Clostridium difficile – Infection, Transmission & Diseases
Clostridium difficile
Clostridium difficile is a Gram-positive, rod-shaped, obligate anaerobic bacterium from the Firmicutes division. The endospore-forming agent is one of the most important nosocomial germs and can lead to the occurrence of antibiotic-associated colitis , especially in a clinical setting .
Was ist Clostridium difficile?
Clostridium difficile is a rod-shaped, gram-positive bacterium and belongs to the Clostridiaceae family. C. difficile is considered a facultative pathogen that can lead to life-threatening inflammation of the colon (pseudomembranous colitis), especially after taking antibiotics. This makes it one of the most relevant nosocomial pathogens (“hospital germs”), since broad -spectrum antibiotics are often used in hospitals and the duration of therapy with antibiotic drugs is generally longer.
C. difficile is one of the obligate anaerobic bacteria and therefore has no chance in an oxygen-containing (oxic) environmentactiveoperate metabolism. Even small amounts of oxygen can be toxic to the bacterium.
In addition, this Clostridia species has the ability to form endospores that are very resistant to various environmental influences. The cell takes onestrengthenWhen stress is true, the strictly regulated process of sporulation is initiated (sporulation). During sporulation, the vegetative cell forms an additional cell compartment, which contains, among other things, the DNA and important proteins in the mature spore with a very stable cell envelope. The spore is released after the mother cell dies and thus ensures the survival of the cell.
This metabolically inactive form of persistence means that stress factors such as heat, oxygen, drought or many alcohol- based disinfectants can be tolerated until the spore can return to the vegetative state under more favorable environmental conditions.
Occurrence, Distribution & Properties
Clostridium difficile is basically spread all over the world (ubiquitous) and occurs in the environment mainly in soil, dust or surface water. C. difficile can also be found in the intestines of humans and animals. A little under 5% of all adults carry the bacterium, mostly unnoticed. On the other hand, the germ was found in about 80% of all infants, which means that it is probably one of the first bacteria to colonize the intestines of a newborn.
A serious problem is the high prevalence in hospitals. The bacterium can be detected in 20% – 40% of all patients and many patients also experience recolonization with C. difficile there, but without immediately developing symptoms. It is reported that the frequency and severity of C. difficile infections has increased over the past several years. The very resistant spores, which are even resistant to many common alcohol-based disinfectants, have a high persistence in dirt, dust, on clothing or floors. This, together with the partly insufficient hygiene in hospitals, contributes to a rapid spread among patients.
This high rate of spread becomes problematic when one considers the prerequisites for an acute infection with C. difficile. In healthy people, a natural colonization of the (large) intestine with apathogenic bacteria (intestinal microbiota) represents protection against other, harmful types of bacteria. Through adaptation and interaction with the human host , this microbiota can restrict the growth of undesirable germs to a certain extent. Our normal intestinal microbiota includes bacteria of the genera Bacteroides , Faecalibacterium or Escherichia , as well as Clostridium species, but not Clostridium difficile.
If this microbiota is partially or completely killed off by taking antibiotics , C. difficile spores can germinate and proliferate in the anoxic environment of the colon .
Even if the increase after taking antibiotics is the most common cause of an acute infection, older or immunocompromised patients are also at risk. In addition, in patients who take proton pump inhibitors to regulate gastric acid, there is a risk that the bacterium will not be killed by the gastric acid and reach the intestine.
C. difficile infection usually causes severe diarrhea and inflammation of the colon. If the bacterium returns to an oxygen-rich environment via the stool , sporulation begins immediately due to the oxygen stress. After excretion and sporulation, the spores can thus easily be transferred by the patient to other patients, staff or various surfaces. In this acute phase of the disease there is the highest risk of infection and spread.
Diseases & Ailments
Under certain circumstances described above, Clostridium difficile can cause a specific form of intestinal inflammation (pseudomembranous or antibiotic-associated colitis). Typical symptoms include abrupt onset of diarrhea, fever , lower abdominal pain , and dehydration and electrolyte depletion associated with diarrhea . In mild forms, mushy-liquid diarrhea occurs, in more severe cases life-threatening inflammation and swelling of the entire large intestine (toxic megacolon), intestinal perforations or blood poisoning (sepsis) can occur.
It is important for the doctor to distinguish Clostridium difficile from other potential pathogens. Risk factors such as age, immunosuppression , taking antibiotics, proton pump inhibitors or anti- inflammatory drugs serve as important indicators. Together with microbiological tests and the detection of specific toxins produced by C. difficile, they can confirm a diagnosis.
The toxins are two of the main virulence factors of C. difficile: TcdA (toxin A) and TcdB (toxin B). These are largely responsible for the damage to the intestinal tissue, although there are strains that do not produce toxin A and can still lead to severe disease progression. Studies have also shown that toxin B is the more relevant factor and that toxin A supports its effect.
Both toxins can penetrate into the epithelial cells of the intestine, where they change both important structural proteins (actins) and signaling pathways within the cell (various GTPases involved in the organization of the actin skeleton). As a result, the cells lose their original shape (change in cell morphology) and important intercellular connections (tight junctions) can be destroyed. This leads to cell death ( apoptosis ), leakage of fluid and allows toxins or pathogens to penetrate deeper tissue layers and further damage the mucosa . The damaged cells form along with cells of the immune system and fibrinsthe typical pseudomembrane, which can be used in endoscopic diagnostics as a sufficiently clear identification of a C. difficile infection.
Hello! I am Lisa Newlon, and I am a medical writer and researcher with over 10 years of experience in the healthcare industry. I have a Master’s degree in Medicine, and my deep understanding of medical terminology, practices, and procedures has made me a trusted source of information in the medical world.