Sodium Difficile Research Paper

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).

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

Clostridium difficile is a spore forming, anaerobic, toxin-producing, gram-positive bacillus that is the most common cause of nosocomial, antibiotic-associated diarrhea (15-25%).1,2,3 The pathogenesis of C. difficile-associated diarrhea (CDAD) is the result of broad spectrum antibiotics, such as clindamycin, flouroquinolones or ceftriaxone, which reduces the population of normal bowel flora and allowing for an overgrowth of C. difficile.1,2 The toxins synthesized by C. difficile, A and B, lead to the inflammation and damage of the intestinal mucosa creating the symptoms of C. difficile infection (CDI). These symptoms can range from asymptomatic carriers, to mild diarrhea to sudden and occasionally deadly colitis. The clinical practice guidelines for the treatment of CDAD recommends the use of metronidazole (MET) and vancomycin (VAN) that is dependent upon the severity of the CDI.1,2,3

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

Clostridium difficile involves a gram-positive spore-forming bacterium, which is a normal element of the colon flora in people. The Clostridium difficile can cause antibiotic-associated diarrhea when the competing bacteria in the gut flora are all killed by antibiotic treatment. The Clostridium difficile infection is one of the serious healthcare-related infection and also a rising health care problem. In the early 1970s, the Clostridium difficile has been known to have the ability to cause pseudomembranous colitis. As stated, the infection is the most cause of nosocomial infectious diarrhea (Aktories & Wilkins, 2000). Individuals that are colonized with clostridium difficile serve as the reservoir for infection and this is by contaminating the environment with spores of such bacteria. This will lead to the spread of the organism on the health care worker’s hands or even through the use of medical equipment. In this paper, we are going to focus on the effective prevention strategies for clostridium difficile. What are the effective prevention strategies for clostridium difficile?

difficile lies within the 19.6 kb pathogenicity locus (PaLoc) and codes for two major virulence factors and three accessory proteins [9]. 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 [10]. Both catalyze the inactivation of Rho-GTPases, which are essential for the regulation of eukaryotic cell cytoskeleton [9]. The inactivation of Rho-GTPases causes cell death via cytoskeletal disorganization [9]. 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

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).

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

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 (C. diff) is a type of bacterium that can cause a person to endure diarrhea like symptoms to more drastic symptoms that may involve inflammation of the colon. Most people who come across C. diff are expected to be in a hospital setting for an extensive period of time. It is more accessible to acquire C. diff when a person is of old age, in a hospital setting, and taking antibiotic medication (Mayo Clinic, 2016). Normally, one would think that taking antibiotics would not cause any harm to the body, but would instead help the body fight off diseases. However, once a person who has been taking antibiotics for a long period of time stops taking them, such as in a nursing home or hospital setting, that person can develop some reactions in the absence of those antibiotics (Bartlett, 2012). This reaction, then allows the person to experience diarrhea symptoms, which lead to inflammation of the colon and more drastic colon problems.

“Clostridium difficile is a gram positive, spore forming anaerobic bacillus, which may or may not carry the genes for toxin A-B production” (Patel 102). In the 1930’s, Hall and O’Toole

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 infection is a suprainfection cause by prolong use of antibiotics. Board spectrum antibiotic such as Penicillins, clindamycin, and cephalosporins are the antimicrobial drugs most commonly associated with C difficile colitis. According to Owens, in his research, C. difficile is primarily acquired in hospitals. Spread by spores, it can colonize a patient’s gut after helpful gut bacteria are killed by antibiotics. Its toxins can cause severe diarrhea and colitis, and it can be fatal (Owens 2013). On the other hand Kim in his research agreed clostridium difficile infection has been considered a hospital-acquired infection. However, a recent population-based study found 41% of CDIs were actually community acquired. It is becoming apparent that community acquired CDI affects populations previously thought to be at low risk; younger patients and patients who had no exposure to antibiotics in the 12 weeks before the infection. Thus, it is necessary to advocate and teach patient about

Each year in the United States, many people require hospitalization due to various medical reasons. Often times, patients must undergo a course of antibiotics to treat the medical condition that warranted the hospitalization. The combination of the necessity to be admitted to a health care facility along with the administration of an antibiotic may result in a Clostridium difficile infection (CDI). The purpose of this paper is to provide an overview of a CDI, including an overview of the microbiology of Clostridium Difficile (C- diff), as well as the epidemiology, pathophysiology, signs, symptoms, treatment and prevention of the infection.

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).