Bacteria invasion

Bacteria cause disease of the gut as a result of either mucosal invasion or toxin produchon or a combinahon of the two mechanisms as summarized in Table 6.4. Treatment is largely directed at replacing and maintaining an adequate intake of fluid and electrolytes. Anhbiohcs are generally not recommended for infechve gastroenterihs. 

Brannstrom, M. Vojinovic, O. (1976). Responses of the dental pulp to invasion of bacteria around three filling materials. Journal of Dentistry for Children, 43, 83-9. 

Stool may also be analyzed for mucus, fat, osmolality, fecal leukocytes, and pH. The presence of mucus suggests colonic involvement. Fat in the stool may be due to a malabsorption disorder. Fecal leukocytes can be found in inflammatory diarrheas including infections caused by invasive bacteria (e.g., E. coli, Shigella, and Campylobacter species). Stool pH (normally greater than 6) is decreased by bacterial fermentation processes. 

Returning to bacteria, PC also appears to play a role in infection of humans by pathogenic strains/species by allowing colonization and invasiveness due to interaction with appropriate receptors on host endothelial cells (reviewed by Harnett and Harnett, 1999). This may act as a double-edged sword, however, as the PC on the surface of the bacteria can be targeted by both the innate and adaptive immune responses and indeed such responses appear to play a role in the control of H. influenzae and S. pneumoniae, respectively, in humans (reviewed by Harnett and Harnett, 1999). 

EPEC causes a degeneration of the microvillus brush border, with cupping and pedestal formation of the plasma membrane at the sites of bacterial attachment and reorganization of cytoskeletal proteins [43, 44], Invasion has been observed in some clinical specimens, but the mechanism of how this bacteria produces diarrhea is not fully understood. Some possibilities include an increase in permeability and loss in microvilli leading to malabsorption. 

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]. 

The exact mechanism of bacterial infection of the prostate is not well understood. The possible routes of infection include ascending infection of the urethra, reflux of infected urine into prostatic ducts, invasion by rectal bacteria through direct extension or lymphatic spread, and by hematogenous spread. 

The Gram-positive bacterium Streptococcus pneumoniae is an important cause of respiratory tract infections, bacteremia, and meningitis. In this strain, the cell wall anchored pneumococcal surface protein A (PspA) has been demonstrated to bind lactoferrin [181]. PspA and closely related proteins in a variety of pneumococcal isolates are most likely involved in the sequestration of iron from lactoferrins, and finally contribute to the virulence of these bacteria. However, the means by which the pneumococcus acquires iron at the mucosal surface during invasive infection is not well understood at the molecular level [182],... 

FnBP-mediated internalization of S. pyogenes (Ozeri et ah, 1998). Additionally, Sfbl has been shown to recruit other ECM components like collagen I and IV that aid in escaping the host immune system (Dinkla et ah, 2003). Around 50% of fhe S. pyogenes clinical isolates express the sfbl gene (Natanson et ah, 1995). However, only five differenf FnBPs contain FnBRs that can potentially assist bacteria in adherence and invasion (Schwarz-Linek et ah, 2006). 

Bernet, M. F., Brassart, D., Neeser, J. R., and Servin, A. L. (1994). Lactobacillus acidophilus Lai binds to cultured human intestinal cell lines and inhibits cell attachment and cell invasion by enterovirulent bacteria. Gut 35, 483-489. 

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