Fecal lactoferrin is sensitive and specific for detecting inflammation in chronic IBD. This noninvasive test may prove useful in screening for inflammation in patients presenting with abdominal pain and diarrhea.

Data presented here demonstrate that FLA is a sensitive and specific biochemical marker of inflammation for use in the diagnosis and interval assessment of pediatric patients with IBD, and its level correlates well with both clinical disease activity indices and ESR. Elevated levels of FLA may also identify patients at greater risk for the development of subsequent clinical flares.

Background Clostridium difficile is the most common known cause of antibiotic-associated diarrhea. Upon the disturbance of gut microbiota by antibiotics, C. difficile establishes growth and releases toxins A and B, which cause tissue damage in the host. The symptoms of C. difficile infection disease range from mild diarrhea to pseudomembranous colitis and toxic megacolon. Interestingly, 10–50 % of infants are asymptomatic carriers of C. difficile. This longitudinal study of the C. difficile colonization in an infant revealed the dynamics of C. difficile presence in gut microbiota.MethodsFifty fecal samples, collected weekly between 5.5 and 17 months of age from a female infant who was an asymptomatic carrier of C. difficile, were analyzed by 16S rRNA gene sequencing.ResultsColonization switching between toxigenic and non-toxigenic C. difficile strains as well as more than 100,000-fold fluctuations of C. difficile counts were observed. C. difficile toxins were detected during the testing period in some infant stool samples, but the infant never had diarrhea. Although fecal microbiota was stable during breast feeding, a dramatic and permanent change of microbiota composition was observed within 5 days of the transition from human milk to cow milk. A rapid decline and eventual disappearance of C. difficile coincided with weaning at 12.5 months. An increase in the relative abundance of Bacteroides spp., Blautia spp., Parabacteroides spp., Coprococcus spp., Ruminococcus spp., and Oscillospira spp. and a decrease of Bifidobacterium spp., Lactobacillus spp., Escherichia spp., and Clostridium spp. were observed during weaning. The change in microbiome composition was accompanied by a gradual increase of fecal pH from 5.5 to 7.ConclusionsThe bacterial groups that are less abundant in early infancy, and that increase in relative abundance after weaning, likely are responsible for the expulsion of C. difficile. Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-016-0198-6) contains supplementary material, which is available to authorized users.

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The glycoprotein lactoferrin is found in many body fluids but also in the granules of neutrophilic granulocytes. Fecal lactoferrin levels increase quickly with the influx of leukocytes into the intestinal lumen during inflammation. This biomarker has recently been shown to be a sensitive and specific marker of disease activity in chronic inflammatory bowel disease. Our aim was the determination of fecal lactoferrin as a marker of intestinal inflammation and therapeutic response following infliximab therapy in pediatric patients with Crohn's disease (CD). A total of five patients (ages 10-15 years) with severe Crohn's disease as defined by the Pediatric Crohn's Disease Activity Index (PCDAI) was enrolled in the study. The fecal lactoferrin levels were determined before and after therapy with infliximab by a quantitative lactoferrin ELISA (IBD-SCAN; TechLab, Inc.). Of the five patients on infliximab therapy, three received a single infusion and the remaining two underwent a regime with three maintenance infusions. All five patients responded to infliximab clinically after the first infusion, and in all patients, fecal lactoferrin levels significantly and rapidly decreased from elevated to near baseline in parallel to clinical assessment and the PCDAI. The reduction in fecal lactoferrin at days 7-10 was 93.43 +/- 4.49%, in comparison with the level before infliximab therapy, and correlated with a mean decrease in the PCDAI from 48.50 to 14.0. For the patients followed during multiple infusions, one remained with mild disease and the other reached remission (subjective and PCDAI). Fecal lactoferrin is a sensitive and specific biomarker representing intestinal inflammation and response to therapy in pediatric patients with Crohn's disease. It may be a helpful noninvasive diagnostic tool for monitoring therapeutic efficiency in pediatric IBD patients. Future studies are needed to further establish the relationship between endoscopic changes and the level of fecal lactoferrin as well as the possible role of lactoferrin as being an early and preclinical indicator of relapse.

Faecal biomarkers FLA, CAL, and PMN-e were able to distinguish between UC patients with mucosal healing from clinical remission and mild disease, showed significant correlations with endoscopy, and were predictive of a flare.

We evaluated Clostridium difficile prevalence rates in 2,807 clinically indicated stool specimens stratified by inpatient (IP), nursing home patient (NH), outpatient (OP), age, gender, and specimen consistency using bacterial culture, toxin detection, and polymerase chain reaction (PCR) ribotyping. Rates were determined based on the detection of toxigenic C. difficile isolates. We identified significant differences in the rates between patient populations and with age. Specimens from NH had a higher rate (46%) for toxigenic C. difficile than specimens from IP (18%) and OP (17%). There were no gender-related differences in the rates. Liquid specimens had a lower rate (15%) than partially formed and soft specimens (25%) and formed specimens (18%) for the isolation of toxigenic C. difficile. The nontoxigenic rate was lowest for NH (4%) and highest for patients<20 years of age (23%). We identified 31 different toxigenic ribotypes from a sampling of 190 isolates that showed the lowest diversity in NH. Fluoroquinolone resistance was observed in 93% of the 027 isolates, all of the 053 isolates, and in four other ribotypes. We observed different rates for toxigenic C. difficile in stratified patient populations, with the highest rate for NH, a low overall nontoxigenic rate, and fluoroquinolone resistance.