Laboratory-acquired Helicobacter pylori infection.
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Biomedical subjects
Publications and source records attributed to F Mégraud.
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Seventeen Campylobacter strains isolated from 16 children hospitalised with acute diarrhea were analysed by in vitro enzymatic amplification using two sets of oligonucleotide primers specific for Campylobacter jejuni and Campylobacter coli, respectively. Thirteen strains (76%) were identified as Campylobacter jejuni and four strains (24%) as Campylobacter coli. Subsequent bacteriological identification confirmed the identity of the same 13 Campylobacter jejuni strains and the 4 Campylobacter coli strains. Thus, these PCR methods enabled rapid and specific detection of all the Campylobacter jejuni and Campylobacter coli strains without any false-positive or false-negative results.
BACKGROUND: The role of Helicobacter pylori in chronic gastric and duodenal ulcer disease has now been proven in adults as well as in children. MATERIAL AND METHODS: H pylori has been looked for during endoscopy in 130 children suffering from recurrent abdominal pain (78 patients) or other symptoms (52 patients). Biopsy samples were taken from the antrum and the fundus, and were examined for histology and bacteriology (Gram staining, urease test, culture). RESULTS: H pylori was found in 30 cases (H pylori+ group, medium age: 12 years) and was absent in the 100 other cases (H pylori- group, medium age: 6 years). H pylori was present in 27% of children suffering from recurrent abdominal pain and 17% of children with other symptoms. Epigastric location of the pain and vomiting were equally frequent in both groups. Endoscopic gastritis, often nodular, was noted in 60% of the cases in the H pylori+ group and in 46% in the H pylori- group (NS). Chronic gastritis was noted in 90% of the cases in the H pylori+ group, and in 32% of the cases in the H pylori- group (p < 0.01). Culture was positive in 27 out of 28 cases (97%) in the H pylori+ group, including 3 cases with negative histologic examination. Twenty-two children in the H pylori+ group were treated with amoxicillin and metronidazole. Endoscopy performed about 2 months later showed eradication of H pylori in 63% of the cases, associated with disappearance of histologic lesions in 6 out of 14 cases and of symptoms in 5 out of 7 cases. CONCLUSIONS: H pylori is associated with some pediatric cases of antral gastritis. Further studies are needed to determine the influence of its eradication on symptoms and the interest to search this pathology (by serology) in children suffering from chronic abdominal pain.
Helicobacter pylori is present worldwide but few large population studies exist on the epidemiology of the infection. A random cross sectional study was performed of H pylori infection in the adult population of San Marino, a European country with high gastric cancer rate, to assess its prevalence and to evaluate its relations with gastrointestinal disease. In 2237 subjects (77% of the initial sample) H pylori IgG antibodies were detected with enzyme linked immunosorbent assay (ELISA) and immunoblotting. A questionnaire including questions about occupation, place of birth, and smoking was given to all subjects. Dyspepsia, peptic ulcer, and gastric cancer in the subjects, relatives, and partners as well as use of drug, dental treatment/prostheses, and gastrointestinal endoscopies, were evaluated by multivariate analysis. H pylori prevalence was of 51%, increased with age from 23% (20-29 years) to 68% (> or = 70 years), and was higher among manual workers. H pylori was independently associated with ulcer (OR = 1.63, 95% confidence intervals (CI) = 1.16 to 2.27), H2 antagonists (OR = 1.94, 95% CI = 1.21 to 3.10), and benzodiazepines (OR = 1.57, 95% CI = 1.02 to 2.42), dental prostheses (OR = 1.25, 95% CI = 1.05 to 1.49), gastroscopy in the past five years (OR = 1.50, 95% CI = 1.05 to 2.14), peptic ulcer in siblings (OR = 1.52, 95% CI = 1.09 to 2.12), gastric cancer in father (OR = 1.61, 95% CI = 1.02 to 2.52). The association of seropositivity with history of ulcer, gastric cancer in family, gastroscopy, and H2 antagonists suggests that H pylori is an epidemiological key factor in the pathogenesis of gastroduodenal diseases in this area.
Helicobacter pylori infection has a widespread distribution but the prevalence varies considerably between developed and developing countries. The infection is probably acquired in childhood. The prevalence curves of infection according to age observed in developing countries may be explained by a generation effect, taking into account that the risk of infection has decreased in recent decades. The major risk factors are overcrowding, lack of education and poor sanitation. The exact mode of transmission is not yet understood fully but is thought to be from person to person.
We aimed to produce a unifying hypothesis to explain the different locations of peptic ulcer and gastritis observed in different populations. The pre-Helicobacter pylori literature on patterns of gastroduodenal disease was reviewed and compared with recent human and animal findings on H. pylori infection. Early observations revealed that duodenal and non-pre-pyloric ulcers tend to be mutually exclusive. In duodenal ulcer patients, gastritis is usually restricted to the antrum, while gastric ulcer patients experience more severe pangastritis. The manipulation of acid output by surgery or acid suppressive therapy alters the distribution of gastritis. Recent experimental evidence in humans and animals has shown that these changes parallel changes in the distribution and cellular responses to H. pylori infection. We propose that the most important factor in the ecology of the H. pylori-infected stomach is local acid production. Local acid production determines the location and severity of inflammation and the clinical outcome of this bacterial infection. Priority research areas should be the investigation of the in vivo behaviour of H. pylori in the acid and the non-acid producing areas of the stomach and the measurement of acid output in populations known to have different patterns of gastroduodenal disease.
The recognition of Helicobacter pylori (H. pylori) as a major cause of gastroduodenal diseases has led to the use of antibiotics to treat these diseases. However, antibiotics used alone are not very effective, and adjuvant therapy is required. The most potent adjuvant therapy consists of increasing the stomach pH with proton pump inhibitors (PPIs). In addition to this action on stomach pH, PPIs, and especially lansoprazole, have been found to have antimicrobial activity against H. pylori. At high concentrations, they are even bactericidal. Furthermore, they can inhibit H. pylori urease activity. These properties, as well as their antisecretory activity, provide the grounds for their use in eradication of H. pylori.
OBJECTIVES: Reduction of gastric acid secretion by maintenance therapy and eradication of Helicobacter pylori by antibiotic treatment have been shown to reduce duodenal ulcer relapse. This study compared the effect of two regimens, a 6-month maintenance on an H2 receptor antagonist versus a one-week antibiotic therapy, on the rate of duodenal ulcer relapse in duodenal ulcer patients with gastric H. pylori infection. METHODS: We conducted a 30-week, double-blind, double-dummy, multicentric clinical trial involving 119 patients (97 M, 22 F, mean age 39 +/- 14 years) randomly assigned to a daily dose of 40 mg famotidine for 6 weeks supplemented with, during the first week, either antibiotics (500 mg amoxicillin q.i.d. and 500 mg tinidazole t.i.d.-antibiotic group) or their placebo (maintenance group). Healed patients after 6 weeks entered the 6-month maintenance phase: the maintenance group received 20 mg famotidine at bedtime and the antibiotic group, a placebo. Endoscopy with antral biopsies was performed to allow a rapid urease test, culture and histological examination upon entry, after 6 weeks, 3 months, and 6 months and, whenever symptoms recurred. H. pylori status was regarded as positive if any one of these three tests was positive, and negative if all tests were negative. RESULTS: The 2 treatment groups were well balanced for all baseline characteristics. After 6 weeks, H. pylori was eradicated in 25 (45%) patients in the antibiotic group, and in 1 (2%) in the maintenance group (P < 0.01). In term of intention-to-treat, there was no significant difference in the healing rate after 6 weeks (93 and 83% in the antibiotic and maintenance groups, respectively; P = 0.15) or in the relapse rate after 6 months (13 and 28% in the antibiotic and maintenance groups, respectively; P = 0.17 Log-rank test). However, the overall failure rate (absence of healing, relapse) was lower (P = 0.04, Log-rank test) in the antibiotic group in which all relapses but one were observed in H. pylori positive patients. The rate of ulcer relapse (1/20) in patients of antibiotic group who remained free of H. pylori during the study, was significantly (P < 0.01) lower compared with that of H. pylori positive patients in the maintenance group (11/44). During the first 6-week period, more side effects were observed in the antibiotic group than in the maintenance group (4 vs 1 patient, respectively). CONCLUSIONS: Our results indicate no significant difference between ulcer relapse rates after 6 months following a one-week antibiotic therapy or long-term maintenance therapy. Short-term antibiotic therapy should be considered as a valuable alternative to the long-term maintenance therapy.
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PURPOSE: To review the various toxic factors produced directly or indirectly by Helicobacter pylori and discuss their relative importance in H. pylori infection. RESULTS: The toxic factors produced by H. pylori can act at different levels. At the epithelial cell level H. pylori enzymes generate toxic molecules: ammonia (urease), lysolecithin (phospholipases) and acetaldehyde (alcohol dehydrogenase). The harmful effects of ammonia have been studied the most intensively and seem to be a likely mechanism of pathogenicity. A vacuolating cytotoxin is expressed in 50-60% of the strains while the gene is present in all. Despite the fact that its potential toxic effect is low, the cytotoxin is associated with ulcer development. Another protein, CagA is a marker for the presence of the toxin. H. pylori can also produce a hemolysin, a platelet-activating factor and a factor that alters parietal cell function. At the mucus level, it does not seem that H. pylori enzymes degrade mucin, and the thinness of the layer could be due to inhibition of mucus exocytosis. CONCLUSION: H. pylori have a wide range of toxic factors which can act together but no one factor is considered sufficient alone to explain the observed lesions.
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Former studies have shown that Helicobacter pylori can induce vacuolation of vacuolation of epithelial cells in vitro and possibly in vivo, either by direct action of a cytotoxin or by the action of its strong urease, which breaks down the urea physiologically present in the stomach into cytotoxic ammonia. We have developed a test using HEp2 cells with adherent H. pylori bacteria in order to compare the effects of an H. pylori urease-negative variant with those of its urease-positive parent strain in the presence of 10 mM urea. The level of ammonia production as well as cell vacuolation and viability were monitored for 72 h. The ammonia produced (20 mM) was found to be the essential determinant of the degree of cell vacuolation and viability of HEp2 cells. However, the addition of acetohydroxamic acid (200 mg/liter), a potent urease inhibitor which inhibits ammonia production, did not completely restore cell growth, suggesting the difficulty of neutralizing the ammonia in the vicinity of the cells. Antibodies directed against H. pylori did not neutralize the urease activity. When H. mustelae was tested in the same manner, the detrimental effects were not observed because a lower quantity of ammonia (5 mM) was generated. This was due to a lower urease activity, although the adherence properties of H. mustelae were different from those of H. pylori both quantitatively (greater adherence) and qualitatively (localized instead of diffuse adherence). We conclude that H. pylori-induced ammonia is an essential determinant of its cell toxicity as well as its adherence properties, which allow a high concentration of ammonia at the cellular level.
A sentinel health information system using telematics and a network of general practitioners was set up in Aquitaine in south western France in 1986. Among the health problems under surveillance was acute diarrhoea. Data for each patient who fulfilled the usual case definition for acute diarrhoea were reported by general practitioners using home terminals (Minitels) connected to a central computer by telephone. Over one year 2234 cases of diarrhoea were reported, the incidence varying from 0.8 to 1.5 cases per doctor per week. Seasonal variations in incidence were observed, with peaks in the winter and in the summer. Only 379 (17%) episodes of diarrhoea were classified as severe, and these patients consulted their general practitioners earlier than patients whose diarrhoea was less severe. Foreign travel was rarely found in the patients' histories, but clusters of cases were found in communities (4.6%) and in families (22.3%). The advantages of this system were easy reporting and immediate feedback, but it was difficult to extrapolate the data, and the system was inadequate for intervening in outbreaks of diarrhoeal disease. Our knowledge of diarrhoeal diseases in south west France improved.
An unusual campylobacter strain, a urease positive thermophilic variant of Campylobacter lari, was isolated from the urine of a patient with urinary tract infection who was hospitalized because of cirrhosis and haemorrhage. The strain was isolated from urine specimens on three separate occasions. A significant serological response to the organism was also detected. This is the first documented case of extra-intestinal infection due to this group of organisms.
A case-control study aimed at comparing the incidence of campylobacter infection with that of other enteropathogens in infants was performed in Oran, Western Algeria. During a one-year period, infants consulting in a health centre were included if they had acute diarrhoea. The controls comprised infants going to the same centre for vaccination. Butzler medium Virion was used to look for thermophilic campylobacters. Campylobacters were isolated in 17.7% of the 411 patients and in 14.9% of the 247 controls. No statistically significant difference was found after stratification by age. In contrast, other enteropathogenic bacteria were rarely present. Among the potential factors of clinical expression of infection, breast feeding appeared to have a protective effect which was higher for campylobacter diarrhoea than that observed for other causes of diarrhoea. These data contrast with those previously published in Bangladesh and could be an incentive for promoting breast feeding in this country, where the tradition is decreasing far below the standard which is generally accepted.