Clostridium Difficile Is A Gram Positive

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 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).

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 (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.

761). Since the nutrients in the intestines are available due to the good bacteria being destroyed, Clostridium difficile uses the nutrients to multiply and releases the toxins , which attack the lining of the intestines, thus causing colitis (Fordtran, 2006, pp. 3).

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

Clostridium difficile is a gram-positive spore-forming bacteria; first isolated and published in 1935 by Hall and O’Toole. This was accomplished from the stool of a healthy infant. However, it was not until 1978 that C. difficile was identified as being associated with many cases of antibiotic-resistant diarrhea.1 C. difficile has since become one of the leading causes of nosocomial infections in the United States. A study conducted in 2015 has estimated that C. difficile infection has an incident of 453,000 (95% confidence interval) in the United States.2 This has placed a tremendous burden on the US healthcare system. According to data from 2008, C. difficile infections have accumulated an excess cost of $4.8 billion to the US healthcare system.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).