Search PubMed⌕ Search

Biomedical subjects

W Opferkuch

Publications and source records attributed to W Opferkuch.

At least 55 records · Page 3Linked to original sources
PubMed1989

[Serodiagnosis of Campylobacter pylori].

The colonization of gastric mucosa with Campylobacter pylori can be detected by serological methods. ELISA and immunoblot methods are currently being employed for detection of antibodies against Campylobacter pylori. In general, both tests will differentiate between Campylobacter pylori positive and Campylobacter pylori negative patients. However, 5-10% of persons with negative cultures for Campylobacter pylori have positive serological tests, but only very few patients with Campylobacter pylori associated with chronic gastritis have negative serological tests. This is true for tests detecting IgG and IgA antibodies. Tests for IgM antibodies have not been found to be useful. Immunoblot analyses have shown that detection of antibodies against a 100-120 KD antigen has a high specificity for Campylobacter pylori infection. In a small study we evaluated the possible use of serological testing for follow-up studies on patients after Campylobacter pylori therapy. We found that patients who became Campylobacter pylori negative after therapy showed a significant decline of serum IgG titers against Campylobacter pylori.

Antibodies, Bacterial↗
PubMed1989

[Campylobacter pylori: clinical correlations and prospective comparative studies of various diagnostic techniques].

The diagnostic performance of two different urease tests and of histologic search after modified Giemsa staining to detect Campylobacter pylori (CP) colonization of the upper gastrointestinal tract was prospectively investigated in 215 esophagogastroduodenoscopies, by using a sensitive culture technique as reference. Single antral urease tests had a high specificity of 95-96%, but a limited sensitivity of 78-83%, which increased to 91-94%, when one antral and one additional body biopsy were submitted to the biochemical tests. Giemsa stains were very sensitive, but less specific. The rate of colonization was similar in antrum and body biopsies, and increased with age. There was a close association of Campylobacter pylori colonization with duodenal and to a lower degree with gastric ulcer disease, but especially with gastritic mucosal changes. CP was never detected in patients without gastritis. Therefore, submitting one antral and one body biopsy specimen to validated urease tests represents a sensitive (91-94%) and specific (93%) method to detect Campylobacter pylori colonization, which appears to be a diffuse phenomenon affecting antral and body mucosae with similar frequency.

Biopsy↗
PubMed1988

Two different mechanisms of serum resistance in Escherichia coli.

Fifty-three serum-resistant strains of E. coli which were all able to grow in at least 50% normal human serum (NHS) were tested in respect to binding and consumption of C3b, factor H, C5, and C6 after incubation in pooled NHS. The results of immunofluorescence tests, hemolytic assays, and binding studies using radiolabeled components were comparable. The different binding patterns allowed us to divide the strains into three different groups. The main features of group I were the attachment of C3, C5, and C6 to the bacterial cells as well as consumption of C3 and C5, whereas factor H did not bind at all or only in small amounts. In addition, released MAC was detectable in the supernatant of reaction mixtures containing bacteria of a group I strain and NHS. In group II factor H was easily bound to the bacteria, but no C3, C5, and C6 binding or C5 consumption was detectable. In addition, strains of group III bound C3 and factor H and some strains also bound and consumed C5. Because of the inhomogeneity of group III, this investigation was restricted to a comparison of groups I and II. From the results presented in this study we conclude that group I bacteria activate the whole complement cascade, whereas with bacteria of group II, complement activation is interrupted at the C3 level. These findings therefore indicate a second, alternative mechanism of serum resistance in E. coli.

Blood↗
PubMed1988

Studies on serum resistance in Escherichia coli.

Serum-sensitive mutants and their serum-resistant smooth parental E. coli strains (Wf8, Wf26, and WF 52) have been investigated in respect to their binding of different complement components. These pairs consisting of a wild-type and its mutants represent a better model for the investigation of the mechanism of serum resistance than the comparison of unrelated strains. Both strains of a pair bind equivalent amounts of C3. In binding assays using radiolabeled terminal components C6, C7, C8, and C9, the serum-sensitive strains do bind more late acting components than their resistant parental strains. An active membrane attack complex stably bound to the cell surface was found on the mutants, whereas with wild-type bacteria a complex could be isolated from the supernatant which is composed of the late acting complement components and S-protein. This complex is released from the surface of the wild-type bacteria without participation of C9.

Blood Bactericidal Activity↗
PubMed1988

Cloning and characterization of a new type of fimbria (S/F1C-related fimbria) expressed by an Escherichia coli O75:K1:H7 blood culture isolate.

The Escherichia coli blood culture isolate BK658 (O75:K1:H7) expresses F1A and F1B fimbriae as well as a third fimbrial type which reacts with anti-S-fimbrial antiserum but fails to show S-specific binding properties (i.e., agglutination of bovine erythrocytes). To characterize these fimbriae, we cloned the respective genetic determinant in E. coli K-12. The resulting recombinant clone HB101(pMMP658-6) expresses fimbriae of 1.2-micron length and a diameter of approximately 7 nm. The determinant codes for the fimbrillin subunit, a protein of 17 kilodaltons in size, and for at least five other proteins of 87, 31, 23, 14.3, and 13.8 kilodaltons. By restriction analysis and by DNA-DNA hybridization, it could be shown that the cloned fimbrial determinant of strain BK658 exhibits a high degree of sequence homology to the gene clusters coding for S fimbrial adhesins (sfa) and F1C fimbriae (foc). By using the Western blot (immunoblot) technique and a quantitative enzyme-linked immunosorbent assay, it could be further demonstrated that the cloned fimbriae of BK658, S fimbriae, and F1C fimbriae share cross-reactive epitopes as well as antigenic determinants specific for each fimbrial type. No antigenic cross-reactivity with F1C fimbriae could be detected. The results indicate a genetical and serological relatedness of the cloned fimbriae to S fimbriae and F1C fimbriae. Therefore, this new type of fimbriae is preliminarily termed S/F1C-related fimbriae (Sfr).

Antigens, Bacterial↗
PubMed1988

Comparable evaluation of orally active beta-lactam compounds in ampicillin-resistant gram-positive and gram-negative rods: role of beta-lactamases on resistance.

The antibacterial activity of the recently developed cephems cefixime and cefetamet-pivoxyl was evaluated in 408 gram-positive and gram-negative rods, all isolated recently from clinical specimens, and compared to that of other orally active agents such as ampicillin, amoxycillin + clavulanic acid, cefaclor, cefuroxime-axetil and to ceftriaxone. With regard to ampicillin-resistant Enterobacteriaceae ceftriaxone proved to be the most active agent, followed by cefixime and cefetamet, whereas cefuroxime was less active. Cefaclor and amoxycillin + claculanic acid were active against ampicillin-resistant Escherichia coli, Klebsiella pneumoniae, and Proteus ssp. isolates. All beta-lactam compounds exhibited poor activity against Acinetobacter anitratus isolates, but were highly active against Haemophilus influenzae with the exception of cefaclor. Both cefixime and cefetamet were poorly active against Staphylococcus aureus, but highly active against beta-hemolytic streptococci. Moreover, both compounds remained unaffected by the production of plasmid-mediated beta-lactamases such as the TEM or OXA enzymes. Resistance to both agents was observed in Enterobacteriaceae that produced large amounts of chromosomally mediated enzymes; their affinity to the class I enzyme from Enterobacter cloacae was somewhat lower than that of other third-generation cephalosporins. However, in contrast with these agents breakdown of cefixime and cefetamet by a class IIIa enzyme form Proteus vulgaris was marginal. In methicillin-resistant S. aureus isolates there was a complete cross-resistance between all beta-lactam compounds included in this study.

Ampicillin Resistance↗
PubMed1988

[Microbiology of Campylobacter pylori].

Campylobacter pylori is a hitherto unknown spiral bacterium. It is implicated in the pathogenesis of chronic antral type B gastritis and also of duodenal and gastric ulcer disease. However, its causal role has not yet been unequivocally established. Taxonomically, C.pylori appears to belong to a genus different from genuine campylobacters, but a precise classification is likewise lacking. The in vitro sensitivity analyses of various antibiotics are complicated by a number of technical difficulties. This is one of the reasons, that results of in vivo eradication trials have to be interpreted with considerable caution.

Campylobacter↗
PubMed1987

An immunological study of otitis media with effusion. Antibodies directed against coagulase-negative staphylococci in the effusion fluid.

From 14 chronic middle ear effusions (MEEs), 17 strains of coagulase-negative staphylococci (CS) were isolated. We then used an ELISA method to determine the antibody titers against these microorganisms in the corresponding effusion fluids and the blood sera of the patients and compared them to the antibody titers against a group of standard CS. In most cases, no specific immune response could be detected against the infecting CS in either the effusion fluids or in the sera. Our results can be explained by the inability of most CS strains to provoke a specific immune response in chronically inflamed middle ears due to their inhibition by non-specific antibodies, which reach the middle ear cavity by plasma leakage. The non-specific antibody titer against Staphylococcus hominis, however, seems to be much lower than against the other CS species. We found a high specific antibody titer against the infecting CS in the effusion fluid of a single case, but not in the serum. This finding supports the hypothesis that the middle ear mucosa has the ability to produce autonomous, local antibodies which are independent of a systemic immune response.

Adolescent↗
PubMed1987

A bacteriological study of otitis media with effusion. Concurrent coagulase-negative staphylococcal infections in the middle ear.

We investigated the bacteriology of 50 chronic middle ear effusions from 30 children (mean age, 5 years 4 months) and compared this with the microorganisms present in the external ear canals and adenoids of each patient to distinguish pure middle ear bacteria from probable contaminations. Coagulase-negative staphylococci (CS), formerly considered to be non-pathogens, were the most frequently isolated bacteria in the middle ear effusions and were followed in incidence by alpha-hemolytic streptococci and group D streptococci. CS were found in 24% of all effusions and in 44% of the infected effusions. Most of the CS strains belonged to the species of Staphylococcus epidermidis. Although the majority of CS isolated from the middle ear effusions studied proved not to be contaminants, the populations of CS in the middle ear and external ear canal showed similar biochemical reaction patterns, antimicrobial susceptibilities, and in vitro production of mucus. No correlation was found between the bacteria present in adenoidal tissue and middle ear effusions.

Adolescent↗
PubMed1987

Interaction of Escherichia coli and macrophages: alteration by treatment of bacteria with beta-lactam antibiotics.

Antibiotics are known to exert an influence on the host-parasite relationship either by impairment of immunocompetent cells or by alteration of the bacterium, such as changes of surface properties or the production of toxins. The main problem in investigating the effect of antibiotics on the surface properties of bacteria consists in morphological changes of bacteria (round cell or filament formation) after treatment e.g. with beta-lactam antibiotics. These changes of morphology lead to problems in the comparison of such bacterial forms with untreated organisms. Therefore, in this study outer membrane vesicles from bacteria were used as a model to investigate the effect of antibiotics on the surface properties of Escherichia coli with regard to the interaction with mouse peritoneal macrophages tested by chemiluminescence reaction. It could be shown that these membrane vesicles induce a luminol dependent chemiluminescence response. Treatment of E. coli with different beta-lactams lead to an increase of the stimulating properties. The relative effectiveness of certain antibiotics depended on the particular E. coli strain. Analysis of the different adhesions involved in the stimulation of macrophages revealed that only mannose-sensitive adhesins were increased after treatment with beta-lactam antibiotics. No stimulation of the membrane-bound NAD(P)H-oxidase could be found following the reaction with outer membrane vesicles. Even the treatment of bacteria with antibiotics did not evoke such a reaction.

Animals↗
PubMed1987

Imipenem resistance in Pseudomonas aeruginosa resulting from diminished expression of an outer membrane protein.

The mechanism of Pseudomonas aeruginosa resistance to imipenem in five imipenem-susceptible clinical isolates and in their resistant counterparts was investigated. The frequency for selecting imipenem-resistant variants ranged from 2.7 X 10(-5) to 2.1 X 10(-8) and was comparable to those for other beta-lactams. Cross-resistance between imipenem and other beta-lactam compounds was not observed. In all imipenem-resistant variants, induction of chromosomal beta-lactamase by imipenem was markedly diminished compared with that in the susceptible parent strain. This was not the case for other inducers such as ampicillin or cefoxitin, suggesting an impaired uptake of imipenem as an explanation for resistance. Analysis of the outer membrane proteins revealed a marked decrease of either a 46- or a 45-kilodalton protein. The lipopolysaccharide of the outer membrane in the imipenem-resistant variants was not altered.

Anti-Bacterial Agents↗