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== Prevalence ==
== Prevalence ==
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C. Difficile is commonly a nosocomial pathogen found in a hospital or similar healthcare facility. Colonization rate of healthy adults is estimated to be 2% while the prevalence of hospitalized adults can be high as 40%. Nearly a third of all C. Difficile infections are community acquired which suggests a recent increase in non-nosocmial infections. Risk factors for the disease are: prolonged antibiotic use (>2 months), advanced age (>65), hospitalization, and residency in a long-term care facility. Prolonged antibiotic exposure is considered the most significant risk factor at this time. Several recent studies have identified patients taking proton pump inhibitors (PPI) are much more susceptible to colonization than those who are not. Asseri et al found patients taking PPIs were 3.6 times more likely to acquire a C. Difficile infection than those who were not. Although, some researchers theorize that acid suppression is not responsible for increased infection rate, but is a marker of other co-morbidities that increase risk of C. Difficile infection (CDI). <br> As noted earlier prolonged antibiotic use and advanced age are two significant risk factors for CDI. Though prolonged antibiotic use seems to be most significant for initial infection, patients with advanced aged are most susceptible for disease reoccurrence. This increased infection and reoccurrence rate in the elderly is likely due to ineffective immune responses as well as insufficient recovery of commensal microbiota following treatment with anti-CDI antibiotics. Recurrent CDI typically occurs shortly after cessation of anit-CDI antibiotic pharmaceuticals with a reappearance of symptoms within 14-45 days. Reoccurance following anti-biotic therapy is primarily contributed to persistent alteration in gut flora of the patient. The causative strain of the CDI reoccurrence is molecularly identical to the original strain in many patients. First time reoccurrence rates have been documented as 33% and infection following previous reoccurrence as high as 45%.<br> A trend of increasing CDI rates was reported throughout the United States in the early 2000’s. Various studies aimed to identify the cause of this significant increase in infection rate and were able to identify particularly strains that were associated with higher rates of infection. Specifically, BI/NAP1/027 strain was identified as a strain primarily responsible for the increased infection rate. This particular strain exhibited an increased resistance to antibiotics used to treat CDI and produced more than twenties times more toxin than historical strains. This strain is also associated with infection of people not previously considered at risk including young, seemingly healthy individuals not exposed to a healthcare environment or prolonged antibiotic treatment. There is also an increased mortality rate in patients infected with BI/NAP1/027 when compared to traditional strains, especially in people 60-90 years old.<br>
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== Characteristics/Clinical Presentation ==
== Characteristics/Clinical Presentation ==
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Manifestations of CDI range from symptomless carriage, to mild-moderate diarrhea, to fatal pseudomembranous colitis. Fever, cramping, abdominal discomfort, and peripheral leukcytosis are common though found in less than half of patients with CDI. The passage of musucs, melena, or hematochezia are rare. Non-GI related symptoms such as arthritis and bacteremia have very rarely been reported in the literature. Patients who have undergone a complete colectomy have been reported to develop C. Difficile ileitis or puchitis in rare instances. Severe CDI can cause: dehydration, electrolyte disturbances, hypoalbuminemia, toxic megacolon, bowel perforation, hypotension, renal failure, sepsis, clonic ileus, toxic dilatation, systemic inflammatory response syndrome, and death. Patients presenting with unexplained leukocytosis should alarm the clinician and prompt them to request stool samples sent for diagnostic testing.
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== Associated Co-morbidities ==
== Associated Co-morbidities ==
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Co-morbidities such as cancer, old age, and renal disease were significantly correlated with a higher rate of mortality from CDI in an English Cohort study of over 2,000 people . Other significant risk factors mentioned in previous sections including: inflammatory bowel disease, immunocompromise, chemotherapy, abdominal surgery, gastrointestinal procedure, previous C. Difficile infection.
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== Medications ==
== Medications ==
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- Vancomycin (Glycopeptide Antibiotics)<br>-Metroidazole (Nirtoimidazole Antibiotic)<br>- Rifamimin (Antimicrobial)<br>-Probiotics<br>-Immunosuppressants<br>
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== Diagnostic Tests/Lab Tests/Lab Values ==
== Diagnostic Tests/Lab Tests/Lab Values ==
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For definitive diagnosis a stool sample must be collected and tested for the antigen glutamate dehydrogenase (GDH). Testing for this antigen can be completed several different ways and is commonly done so via enzyme-linked immunisirbent assay (ELISA) or immunochromatographic assay. GD functions as cell-wall protein produced by the C. Difficile bacteria in considerably higher amounts than toxins. If GDH, TcdA, and TcdB are all present the physician can definitively diagnose the patient with CDI. There are a number of different tests used for identification of these markers, all of which have varying levels of psychometric properties. If all three markers are not present subsequent tests will be performed that are more specific to the missing markers before CDI is ruled out by the physician. Other tests occasionally used are sigmoidoscopy and colonoscopy. These tests are not frequently used because only ~50% of CDIs have visible pseudomembrane formation. Thickening of the colon wall and pericolonic stranding are sometimes evident on radiographs and referred to as “accordion sign” and or “double-halo sign.”
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== Etiology/Causes ==
== Etiology/Causes ==
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== Differential Diagnosis
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== Differential Diagnosis
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<div> Diarrhea is defined as an abnormal increase in stool frequency and liquidity. This can be accompanied by incontinence, urgency, and perineal discomfort. There are numerous causes of diarrhea including: food, alcohol, use of laxativies, pharmaceutical side effects, and travel. When an acute episode of diarrhea is associated with fever, cramps, and blood or pus in the stool can be indicative of an invasive enteric infection. Chronic diarrhea associated with weight loss and nigh pain may be indicative of a neoplasm or inflammatory bowel disease. Extraintestinal symptoms such as arthritis as well as lesions to the skin and eye are also commonly present in inflammatory bowel disease. <br> A more comprehensive list of potential causes of diarrhea and potential differential diagnoses include: pancreatitis, pancreatic carcinoma, Crohn’s disease, Irritable bowel syndrome, diabetic enteropathy, hyperthyroidism, caffeine, incomplete obstruction, fecal impaction, muscular incompetency, ileal bypass, viral infection, bacterial infection, parasitic infection, protozoal infection (Giardia), ulcerative colitis, diverticulitis, food allergy, creatine use, chemotherapy, lactose intolerance, psychogenic (nervous tension). A thorough assessment of patients history, signs, symptoms, risk factors, and lab tests are necessary for an accurate diagnosis. <br><br></div>
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== Case Reports/ Case Studies ==
== Case Reports/ Case Studies ==
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A. Loshkajian. Pseudomembranous Colitis. Available at: http://www.eurorad.org/eurorad/
case
.php?id=1368. Accessed March, 17, 2014<br>Pron B, Merckx J, Gaillard J, et al. Chronic septic arthritis and osteomyelitis in a prosthetic knee joint due to Clostridium difficile. European Journal Of Clinical Microbiology & Infectious Diseases: Official Publication Of The European Society Of Clinical Microbiology [serial online]. July 1995;14
(
7):599-601. Available from: MEDLINE, Ipswich, MA. Accessed March 12, 2014.<br>
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Bermejo C, Maseda E, Salgado P, Gabilondo G, Gilsanz F. [Septic shock due to a community acquired Clostridium difficile infection. A
case
study and a review of
the
literature.]. Revista Espanola De Anestesiologia Y Reanimacion
[
serial online]. June 1, 2013;Available from: MEDLINE, Ipswich, MA. Accessed March 12, 2014.<br>
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Leonard A, Ho K, Flexman J. Proton pump inhibitors and diarrhoea related to Clostridium difficile infection in hospitalised patients
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a
case
-control
study
. Internal Medicine Journal [serial online
]
. May 2012;42(5):591-594. Available from: Academic Search Premier, Ipswich, MA. Accessed March 12, 2014.<br>
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De Almeida M, Heffernan H, Roberts S, et al. Severe Clostridium difficile infection in New Zealand associated with an emerging strain, PCR-ribotype 244. The New Zealand Medical Journal [serial online
]
. August 16, 2013;126(1380
)
:9-14. Available from: MEDLINE, Ipswich, MA. Accessed March 12, 2014.<br>
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== Resources <br> ==
== Resources <br> ==
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http://www.cdc.gov/HAI/organisms/cdiff/Cdiff_infect.html
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http://www.apic.org/Professional-Practice/CDIresources
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http://www.in.gov/isdh/files/CDI_ResourceManual.pdf<br><br>
== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed]) ==
== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed]) ==
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== References ==
== References ==
see [[Adding References|adding references tutorial]].
see [[Adding References|adding references tutorial]].
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ref name="Cohen">Cohen S, Gerding D, Wilcox M, et al. Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA). Infection Control & Hospital Epidemiology [serial online]. May 2010;31(5):431-455. Available from: CINAHL, Ipswich, MA. Accessed March 12, 2014.<
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[[Category:Bellarmine_Student_Project]]
[[Category:Bellarmine_Student_Project]]