the gut microbiota consists of bacteria, viruses, and fungi, most publications addressing the microbiota-gut-brain axis in irritable bowel syndrome (IBS) have a sole focus on bacteria. This may relate to the relatively low presence of fungi and viruses as compared to bacteria. Yet, in the field of inflammatory bowel disease research, the publication of several papers addressing the role of the intestinal mycobiome now suggested that these low numbers do not necessarily translate to irrelevance. In this review, we discuss the available clinical and preclinical IBS mycobiome data, and speculate how these recent findings may relate to earlier observations in IBS. By surveying literature from the broader mycobiome research field, we identified questions open to future IBS-oriented investigations.

Human milk oligosaccharides alleviate stress-induced visceral hypersensitivity and associated microbiota dysbiosis.

Pain-related functional gastrointestinal disorders (FGIDs) are characterized by visceral hypersensitivity (VHS) associated with alterations in the microbiota-gut-brain axis. Since human milk oligosaccharides (HMOs) modulate microbiota, gut and brain, we investigated whether HMOs impact VHS, and explored the role of gut microbiota. To induce VHS, C57BL/6JRj mice received hourly water avoidance stress (WAS) sessions for 10 d, or antibiotics (ATB) for 12 d. Challenged and unchallenged (Sham) animals were fed AIN93M diet (Cont) or AIN93M containing 1% of a 6-HMO mix (HMO6). VHS was assessed by monitoring the visceromotor response to colorectal distension. Fecal microbiome was analyzed by shotgun metagenomics. The effect of HMO6 sub-blends on VHS and nociceptive pathways was further tested using the WAS model. In mice fed Cont, WAS and ATB increased the visceromotor response to distension. HMO6 decreased WAS-mediated electromyographic rise at most distension volumes and overall Area Under Curve (AUC=6.12±0.50 in WAS/HMO6 vs. 9.46±0.50 in WAS/Cont; P<.0001). In contrast, VHS in ATB animals was not improved by HMO6. In WAS, HMO6 promoted most microbiota taxa and several functional pathways associated with low VHS and decreased those associated with high VHS. Among the sub-blends, 2'FL+DFL and LNT+6'SL reduced visceromotor response close to Sham/Cont values and modulated serotoninergic and CGRPα-related pathways. This research further substantiates the capacity of HMOs to modulate the microbiota-gut-brain communication and identifies mitigation of abdominal pain as a new HMO benefit. Ultimately, our findings suggest the value of specific HMO blends to alleviate pain associated FGIDs such as infantile colic or Irritable Bowel Syndrome.

Isolated gastrointestinal histoplasmosis: A rare diagnosis of pediatric chronic abdominal pain.

Gastrointestinal (GI) histoplasmosis usually occurs as a part of disseminated histoplasmosis in immunocompromised or elderly subjects. Isolated histoplasmosis involving the GI tract in an immunocompetent host is very rare. It is also not considered as an etiology for chronic abdominal pain in children. Here we present an 8-year-old boy with abdominal pain and weight loss who underwent treatment for tuberculosis but on reinvestigation was diagnosed as GI histoplasmosis. He responded well to treatment and achieved good catch up growth.

An 11-Year-old Male With X-linked Agammaglobulinemia and Persistent Abdominal Pain.

Metagenomic next-generation sequencing is a promising tool for detecting pathogens that are difficult to isolate by traditional modalities, particularly in the diagnosis of complex infections in immunocompromised children. We describe a child with X-linked agammaglobulinemia and chronic abdominal pain diagnosed with a multiorganism infection (Helicobacter cinaedi, Campylobacter coli and Parainfluenza) identified by various diagnostic tools, including plasma metagenomic next-generation sequencing.

The gut microbiome: a missing link in understanding the gastrointestinal manifestations of COVID-19?

Coronavirus disease 2019 (COVID-19), which is caused by infection with SARS-CoV-2, presents with a broad constellation of both respiratory and nonrespiratory symptoms, although it is primarily considered a respiratory disease. Gastrointestinal symptoms-including nausea, abdominal pain, vomiting, and diarrhea-rank chief among these. When coupled with the presence of viral RNA in fecal samples, the presence of gastrointestinal symptoms raises relevant questions regarding whether SARS-CoV-2 can productively infect the upper or lower gastrointestinal tract. Despite the well-documented prevalence of gastrointestinal symptoms and the high rate of SARS-CoV-2 fecal RNA shedding, the biological, clinical, and epidemiological relevance of these findings is unclear. Furthermore, the isolation of replication-competent virus from fecal samples has not been reproducibly and rigorously demonstrated. Although SARS-CoV-2 shedding likely occurs in a high proportion of patients, gastrointestinal symptoms affect only a subset of individuals. Herein, we summarize what is known about gastrointestinal symptoms and fecal viral shedding in COVID-19, explore the role of the gut microbiome in other respiratory diseases, speculate on the role of the gut microbiota in COVID-19, and discuss potential future directions. Taking these concepts together, we propose that studying gut microbiota perturbations in COVID-19 will enhance our understanding of the symptomology and pathophysiology of this novel devastating disease.

Local immune response to food antigens drives meal-induced abdominal pain.

Up to 20% of people worldwide develop gastrointestinal symptoms following a meal1, leading to decreased quality of life, substantial morbidity and high medical costs. Although the interest of both the scientific and lay communities in this issue has increased markedly in recent years, with the worldwide introduction of gluten-free and other diets, the underlying mechanisms of food-induced abdominal complaints remain largely unknown. Here we show that a bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine. Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain. This aberrant pain signalling resulted from histamine receptor H1-mediated sensitization of visceral afferents. Moreover, injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation. Our results identify and characterize a peripheral mechanism that underlies food-induced abdominal pain, thereby creating new possibilities for the treatment of irritable bowel syndrome and related abdominal pain disorders.

Self-reported bowel symptoms are associated with differences in overall gut microbiota composition and enrichment of Blautia in a population-based cohort.

BACKGROUND AND AIM: Altered gut microbiota have been suggested as part of an etiology of irritable bowel syndrome (IBS), but studies have shown contrasting results. Our aim was to examine gut microbiota composition in a large population-based cohort, with respect to presence and severity of bowel symptoms. METHODS: The study cohort consisted of 1988 participants of the Malmö Offspring Study (mean age 40 years, 53% women). From a questionnaire, 19% reported having bowel symptoms the last 2 weeks and 15% reported having IBS. Bowel symptoms were assessed by a validated set of questions with visual analog scales. Gut microbiota was assessed by 16S rRNA gene sequencing (300 bp*2 in V1-V3 region) from fecal samples. The association between abundance of bacteria at genus level and bowel symptoms was calculated by logistic regression or general linear model, adjusted for false discovery rate (q < 0.05). RESULTS: Self-reported bowel symptoms (P = 0.003) and IBS (P = 0.031) were associated with difference in overall gut microbiota composition (beta-diversity). Additionally, bowel symptoms and IBS were associated with increased abundance of Blautia, and bowel symptoms also with a genus in the SHA98 order and Butyricimonas. Pain was associated with increased abundance of Fusobacterium. Diarrhea was associated positively with [Prevotella] and Blautia and negatively with a genus in the SHA98 order and a genus in the Christensenellaceae family. CONCLUSION: Self-reported bowel symptoms are associated with differences in overall gut microbiota composition and abundancy of a few specific bacteria at genus level in a population-based cohort. Diarrhea is the individual symptom with most associations.

The Effect of Helicobacter pylori on the Presentation and Clinical Course of Coronavirus Disease 2019 Infection.

OBJECTIVES: Novel coronavirus 2019 (corona virus disease 2019 [COVID-19]) binds angiotensin-converting enzyme-2 (ACE-2) receptors to enter the cell. These receptors are widely expressed in the intestine, and COVID-19 may cause gastrointestinal symptoms via these receptors during the course of the disease. Helicobacter pylori is known to increase the expression of ACE-2 receptors in the gastrointestinal tract. The aim of this study was to investigate the effects of H pylori on the presentation and clinical course of COVID-19 infections. METHODS: This study was carried out from June 1 to July 20, 2020. Patients diagnosed with COVID-19 infections by PCR tests were included in the study. Antigen screening tests were performed on stool samples to determine the presence of H pylori. All patients were evaluated for manifestations of COVID-19 infection, severity of the course, hospitalized days because of the virus and outcome of the disease process. RESULTS: Of 108 COVID-19 positive patients evaluated, 31 with a mean age of 49.54 ±â€Š17.94 years were H pylori-positive (8 girls [25.8%]) and 77 with a mean age of 47.85 ±â€Š20.51 years; (31 girls [40.3%]) were H pylori-negative. Abdominal pain (19.4% vs 2.6%) and diarrhea (32.3% vs 9.1%) were significantly higher in patients with H pylori than those without (P = 0.007 and P = 0.006, respectively). There was no statistically significant difference between H pylori positivity and the number of hospitalized days, the severity of the course of COVID-19 infection, or the outcome of the disease (P > 0.05). CONCLUSION: Our results revealed that the findings of abdominal pain and diarrhea strongly correlated with the presence of H pylori in COVID-19 patients.

Clinical diagnosis and endoscopic analysis of 10 cases of intestinal tuberculosis.

To analyze the clinical characteristics of intestinal tuberculosis (ITB), pay attention to the diagnostic value of endoscopy and mucosal biopsy, improve the recognition of atypical manifestations of ITB under endoscopy, and reduce misdiagnosis and missed diagnosis.The clinical data of 10 patients who were hospitalized in Changzhou second people's Hospital and finally diagnosed as ITB from January 1, 2015 to present were analyzed retrospectively. The basic information, medical history, clinical manifestations and computed tomography (CT), endoscopy of the patients was analyzed retrospectively. The results of pathological examination were analyzed and sorted out.Among the 10 patients, the ratio of male to female was 7:3, 10 (100%) had abdominal pain, 3 (30%) had diarrhea and 2 (20%) had bloody stool. The positive rate of tuberculosis T cell test was 75% (6/8), the diagnostic rate of chest high resolution CT was 60%, and the abnormal rate of abdominal high-resolution CT was 66.7% (6/9). Colonoscopy showed that the lesions mainly involved ileocecum (70%) and ascending colon (60%). Most of the lesions were intestinal stenosis (60%) and circular ulcer (50%). In a few cases, cold abscess (20%) and scar diverticulum (10%). Most of the pathological manifestations were granuloma formation and multinucleated giant cells (60%). The detection rate of caseous granuloma was 20%.The general condition and clinical manifestations of patients with ITB are not specific. Endoscopy and mucosal biopsy are of great significance for its diagnosis. The clinical manifestations and endoscopy of some patients showed atypical signs. Therefore, the combination of multi-disciplinary team models and the enhancement of clinician's recognition of the characteristics of endoscopic examination of ITB can improve us the diagnosis level of ITB.

Randomised clinical trial: linaclotide vs placebo-a study of bi-directional gut and brain axis.

BACKGROUND: Linaclotide, a guanylate cyclase C agonist relieves irritable bowel syndrome with predominant constipation (IBS-C) symptoms, but how it improves pain in humans is unknown. AIMS: To investigate the effects of linaclotide and placebo on the afferent and efferent gut-brain-gut signalling in IBS-C patients, in a randomised clinical trial. METHODS: Patients with IBS-C (Rome III) and rectal hypersensitivity were randomised (2:1) to receive linaclotide (290 µg) or placebo for 10 weeks and undergo bi-directional gut and brain axis assessment using anorectal electrical stimulations and transcranial/transspinal-anorectal magnetic stimulations. Rectal sensations were examined by balloon distention. Assessments included abdominal pain, bowel symptoms and quality of life (QOL) scores. Primary outcomes were latencies of recto-cortical and cortico-rectal evoked potentials. RESULTS: Thirty-nine patients participated; 26 received linaclotide and 13 received placebo. Rectal cortical evoked potentials latencies (milliseconds) were significantly prolonged with linaclotide compared to baseline (P1:Δ 19 ± 6, P < 0.005; N1:Δ 20 ± 7, P < 0.02) but not with placebo (P1:Δ 3 ± 5; N1:Δ 4.7 ± 5,P = 0.3) or between groups. The efferent cortico-anorectal and spino-anorectal latencies were unchanged. The maximum tolerable rectal volume (cc) increased significantly with linaclotide compared to baseline (P < 0.001) and placebo (Δ 29 ± 10 vs 4 ± 20, (P < 0.03). Abdominal pain decreased (P < 0.001) with linaclotide but not between groups. Complete spontaneous bowel movement frequency increased (P < 0.001), and IBS-QOL scores improved (P = 0.01) with linaclotide compared to baseline and placebo. There was no difference in overall responders between linaclotide and placebo (54% vs 23%, P = 0.13). CONCLUSIONS: Linaclotide prolongs afferent gut-brain signalling from baseline but both afferent and efferent signalling were unaffected compared to placebo. Linaclotide significantly improves rectal hypersensitivity, IBS-C symptoms and QOL compared to placebo. These mechanisms may explain the effects of linaclotide on pain relief in IBS-C patients. ClinicalTrials.Gov: Registered at Clinical trials.gov no NCT02078323.

Lactobacillus reuteri DSM 17938 is effective in the treatment of functional abdominal pain in children: Results of the double-blind randomized study.

BACKGROUND & AIMS: Possible therapeutic effect of Lactobacillus (L.) reuteri DSM 17938 has been reported in children with functional abdominal pain (FAP) but data are inconclusive. METHODS: This is a randomized double-blinded controlled trial (RCT) which assessed effect of L. reuteri DSM 17938 (dose 108 CFU/day) in children (age 4-18 years) on FAP during an intervention period of 12 weeks and follow-up of 4 weeks. This study was performed after the interim analysis and had different labeling of products and a new randomization. Data presented here are results of this RCT and pooled data from both RCTs (before and after interim analysis). RESULTS: This RCT included 46 children (median age 10.1 vs 10.6 years; 11 vs 13 girls). Abdominal pain was less severe in intervention group during the 4th month of the study and there was significant increase in the number of days without pain. Pooled data from both parts of the study included 101 children. Number of days without pain was significantly higher in the L. reuteri group (mean difference 26.42 days, 95% CI 22.47-30.17). Significant difference in the pain intensity was found after 2nd, 3rd and 4th month of the intervention. There was no difference between groups in the number of children in whom symptoms completely ceased (Risk Ratio 1.09, 95% CI 0.75-1.58). CONCLUSION: Administration of L. reuteri DSM 17938 was associated with the reduction in the intensity of pain and with significantly increase in pain-free days in children with FAP.