Intestinal spirochaetosis.
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Antibodies, Bacterial↗
Biomedical subjects
L Engstrand
Publications and source records attributed to L Engstrand.
An in vivo model for gastric physiological and pathophysiological studies in the mouse.
AIM: In vivo models for studying gastrointestinal physiology and pathophysiology are well established in rats. Since a number of genetically modified mice are available there is a need for reliable mouse models. The aim of this project was to develop an in vivo mouse model for gastrointestinal studies. METHODS: C57bl/6, NMRI and transgenic FVB/N (expressing human alpha-1,3/4-fucosyltransferase) mice were anaesthetized with isoflurane and the gastric mucosa exteriorized for intravital microscopy. Acid-base status and acid secretion were measured and blood pressure was continuously monitored. Gastric mucosal blood flow was recorded by laser-Doppler flowmetry. Mucus thickness and accumulation rate were measured with micropipettes. RESULTS: We have developed an in vivo mouse model for studies of the gastric mucosa. With isoflurane anaesthesia the preparation can be studied for up to 5 h with stable blood pressure and mucosal blood flow. Acid-base status agrees with results from other laboratories. Blood flow increased in both C57bl/6 and alpha1.3/4-FT mice in response to luminal HCl, and the mucus gel could be divided into a firmly and a loosely adherent layer, all comparable with results in the rat. However, the firmly adherent mucus layer was thinner (45 +/- 2 microm), and the mucus accumulation rate lower, than in the rat. Furthermore, both basal and stimulated acid secretion showed lower outputs than in the rat. CONCLUSIONS: This model has great potential for investigations of gastrointestinal physiology and pathophysiology and can be applied for Helicobacter pylori infection studies.
Acid-Base Equilibrium↗
Assessment of the cag pathogenicity island status of Helicobacter pylori infections with serology and PCR.
The serological characterisation of Helicobacter pylori strains has been questioned, e.g., when the presence or absence of the cag pathogenicity island (PAI) is determined. This study compared CagA-reactive serum antibodies, assessed with immunoblot, with cag PAI status, as determined by PCR. CagA serology results were available for 101 individuals contributing 202 bacterial samples for cag PAI PCR. There was a high degree of correlation between the two methods (kappa coefficient, 0.82; 95% confidence interval, 0.68-0.97). Combined with suggested biological explanations for the discrepancies, this finding supports the application of well-evaluated serological assays in the assessment of the cag PAI status of H. pylori infections in clinical and epidemiological studies.
Antibodies, Bacterial↗
Management issues in dyspepsia: current consensus and controversies.
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Breath Tests↗
Microbial translocation and inflammatory response in patients with acute peritonitis.
BACKGROUND: In peritonitis, increased production of cytokines and changes in the splanchnic cellular immune system may cause translocation of bacteria and endotoxins. The aims of this study were to assess the frequency of translocation and relate translocation to the immune response in patients with acute peritonitis. METHODS: Patients with local (LP, n=20) or general peritonitis (GP, n=15) were compared with controls (C, n=12). Blood was obtained preoperatively for cultures, and analyses of endotoxin and cytokines (tumour necrosis factor-alpha, interleukins 6 and 10). Mesenteric lymph nodes (MLNs) were excised for culturing and immunohistochemistry using antibodies CD4, CD8 and CD68. RESULTS: Positive blood and MLN cultures were not obtained in controls. DNA typing proved bacterial translocation in one patient with local and one patient with general peritonitis. Thus translocation was proven to occur in 6% of patients with peritonitis. Endotoxaemia was predominantly found in the GP group. Cytokines increased during peritonitis and more so in patients with GP than in those with LP. More CD8 and CD68 cells were found in MLNs from LP patients than in C patients and more CD4 and CD8 cells in LP patients than in GP patients. There was no significant difference in this regard between the GP and C groups. CONCLUSIONS: Bacterial translocation occurs during acute peritonitis but seems to be fairly infrequent. Peritonitis causes significant inflammatory cellular reactions.
Acute Disease↗
Valid symptom reporting at upper endoscopy in a random sample of the Swedish adult general population: the Kalixanda study.
BACKGROUND: Upper oesophagogastroduodenoscopy is considered to be the gold standard for upper gastrointestinal disease assessment, but is currently seldom used in epidemiological studies. One concern is that the procedure may bias sampling among volunteers in a general adult population. The aim of this study was to explore whether the procedure affects symptom reporting. METHODS: A random sample of 3000 adults aged 20-81 years (mean age 50.4), from two Swedish municipalities (n=21,610) was surveyed using a validated postal questionnaire (the Abdominal Symptom Questionnaire) assessing gastrointestinal symptoms. A subsample of the responders was invited, in random order, to undergo an upper endoscopy and repeated symptom reporting using the same questionnaire, as well as a serology test for Helicobacter pylori. RESULTS: The response rate to the initial questionnaire was 74.2% and the participation rate for those eligible for the upper endoscopy was 73.3% (n = 1001, mean age 54.0 years, 48.8% male). No major social or symptom sampling error was encountered from the selection process, with the exception of an excess of symptom reporters among the youngest subjects. The prevalence of reflux symptoms, dyspeptic symptoms and irritable bowel symptoms was 40%, 37.6% and 29.6%, respectively, which is relatively high, but in no way extreme. CONCLUSIONS: The upper endoscopy survey strategy was successful. The response rate was high and there was no major selection bias of clinical relevance. The cohort selected for this study appears to be representative of the general Swedish adult population.
Adult↗
Infection with cagA-positive and cagA-negative types of Helicobacter pylori among children and adolescents with gastrointestinal symptoms in Latvia.
In order to determine the prevalence of concomitant cagA-positive and cagA-negative Helicobacter pylori genotypes in individual subjects, a group of 56 symptomatic patients (aged 8-18 years) was studied. Among 31 patients culture-positive for Helicobacter pylori, only cagA-positive colonies were isolated from 18 patients, both cagA-positive and cagA-negative genotypes were isolated from 4 patients, and in 9 patients all of the individual colonies isolated were cagA-negative, but in seven of them a pool of colonies was positive for cagA. Thus, the presence of both cagA-positive and cagA-negative genotypes in the same individual was identified in 11 of the 31 culture-positive patients tested, and most of the patients predominantly colonized by cagA-negative strains also harbored a small amount of cagA-positive strains. Previous or current infection with cagA-positive strains of Helicobacter pylori was observed in 50 of the 56 patients studied.
Adolescent↗
Helicobacter pylori: resurrection of the cancer link.
Helicobacter pylori is one of the most common pathogenic bacterial infections, colonizing an estimated half of all humans. In a subset of individuals, the infection leads to serious gastroduodenal disease such as peptic ulcers and gastric adenocarcinoma. The factors contributing to skewing this, in most cases benign, relationship into disease development are largely unknown. However, factors emanating from the bacterium, host and the environment have been shown to affect the risk for disease, although no factor can be singled out to be most important. The known factors are associated with affecting the risk of disease, and are not absolute. Virulence of H. pylori is affected by the existence and regulation of certain genes present in the bacterial population in a stomach. The effects of H. pylori on gastric cancer development have been challenged and the risk associated with infection with virulent (i.e. Cag PAI positive) H. pylori has likely been underestimated.
Adenocarcinoma↗
Does the method of Helicobacter pylori detection influence the association with gastric cancer risk?
BACKGROUND: The exact role of Helicobacter pylori as a causative agent of gastric cancer is still under debate. The aim of this study was to determine how the use of different diagnostic methods for detection of H. pylori influences the measures of prevalence of the infection and thus the association with risk of gastric adenocarcinoma. METHODS: We included 72 cases and 324 controls in an endoscopy clinic-based matched case-control study. Culture of H. pylori and immunohistochemical staining were performed on gastric biopsies. Serum samples were tested for H. pylori IgG by conventional ELISA and by immunoblotting. RESULTS: The overall prevalence of H. pylori was 68% based on all 4 diagnostic methods, 79% in the cases and 66% in the controls. Highest agreement, 91%, was observed between culture and immunohistochemistry with a Kappa value of 0.81. Immunoblotting detected the highest number of H. pylori-positive subjects in both cases and controls. The association of H. pylori positivity with gastric cancer was generally weaker and statistically non-significant using culture and immunohistochemistry compared with the serological tests, of which IgG ELISA yielded the higher odds ratio (OR 2.5, 95% confidence interval 1.4-4.4). CONCLUSION: The study shows that relative risk estimates for the association between H. pylori and gastric cancer risk are to some extent determined by the diagnostic method used to detect H. pylori infection.
Adenocarcinoma↗
[Anthrax--the Swedish perspective].
The recent occurrence in the USA of deliberate release of virulent Bacillus anthracis in letters sent to three media corporations and to the American senate has led to a great anxiety in Sweden and elsewhere in Europe. Numerous letters have been suspected to contain B. anthracis spores and several have contained powder of different types. In none of the tested letters collected by the Swedish police have we been able to detect anthrax bacilli. Powder containing letters have been tested with either bacterial isolation and/or B. anthracis specific PCR. Anthrax is a disease found naturally in herbivores and is occasionally spread to humans. It is caused by the gram-positive rod B. anthracis that was discovered by Robert Koch in 1876. Beginning in the 1930s many states have developed B. anthracis for use as a weapon. A few releases of the bacteria have been reported before October 2001. B. anthracis causes three forms of disease, cutaneous, pulmonary and gastro-intestinal. The pulmonary form is the most dangerous and may lead to death merely one to two days after onset of severe symptoms. This is due to the rapid growth and release of several potent toxins that engage the immune system and promote tissue destruction. B. anthracis infection can be treated with several antibiotics, among which quinolones and tetracyclins have been recommended. Diagnosis can readily be achieved by microscopy, bacterial isolation and PCR at the Swedish Institute for Infectious Disease Control and the Swedish Defence Research Agency. Antibiotics relevant for treatment of B. anthracis infections are already stockpilled in our country. Further actions to strengthen our capability to deal with bioterrorism are ongoing.
Anthrax↗
Mutation frequency and biological cost of antibiotic resistance in Helicobacter pylori.
Among the several factors that affect the appearance and spread of acquired antibiotic resistance, the mutation frequency and the biological cost of resistance are of special importance. Measurements of the mutation frequency to rifampicin resistance in Helicobacter pylori strains isolated from dyspeptic patients showed that approximately 1/4 of the isolates had higher mutation frequencies than Enterobacteriaceae mismatch-repair defective mutants. This high mutation frequency could explain why resistance is so frequently acquired during antibiotic treatment of H. pylori infections. Inactivation of the mutS gene had no substantial effect on the mutation frequency, suggesting that MutS-dependent mismatch repair is absent in this bacterium. Furthermore, clarithromycin resistance conferred a biological cost, as measured by a decreased competitive ability of the resistant mutants in mice. In clinical isolates this cost could be reduced, indicating that compensation is a clinically relevant phenomenon that could act to stabilize resistant bacteria in a population.
Adenosine Triphosphatases↗
Gastric cancer and human leukocyte antigen: distinct DQ and DR alleles are associated with development of gastric cancer and infection by Helicobacter pylori.
DNA and sera from 130 cases of gastric cancer and 263 population-based controls were analyzed to study the association of HLA class II DR-DQ alleles with Helicobacter pylori (Hp) infection and the risk for gastric cancer. Presence of the DQA1*0102 allele was inversely and significantly associated with Hp seropositivity (P = 2 x 10(-5)), which is an independent replication of previous findings. However, this inverse relationship with Hp did not correspond with a reduced risk of gastric cancer. At the DRB1 locus, the *1601 allele was significantly associated with an increased gastric cancer risk with an odds ratio (95% confidence interval) of 8.7 (range, 2.7-28.0). The effect of *1601 was more pronounced among Hp-negative subjects, and the association was stronger with the diffuse, rather than with the intestinal, histological type of gastric cancer. Because none of the HLA alleles were associated with both Hp infection and gastric cancer, the HLA DR-DQ alleles are linked with gastric cancer risk through other mechanisms than an increased susceptibility to Hp infection.
Adenocarcinoma↗
Effects of pH, nitrite, and ascorbic acid on nonenzymatic nitric oxide generation and bacterial growth in urine.
Nitrite may be generated by bacteria in urine during urinary tract infections. Acidification of nitrite results in the formation of nitric oxide (NO) and other reactive nitrogen oxides, which are toxic to a variety of microorganisms. We have studied NO formation and bacterial growth in mildly acidified human urine containing nitrite and the reducing agent vitamin C. Urine collected from healthy subjects was incubated in closed syringes at different pH values with varying amounts of nitrite and/or ascorbic acid added. NO generation was measured in headspace gas using a chemiluminescence technique. A similar setup was also used to study the growth of three strains of bacteria in urine. Mildly acidified nitrite-containing urine generated large amounts of NO and this production was greatly potentiated by ascorbic acid. The growth of Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus saprophyticus was markedly reduced by the addition of nitrite to acidified urine. This inhibition was enhanced by ascorbic acid. In conclusion, we show that the growth of three common urinary pathogens is markedly inhibited in mildly acidified urine when nitrite is present. The bacteriostatic effect of acidified nitrite is likely related to the release of NO and other toxic reactive nitrogen intermediates. These results may help to explain the well-known beneficial effects of urinary acidification with, e.g., vitamin C in treatment and prevention of urinary tract infection.
Adult↗
Helicobacter in water and waterborne routes of transmission.
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Culture Media↗
Helicobacter pylori in gastric cancer established by CagA immunoblot as a marker of past infection.
BACKGROUND & AIMS: Helicobacter pylori may disappear spontaneously with progressing precancerous changes and invalidate serologic studies of its association with gastric cancer. We reestimated the strength of the H. pylori-gastric cancer relationship, using both conventional immunoglobulin (Ig) G enzyme-linked immunosorbent assay (ELISA) and immunoblot (against cytotoxin-associated antigen A [CagA] antibodies that prevail longer after eradication) to detect past H. pylori exposure more relevant for time at cancer initiation. METHODS: In our population-based case-control study, the seroprevalence among 298 gastric adenocarcinoma cases was 72% (IgG ELISA) and 91% (immunoblot) vs. 55% and 56% among 244 controls frequency-matched for age and gender. RESULTS: Using IgG ELISA only, the adjusted OR for noncardia gastric cancer among H. pylori-positive subjects was 2.2 (95% confidence interval [CI], 1.4-3.6). When ELISA-/CagA+ subjects (odds ratio [OR], 68.0) were removed from the reference, the OR rose to 21.0 (95% CI, 8.3-53.4) and the previous effect modification by age disappeared. ELISA+/CagA- subjects had an OR of 5.0 (95% CI, 1.1-23.6). There were no associations with cardia cancer. CONCLUSIONS: The weaker H. pylori-cancer relationships in studies based on IgG ELISA rather than CagA may be caused by misclassification of relevant exposure. A much stronger relationship emerges with more accurate exposure classification. In the general Swedish population, 71% of noncardia adenocarcinomas were attributable to H. pylori.
Adenocarcinoma↗
An update on Helicobacter pylori microbiology and infection for the new millennium.
The finding of the bacterium Helicobacter pylori in patients with symptomatic gastric diseases was a breakthrough for both treatment of peptic ulcer disease and studies of other infectious diseases. Helicobacter pylori infection is rare among the young, indicating that improved childhood living conditions have halted the transmission of the bacterium within families, with a parallel decrease in symptomatic gastroduodenal diseases. Extensive strain variation in H. pylori has been demonstrated at both the genomic and the protein level, and the interstrain variation is higher than in any other bacterium studied so far. Pathogenic markers in H. pylori and host genetics are both of importance for disease outcome. Genotypic or phenotypic markers of H. pylori strains may be used to discriminate patients who should undergo eradication therapy from those who might not benefit from it. Possible positive effects of the infection are still under investigation, and several hypotheses regarding the etiology of diseases in different parts of the stomach have been proposed. To be able to separate the disease-causing infections from the silent infections is a real challenge for the new millennium, and one of the most important issues for therapy and prevention, in the research field of H. pylori.
Age Factors↗
In vitro pharmacodynamic studies of activities of ketolides HMR 3647 (Telithromycin) and HMR 3004 against extracellular or intracellular Helicobacter pylori.
The pharmacodynamic properties of the ketolides HMR 3647 (telithromycin) and HMR 3004 were studied against Helicobacter pylori. Both ketolides showed a pronounced concentration-dependent killing, a significant postantibiotic effect, a long postantibiotic sub-MIC effect, and a reduction of intracellular H. pylori.
Anti-Bacterial Agents↗
Comparison of genetic divergence and fitness between two subclones of Helicobacter pylori.
Helicobacter pylori has a very plastic genome, reflecting its high rate of recombination and point mutation. This plasticity promotes divergence of the population by the development of subclones and presumably enhances adaptation to host niches. We have investigated the genotypic and phenotypic characteristics of two such subclones isolated from one patient as well as the genetic evolution of these isolates during experimental infection. Whole-genome genotyping of the isolates using DNA microarrays revealed that they were more similar to each other than to a panel of other genotyped strains recovered from different hosts. Nonetheless, they still showed significant differences. For example, one isolate (67:21) contained the entire Cag pathogenicity island (PAI), whereas the other (67:20) had excised the PAI. Phenotypic studies disclosed that both isolates expressed adhesins that recognized human histo-blood group Lewis(b) glycan receptors produced by gastric pit and surface mucus cells. In addition, both isolates were able to colonize, to equivalent density and with similar efficiency, germ-free transgenic mice genetically engineered to synthesize Lewis(b) glycans in their pit cells (12 to 14 mice/isolate). Remarkably, the Cag PAI-negative isolate was unable to colonize conventionally raised Lewis(b) transgenic mice harboring a normal gastric microflora, whereas the Cag PAI-positive isolate colonized 74% of the animals (39 to 40 mice/isolate). The genomic evolution of both isolates during the infection of conventionally raised and germ-free mice was monitored over the course of 3 months. The Cag PAI-positive isolate was also surveyed after a 10 month colonization of conventionally raised transgenic animals (n = 9 mice). Microarray analysis of the Cag PAI and sequence analysis of the cagA, recA, and 16S rRNA genes disclosed no changes in recovered isolates. Together, these results reveal that the H. pylori population infecting one individual can undergo significant divergence, creating stable subclones with substantial genotypic and phenotypic differences.
Adhesins, Bacterial↗