Clostridium difficile case report

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A 76-Year-Old Man With Recurrent Clostridium difficile–Associated Diarrhea :

A 76-Year-Old Man With Recurrent Clostridium difficile– Associated Diarrhea Done by: Hassan Mohammed Abu Helal Supervised by : Dr. Abdelraouf El Manama

Case History:

Case History Mr S is a 76-year-old man with hypertension , hypertensive renal disease with cadaveric renal transplantation in 1988 . again in 1998, spinal stenosis , urinary retention due to the spinal stenosis and to benign prostatic hypertrophy (treated with an indwelling Foley catheter), recurrent Clostridium difficile infection .

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current illness began when he was admitted to the hospital with a urinary tract infection. He received ceftriaxone and ciprofloxacin. after discharge, he developed diarrhea . After several weeks of diarrhea, his nephrologist treated him empirically for CDI with a 10-day course of metronidazole ; he improved and his stools initially became formed.

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about a month after discharge , he was still having 4 to 5 loose stools daily along with poor appetite, weight loss, fever, chills, and weakness. He was readmitted to the hospital and a stool sample was found to be positive for C difficile toxin. He was placed on contact precautions and treated with oral vancomycin and again improved , but again relapsed and was treated with a long (6-8 weeks) course of oral vancomycin followed by a tapering dose.

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Four days after stopping the oral vancomycin , Mr. S again began experiencing diarrhea . In the ensuing months, he had several hospitalizations for diarrhea. he also had another urinary tract infection and was treated first with cefpodoxime and then with ciprofloxacin.

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Mr. S also has arthritis of his left shoulder with severe shoulder pain, and he is mostly confined to a wheelchair. Further evaluation of his urinary problems during his recent hospitalization revealed a neurogenic bladder thought to be due to his spinal stenosis .

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Mr. S's medications include prednisone, 4 mg daily; cyclosporine, 50 mg daily; and diltiazem , trazodone , atenolol , minoxidil , furosemide , long-acting nitrates, finasteride , and erythropoietin, along with the standing vancomycin and rifaximin . He does not smoke and he drinks only 1 alcoholic beverage per month.

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His stool studies were positive for C difficile toxin A during his initial hospitalization for diarrhea; subsequent samples obtained when symptoms have recurred have been negative. Mr S's most recent urine culture showed resolution of a previous Pseudomonas infection.

Disease Pathogenesis :

Disease Pathogenesis Clostridium difficile is a gram-positive , spore-forming , anaerobic bacillus first isolated in 1935 from the stool of a healthy neonate. The species was named “difficile” because initially it was hard to culture . Clostridium difficile infection is now by far the most common known cause of infectious diarrhea in hospital patients in North America and Europe. the incidence and severity of disease have increased alarmingly since 2000.

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only 1% to 4% of healthy adults carry this organism. Neonates , lacking an established intestinal microflora , frequently have C difficile colonization but, interestingly, seldom experience C difficile toxin–induced diarrhea or colitis, possibly because of a lack of toxin receptor expression in the immature gut. In adults , loss of colonization resistance to CDI is most often the result of antimicrobial therapy.

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All antimicrobials are not equal in this regard . The ability of clindamycin to impair colonization resistance and induce CDI is well known. However, in current medical practice, second- and third-generation cephalosporins and fluoroquinolones are more frequently used to treat infections in hospital patients and, as in the case of Mr S, most frequently cause CDI.

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It is important to be aware that disease onset can be delayed for 2 or, in rare cases, even 3 months, as these late presentations can lead to misdiagnosis. Although the majority of CDI results from antimicrobial use , other events may impair colonization resistance, including: * bowel preparation for colonoscopy or surgery, * cytotoxic chemotherapy, * colitis caused by inflammatory bowel disease.

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Pathogenic strains of C. difficile produce 2 large protein exotoxins , toxin A and toxin B. They are antigenically distinct . Hence, enzyme immunoassays (EIAs) directed against one toxin cannot recognize the other. Commonly used tests that detected toxin A by EIA yielded false-negative results in a majority of patients in those outbreaks. Most, but not all, currently used EIAs detect both toxins.

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Clostridium difficile infection caused by toxin A–negative, toxin B–positive strains has dispelled the long-held belief that intestinal disease is caused by toxin A alone. In fact, both toxins are highly injurious to the human colon, causing enterocyte cell death , a marked acute inflammatory response, and severe mucosal injury .

Pathogenesis of Clostridium difficile Infection.:

Pathogenesis of Clostridium difficile Infection.

Epidemiology and Risk Factors :

Epidemiology and Risk Factors The risk of developing CDI as a complication of antimicrobial use depends on 3 groups of factors: (1) impairment of colonization resistance, as already discussed; (2) risk of exposure to toxigenic C difficile or its spores; and (3) host health and immune status. Mr S developed CDI after his hospitalization for a urinary tract infection.

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The risk of developing CDI during or after antimicrobial use in the hospital is far greater than after the use of the same agents in the community. In community-based studies , CDI complicated fewer than 1 in 5000 antimicrobial prescriptions, leading to 7.6 CDI cases per 100 000 person-years. In contrast, CDI complicates 0.5% to 1% of hospital admissions.

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The environment of hospitals and other health care facilities is contaminated by C difficile spores. These spores are resistant to drying, temperature fluxes, and many antiseptic solutions, yet remain viable for long periods in the environment and cause CDI when ingested. Advancing age as well as acute and comorbid diseases are prominent risk factors for CDI and, as in Mr S's case, the disorder disproportionately affects older and frail patients.

Host factors that increase susceptibility to C difficile –associated diarrhea :

Host factors that increase susceptibility to C difficile –associated diarrhea Age greater than 65 years Chronic debilitation or critical illness Alteration in gut motility (1) Agents that affect the bowel, including enemas, stool softeners, and opioids , are identified as risk factors for disease development. (2) Patients who have undergone abdominal surgery with subsequent ileus are also at increased risk.

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Receipt of enteral tube feeds. Use of proton-pump inhibitors (These may increase the rate of successful colonization after ingestion.) Cancer chemotherapeutic agents are associated with an increased risk of C difficile disease. This may be due to the antimicrobial activity of some of these agents or due to impaired immunity with neutropenia . Impaired humoral immunity (especially of the IgG subclasses) may increase the susceptibility to relapsing disease. HIV infection : C difficile infection has become one of the most common causes of infectious diarrhea in persons with HIV.

Risk Factors for Clostridium difficile–Associated Diarrhea: :

Risk Factors for Clostridium difficile–Associated Diarrhea: Admission to intensive care unit Advanced age Antibiotic therapy Immunosuppressive therapy Multiple and severe underlying diseases Placement of a nasogastric tube Prolonged hospital stay Recent surgical procedure Residing in a nursing home Sharing a hospital room with a C. difficile–infected patient Use of antacids

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According to the US National Hospital Discharge Survey , 31 CDI-associated hospitalizations were reported per 100 000 population in 1996 compared with 61 per 100 000 in 2003 and 84 per 100 000 in 2005 (the latest year for which data are available). This represents an approximate 25% annual increase each year since 2000.

Clinical Presentation :

Clinical Presentation Diarrhea is usually fairly mild, with 3-6 stools per day. However, severe cases may have more than 20 stools per day. Leukocytosis is found in 50-60% of patients. Fever affects 30-50% of patients. Abdominal pain or cramping affects 20-33% of patients and may have various presentations.

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Other common findings include nausea , malaise , and anorexia . Severe disease may lead to electrolyte disturbances, dehydration, hypotension, renal failure, sepsis, and death. Constipation with or without dyspepsia is an atypical presentation, occurring in less than 1% of cases . Colitis can be present without accompanying diarrhea, particularly in patients with right-sided colonic involvement. Toxic megacolon can complicate severe infection and can lead to bowel perforation. Extraintestinal manifestations are rare and include the following: Bacteremia , generally polymicrobial Splenic abscess Osteomyelitis Reactive arthritis or tenosynovitis

Pseudomembranous Colitis Differential Diagnoses :

Pseudomembranous Colitis Differential Diagnoses Amebiasis . Campylobacter infection. Crohn’s disease. Cryptosporidiosis. Diverticulitis. Dumping syndrome. Food poisoning. Gastroenteritis. Ileus . Vibrio infection. Inflammatory bowel dz. Intra-abdominal sepsis. Irritable bowel syndrome. Ischemic colitis. L. monocytogenes . Megacolon (toxic). Salmonellosis . Shigellosis. Typhoid fever. Ulcerative colitis.

Diagnosis :

Diagnosis confirmation of CDI should be obtained by demonstrating the presence of C difficile or its toxins in a stool sample. Most clinical laboratories use EIA to detect toxin A and toxin B. these assays have the advantages of being relatively quick and easy to perform so that same-day results are feasible.

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However, they are often insensitive (66% sensitivity in 1 study), leading to frequent false-negative results. Hence, negative test results do not override a strong clinical suspicion for CDI, as in the case of Mr S, who had several negative stool test results after initial treatment.

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More accurate stool assays are available, including the tissue culture cytotoxicity assay , often used as a gold standard test, that identifies toxin effects at a cellular level using living cells in tissue culture and can detect toxin concentrations that are 100 to 1000 times lower than those detected by EIA. However, these more accurate techniques require greater laboratory resources and personnel training, take longer (24-48 hours) to provide a result, and are more than twice as expensive.

Treatment :

Treatment Treatment of CDI can be stratified according to the severity of illness. Mild CDI in an otherwise healthy individual can be managed by discontinuing the antimicrobial agent responsible for causing the infection, requesting stool testing to confirm CDI, and monitoring the patient's progress.

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Oral metronidazole , 500 mg every 6 hours for 10 to 14 days, is the treatment of choice for moderately severe CDI. In a large randomized controlled trial, the response rate to metronidazole , as determined by resolution of diarrhea at day 10 of therapy, was 77% in mild and moderate CDI.

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Oral vancomycin , 125 mg every 6 hours for 10 to 14 days, is also effective in mild to moderate CDI, with a response rate (82%) similar to metronidazole . Oral vancomycin is the second-line agent in this situation because of greater cost and lingering concerns regarding encouraging vancomycin resistance, especially in a nosocomial setting.

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The indications for using oral vancomycin to treat CDI include : (1) severe disease, (2) metronidazole contraindications or intolerance, (3) inadequate response to metronidazole treatment. Oral vancomycin has been recommended as the optimal first-line treatment for severe CDI for more than 2 decades.

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In 2 randomized controlled trials, individuals with mild to moderate CDI responded similarly to metronidazole compared with vancomycin . However, in severe CDI, both studies demonstrated a significant advantage of vancomycin over metronidazole , with response rates of 97% vs 76%, respectively.

Prevention :

Prevention prudent use of antimicrobials is the first step in risk reduction. Probiotics have been used by antibiotic recipients in an attempt to conserve colonization resistance and avoid both CDI and simple antibiotic-associated diarrhea. Probiotic preparations containing viable lactobacilli or Saccharomyces species taken in conjunction with antimicrobials can halve the incidence of antibiotic-associated diarrhea.

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In health care facilities, barrier precautions should be used for patients with CDI and diarrhea and a single room provided if possible. hand-washing before and after patient contact are essential in reducing infection transmission. In high-risk situations, hand hygiene using soap and running water is preferred to alcohol-based hand cleansers for removing C difficile spores.

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Thank you