SEARCH · PubMed Health
Results for “Bacterial Capsules”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Biochemistry and expression of bacterial capsules.
Explore the source record for details and available documents.
Capsules of Escherichia coli, expression and biological significance.
Escherichia coli may cause intestinal or extraintestinal infections. Generally, extraintestinal E. coli are encapsulated. The capsules are important virulence determinants, which enable the pathogenic bacteria to evade or counteract the unspecific host defense during the early (preimmune) phase of infection. They interfere with the action of complement and phagocytes. This effect is generally transient and overcome by capsule-specific antibodies in the immune phase of the host defense. In some cases, capsules are not or only poorly immunogenic, as a result of structural relationship or identity with host material. Strains with such capsules (e.g., K1 or K5) are very virulent. Bacterial capsules consist of acidic polysaccharides, which are made up from oligosaccharide repeating units. The capsules of E. coli are divided into two groups, which differ in chemistry, biochemistry, and genetic organization. All capsular polysaccharides are chromosomally determined: those of group I close to his and those of group II close to serA. The biosynthesis and surface expression have been extensively studied with representatives of group II capsular polysaccharides. It could be shown that their biosynthesis is directed from a gene block that determines the synthesis of the polysaccharide, its translocation across the cytoplasmic membrane, as well as its surface expression in a coordinate process. The chemical nature of group II capsular polysaccharides, as well as the mechanism(s) of their biosynthesis and expression, is presented.
Intracellular growth of Mycobacterium avium in human macrophages is linked to the increased synthesis of prostaglandin E2 and inhibition of the phagosome-lysosome fusions.
A virulent strain of Mycobacterium avium grew actively inside human adherent peripheral blood monocyte-derived macrophages. Bacteria were always confined to the phagosome compartment and were encapsulated. Cytochemical labeling of acid phosphatase using transmission electron microscopy showed a strong inhibition of the phagosome-lysosome fusions (PLF) in macrophages as not more than 25-30% bacteria containing phagosome at any time effectively fused with lysosomes. In case of a positive fusion event, the bacterial capsule prevented the diffusion of the lysosomal contents to the bacterial surface. Moreover, the infection of macrophages both by living and gamma-killed M. avium was linked to an increased synthesis of prostaglandin E2 (PGE2); however the total amount of PGE2 synthesized in the latter case was significantly lower than that observed with viable organisms. Our results suggest that the inability of human macrophages to control M. avium infection is linked to immunosuppressive pathways, e.g. enhanced synthesis of PGE2 and also to an impairment of normal microbicidal functions of the infected macrophages.
An electron microscopic India ink technique for demonstrating capsules on microorganisms: studies with Streptococcus pneumoniae, Staphylococcus aureus, and Neisseria gonorrhoeae.
A technique using India ink in electron microscopic preparations was used to study bacterial capsules. Capsules were demonstrated on Streptococcus pneumoniae and Staphylococcus aureus (strain M and the Smith diffuse variant) from in vitro cultures. Two types of false capsules were observed on Neisseria gonorrhoeae grown in vitro or obtained from human urethral exudates. No true capsules were definitively identified on gonococci from these sources. The technique described does not require the use of specific anticapsular antibody or specific polysaccharide stains and permits the detection of artifacts that may, by the use of light microscopic methods, be misinterpreted as capsules.
Molecular order of carbohydrate components in cell walls of bacteria, fungi and algae according to the topo-optical reaction of the vicinal OH groups.
Selective topo-optical staining of vicinal OH groups with aldehyde-bisulphite-toluidine blue (ABT) has been used for studying the molecular structural order of polysaccharide components in microbial cell walls and capsules. (i) By intensive metachromatic staining in the light microscope, the method demonstrates carbohydrates, containing free vicinal OH or acylaminohydroxyl groups. (ii) The birefringence induced by oriented toluidine blue binding of the ABT reaction, provides information about the linear order of the reacting carbohydrate chains, a possibility not offered by other ultrastructural methods. Furthermore the different optical character of birefringence induced by ABT is indicative of the presence of (a) tangentially oriented polysaccharide chains in the cell wall of the molds and bacterial capsules; or (b) radially oriented OH groups suggesting helical glycan chains of peptidoglucomannane and mucopeptide in the yeasts and bacterial cell walls.
Differential handling of bacterial antigens in macrophages infected with Mycobacterium leprae as studied by immunogold labeling of ultrathin sections.
Mycobacterium leprae were purified from the livers of experimentally infected armadillos, and the purity of the bacterial preparation was established by electron microscopy, immunoelectrophoresis of purified bacilli with rabbit serum raised against liver tissues from a noninfected armadillo, and gas chromatography. Such purified and intact bacilli were fixed and embedded by a gelatin-Lowicryl method for electron microscopy which preserved the mycobacterial antigens. Ultrathin sections were labeled with antisera raised in rabbits against the total antigens of the following species of mycobacteria: M. leprae, M. bovis BCG, M. avium, and a rapid-growing, nonpathogenic species, M. fallax. Bacteria were also labeled using serum raised against 2,3-diacyl-trehalose-2'-sulfate (sulfolipid-IV or SLIV) isolated and purified from M. tuberculosis. The immunolabeling was visualized under the electron microscope (EM) by using a secondary probe (goat-antirabbit IgG, H+L, coupled to 5 nm gold particles; GAR-5). EM results showed that M. leprae bacilli were highly labeled with all of the antisera used except SLIV, which was present only in discrete amounts. All of the antisera used labeled the bacterial "capsule," showing that this structure was not an artifact since it contained mycobacterial antigens. In parallel experiments, the murine J-774 macrophage cell line was infected with purified M. leprae, and fixed for EM at various time intervals for 1 week. Although the phagocytized bacteria did not multiply during the 1-week experiment, macrophages were unable to lyse them. Immunogold labeling of bacterial antigens in ultrathin sections of infected macrophages helped us to conclude: a) bacterial death and/or lysis is not a prerequisite for processing of antigens by infected macrophages; b) there was conclusive evidence for a differential antigen handling, i.e., some antigens were rapidly released (within 2 days, mostly capsular antigens) inside infected macrophages and transported to the macrophage surface, whereas others (the majority of them located in the cell-wall skeleton and in deeper bacterial structures) remained unreleased even after 4 to 7 days of infection; c) although relatively fewer epitopes reacting with anti-SLIV antibodies were found, they were rapidly released (within 2 days) inside macrophages, and exocytized to the macrophage surface. These novel findings are discussed in relation to leprosy and the current knowledge about the processing of bacterial antigens.
Complement deposition by antibodies to Pseudomonas aeruginosa mucoid exopolysaccharide (MEP) and by non-MEP specific opsonins.
The failure of cystic fibrosis patients to limit chronic infection due to mucoid Pseudomonas aeruginosa might be due to ineffective opsonins produced against this bacterium. Nonopsonizing antibody to the bacterial capsule, mucoid exopolysaccharide (MEP), appears at elevated titers during chronic colonization of cystic fibrosis patients, as do opsonins not specific for MEP. Nonopsonic antibodies to MEP occur naturally in most adults and can be induced in animals by immunization. A limited number of humans produce MEP-specific opsonic antibodies after immunization. The purpose of this study was to compare the activation and deposition of C components onto the bacterial surface in the presence of these different antibodies. Opsonic killing uses the classical C pathway. MEP-specific opsonic and nonopsonic antibodies bound to whole bacteria and activated C to a comparable degree, but opsonic antibody deposited 3 to 40 times more C3 onto bacteria, mostly as C3bi, compared to nonopsonic antibody. In addition, two to three times as much nonopsonic mAb as opsonic mAb (both IgG2b) bound to the bacteria at comparable input concentrations, indicating the difference in C deposition was not due to differences in antibody binding. Non-MEP-specific opsonins also bound C3 to the bacteria, but only a mean of 27 +/- 14% was ester linked, compared with 81 +/- 11% of C3 deposited by MEP-specific opsonins. Immunoprecipitation experiments indicated that two-thirds of the C3 bound in the presence of MEP-specific opsonins was linked to MEP, whereas non-MEP-specific opsonins obtained from infected patients deposited the C3 onto LPS and other unidentified Ag. These data show that MEP-specific opsonins function by depositing C3 onto the outer bacterial surface that differentiates them from non-MEP-specific opsonins produced in response to chronic infection.
Antigenic homology among gram-negative organisms isolated from cattle with clinical mastitis.
This study examined the degree of serologic homology among mastitis pathogens. Antibodies were raised against the Rc mutant, Escherichia coli O111:B4 (strain J5) and affinity purified against lipopolysaccharide derived from the Ra mutant, Salmonella typhimurium TV119. These antibodies reacted with a battery of unrelated Gram-negative bacteria in whole cell ELISA. Bacteria with strong cross-reactions included a heterologous, smooth E. coli, Salmonella dublin, S. typhimurium, Salmonella newport, and Pseudomonas aeruginosa. Recognition of Klebsiella pneumoniae and Bordetella bronchisepticum was observed, but reactions were weaker than with the other isolates. The reduced recognition of these isolates probably reflects a masking effect of the bacterial capsule and variations in lipopolysaccharide structure. The polyclonal antibody did not recognize a Gram-positive isolate, Staphylococcus aureus. These immunoglobulins were then tested using whole cell ELISA against a panel of bacteria recovered from the mammary glands of cattle with clinical mastitis. Marked reactivity was noted against a variety of Gram-negative pathogens. Gram-positive isolates had lower recognition by Gram-negative core antigen specific immunoglobulin. The results suggest immunization with rough mutant bacteria may have broad application in the prevention of coliform mastitis.
[Immunology and diagnostic test results in Lyme borreliosis].
Borrelia burgdorferi (B. burgdorferi), the etiologic agent of Lyme borreliosis, shows both a variety of outer surface proteins with molecular weights between 16 and 100 kiloDalton (kD) and a 41 kD flagellar protein, which induce the immunologic response. Lipopolysaccharides, another constituent of the bacterial capsule, are responsible for the inflammatory reaction, constitutional symptoms and for the Jarisch-Herxheimer reaction. First a vigorous T-cell immune response develops, followed later by a more slowly evolving humoral B-cell immune response. The delayed onset of the humoral immune response may explain why antibodies against B. burgdorferi could not be detected early in the course of the disease. But the antibody titers increase with duration of the illness. The humoral response shows the usual pattern of IgM appearing first, followed by IgG and IgA. The IgM titer normalizes after recovery while the IgG titer could persist over years or decades. It is hardly possible to detect B. burgdorferi microscopically or by cultivation from blood, joint or cerebrospinal fluid. For routine diagnosis the fluorescent antibody staining and the ELISA methods are available which detect IgM or IgG antibodies against B. burgdorferi. But the sensitivity and specificity of these tests are still unsatisfactory. Other methods such as the ELISA-capture method, complement binding reaction, passive hemagglutination or the polymerase chain reaction are not yet established for routine purposes. Western blot analysis did not yield an essential diagnostic advantage but may be helpful in long term observation or in special cases. The measurement of the cellular immune response by T-cell proliferation tests remains controversial. First of all Lyme borreliosis has to be diagnosed by clinical findings and by elimination through differential diagnosis. An elevated antibody titer or a positive T-cell proliferation test may confirm the diagnosis but cannot prove it. Without consistent clinical findings they are of no practical significance. Some general guidelines for interpretation of laboratory results are given.
Protective efficacy of Haemophilus influenzae type b polysaccharide-diphtheria toxoid-conjugate vaccine.
We estimated the relative protective efficacy of Haemophilus influenzae type b polysaccharide (PRP) vaccine and PRP-diphtheria toxoid-conjugate (PRP-D) vaccine using data from reports of cases of invasive Haemophilus disease occurring in vaccinated children submitted to the Food and Drug Administration, Rockville, Md, and Washington University, St Louis, Mo. During the first 13 months following licensure of each of the vaccines, there were 127 cases reported in recipients of PRP vaccine vs 17 cases in recipients of PRP-D vaccine. The total number of reported cases for each vaccine is not necessarily comparable, since the extent of vaccine use in the population and the extent of reporting of cases may have been different during the two periods. However, the proportion of reported cases occurring equal to or 14 days or more after vaccination (a period considered sufficient to develop immunity) was significantly greater for PRP vaccine (106 [83%] of 127 cases) compared with PRP-D vaccine (7 [41%] of 17 cases). Based on the ratio of late-onset to early-onset cases observed for PRP vaccine, we would have expected 50 late-onset cases after PRP-D vaccination. Since only 7 late-onset PRP-D vaccine failures were reported (86% fewer than expected), the data suggest that PRP-D vaccine was more effective in preventing disease 14 days or more after vaccination than was PRP vaccine.
Immunization response varies with intensity of acute lymphoblastic leukemia therapy.
Twenty-four children receiving maintenance chemotherapy for acute lymphoblastic leukemia were given booster doses of tetanus-diphtheria combined toxoids. One month later, 19 of the 24 children were given Haemophilus influenzae B oligosaccharide-cross-reacting material conjugate vaccine. Following immunization, all patients had protective antibody titers against tetanus, 92% had protective antidiphtheria titers, and 84% had protective titers against H influenzae. Preimmunization titers, postimmunization titers, and response to immunization varied according to the intensity of therapy. There was no correlation with duration of therapy or quantitative hematologic values in the peripheral blood. These observations support the recommendation that children treated for acute lymphoblastic leukemia should be immunized against H influenzae B.
Response of 7- to 15-month-old infants to sequential immunization with Haemophilus influenzae type b-CRM197 conjugate and polysaccharide vaccines.
OBJECTIVE: To evaluate the immunologic potential of infants 7 to 15 months of age to respond to Haemophilus influenzae type b polysaccharide vaccine following immunization with H influenzae b oligosaccharide-CRM197 conjugate vaccine. STUDY DESIGN: One hundred seventy-one infants, aged 7 to 15 months, were consecutively and alternatively assigned to one of three immunization protocols. Group 1 (n = 71) received three doses of H influenzae b oligosaccharide-CRM197 conjugate vaccine, group 2 (n = 47) received two doses of H influenzae b oligosaccharide-CRM197 conjugate vaccine followed by one dose of H influenzae type b polysaccharide vaccine, and group 3 received one dose of H influenzae b oligosaccharide-CRM197 conjugate vaccine followed by two doses of H influenzae type b polysaccharide vaccine. Immunizations were given on day 0 and at 2 months and 6 months. Anti-H influenzae type b polysaccharide antibody levels were measured on day 0 and 2, 3, 6, 7, and 12 months after the study began. RESULTS: Haemophilus influenzae type b polysaccharide vaccine given as a second dose stimulated an antibody rise but did so less effectively than H influenzae b oligosaccharide-CRM197 conjugate vaccine. Two doses of H influenzae b oligosaccharide-CRM197 conjugate vaccine were highly immunogenic; geometric means were 31 and 35 micrograms/mL in the 7- to 11-month and 12- to 15-month age groups, respectively. Following two doses of H influenzae b oligosaccharide-CRM197 conjugate vaccine, both immunization protocols resulted in (1) equally high geometric mean antibody levels 1 month after immunization and (2) similar geometric mean antibody levels 6 months after immunization. CONCLUSIONS: Haemophilus influenzae b oligosaccharide-CRM197 conjugate vaccine induces antibody levels that would be expected to protect infants from initial invasion and primes the immune system for an anamnestic response. Our data indicate that if a booster immunization is needed, H influenzae type b polysaccharide vaccine could be an alternative to H influenzae b oligosaccharide-CRM197 conjugate vaccine.
Genetics of capsular polysaccharide production in bacteria.
Explore the source record for details and available documents.
Haemophilus influenzae epiglottitis occurring simultaneously in two siblings.
Intrafamilial spread of Haemophilus influenzae type B disease has often been described for meningitis, but rarely for epiglottitis. Here we report for the first time epiglottitis occurring simultaneously in two siblings and comment on the value of chemoprophylaxis and vaccination to prevent secondary and primary disease.
Virulence factors in anaerobic bacteria.
Various surface structures can be expressed in Bacteroides fragilis, but little is known about capsular structures in other non-spore-forming anaerobes. Fimbriae have been isolated from Bacteroides fragilis and Porphyromonas gingivalis. The importance of iron-repressible outer membrane proteins as virulence factors in Bacteroides fragilis is under study. The low endotoxic activity of Bacteroides fragilis lipopolysaccharide can be attributed to the chemical composition of this organism's lipid A. A tissue culture system for the demonstration of Bacteroides fragilis enterotoxin has recently been described. The toxins A and B of Clostridium difficile are immunologically distinct. The importance of IgA proteases and other enzymes as virulence factors in anaerobic bacteria remains unclear.
Immunogenicity of Haemophilus influenzae type b capsular polysaccharide and its tetanus toxoid conjugate in patients with recurrent infections or humoral immunodeficiency.
The antibody response to the capsular polysaccharide of Haemophilus influenzae type b was evaluated after vaccination with the capsular polysaccharide or its tetanus toxoid conjugate in 41 randomized patients with recurrent infections, IgA deficiency, common variable immunodeficiency, or the Wiskott-Aldrich syndrome. Serum antibodies were measured using a Farr assay for total antibodies and an enzyme-linked immunosorbent assay for antibodies of the three main immunoglobulin classes and of each IgG subclass. Antibody levels reached concentrations generally considered as protective in the majority of cases, the best response being observed after two injections of the conjugate vaccine with a 1-month interval. Vaccination with the conjugate therefore seems to be promising for the prevention of Haemophilus influenzae type b infections in such patients.
Synthesis of two phosphate-containing "heptasaccharide" fragments of the capsular polysaccharides of Streptococcus pneumoniae types 6A and 6B.
The "heptasaccharides" O-alpha-D-galactopyranosyl-(1----3)- O-alpha-D-glucopyranosyl-(1----3)-alpha, beta-L-rhamnopyranose 2''-[O-alpha-D-galactopyranosyl-(1----3)-O-alpha-D-glucopyranosyl- (1----3)-O-alpha-L-rhamnopyranosyl-(1----3)-D-ribit-5-yl sodium phosphate] (25) and O-alpha-D-galactopyranosyl- (1----3)-O-alpha-D-glucopyranosyl-(1----3)-alpha, beta-L-rhamnopyranose 2''-[O-alpha-D-galactopyranosyl-(1----3)-O-alpha-D-glucopyranosyl- (1----3)-O-alpha-L-rhamnopyranosyl-(1----4)-D-ribit-5-yl sodium phosphate] (27), which are structural elements of the capsular polysaccharides of Streptococcus pneumoniae types 6A and 6B ([----2)- -alpha-D-Galp-(1----3)-alpha-D-Glcp-(1----3)-alpha-L-Rhap- (1----X)-D-RibOH-(5-P----]n; 6A X = 3, 6B X = 4), respectively, have been synthesized. 2,4-Di-O-acetyl- 3-O-[2,4,6-tri-O-acetyl-3-O-(2,3,4,6-tetra-O-acetyl-alpha-D- galactopyranosyl)-alpha-D-glucopyranosyl]-alpha-L-rhamnopyranosyl trichloroacetimidate (13) was coupled with 5-O-allyloxycarbonyl-1,2,4-tri-O- benzyl-D-ribitol (10), using trimethylsilyl triflate as a promotor (----14), and deallyloxycarbonylation (----15) and conversion into the corresponding triethylammonium phosphonate then gave 16. Condensation of 16 with 4-methoxybenzyl 2,4-di-O-benzyl-3-O-[2,4,6-tri-O-benzyl-3-O-(3,4,6-tri-O-benzyl-alpha-D- galactopyranosyl)-alpha-D-glucopyranosyl]- alpha-L-rhamnopyranoside (22) followed by oxidation and deprotection afforded 25. 5-O-Allyl-1-O-allyloxycarbonyl-2,3-di-O-benzyl-D-ribitol (12) was coupled with 13, using trimethylsilyl triflate as a promoter, the resulting tetrasaccharide-alditol derivative 17 was deallyloxycarbonylated (----18), acetylated (----19), and deallylated (----20), and the product was converted into the triethylammonium phosphonate derivative 21. Condensation of 21 with 22 followed by oxidation and deprotection afforded 27.