Clostridium difficile

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Clostridium difficile
Clostridium Difficile on blood agar
Morphology Gram-positive rods , sporulating
Relation to oxygen strictly anaerobic
Cultivation selective soils with cefoxitin and cycloserine, soils with vit. K and hemin (green fluorescence under UV light)
Virulence factors thermolabile toxins: toxin A (enterotoxin, encoded chromosomally), toxin B (necrotizing cytotoxin)
Source colonized or infected person
Transmission alimentary tract (ingestion of spores that are excreted in the faeces)
Disease postantibiotic colitis, pseudomembranous colitis , toxic megacolon
Diagnostics Demonstration of toxins in stool, macroscopic picture in colitis (colonoscopy), stool cultivation on selective soils
Therapy discontinue current ATB treatment, probiotics, nitromidazole ATB, vancomycin
MeSH ID D016360

Template:Infobox - bakterie C. difficile is a gram-positive sporulating anaerobic rod. It is present in the intestines of 5% of healthy adults and slightly more in children and infants. With its toxins, it is able to cause disability, which can manifest as mild diarrheal disease, but also as life-threatening pseudomembranous enterocolitis.

These diseases often arise in connection with the administration of antibiotics (clindamycin , penicillins and cephalosporins), which eliminate the normal intestinal microflora. C. difficile is relatively resistant and in case of elimination of normal intestinal microflora, overgrowth occurs, which subsequently leads to the development of clinical symptoms.

Morphology[edit | edit source]

Bacillus type bacteria - slender rods, the size is quite variable. It easily sporulates in the presence of bile salts. The vegetative cell is easily bulged by spores that are relatively non-resistant.

Cultivation[edit | edit source]

This clostridium is named after the difficult cultivability, but today it is no longer justified when using suitable soils. C. difficile is cultured from faeces on soils containing the antibiotic cefoxitin, which eliminates the accompanying microflora, but C. difficile is resistant to it. It is also resistant to clindamycin. It requires an anaerobic atmosphere for cultivation.

Pathogenesis[edit | edit source]

Pseudomembranous enterocolitis caused by Clostridium difficile on a histological specimen

Some strains release toxins (toxin A and B), which are released into the environment by the breakdown of cells. Other strains produce both toxins at the same time, but most strains do not produce any toxins. Toxins cause intestinal damage that can result in pseudomembranous enterocolitis . The formation of classical pseudomembranous enterocolitis occurs by the interaction of both toxins (toxin A damages the cells of the intestinal epithelium and reduces the efficiency of the immune system, toxin B completely destroys the damaged cells). This creates necrosis and ulcerations covered with poppies. Diarrhea, painful abdominal tension and fever appear.

Pseudomembranous enterocolitis can result in:

  • toxic megacolon
  • ileus
  • intestinal rupture endangering the patient's life

According to some sources, the hypervirulent strain C. difficile PCR ribotype 027 in particular poses a major epidemiological threat in the near future . The higher frequency of clinical forms is probably related to the high production of toxins.[1]

Diagnostics[edit | edit source]

We perform the c.diff card from a stool sample on selective soils in an anaerobic atmosphere. We use latex agglutination or ELISA test to detect the toxin. The test on human embryonic lung fibroblast culture is more sensitive, where the toxin produces a significant cytopathic effect and it is possible to perform a neutralization test with a specific antiserum.

Therapy[edit | edit source]

We use the antibiotics metronidazole and vancomycin for the treatment of enterocolitis. Furthermore, the patient should be treated symptomatically.

Restoration of the normal intestinal microflora is also essential, especially in patients treated with antibiotics. We'll do it by giving probiotics. The success of faecal transplant therapy from a healthy donor is also discussed.[2]

Links[edit | edit source]

References[edit | edit source]

  1. O. Nyč, B. Macková, V. Jindrák: Zprávy CEM (SZÚ, Praha) 2006; 15(10-11): 457
  2. Transplantace faeces,

Related[edit | edit source]

External[edit | edit source]

References[edit | edit source]

  • VOTAVA, Miroslav, et al. Medical microbiology special. 1st edition. Brno: Neptun, 2003. 495 pp. 150-151. ISBN 80-902896-6-5 .
  • . Nyč, B. Macková, V. Jindrák: Zprávy CEM (SZÚ, Praha) 2006; 15(10-11): 457
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