The Mucosal Epithelial Cell Lab Report

Clostridium difficile associated disease will resolve when the patient discontinues taking the antibiotics to which he/she has been previously exposed (Nipa, 2010). Administration of a different antibiotic is used to treat the infection (Grossman, 2010). The infection can usually be treated with an appropriate course of about 10 days of antibiotics including metronidazole or vancomycin administered orally (Nipa, 2010). On occasion intravenous vancomycin may be necessary (Gould, 2010). The nurse should ensure patients are not only taking the newly prescribed antibiotic, but also responding to the treatment by showing a decrease in symptoms. Symptoms can recur despite antibiotic therapy, close monitoring is essential. In order to avoid risk of further complications, nursing interventions would include careful assessment of white blood cell count, temperature, and hydration status; meticulous skin care and assistance with bowel elimination given the loose frequent stools; and management of abdominal discomfort (Grossman, 2010).

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 (C-Diff) is considered one of the most common infections a patient can acquire within their hospital stay. It is estimated that C-Diff is responsible for 337,000 infections and 14,000 deaths a year (Centers for Disease Control and Prevention, 2012). Working in the emergency department (ED), I have witness first hand how debilitating this gastrointestinal infection can be. Patients are admitted to the ED for having severe watery diarrhea, abdominal pain, and fever. Elderly patients are at increase risk for sepsis and dehydration related to recurrent infections. Appropriate management and education of C-Diff is optimal for patient survival and decrease contamination across lifespan.

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).

C. difficile is a spore-forming and strict anaerobe gram-positive bacillus [4], capable of excreting pathogenic toxins, as discussed below [3]. This spore forming ability is a method of bacterial persistence within the human body. C. difficile is able to resist and survive a variable environment when various other microbes cannot. Three important factors affecting the risk of CDI include the use of antibiotics, length of hospital-environment exposure and age [1]. The use of broad range antibiotics affects the composition and lively-hood of normal

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

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

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

Clostridium difficile, or C. difficile for short, are words that every healthcare worker hates to hear that their patient has, or may potentially have. This spore forming bacterium has significant healthcare-associated infection potential. An especially virulent strain has affected health care facilities throughout the U.S. and North America in the past few years. What C. difficile is, its symptoms, how it is transmitted, and the prevention transmission are important issues to all healthcare workers. These questions and issues will be covered in this paper.

In patients with C. difficle should have a separate room and with other patients. Those to come in contact with patients should take precaution like wearing disposable gloves and isolation gowns

Clostridium difficile is a Gram-positive anaerobe bacteria meaning it does not have the ability to grow in the presence of oxygen. There are two different exotoxins produced by the organism Clostridium difficile, toxin A and toxin B. The organism produces spores which are the contagious particles of the bacterium. These spores are found all over our environment and in feces of both animals and humans. It is very hard to annihilate these spores due to them being resistant to alcohol, disinfectants, heat and radiation (Awad, 2014). Infection by C. difficile occurs through the fecal-oral route during ingestion of spores. As these spores pass through the gastrointestinal system, bile acids and other substances stimulate their germination. Toxins may be produced depending on the microflora that exists in the gastrointestinal tract. Colonization and proliferation, which are likely to involve numerous surface structures and adhesions, primarily occur in the suitably anaerobic

In the United States, Clostridim difficile has cost the healthcare system possible more than 1 billion dollars annually, and in developing countries it is the leading cause of illness that occurred in hospitals; with cases that have C. difficile link to it is estimated to cause over 3600 dollars in health care fees (Heinlen and Ballard, 2010). According to data that was reported by Center for Disease Control and Prevention, C. difficile start from a low of 31 cases out of 100,000 people per yer in 1996 to an increase in 2003 with 61cases out of 100,000 people per year (Heinlen and Ballard, 2010). In the United States alone, it have been estimated that 500,000 cases have occurred per year (Heinlen and Ballard, 2010). C. difficile infections (CDI) have also increased by 25% with an estimate of 15,000- 20,000 people die per year in

The rate of costridium difficile infection has increased in both hospital and community settings during the last two decades. The main caused of C. difficle is inappropriate use of antibiotic usage. Doctors are prescribing antibiotics for virus related SXS and environmental factors. The first step to treating C. difficile is stop taking the antibiotic that triggered the infection. For severe and recurrent cases Doctors usually prescribe Vancomycin according to the CDC. This antibiotic is gradually tapered dose given once every few days. If the antibiotic does not work and C. difficle caused damage to organs and interfere with electrolyte balance than surgery can be done to remove the part of the intestine that is damaged. Another way to treat

The use of C. difficile phages as a treatment for CDI would involve orally giving patients a C. difficile specific phage preparation. The phages would attach to the receptors on the C. difficile cells, and following the phage DNA entering the cell, would undergo replication and ultimately lyse the bacterial cell, releasing phage virions to infect surrounding C. difficile cells. This infection and lysis process would be repeated until all the C. difficile cells are killed and the infection is cleared. Phage therapy offers select advantages over existing antibiotic treatments. They include the specific nature of the phage–bacterial interaction, which would avoid exacerbating the gut dysbiosis (disruption of gut microbiota) that can be associated

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).