Clostridium Difficile

Clostridium difficile infection or CDI is a disease that is caused from a severe mishap of the microbiota in the gut by antibiotics. This causes the patient to have persistent diarrheal problems from mild symptoms to very extreme and severe symptoms. In the past twenty years, this infection has been on the rise in numbers of problems in public health and has even caused a number of deaths. Although this is not the only infection the transplant can help conquer, C.difficile a great example to portray since in the past ten years it has become a growing health problem.

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).

This paper will mainly explain what Clostridium difficile is, its causal agent, epidemiology, ways of transmission, some clinical features, diagnoses and how to test for the bacterium, treatment, prognosis, and preventative measures. There are treatments available for this

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.

Many Americans die each year from complications connected to Clostridium difficile. It can ill a significant number of individuals as well as animals. The Clostridium difficile infection is the result of poor hygiene, misuse, overuse of antibiotics and an aging population. In this paper I will be discussing the following topics, what clostridium difficile means, what it causes, signs and symptoms, complications, treatment and the prevention.

Clostridium difficile is a gram-positive, spore-forming, anaerobic bacillus. Since the turn of the 21st century, there has been a dramatic increase in the number of nosocomial infections associated with antibiotic exposure and an increase in the severity of the disease. Challenges of disease containment include emerging risk factors and recurrence. In 2008 the acute care costs, not including the economic burden placed outside of the hospital, was estimated to be around $4.8 billion in the US. As such, it has become clear that preventative measures are needed to monitor and reduce the risk of infection and recurrence.

Clostridium difficile, also known as C. diff, is a bacterium that causes severe symptoms, including inflammation of the colon, which can be life threatening (Centers for Disease Control and Prevention, 2015). It is a very common infection that affects hundreds of thousands in the United States alone. If not caught and treated early, it can be deadly. I kills thousands of people in the United States every year (Mayo Clinic Staff, 2017). It is extremely important to learn the signs and symptoms of this infection so treatment can begin as early as possible.

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?

The healthcare professional can expect to encounter various conditions within their scope of experience. Clostridium difficile represents one of the most common and challenging nosocomial infections that can cause life-threatening complications such as hypervolemia, sepsis, pain, and peritonitis (Grossman and Mager 155). The recognition, diagnosis, treatment and inhibition of transmission of this bacterium are imperative in order to limit infection and prevent death.

Ample literature has been published to elucidate the pervasive nature of Clostridium difficile and its relationship with inadequate health-care practices. Clostridium difficile-associated disease: New challenges from an established pathogen by Sunshine and McDonald, published in the Cleveland Clinic Journal of Medicine discusses the concern over Clostridium difficile. It includes a case report involving infection caused by the bacterium and important guidelines for prevention and treatment associated with the bacterium.

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, a nosocomial pathogen, is of critical importance. By 2010 it was the most prevalent healthcare-related pathogen globally [1], accounting for 20-30% of antibiotic-associated diarrheal cases in healthcare settings [2]. Symptoms of C. difficile infection (CDI) are significant and include severe diarrhea and dehydration. In more serious cases, CDI can result in pseudomembranous colitis, bowel perforation, sepsis and even death [3, 4].Beyond serious impact upon patients, CDI is costing multiple billions of dollars in hospital care in the United States alone [5]. Clearly the need exists to identify and characterize the infection and toxicity pathways of C. difficile.

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

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).