Klebsiella oxytoca as a causative organism of antibiotic-associated hemorrhagic colitis.

BACKGROUND: Antibiotic-associated hemorrhagic colitis is a distinct form of antibiotic-associated colitis in which Clostridium difficile is absent. Although the cause is not known, previous reports have suggested a role of Klebsiella oxytoca. METHODS: We studied 22 consecutive patients who had suspected antibiotic-associated colitis and who were negative for C. difficile. Patients underwent diagnostic colonoscopy, and among those who received a diagnosis of antibiotic-associated hemorrhagic colitis, stool samples were cultured for K. oxytoca. We isolated K. oxytoca strains and tested them for cytotoxin production using a tissue-culture assay. In addition, we also cultured stool samples obtained from 385 healthy subjects for K. oxytoca. An in vivo animal model for antibiotic-associated hemorrhagic colitis was established with the use of Sprague-Dawley rats. RESULTS: Of the 22 patients, 6 had findings on colonoscopy that were consistent with the diagnosis of antibiotic-associated hemorrhagic colitis, and 5 of these 6 patients had positive cultures for K. oxytoca. No other common enteric pathogens were found in the five patients. Before the onset of colitis, all five were receiving penicillins, and two were also taking nonsteroidal antiinflammatory drugs (NSAIDs). All isolated K. oxytoca strains produced cytotoxin. K. oxytoca was found in 1.6% of the healthy subjects. In the animal model, K. oxytoca was found only in the colon of rats that received amoxicillin-clavulanate in addition to being inoculated with K. oxytoca. In these rats, infection with K. oxytoca induced a right-sided hemorrhagic colitis that was not observed in uninfected animals that received amoxicillin-clavulanate, indomethacin (an NSAID), or both. CONCLUSIONS: Our fulfillment of Koch's postulates for cytotoxin-producing K. oxytoca suggests that it is the causative organism in at least some cases of antibiotic-associated hemorrhagic colitis. Infection with K. oxytoca should be considered in patients with antibiotic-associated colitis who are negative for C. difficile.

Role of Klebsiella oxytoca in antibiotic-associated diarrhea.

BACKGROUND: Klebsiella oxytoca was recently shown to be the causative agent of antibiotic-associated hemorrhagic colitis. Because it is unclear whether K. oxytoca also causes nonhemorrhagic antibiotic-associated diarrhea, our study investigated a possible association between K. oxytoca and that disorder. METHODS: A total of 371 consecutive patients were recruited into 4 study groups: (1) group A+D+ (patients who received antibiotics and experienced diarrhea; n = 107), (2) group A+D- (patients who received antibiotics but did not experience diarrhea; np93), (3) group A-D+ (patients who experienced acute-onset diarrhea but did not receive antibiotics; n = 60), and (4) group A-D- (patients without diarrhea who did not receive antibiotics; n = 111). Stool samples were plated on MacConkey agar and K. oxytoca was identified using a standard test kit. Clostridium difficile was detected by a toxin A/B antigen test. K. oxytoca strains were tested for cytotoxicity with use of cell-culture assays. RESULTS: In 15 of 371 stool samples, K. oxytoca strains were isolated during the study period. There was no significant difference in the distribution of K. oxytoca among the 4 study groups. Six of the 15 strains were found to be toxin producing. Three of the toxin-producing strains caused antibiotic-associated hemorrhagic colitis. No case of nonhemorrhagic antibiotic-associated diarrhea due to toxin-producing K. oxytoca was detected. CONCLUSION: K. oxytoca is not the causative agent of nonhemorrhagic antibiotic-associated diarrhea. This is in contrast to the distinct clinical entity of antibiotic-associated hemorrhagic colitis. Testing for K. oxytoca is therefore only warranted for patients who experience bloody diarrhea during antibiotic therapy.

Renal cell carcinoma metastatic to the stomach: single-centre experience and literature review.

OBJECTIVES: To investigate the incidence, clinical presentation and therapy of gastric metastases, an uncommon finding, in a large group of patients with renal cell carcinoma (RCC). PATIENTS AND METHODS: We systematically searched the computerized RCC database of our institute, covering 2082 patients (1180 men and 902 women) who had surgery between January 1984 and September 2005, to identify those with a synchronous and/or metachronous diagnosis of cancer in gastric biopsies or resection specimens. The histopathological slides of both renal and gastric cancer probes, and the clinical presentation, treatment and outcome of affected patients, were reassessed. RESULTS: Twelve patients with primary gastric cancer, one with local RCC recurrence affecting the antrum and five with clear cell RCC (three men and two women; mean age 73 years, range 65-83) with haematogenous cancer spread to the stomach were detected. The mean (range) time to gastric metastasis was 6.9 (1.7-13.1) years. There were metastases to other organs, most often the lung, in all patients. Three patients presented with symptoms of gastrointestinal bleeding, which was successfully controlled by local endoscopic therapy. Four patients died from disease at 3-19 months after diagnosis. One patient is still alive with disease after approximately 2 years. CONCLUSIONS: Gastric metastasis in patients with RCC appears to be a late event in the course of the disease. Most patients show concomitant tumour spread to other organs, and the outcome is generally poor. The use of targeted drugs might offer a new perspective for affected patients.

Juvenile polyposis of the stomach causing recurrent upper gastrointestinal bleeding.

We present the case of a 42-year-old man who suffered from recurrent severe upper gastrointestinal bleeding starting from February 2003. Endoscopy showed multiple glassy polyps in the stomach, which corresponded to a diffuse mucosal thickening detected by endosonography. The duodenum was normal. In February 2006, life-threatening acute gastrointestinal bleeding prompted total gastrectomy. The resection specimen showed the gastric mucosa carpeted by numerous glassy pedunculated polyps, measuring 2 cm in largest diameter. Histologically, the polyps were characterized by an abundant loose stroma and by elongated, twisting foveolae, covered by hyperplastic epithelium. Colonoscopy including the terminal ileum revealed a single tubulovillous adenoma, but no hamartomatous polyps, rendering a final diagnosis of juvenile polyposis of the stomach. This case represents the first description of juvenile polyposis causing life-threatening gastric haemorrhage. Thus, although rare, the disease has to be considered in the differential diagnosis of patients with acute upper gastrointestinal tract bleeding.

Complete remission of a metastatic gastrointestinal stromal tumour with the tyrosine kinase inhibitor imatinib (STI 571): effect of low dosage in an advanced tumour with exon 11 mutation.

We report a 51-year-old man with an advanced malignant metastatic gastrointestinal stromal tumour, who showed a complete response after 5 months of treatment with imatinib at a dose of 400 mg per day. An early treatment response was demonstrated in an 18fluorodeoxyglucose positron emission tomography scan after 1 month of therapy. Complete remission was documented histologically by negative serial biopsies of residual tumour nodes after 5 months of therapy. No serious side effects were seen with imatinib. A 21 bp, exon 11, in-frame mutation of the c-kit gene was found by DNA sequence analysis of tumour tissue.