Clostridium difficile (C. difficile) is an anaerobic, Gram-positive, bacillus-shaped bacterium that causes the disease Clostridium Difficile Infection (CDI). One of the reasons this particular species is so successful and disease-causing is because it possesses the ability to form spores, which makes it very difficult to eradicate, as these spores are able to survive extreme conditions. C. difficile flourishes in the gastrointestinal tracts of individuals who have been prescribed broad spectrum antibiotics, as these tend to disrupt the normal microbiota. If an individual has previously contracted CDI, the likelihood of future infection(s) is more likely than if it were never contracted, at a rate of ~35%. The aim of this study, which is actually the first of its kind, is to utilize the probiotic Lactobacillus casei Shirota (L. casei Shirota) to attempt to suppress the recurrence of CDI after an initial infection. Probiotics contain a live strain(s) of “healthy” bacteria that help rather than harm an individual, and they work by competing with C. difficile’s
Clostridium difficile is a Gram-positive, spore-forming, rod-shaped bacillus that is renowned for being the leading cause of hospital-acquired diarrhea in adult patients. C. difficile is present as normal intestinal flora within 3% to 5% of healthy people2, while its spores are ubiquitous in the environment, especially in hospital settings. It grows at an optimal temperature and pH of 37ºC and 6.5–7.5 respectively.1 It is an obligate anaerobic as it thrives in the absence of oxygen. It is highly motile with the presence of peritrichous flagella, which are evenly spread out along its surface. As briefly mentioned above, this evolving pathogen produces endospores. The bacterium produces dormant spores, which are extremely hardy and resistant to antibiotics, the host’s innate immune system, and once shed into the environment through the host’s feces, they are resistant to unfavorable aerobic conditions3 as well as several types of bleach-free disinfectants, which are commonly used in hospitals.3 The spores will germinate under the favorable conditions of the intestinal tract, resulting in the multiplication of vegetative cells, colonizing in the gastrointestinal tract. The vegetative cells release two powerful exotoxins upon adherence to the epithelial cells of the GI tract. Pathogenic strains of C. difficile produce two exotoxins: toxin A and toxin B. Toxin A is an enterotoxin that causes fluid excretion, resulting in fluid accumulation and watery diarrhea. Toxin B is a potent
C-Diff is an anaerobic gram-positive spore forming bacterium, which affects and grows in the gastrointestinal tract after the normal intestinal flora, has been changed by antibiotic therapy or by contact through the fecal- oral route (Kelly & Lamont, 2014). The C-Diff organism, releases two different toxins, toxins A & B. Both toxins are cytotoxic for many different cells. Toxin B is more potent then A, both toxins cause increased vascular permeability by opening tight junctions between cells, which cause hemorrhage, these toxins also stimulate the
Clostridium difficile also known as C-diff is a pathogen. According to Doctor Michelle Wright, It lives harmlessly in the gut of many people. About three in hundred healthy adults and as many as seven in ten healthy babies have a number of c difficile bacteria living in their gut (2015). Healthy people normally have a certain number of c-diff bacterium living in their gut, but this bacterium is usually kept in check by all the other harmless bacteria that lives in our gastrointestinal tract. Clostridium difficile
Clostridium difficile is a gram positive, spore forming anaerobic bacillus, which may or may not carry the genes for toxin A-B production (Nipa, 2010). These two types of protein exotoxins produced by the Clostridium difficile bacillus, toxin A and toxin B, can have an infectious form and a non-active, non-infectious form (Grossman, 2010). The infectious form can survive for a short duration of time in the environment. The spores can survive for a longer period of time in the environment and are not infectious unless and until they are ingested or are transformed into an infectious state (Nipa, 2010).
Ingestion of the endospore causes infection. Once it reaches the preferred anaerobic environment of the gut, the endospores germinate and begin releasing toxins A and B (Burns & Minton 2011). The presence of C. difficile does not necessarily mean infection. A patient can be positive for C. difficile but have normal stool, which means there is colonization without infection. Patients who have the C. difficile pathogen without experiencing any symptoms allow it to be passed along undetected which contributes to the ongoing spread to others. Only when toxin A and toxin B are released at suitable levels does C. difficile become pathogenic to humans. Once infected, typical symptoms include watery diarrhea, abdominal pain, colitis, fever, and fecal leukocytes. Moderate to severe Clostridium difficile infection (CDI) consist of profuse diarrhea, abdominal distention, leukocytosis, systemic inflammatory response, pseudomembranous colitis, megacolon and death (Sunenshine & McDonald, 2006). With the combination of a highly resilient endospores, and asymptomatic carriers, this allows C. difficile to persist in the environment and spread to patients with compromised immune systems, or older patients who have a high risk of contracting CDI with a higher severity than healthy adults (Laffan, Bellantoni, Greenough, Zenilman, 2006).
difficile lies within the 19.6 kb pathogenicity locus (PaLoc) and codes for two major virulence factors and three accessory proteins . Genes tcdA and tcdB encode Toxin A and Toxin B, respectively, the two major virulence factors which are part of the clostridial glucosylating toxin family . Both catalyze the inactivation of Rho-GTPases, which are essential for the regulation of eukaryotic cell cytoskeleton . The inactivation of Rho-GTPases causes cell death via cytoskeletal disorganization . The accessory gene functions are as follows; tcdE as a putative holin protein; tcdD as a positive regulator and tcdC as a negative regulator, both of which are controlling Toxin A and B gene expression
Clostridium difficile is a gram-positive bacterium which causes diarrhoea. It also known as antibiotic associated diarrhoea and also pseudomembranous colitis. The bacterium secretes large protein toxin that also causes toxic mega colon. Clostridium difficile is caused by when a person is given one of the following antibiotics: Cephalosporin, penicillin (particularly Ampicillin or Amoxicillin), Clindamycin and Fluoroquinolone. The antibiotic will remove the entire normal flora in the colon. The lack of normal flora will make the person vulnerable to infection especially to Clostridium difficile because Clostridium difficile produces hardy spores
CDI cannot be treated with many antibiotics, and as early as 2000 another strain appeared that was resistant to even more antibiotics, including fluoroquinolones (“Antibiotic/Antimicrobial Resistance.”). This new strain creates more toxins and can show up in people not normally considered at risk for CDI infection, like those who have not been hospitalized or treated with antibiotics (“C. difficile infection.”). This aggressive strain only adds more danger to an already resistant bacteria. As antibiotics became more common, they were prescribed for thousands of common illnesses. Over time, Clostridium difficile has built up a resistance to antibiotics to become a major concern. Even more frightening, it has started to appear in the community. In fact, the Centers for Disease Control rate it as an urgent threat. Superbugs like CDI are becoming a more ever-present threat and we must continually work towards newer and more effective treatments to counteract the bacterias frightening ability to resist us (“Antibiotic/Antimicrobial Resistance.”). CDI is just one of many superbugs, however, and others pose just as great a
C-Diff is an opportunistic infection, it will affect an individual whose flora in the intestines has been compromised by the treatment of antibiotics for a different infection like pneumonia, MRSA, etc... Antibiotics do not know what bacterial are good and what is bad. They kill all bacteria. This gives the C-Diff spores the opportunity to then take over the flora in the intestine that are being killed by the current regiment of antibiotics. C-Diff affects the flora of the large intestine
Clostridium difficile is a gram positive, anaerobic, spore forming bacillus. In 1935 it was first described as member of the intestinal flora in healthy neonates  , and then in 1978 it was recognised as a cause of diarrhoea . Today it is widely acknowledged as the leading cause of hospital-acquired diarrhoea. This organism can cause a variety of diseases, from mild diarrhoea to severe pseudomembranous colitis, and collectively these are known as C. difficile infections (CDIs) . It is known that the symptoms seen in patients infected with C. difficile are due to the toxins (toxin A and toxin B) that are produced by the organism . Some strains of C. difficile seem to have an increased virulence which can be associated with increased severity, recurrence and increased mortality. This increased virulence is thought to be a result of increased expression of toxins A, B . There is also another toxin produced by C. difficile known as binary toxin, this is also thought to contribute towards increased virulence . A particular strain of C. difficile that does seem to have increased virulence is the strain known as PCR ribotype O27 or North American pulsed (NAP)-field type 01. In Europe PCR ribotype O27 is the sixth most common ribotype , and new ribotypes are being detected that appear to have evolved from the O27 lineage , making the need for a method to demonstrate strain relatedness highly important. In a hospital setting knowing the
The presence of C. difficile in the bacterial flora of human gut normally causes no harm. C. difficile represents a problem when overgrows due to the used of antibiotics, which destroy the normal flora that held C. difficile in balance. This makes C. difficile grow faster and colonizing the human colon. When colonization occurs, the toxins from C. difficile cause diarrhea and life-threatening colitis (Nazarko, 2015, p. 21).
Clostridium difficile colitis or another name pseudomembranous colitis is colitis. That mean colitis is inflammation of the large intestine and the cause infection with Clostridium difficile bacteria. Clostridium difficile bacteria is type of microorganisms normal flora in intestinal is harmless or even beneficial under normal circumstances. But when occur defect in balance of organisms in the intestines, the bacteria can be detrimental and can grow out of control and cause infection from through realase toxins that attack the lining of the intestines., causing a condition called Clostridium difficile colitis. Taxonomy of Clostridium difficile bacteria is phylum firmicutes, class clostridia, order clostridiales. Family clostridiaceae, genus clostridium. Historical synonym: Bacillus difficile.
Most of the public have heard of broad-spectrum drugs, especially in terms of antibiotic resistance, because they fight a wide range of bacteria but also kills normal flora in the gut (Haddox, 2013). The loss of this gut flora can lead to an abnormal growth of harmful bacteria such as clostridium difficile (C-Diff). The four “C” antibiotics that have a high risk for patient to develop C-diff are clindamycin, cephalosporins, coamoxiclav, and ciprofloxacin (Haddox, 2013). These antibiotics have the highest risk of leading to C-diff development, however all antibiotics increase a patient’s likelihood of a C-diff infection. This effect can last up to 12 weeks post antibiotic administration (Haddox, 2013).