• The Journal of the Korea Contents Association
• /
• v.10 no.5
• /
• pp.259-266
• /
• 2010

Clostridium difficile-associated disease (CDAD) is an important nosocomial infectious diarrhea and is associated with antibiotic use. Recently, incidence of C. difficile has been increasing in hospitals. A total of 1,329 stool specimens were examined from January, 2005 to December, 2008. This study analyzed the incidence and clinical characteristics of C. difficile infections on them. Out of 1,329 stool specimens, 283 specimens showed toxin A/B positive, using EIA. The positive rate was 21.2%; with the highest incidence among and above the 70years old. On endoscopy, psedo membranous colitis was found in 57.7%, and 19.5% of patients were normal. Pathologic finding showed PMC in 26.8% of patients, AAC in 52.2%. C. difficile was associated with PMC, however, endoscopic and pathologic findings tests showed normal to PMC.

• Clinical and Experimental Pediatrics
• /
• v.53 no.2
• /
• pp.184-189
• /
• 2010

Purpose : Pseudomembranous colitis (PMC) occurs rarely in children, but its incidences are increasing due to frequent antibiotic use. We investigated the incidence and clinical characteristics of PMC accompanied by bacterial enteritis-like symptoms in children. Methods : Between November 2003 and July 2007 at the Department of Pediatrics, Dongsan Medical Center, we analyzed the medical records of consecutive patients who received antibiotics in the past 1 month, developed bacterial enteritis-like symptoms, and were diagnosed with PMC based on sigmoidoscopy examination and histological findings. Results : Among 22 patients who underwent sigmoidoscopy and biopsy examinations, 11 (50%) were diagnosed with PMC. These 11 patients were aged 2 months-12 years, among whom 5 patients (45.5%) were less than 1 year old. The clinical symptoms were bloody diarrhea (28.6%), abdominal pain or colic (28.6%), watery or mucoid diarrhea (23.8%), vomiting (9.5%), and fever (9.5%). The antibiotics used were penicillins (55.6%), macrolides (27.8%), cephalosporins (11.1%), and aminoglycosides (5.6%). The period of antibiotic use was 3-14 days. The interval between the initial antibiotic exposure and the onset of symptoms was 5-21 days. The results of stool examination of all patients were negative for Clostridium difficile toxin A. Patient distribution according to the degree of PMC was as follows: grade I, 18.2% (2 cases); grade II, 27.3% (3); grade III, 36.4% (4); and grade IV, 18.2% (2). PMC did not recur in any case.Conclusion : PMC is not a rare disease in children. If pediatric patients receiving antibiotics manifest symptoms like bacterial enteritis, PMC should be suspected. Endoscopy and biopsy should be applied as aggressive diagnostic approaches to detect this condition.

• Tuberculosis and Respiratory Diseases
• /
• v.69 no.2
• /
• pp.115-118
• /
• 2010

Paclitaxel has been widely used for treating many solid tumors. Although colonic toxicity is an unusual complication of paclitaxel-based chemotherapy, the reported toxicities include pseudomembranous colitis, neutropenic enterocolitis and on rare occasions ischemic colitis. $Genexol-PM^{(R)}$, which is a recently developed cremophor-free, polymeric micelle-formulated paclitaxel, has shown a more potent antitumor effect because it can increase the usual dose of paclitaxel due to that $Genexol-PM^{(R)}$ does not include the toxic cremophor compound. We report here on a case of a 57-year-old man with advanced non-small cell lung cancer and who developed ischemic colitis after chemotherapy with $Genexol-PM^{(R)}$ and cisplatin. He complained of hematochezia with abdominal pain on the left lower quadrant. Colonoscopy revealed diffuse mucosal hemorrhage and edema from the sigmoid colon to the splenic flexure. After bowel rest, he recovered from his symptoms and the follow-up colonoscopic findings showed that the mucosa was healing. Since then, he was treated with pemetrexed monotherapy instead of a paclitaxel compound and platinum.

• Journal of Microbiology and Biotechnology
• /
• v.24 no.5
• /
• pp.696-703
• /
• 2014

Clostridium difficile causes mucosal damage and diarrhea by releasing two exotoxins: toxin A and toxin B. C. difficile colitis is associated with alterations in bowel flora and the failure to mount an effective antibody response. The aim of the current study was to investigate whether antitoxin sera prevent toxin-A-induced apoptosis, cytoskeletal disaggregation, cell detachment, and tight junction loss in cultured colonic epithelial cells. Serum samples were isolated from mice that survived a C. difficile infection following antibiotic treatment, and the antitoxin effects of these samples were investigated in toxin-A-exposed HT29 colonic epithelial cells and a toxin-A-induced animal model of gut inflammation. Unchallenged mice did not produce IgG against toxin A, whereas serum (antiserum) from C. difficile-challenged mice showed significant IgG responses against toxin A. Treatment with the antiserum markedly inhibited mucosal damage and inflammation in the toxin-A-treated mouse model. In contrast to control mouse serum, the antiserum also markedly inhibited toxin-A-induced DNA fragmentation, dephosphorylation of paxillin and Epo receptor (EpoR), deacetylation of tubulin, and upregulation of p21(WAF1/CIP1) and p53. Taken together, these results reveal that the generated antitoxin serum has biotherapeutic effects in preventing various C. difficile toxin-A-induced cellular toxicities.

• Korean Journal of Clinical Pharmacy
• /
• v.26 no.1
• /
• pp.46-52
• /
• 2016

Background: The use of acid suppressive agents became a standard therapy in an intensive care unit (ICU) to prevent stress related gastrointestinal mucosal damage. However, the risk of infectious diseases has been concerned. Objective: The study was to determine the differences between histamine 2 receptor antagonists (H2RA) and proton pump inhibitors (PPI) in incidence of nosocomial pneumonia and pseudomembranous colitis (PMC) by Clostridium difficile with patients in ICU. Methods: This is a retrospective comparative study including patients admitted to the ICU who were at least 18 years of age and stayed for more than 48hrs from August 1, 2014 to January 31, 2015. The propensity score analysis and propensity matched multivariable logistic regression were used in analyzing data to control for confounders. Results: A total of 155 patients were assessed. H2RA were prescribed in 110 (53.9%) and PPI were in 45 (22.1%). Nosocomial pneumonia developed in 37 (23.9%); 25 (22.7%) were on H2RA and 12 (26.7%) were on PPI. The unadjusted incidence of nosocomial pneumonia was slightly higher in the patients with PPI (odds ratio (OR) 1.24; 95% confidence interval (CI): 0.54-2.71) compared to them with H2A. After adjusting with propensity score, the adjusted OR with PPI was 1.35 (95% CI: 0.44-4.11). The propensity score matched analyses showed similar results. Conclusion: The uses of PPI and H2RA as a stress ulcer prophylaxis agent showed similarity in the incidence of nosocomial pneumonia and PMC.

• Journal of Yeungnam Medical Science
• /
• v.33 no.1
• /
• pp.48-51
• /
• 2016

Milk-alkali syndrome (MAS), a triad of hypercalcemia, metabolic alkalosis, and renal failure, is associated with ingestion of large amounts of calcium and absorbable alkali. MAS is the third most common cause of hypercalcemia in hospital, after primary hyperparathyroidism and malignant neoplasm. MAS is not often reported in the Korean literature. We describe MAS secondary to intake of calcium citrate for the treatment of osteoporosis with thoracic spine compression fracture. A 70-year-old man presented to our hospital with a 1-week history of general weakness and lethargy. He was found with acute kidney injury (serum creatinine, 4.6 mg/dL), hypercalcemia (total calcium, 14.8 mg/dL), and alkalosis. Laboratory evaluation excluded both hyperparathyroidism and malignancy. Mental status and serum calcium level was normalized within a week after proper hydration and intravenous administration of furosemide. However, he developed aspiration pneumonia, pseudomembranous colitis, and sepsis with multi-organ failure. Despite intensive treatment including inotropics, mechanical ventilation, and renal replacement therapy, he expired with no signs of renal recovery on the 28th hospital day.

• Food Science of Animal Resources
• /
• v.41 no.5
• /
• pp.883-893
• /
• 2021

Clostridium difficile present in feces of food animals may contaminate their meats and act as a potential source of C. difficile infection (CDI) to humans. C. difficile resistance to antibiotics, its production of toxins and spores play major roles in the pathogenesis of CDI. This is the first study to evaluate C. difficile prevalence in retail raw animal meats, its antibiotics susceptibilities and toxigenic activities in Al-Jouf, Saudi Arabia. Totally, 240 meat samples were tested. C. difficile was identified by standard microbiological and biochemical methods. Vitek-2 compact system confirmed C. difficile isolates were 15/240 (6.3%). Toxins A/B were not detected by Xpect C. difficile toxin A/B tests. Although all isolates were susceptible to vancomycin and metronidazole, variable degrees of reduced susceptibilities to moxifloxacin, clindamycin or tetracycline antibiotics were detected by Epsilon tests. C. difficile strains with reduced susceptibility to antibiotics should be investigated. Variability between the worldwide reported C. difficile contamination levels could be due to absence of a gold standard procedure for its isolation. Establishment of a unified testing algorithm for C. difficile detection in food products is definitely essential to evaluate the inter-regional variation in its prevalence on national and international levels. Proper use of antimicrobials during animal husbandry is crucial to control the selective drug pressure on C. difficile strains associated with food animals. Investigating the protective or pathogenic potential of non-toxigenic C. difficile strains and the possibility of gene transfer from certain toxigenic/ antibiotics-resistant to non-toxigenic/antibiotics-sensitive strains, respectively, should be worthy of attention.

• Journal of Life Science
• /
• v.28 no.8
• /
• pp.885-891
• /
• 2018

Clostridium difficile (C. difficile) toxin A is known to cause acute gut inflammation in humans and animals by triggering cytoskeletal disorganization in gut epithelial cells. In human colonocytes, toxin A blocks microtubule assembly by directly increasing the enzymatic activity of histone deacetylase-6 (HDAC-6), a tubulin-specific deacetylase, thereby markedly decreasing tubulin acetylation, which is essential for microtubule assembly. Microtubule assembly dysfunction-associated alterations (i.e., toxin A-exposed gut epithelial cells) are believed to trigger barrier dysfunction and gut inflammation downstream. We recently showed that potassium acetate blocked toxin A-induced microtubule disassembly by inhibiting HDAC-6. Herein, we tested whether acetic acid (AA), another small acetyl residue-containing agent, could block toxin A-induced tubulin deacetylation and subsequent microtubule assembly. Our results revealed that AA treatment increased tubulin acetylation and enhanced microtubule assembly in an HT29 human colonocyte cell line. AA also clearly increased tubulin acetylation in murine colonic explants. Interestingly, the AA treatment also alleviated toxin A-induced tubulin deacetylation and microtubule disassembly, and MTT assays revealed that AA reduced toxin A-induced cell toxicity. Collectively, these results suggest that AA can block the ability of toxin A to cause microtubule disassembly-triggered cytoskeletal disorganization by blocking toxin A-mediated deacetylation of tubulin.

• Journal of Microbiology and Biotechnology
• /
• v.26 no.8
• /
• pp.1446-1451
• /
• 2016

Clostridium difficile toxin A causes acute gut inflammation in animals and humans. It is known to downregulate the tight junctions between colonic epithelial cells, allowing luminal contents to access body tissues and trigger acute immune responses. However, it is not yet known whether this loss of the barrier function is a critical factor in the progression of toxin A-induced pseudomembranous colitis. We previously showed that NADH:quinone oxidoreductase 1 (NQO1) KO (knockout) mice spontaneously display weak gut inflammation and a marked loss of colonic epithelial tight junctions. Moreover, NQO1 KO mice exhibited highly increased inflammatory responses compared with NQO1 WT (wild-type) control mice when subjected to DSS-induced experimental colitis. Here, we tested whether toxin A could also trigger more severe inflammatory responses in NQO1 KO mice compared with NQO1 WT mice. Indeed, our results show that C. difficile toxin A-mediated enteritis is significantly enhanced in NQO1 KO mice compared with NQO1 WT mice. The levels of fluid secretion, villus disruption, and epithelial cell apoptosis were also higher in toxin A-treated NQO1 KO mice compared with WT mice. The previous and present results collectively show that NQO1 is involved in the formation of tight junctions in the small intestine, and that defects in NQO1 enhance C. difficile toxin A-induced acute inflammatory responses, presumably via the loss of epithelial cell tight junctions.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.10 no.2
• /
• pp.206-210
• /
• 2007

Turcot syndrome is characterized by the concurrence of a primary neuroepithelial brain tumor and multiple colorectal polyposis. We report a case of a 24-year-old woman diagnosed with Turcot syndrome. At first, the patient was diagnosed as having a medulloblastoma after a tumorectomy of the 4th ventricle mass. The patient underwent radiotherapy and chemotherapy. After high-dose chemotherapy, neutropenic fever and severe mucositis developed. For an evaluation of the persistent hematochezia and diarrhea, a colonoscopy was performed. It revealed pseudomembranous colitis and multiple polyps in the entire colon. According to the family history, her father had undergone a total colectomy due to colon cancer and polyposis of the entire colon. Her brother also was found to have multiple polyps in the colon by a colonoscopy. The patient was diagnosed with Turcot syndrome.