Gastrointestinal tract bacterial

C2H5OH, ethanol is formed by bacteria in the gastrointestinal tract in low amounts. Most of the ethanol of bacterial source is metabolized during the first liver passage yielding acetaldehyde and subsequently acetic acid. 

As with all drugs, the specific side effects of the quinolones must be considered when they are chosen for treatment of bacterial infections [5]. Reactions of the gastrointestinal tract and the central neivous system are the most often observed adverse effects during therapy with quinolones. It should be underlined, however, that compared with many other antimicrobials, diarrhea is less frequently observed during quinolone treatment. Antibiotic-associated colitis has been observed rarely during quinolone therapy. Similarly, hypersensitivity reactions, as observed during therapy with penicillins and other (3-lactams, is less frequently caused by quinolones. Some other risks of quinolone therapy have been defined and must be considered if a drug from this class is chosen for treatment of bacterial infections. 

It is conceivable that nltrosamlnes can be synthesized In the Intestine, since the precursors are present. While the conditions for aqueous nltrosatlon reactions are not optimum at pH values encountered In the lower gastrointestinal tract, several studies have shown that these reactions can be catalyzed (39, 40, 41). It has been suggested that the Intestine might be a site for the formation of nltrosamlnes by bacterial action (42). Sander (43) has demonstrated the formation of nltrosamlnes by bacterial action from precursor amines and nitrate at neutral pH and Klubes and coworkers have reported the formation of NDMA. upon Incubation of l C-dlmethylamlne and sodium nitrite with rat fecal contents (44, 45). 

The oral cavity and the lower gastrointestinal tract are densely colonized by bacteria with counts exceeding 109 colony-forming units (CFU)/ml, whereas the density in the stomach and proximal small bowel is normally below 105 CFU/ml (fig. 1). Bacterial density increases through... 

Fig-1. The density of bacteria along the gastrointestinal tract of man is shown schematically based on data from references 1-5 in the text. Density is given by logio CFU/ml of luminal contents in the fasting state. TBC = Total bacterial count. 

Drasar BS, Shiner M, Mcloed GM Studies on the intestinal flora. The bacterial flora of the gastrointestinal tract in healthy and achlorhydric persons. Gastroenterology 1969 56 71— 79. 

Berg RD Bacterial translocation from the gastrointestinal tract. Adv Exp Med Biol 1999 473 11-30. 

The /V4-acylatcd sulfonamides, succinylsulfathiazole (4.124) and phtha-lylsulfathiazole (4.125), are poorly absorbed by the gastrointestinal tract. These compounds, which were once used as intestinal antiseptics, are inactive in vitro and must be activated by hydrolysis to sulfathiazole by bacterial hydrolases in the large intestine [78],... 

Clarithromycin is better absorbed and irritates the gastrointestinal tract less than erythromycin. It is presumed that its activity exceeds that of erythromycin by 2-4 times with respect to a number of streptococci and staphylococci, and to a few other microorganisms. It is used for treating bacterial bronchitis, pneumonia, skin and sexual infections. It is believed that clarithromycin is the most active macrolide for treating atypical mycobacteria. Synonyms of this drug are biaxin and others. 

Clindamycin is a chlorine-substituted derivative of lincomycin. However it is more potent and is better absorbed from the gastrointestinal tract and has therefore replaced lincomycin in most situations. Clindamycin is in principle a bacteriostatic agent. Its indications are mainly limited to mixed anaerobic infections. As mentioned above it has a similar mechanism of action as erythromycin. It selectively inhibits bacterial protein synthesis by binding to the same 50s ribosomal subunits. Erythromycin and clindamycin can interfere with each other by competing for this receptor. Also cross-resistance with erythromycin frequently occurs. Resistance is rather chromosomal rather than plasmid mediated and is especially found in cocci and Clostridium difficile. 

The spectrum of gastrointestinal tract infections (GTI) cover a wide spectrum from asymptomatic Helicobacter pylori gastritis to self-limiting viral gastroenteritis to food poisoning to bacterial enterocolitis to antibiotic-associated Clostridium difficile colitis to typhoid fever with sepsis and multi-organ failure. 

Mechanism of Action A third-generation cephalosporin that binds to bacterial cell membranes and inhibits cell wall synthesis. Therapeutic Effect Bactericidal. Pharmacokinetics Rapidly absorbed from the gastrointestinal tract. Protein binding 65%-77%. Excreted primarily in urine. Half-life 2-3 hr. 

More recently, a new test (.HemoQuant) has been developed. This test involves the chemical conversion of stool heme to porphyrins that can be assayed fluorometrically. The Lest also detects porphyrins present in stool as a result of bacterial and enzymatic degradation of hemoglobin as it travels through the intestines. Thus, this new test provides a quantitative measure of all blood that enters the gastrointestinal tract. It appears to be biochemically sound and is considered a methodological breakthrough. 

Mack, D. R., and Sherman, P. M. Hydrophobicity and the gastrointestinal tract Methods of determination, its source and implications for bacterial adherence. Colloids Surfaces B 15 355-363, 1999. 

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