Clostridium intestinal microflora

Rafii F, Smith DB, Benson RW, Cemiglia CE (1992) Immunological homology among azoreductases from Clostridium and Eubacterium strains isolated from human intestinal microflora. J Basic Microbiol 32 99-105... 

Huijghebaert et al. [23] isolated a bile salt sulfatase-producing strain designated, Clostridium S, from rat feces. This bacterium hydrolyzed the 3-sulfates of lithocholic acid, chenodeoxycholic acid, deoxycholic acid and cholic acid but not the 7-or 12-monosulfates. Sulfatase activity required the 3-sulfate group to be in the equatorial position. A free C-24 or C-26 carboxyl group was also required for sulfatase activity in whole cells of this bacterium. The 3-sulfate of cholesterol, Cj,-and Cji-steroids were not hydrolyzed by Clostridium S, [24]. Nevertheless, C,9- and C2]-steroid sulfates are hydrolyzed in the gut by microbial activity suggesting that the intestinal microflora may contain bacteria with steroid sulfatases possessing different substrate specificities. However, it should be noted that enzyme substrate specificity studies carried out in whole cells may reflect both cell wall permeability and enzyme specificity. 

HSDH activities are found rather widely distributed among intestinal bacteria including members of the genera Bacteroides, Eubacterium, Clostridium, Bifidobacterium and Escherichia [25-29]. In the human intestinal microflora, 7a-HSDH appears to be much more widely distributed than 3a-HSDH or 12a-HSDH [17]. Individual species may contain from 1 to 3 different stereospecific HSDHs. However, there is considerable variation between strains regarding the presence and extent of HSDH activity. 

The nature of the Bir-like compounds synthesized by Clostridium tetanomorphum (Hendlin, 1953) is unknown. Clostridia abound in most intestinal microfloras. 

The development of the intestinal microbiota needs to be characterized to define the composition that helps us to remain healthy. Specific aberrations in the intestinal microflora may predispose to disease. Such aberrations have been identified in allergic disease, including decreased numbers of bifidobacteria and an atypical composition of bifidobacterial microflora. Also, aberrations in Clostridium content and composition have been reported to be important. Similar predisposing factors may also exist in the case of microflora and both inflammatory gut diseases and rotavirus diarrhea. Microflora aberrations have also been reported in rheumatoid arthritis, juvenile chronic arthritis, ankylosing spondylitis, and irritable bowel syndrome patients. A thorough knowledge of the intestinal microflora composition will offer a basis for future probiotic development and the search for new strains for human use. Many diseases and their prevention can be linked to the microflora in the gut. 

Nitropyrene Bacteroides sp., Bacteroides thetaiotaomicron, Bacteroides fragilis. Bifidobacterium infantis, Clostridium sp., Clostridium perfringens, Clostridium clostridiiforme, Clostridium leptum, Citrobacter sp., Peptococcus anaerobium, Peptostreptococcus productus. Salmonella typhimurium, Escherichia coli, Lactobacillus sp., Lactobacillus acidophilus. Rat and Human intestinal microflora. 1 -Aminopyrene, 1 -N-Acetyl-1 -aminopyrene, 1 -N-Formyl-1 -aminopyrene. 53, 36, 37, 13, 12, 45, 41, 44, 43, 64, 65, 10. 

N itrobenz [ajanthracene Bacteroides sp., Butyrivibrio sp., Clostridium clostridiiforme, Clostridium nexile, Clostridium paraputrifiicum, Clostridium perfringens, Eubacterium sp., Eubacterium hadrum. Human, Mouse, Pig and Rat intestinal microflora. 7-Aminobenz[a]anthracene, Benz[a]anthracene7,12-dione. 57. 

Nitrobenzo[a]pyrene Bacteroides thetaiotaomicron. Bifidobacterium infantis, Clostridium sp., Citrobacter sp., Clostridium perfringens, Peptostreptococcus productus, Escherichia coli. Rat and Human intestinal microflora. 6-Aminobenzo[a]pyrene, 6-Nitrosobenzo[a]pyrene. 13, 12, 68, 27. 

Penicillins alter the normal bacterial flora in areas of the body, including the respiratory and intestinal tracts. Patients taking oral penicillins may experience nausea, vomiting, or diarrhea. This is usually of little clinical significance because the normal microflora reestablishes itself quickly after cessation of therapy. However, serious superinfection with resistant organisms such as Pseudomonas, Proteus, or Candida can follow long-term therapy with any penicillin. Superinfection with Clostridium difficile can lead to potentially fatal pseudomembranous colitis. 

Microbial numbers and species diversity increases in the distal small intestine, with facultative anaerobes as well as more strict anaerobic species such as bacteroides, clostridia. Gram positive cocci and bifidobacteria reaching population levels of up to 10 colony forming units (CFU)/mL contents. The colon is the main site of microbial colonization in the gut, and the microflora is dominated by the strict anaerobes. This microflora is made up of Bacteroides spp., Eubacterium spp., Clostridium spp., Eusobacterium spp, Peptostreptococcus spp., and Bifidobacterium spp., with lower population levels of anaerobic streptococci, lactobacilli, methanogens and sulphate-reducing bacteria (Figure 6.2). Climax microbial populations occur (up to 10 cells/g) and estimates of diversity range from 400 to 500 different bacterial species. The facultative anaerobes such as lactobacilli, streptococci/enterococci and the Enterobacteriaceae occur in population levels about 100-1000-fold lower than strict anaerobes (Moore and Holdeman 1975 Conway 1995). 

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