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Colonic bacteria

Bird, A.F., Stynes, B.A. and Thomson, W.W. (1980) A comparison of nematode and bacteria-colonized galls induced by Anguina agrostis in Lolium rigidum. Phytopathology IQ, 1104-1109. [Pg.168]

Although theoretically safe, poorly absorbed antimicrobials could become absorbable in the presence of mucosal inflammatory or ulcerative changes [100], like those occurring in IBD or when invasive bacteria colonize the intestine. To verify whether the presence of intestinal lesions would affect rifaximin absorption, the drug was given to rats with experimentally induced colitis [101]. The indomethacin-induced enteropathy did not affect intestinal absorption of rifaximin. However, under the same experimental conditions, systemic bioavailability of neomycin did increase [101]. [Pg.45]

Bacteria colonize only a small proportion of the available particle surface area (0.01 to 5 % range of the data obviously dependent upon the method used for the calculation of surface area cf. Hargrave, 1972 Rublee and Dornseif, 1978 Weise and Rheinheimer, 1978 DeFlaun and Mayer, 1983). Deep pores of wheathered feldspar and clay grains do not appear to be inhabited by bacteria (DeFlaun and Mayer, 1983). Bacteria preferentially... [Pg.142]

Uropathogenic E. coli cause 90% of the urinary tract infections. The bacteria colonize from the feces or perineal region and ascend the urinary tract to the bladder. With the aid of specific adhesins (pyelonephritis-associated pili) they are able to colonize the bladder. Another factor involved in the pathogenicity of the uropathogenic strains of E. coli is their resistance to complement-dependent bactericidal effect of serum. This phenomenon is associated with the presence of a capsule, which decrease the ability of antibodies and/or complement to bind to the bacterial surface, which in turn prevents the phagocytes from recognizing and engulfing the bacterial cells. [Pg.926]

The proximal small intestine (duodenum and jejunum) normally contains few bacteria. Most ingested bacteria do not survive the acidic environment of the stomach and therefore few live organisms normally enter the small bowel. The motfiity of the jejunum prevents fecal-type organisms from progressing up into the jejunum from the cecum. The ileum normally contains some fecal-type bacteria. Colonization of the upper small bowel is described as bacterial overgrowth and usually occurs as a consequence of other abnormalities (structural or motility disorders) of the small intestine (see Box 48-4). Use of PPIs is associated with an increased risk of bacterial colonization. [Pg.1864]

The bacteria colonizing the small bowel (such as Escherichia coli and Bacteroides species) deconjugate and dehydroxylate bde salts, leading to conjugated bde salt deficiency, which causes fat malabsorption. Bacterial metabolism of vitamin B12 may also occur, leading to vitamin B,2 deficiency. The clinical symptoms of bacterial overgrowth are abdominal pain, diarrhea, and steatorrhea. ... [Pg.1865]

Figure 2. Bacteria colonize ear tag wounds (indicated by arrow) two days after i.v. injection of bacteria into mice. Figure 2. Bacteria colonize ear tag wounds (indicated by arrow) two days after i.v. injection of bacteria into mice.
Figure 3. Bacteria colonize tumors (indicated by open arrow) but not inflammatory sites induced by Sephadex (indicated by solid arrow). Figure 3. Bacteria colonize tumors (indicated by open arrow) but not inflammatory sites induced by Sephadex (indicated by solid arrow).
Bacteria causing gastrointestinal infection need to penetrate the mucus layer before attaching themselves to the epithelial surface. This attachment is usually mediated by bacterial fimbriae or pilus structures, although other cell surface components may also take part in the process. Adherent bacteria colonize intestinal epithelium by multiplication and initiation of a series of biochemical reactions inside the target cell through signal transduction mechanisms (with or without the help of toxins) (51). [Pg.262]

Enterotoxins. Toxic proteins formed by bacteria with molecular masses in the range from 27000 to 30000 which are usually excreted into the medium ( exotoxins). E. can be taken up with contaminated food or be formed by the bacteria colonizing the intestinal walls. Finally, the bacteria can penetrate the intestinal walls and then start to excrete the E. Some E. are thermally very stable and survive when food is boiled. E. from Salmonella and Staphylococcus species are the most frequent causes of food poisoning. Shortly after uptake, the symptoms of nausea, vomiting, diarrhea, and circulatory complaints occur. Deaths are rare and occur only when the subject is already in a weakened state. The sites of attack by E. vary, e.g., at intestinal epithelial cells or in the vegetative nervous system. For the production of antitoxins, E. are obtained by lysis of bacterial cells or from cell-free culture filtrates. E. have been detected, e. g., in the following bacterial species Bacillus cereus, Clostridium perfringens, Escherichia coli. Vibrio cholerae. Staphylococcus aureus, and Streptococcus faecalis. [Pg.209]

Macfarlane GT, Macfarlane S. Bacteria, colonic fermentation, and gastrointestinal health. / AOAC Int. 2012 95 50—60. [Pg.13]

Table 4 Bacteria colonizing the mucus layer using glycan-recognizing adhesins. Table 4 Bacteria colonizing the mucus layer using glycan-recognizing adhesins.
Neolithic tartar, medieval tartar, and Industrial Age tartar were compared. A. Gibbons. How sweet it is genes show how bacteria colonized human teeth. 2013. Science 339(6122), p. 896. DOl 10.1126/science.339.6122.896. [Pg.322]

Dragstedt concluded that these bacteria colonized the damaged mucosa after ulcer formation and proposed that they had migrated up from the alimentary tract. He did not believe that they played a substantial role in the etiology of the disease and did not pursue these studies further, choosing rather to focus on the role of vagal innervation in acid-induced ulceration. [Pg.452]


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See also in sourсe #XX -- [ Pg.1615 ]




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