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Bacterial colonization

Bacterial catabolism of oral food residue is probably responsible for a higher [NHj] in the oral cavity than in the rest of the respiratory tract.Ammonia, the by-product of oral bacterial protein catabolism and subsequent ureolysis, desorbs from the fluid lining the oral cavity to the airstream.. Saliva, gingival crevicular fluids, and dental plaque supply urea to oral bacteria and may themselves be sites of bacterial NH3 production, based on the presence of urease in each of these materials.Consequently, oral cavity fNTi3)4 is controlled by factors that influence bacterial protein catabolism and ureolysis. Such factors may include the pH of the surface lining fluid, bacterial nutrient sources (food residue on teeth or on buccal surfaces), saliva production, saliva pH, and the effects of oral surface temperature on bacterial metabolism and wall blood flow. The role of teeth, as structures that facilitate bacterial colonization and food entrapment, in augmenting [NH3J4 is unknown. [Pg.220]

Disruption of these defense mechanisms can lead to bacterial colonization or viral infection. Mucus temperature is important in controlling respiratory infections because decreasing below central body core temperature not only impairs ciliary movement,hut also enhances viral replication,- greatly increasing the likelihood of respiratory infection. Drying of airway mucus also increases the possibility of respiratory infection by reducing mucus thickness and impairing mucociliary clearance, i- i--... [Pg.229]

Figure 7.2. Microradiograpli of Burial 30, periosteal surface at top. Snake Hill bone microradiographs show radiolucent cavities around Haversian canals surrounded by hypermineralized rims, which Baud and Lacotte (1984) argue are characteristic of bacterial colonization. Figure 7.2. Microradiograpli of Burial 30, periosteal surface at top. Snake Hill bone microradiographs show radiolucent cavities around Haversian canals surrounded by hypermineralized rims, which Baud and Lacotte (1984) argue are characteristic of bacterial colonization.
The third topic in polyphosphazene biomaterials that will be described in this article concerns surface implications. One of the major problems in the utilization of polyphosphazenes in solid state is their exploitation in the construction of implantable devices, for which good physical properties, minimum biological response, and good resistance to fungal or bacterial colonization may be required. [Pg.218]

The process, once initiated, is self-sustaining and may become more accelerated with time because the atrophy and intestinal metaplasia are progressive lesions and lead to further loss of parietal cells and incrased bacterial colonization of the mucosa. The initial mutations transform gastric cells into mature intestinal-type cells. Further superimposed mutations transform metaplastic cells into progressively dysplastic cells and eventually into neoplastic cells. This is a process of loss of differentiation which implies a multihit phenomenon which could be explained on the basis of continued formation of minute amounts of nitroso compounds over many years. [Pg.327]

E. L. Nurmiaho-Lassila, S. Timonen, K. Haahtela, R. Sen, Bacterial colonization patterns of intact Pinus. syhe.siris mycorrhizospheres in dry pine forest soil an electron microscopy study. Can. J. Microbiol. 43 1017 (1997). [Pg.295]

Bacterial colonization of pressure sores is common. Because infection impairs wound healing and may require systemic antimicrobial therapy, the clinician must be able to distinguish it from colonization. Table 70-8 describes the clinical presentation of infected pressure sores. [Pg.1084]

When the mechanisms restricting bacterial colonization in the upper gut fail, due to disease or dysfunction, bacterial overgrowth develops. The segmental distribution may be gastric, intestinal or both depending on the type of failure. The consequences for the host vary from none to life-threatening complications, caused by severe water and electrolyte deficiencies and septic manifestations. [Pg.2]

In the present review the gastric lumen is confined to the habitat above the mucus layer, for which the pH of fasting gastric juice is the major defense mechanism against bacterial colonization. This defense mechanism is henceforth denoted the gastric acid barrier. [Pg.4]

The consequences of a failure of the gastric acid barrier for the intestinal microflora emerge from studies of healthy individuals and patient populations with other important defense mechanisms against bacterial colonization intact. [Pg.8]

Shindo et al. [66] treated 19 healthy volunteers with omeprazole 20 mg, cultured gastric and jejunal aspirate, and determined gastric pH and bile acid metabolism. Although motility studies were not performed, it can be assumed that intestinal migrating motor complexes were normal [21] (fig. 4). Bacterial colonization was defined by species density exceeding 105 CFU/0.5 ml, and only reported for those exceeding this limit. [Pg.8]

Fig. 5. Relationship between fasting intestinal motility [x-axis migrating motor complex (MMC) index] and bacterial colonization of small bowel in 41 patients with late radiation enteropathy (LRE) is shown by two plots. Relationship to Gram-negative bacilli (a) and to total bacterial count (b) in the duodenum is shown. Note that no significant Gram-negative colonization was found in patients with normal MMC (index = 3). The vertical dotted lines show the normal limit for MMC index. Increased bacterial counts due to URT flora were found in some patients with normal MMC (b). Tied observations are indicated as follows n = 1 n = 2 1 n = 3 1 n = 4 + n = 6 For n > 6... Fig. 5. Relationship between fasting intestinal motility [x-axis migrating motor complex (MMC) index] and bacterial colonization of small bowel in 41 patients with late radiation enteropathy (LRE) is shown by two plots. Relationship to Gram-negative bacilli (a) and to total bacterial count (b) in the duodenum is shown. Note that no significant Gram-negative colonization was found in patients with normal MMC (index = 3). The vertical dotted lines show the normal limit for MMC index. Increased bacterial counts due to URT flora were found in some patients with normal MMC (b). Tied observations are indicated as follows n = 1 n = 2 1 n = 3 1 n = 4 + n = 6 For n > 6...
Roily and Liebermeister [95] showed that bacteria introduced into the small bowel disappeared rapidly, without bile, pancreatic, and intestinal juices having antibacterial properties alone or mixed. Later studies, of which those by Dack and Petran [96], Dixon [99] and Dixon and Paulley [100] are of particular importance, provided considerable further evidence that intestinal peristalsis is the main line of defense against bacterial colonization of the small bowel. This was also concluded by Donaldson [101-103] when he reviewed host defense mechanisms in 1964. At that time, however, the insights into small bowel motility were confined to the reflex-mediated peristaltic behavior. [Pg.11]

Pharmacological suppression of intestinal peristalsis in experimental animals leads to bacterial colonization of... [Pg.15]

Blood donors with selective IgA deficiency have a normal gastrointestinal microflora without evidence of bacterial overgrowth [191]. In patients with complex immunodeficiency increased bacterial colonization is seen in... [Pg.16]

Dolby JM, Webster ADB, Bordello SP, Barclay FE, Bartholomew BA, Hill MJ Bacterial colonization and nitrite concentration in the achlorhydric stomachs of patients with primary hypogammaglobulinaemia or classic peme-cious anaemia. Scand J Gastroenterol 1984 19 105-110. [Pg.19]

Gilman RH, Partanen R, Brown KH, Spira WM, Khanam S, Greenberg B, et al Decreased gastric acid secretion and bacterial colonization of the stomach in severely malnourished Bangladeshi children. Gastroenterology 1988 94 1308-1314. [Pg.19]

McLoughlin GA, HedeJE, Temple JG, Bradley J, Capman DM, McFarland J The role of IgA in the prevention of bacterial colonization of the jejunum in the vagotomized subject. Br J Surg 1978 65 435-437. [Pg.22]

Gram stain and culture is questionable because some patients have chronic bacterial colonization of the bronchial tree between exacerbations. [Pg.943]

Recently, an approach mimicking the GI tract and feasible for pharmaceutical dissolution studies has been published [47], Coming from the area of nutritional research, this approach reflects some promising aspects, such as relevant luminal pH values, peristalsis, luminal bacterial colonization, and relevant fluid volumes. However, permeation is only reflected by diffusion through hollow fiber membranes and thus is not in the scope of this chapter. Nevertheless, it will be interesting to see whether it will be possible to expand such a perfect in vitro device toward a more realistic intestinal epithelium. [Pg.439]

Newburg, D. S. (2000). Oligosaccharides in human milk and bacterial colonization. /. Pediatr. Gastroenterol. Nutr. 30(Suppl. 2), S8-S17. [Pg.153]

Van Strijp AJP, Van Steenbergen TJM and Ten Cate JM (1997) Bacterial colonization of mineralized and completely demineralized dentine in situ. Caries Res (in press). [Pg.16]

Duffy, L. C., Faden, H., Wasielewski, R., Wolf, J., and Krystofik, D. (1997). Exclusive breastfeeding protects against bacterial colonization and day care exposure to otitis media. Pediatrics 100, E7. [Pg.71]

Bacterial colonization of lower respiratory tract. Cigarette smoke, administered for 3 days before and after intratracheal instillation of bacterial suspension containing six bacterial species (Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumonia, Proteus mirabilis, Haemophilus influenza, Peptostreptococcus spp.) to male Wistar albino rats with or without vitamin E supplements (100 mg/kg/day), signifi-... [Pg.290]


See other pages where Bacterial colonization is mentioned: [Pg.23]    [Pg.1021]    [Pg.118]    [Pg.193]    [Pg.1]    [Pg.2]    [Pg.4]    [Pg.4]    [Pg.9]    [Pg.9]    [Pg.127]    [Pg.725]    [Pg.185]    [Pg.125]    [Pg.242]    [Pg.112]    [Pg.113]    [Pg.151]    [Pg.82]    [Pg.102]    [Pg.372]    [Pg.200]    [Pg.63]   
See also in sourсe #XX -- [ Pg.760 ]

See also in sourсe #XX -- [ Pg.232 ]

See also in sourсe #XX -- [ Pg.156 ]




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