SUMMARY A new spiral bacterium, distinct from Campylobacter pylori, was found in the gastric mucosa ofsix patients with gastrointestinal symptoms. All patients had chronic active type B gastritis and four had oesophagitis. Culture and microscopy for C pylori infection was negative. These unculturable spiral organisms were probably an incidental finding in patients presenting for upper gastrointestinal endoscopy, but it is not possible to say from this small series whether these organisms cause chronic active gastritis.The organism is helical, 3 5-7-5 um long and 0 9 gm in diameter with truncated ends flattened at the tips, and up to 12 sheathed flagella 28 nm in diameter at each pole. It is proposed that this spiral bacterium should be called "Gastrospirillum hominis Gen.nov., Sp.nov." Spiral organisms were first reported in the gastric mucosa of a dog in 1881 by Rappin'; and his observations were confirmed and extended in the dog and other mammalian species by other authors.2' In 1906 Krienitz described three types of spiral bacteria in the base of a gastric ulcer in a patient with gastric carcinoma.5 Since 1983 when Warren6 and Marshall' first described Campylobacter pylori and its association with gastritis, there has been much renewed interest in gastric microbiology and histopathology.89 Between July 1986 and July 1987, while studying patients attending endoscopy clinic for the investigation of upper gastrointestinal symptoms, we found spiral organisms unlike C pylori on Gram stained tissue smears from the gastric mucosa. Following our preliminary report on three patients,'0 we found the bacterium in a further three patients and obtained regional biopsy specimens from three of the six. Material and methodsThe patients were part ofa large study to determine the prevalence of Cpylori in the gastric mucosa ofpatients attending for upper gastrointestinal endoscopy. The study was approved by the Gloucestershire Royal Hospital ethical committee. Patients gave informed consent for endoscopy and biopsy; patients with a contraindication to biopsy were excluded. Demographic details, symptoms, medical, surgical, family, Accepted for publication 2 February 1989 social and drug history were entered on to a computer database. When these unusual spiral organisms were found in Gram stained tissue smears of the gastric mucosa the patients' notes were examined in more detail and four patients were asked to return for a second endoscopy; three agreed (cases 1-3). ENDOSCOPYThe oesophagus, stomach, and duodenum were examined and the appearances noted. Four mucosal specimens were taken from within 5 cm ofthe pylorus. Two specimens were sent for histological examination in 10% formol-saline, and two specimens, placed near the top of a 5 ml bijoux bottle containing 100 pl saline to maintain humidity, were sent for microbiological examination. Between each examination the flexible endoscopes (including all the channels) and biopsy forceps were disinfected by immersion in 2% glutaraldehyde for at least 10 minutes, rinsed in water...
No abstract
Background-Helicobacter pylori is a gastroduodenal pathogen associated with ulceration, dyspepsia, and adenocarcinoma. Recent preliminary studies have suggested that H pylori may be protective for oesophageal adenocarcinoma. In addition, strains of H pylori identified by the presence of the cytotoxin associated gene A (cagA) are shown to have a significant inverse association with oesophageal adenocarcinoma. Given that cagA + H pylori may protect against oesophageal carcinoma, these strains may be protective for oesophagitis, a precursor of oesophageal carcinoma. Aims-The aim of this study was to investigate the association between cagA + H pylori and endoscopically proved oesophagitis. Patients-The study group included 1486 patients attending for routine upper gastrointestinal tract endoscopy. Methods-At endoscopy the oesophagus was assessed for evidence of reflux disease and graded according to standard protocols. Culture and histology of gastric biopsy specimens determined H pylori status. The prevalence of cagA was identified by an antibody specific ELISA (Viva Diagnostika, Germany). Results-H pylori was present in 663/1485 (45%) patients and in 120/312 (38%) patients with oesophagitis. Anti-CagA antibody was found in 499/640 (78%) H pylori positive patients. Similarly, anti-CagA antibody was found in 422/521 (81%) patients with a normal oesophagus and in 42/60 (70%) with mild, 24/35 (69%) with moderate, and 11/24 (46%) with severe oesophagitis. The risk of severe oesophagitis was significantly decreased for patients infected with cagA + H pylori after correction for confounding variables (odds ratio 0.57, 95% confidence interval 0.41-0.80; p=0.001). Conclusions-These results suggest that infection by cagA + H pylori may be protective for oesophageal disease. (Gut 2001;49:341-346)
SUMMARY The presence of C pylon infection was determined in 1445 patients undergoing upper gastrointestinal endoscopy over a 12 month period. The presence of C pylori was detected in gastric mucosal biopsy specimens by the biopsy urease test, microscopy (Gram stained smears and histology) and culture. Two media were used for the biopsy urease test: Christensen's urea broth (for the first 600 patients) and the Christensen's urea broth modified by increasing the concentration of phenol red and omitting the nutrients, glucose and peptone (for the remaining patients). Both the Christensen's urea broth and modified urea broth were almost 100% specific when compared with detection of C pylon by Gram, culture and histopathology. The modified broth was more sensitive (96% sensitivity compared with culture) than the Christensen's broth (92% sensitivity) but this difference was not statistically significant. The modified broth gave significantly more positive results (58%) in less than 30 minutes than the Christensen's broth (48%). Seventy four per cent of positive results were available in less than two hours. Specimens from patients with extensive Cpylori infection gave more rapid results: 86% of specimens that yielded a profuse growth of C pylon and 76% that contained numerous organisms on histological sections had a positive urease test in less than one hour. There was no significant difference between the specificity and sensitivity of our modified urea broth and the other modified broths described in the literature. This test is a cheap and rapid alternative to the diagnosis of C pyloni by Gram stained smears or culture.There is now strong evidence that Campylobacter pylori is an important aetiological factor in gastritis and peptic ulceration.'2 Initially this infection was diagnosed by microscopy of tissue smears or sections, or by prolonged microaerobic culture. These techniques are relatively cumbersome and slow, and a more simple, rapid diagnostic method would seem desirable. Langenberg et al first reported that C pylori produced large amounts of urease3; this character was then used for the rapid identification of C pylori cultures. Our initial observation that there was enough preformed urease produced by the organisms to detect C pylori in biopsy specimens led to a small pilot study that confirmed the ease and
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