Small intestinal bacterial overgrowth syndrome

Human intestinal microbiota create a complex polymi-crobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO).SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastro-intestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacte-riostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insuff iciency, immuno-deficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, f istulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Noninvasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be com-plex, addressing all causes, symptoms and complica-tions, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

Blood pressure and stature in Helicobacter pylori positive and negative persons

To evaluate vital signs and body indices in Helicobacter pylori (H. pylori) positive and negative persons. A total of 22 centres entered the study. They were spread over the whole country, corresponding well to the geographical distribution of the Czech population. A total of 1818 subjects (aged 5-98 years) took part in the study, randomly selected out of 38147 subjects. H. pylori infection was investigated by means of a 13C-urea breath test. Data on height, weight, systolic and diastolic blood pressure and heart rate were collected at the clinics of general practitioners. The overall prevalence of H. pylori infection was 30.4% (402/1321) in adults (≥ 18 year-old) and 5.2% (26/497) in children and adolescents (≤ 17 year-old). Once adjusted for age and gender, only a difference in body mass index remained statistically significant with H. pylori positive adults showing an increase of 0.6 kg/m2 in body mass index. Once adjusted for age and gender, we found a difference in height between H. pylori positive and H. pylori negative children and adolescents. On further adjustment for place of residence, this difference became statistically significant, with H. pylori positive children and adolescents being on average 3.5 cm shorter. H. pylori positive adults were significantly older compared to H. pylori negative subjects. Once adjusted for age and gender, H. pylori infection had no impact on body weight, body mass index and vital signs either in adults or children and adolescents. Chronic H. pylori infection appeared to be associated with short stature in children. H. pylori infection did not influence blood pressure, body weight and body mass index either in adults or children and adolescents.

Bacteriocinogeny in experimental pigs treated with indomethacin and Escherichia coli Nissle

AIM： To evaluate bacteriocinogeny in short-term highdose indomethacin administration with or without probiotic Escherichia coli Nissle 1917 （EcN） in experimental pigs.METHODS： Twenty-four pigs entered the study： Group A （controls）, Group B （probiotics alone）, Group C （indomethacin alone） and Group D （probiotics and indomethacin）. EcN （3.5 × 10^10 bacteria/d for 14 d） and/or indomethacin （15 mg/kg per day for 10 d） were administrated orally. Anal smears before and smears from the small and large intestine were taken from all animals. Bacteriocin production was determined with 6 different indicator strains; all strains were polymerase chain reaction tested for the presence of 29 individual bacteriocinencoding determinants. RESULTS： The general microbiota profile was rather uniform in all animals but there was a broad diversity in coliform bacteria （parallel genotypes A, B1, B2 and D found）. In total, 637 bacterial strains were tested, mostly Escherichia coli （E. coli. There was a higher incidence of non-E：, coli strains among samples taken from the jejunum and ileum compared to that of the colon and rectum indicating predominance of E. coil strains in the large intestine. Bacteriocinogeny was found in 24/77 （31%） before and in 155/560 （28%） isolated bacteria at the end of the study. Altogether, 13 individual bacteriocin types （out of 29 tested） were identified among investigated strains. Incidence of four E. coli genotypes was equally distributed in all groups of E. coil strains, with majority of genotype A （ranging from 81% to 88%）. The following types of bacteriocins were most commonly revealed： colicins Ia/Ib （44%）, microcin V （18%）, colicin E1 （16%） and microcin H47 （6%）. There was a difference in bacteriocinogeny between control group A （52/149, 35%） and groups with treatment at the end of the study： B： 31/122 （25%, P = 0.120）; C： 43/155 （28%, P = 0.222）; D： 29/134 （22%, P = 0.020）. There was a significantly lower prevalence of colicin Ib, microcins H47 and V （probiotics group, P 〈 0.001）, colicin E1 and microcin H47 （indomethacin group, P 〈 0.001） and microcins H47 and V （probiotics and indomethacin group, P = 0.025） compared to controis. Escherichia fergusonil （E. fergusoniO was identi-fled in 6 animals （6/11 isolates from the rectum）. One strain was non-colicinogenic, while all other strains of E. fergusonii solely produced colicin El. All animals started and remained methanogenic despite the fact that EcN is a substantial hydrogen producer. There was an increase in breath methane （after the treatment） in 5/6 pigs from the indomethacin group （C）. CONCLUSION： EcN did not exert long-term liveabilib/ in the porcine intestine, All experimental pigs remained methanogenic, Indomethacin and EcN administered together might produce the worst impact on bacteriocinogeny.