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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During bacteriophage studies on Haemophilus influenzer, it was observed that encapsulated type b and unencapsulated Rb strains released a bactericidal substance acitve against types a, c, d, e, and f H. influenzae, non-typable H. influenzae strains, other Haemophilus species, and certain members of the Enterobacteriaceae. The bactericidal activity was assayed by a plaque test utilizing an Rd strain as an indicator lawn and was also demonstrated in mixed broth cultures of a producer strain and an indicator strain. Immediately lysis of sensitive bacteria by the factor was not evident. The factor is sensitive to trypsin but resistant to deoxyribonuclease, treatment with 2-mercaptoethanol, lipase, alpha-amylase, and heating in a 100 degrees C water bath for 20 min. The activity is not dependent upon increased Ca2+ or Mg2+ concentration as is necessary for HP1C1 and S2 phage propagation. The bactericidal factor is not pelleted by high-speed centrifugation at 150,000 X g for 6 h. Treatment with ultraviolet light or mitomycin C does not result in observable phage, phage-like particles, or increased bactericidal activity. T-HE BACTERICIDAL FACTOR IS NOT A TYPICAL SMALL MOLECULAR WEIGHT "COLICIN-LIKE" BACTERiocin in that it is not inducible, has a wider range of activity, and does not kill by "single-hit" kinetics. On preliminary characterization, it is a thermostable protein toxic to certain bacterial strains.
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PMID:Bactericidal substance produced by Haemophilus influenzae b. 108 28

Capsulated Haemophilus influenzae type b and two spontaneous mutants (classes I and II variants) were characterized by transmission and scanning electron microscopy. When cells were treated with type b-specific antiserum prior to manipulations for electron microscopy, sectioned capsulated cells had electron-dense, fibrous capsular antigen-antibody complexes around them. In negatively stained preparations, the complexes appeared as electron-transparent zones surrounding cells. In contrast, only residual electron-dense, extracellular material was seen in sectioned, untreated, capsulated cells, and electron-dense "bridges" connected adjacent cells in negatively stained preparations. No extracellular capsular material was seen around the class I and II variants. Characteristic electron-translucent regions were always observed within the cytosol of the class I cells, both in thin sections and by negative staining. These areas were located adjacent to the cell envelope separating the plasma membrane from the dense cytoplasmic matrix. At times, electron-dense, thread-like material extended from the dense cytoplasmic matrix to the plasma membrane. No such regions were seen in the capsulated and class II cells. Class I cells fixed with methanol or suspended in NaCl or phosphate-buffered saline prior to treatment with fluorescein-tagged type b-specific antiserum (FTA reagent) exhibited, by immunofluorescence, patches of capsular antigen along their sides. However, when fixed with glutaraldehyde or OsO4 or suspended in tris-(hydroxymethyl)aminomethane plus Ca2+ buffer prior to treatment with FTA reagent, no patches of capsular antigen were seen. Subsequent exposure of the latter cells to methanol followed by treatment with FTA reagent resulted in the reappearance of the patches of capsular antigen. Thus, in the class I variant the capsular antigen is unlikely to be surface located. Scanning electron microscopy revealed that class I and II variant cells within undisturbed colonies were regularly aligned side-by-side, whereas cells within colonies of the capsulated strain were randomly distributed.
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PMID:Ultrastructural characterization of capsulated Haemophilus influenzae type b and two spontaneous nontypable mutants. 108 40

Haemophilus influenza and its extracellular products (EP) did not release histamine from basophil leukocytes in cell suspensions from normal individuals, patients with chronic bronchitis or patients allergic to either house dust mite, grass pollen, cat dander or to their own bacteria. However, the EP was found to enhance their basophil histamine release. IgE-mediated histamine release was examined by stimulation of the cells with anti-IgE or the specific allergens, and non-immunological histamine release by stimulating the cells with the calcium ionophore A23187 or Staphylococcus aureus. In all the experiments EP caused a significant increase in the histamine release. When H. influenzae endotoxins were removed from the EP, the potentiating effect of EP was completely abolished, whereas heating (80 degrees C, 30 min) or treatment of EP with proteinase did not influence the potentiating effect. These results indicate that H. influenzae endotoxin potentiates histamine release caused by IgE-mediated reactions or by non-immunological mechanisms.
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PMID:Endotoxin from Haemophilus influenzae enhances IgE-mediated and non-immunological histamine release. 168 72

Haemophilus influenzae and its extracellular products (EP) did not release histamine in leukocyte suspensions from normal individuals. However, the EP were found to enhance basophil histamine release triggered by anti-IgE and by the calcium ionophore A23187. Experiments with EP indicate that it is the content of endotoxins which is responsible for the potentiating effect. Removal of endotoxin from the EP thus completely abolished the potentiating effect, whereas inactivation of its protease and proteins by heat-treatment or by proteinase K did not change the potentiation. A reinforcement of mediator release by the extracellular products of H. influenzae might play a pathophysiological role in chronic obstructive pulmonary disease.
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PMID:Haemophilus influenzae potentiates basophil histamine release possibly by its endotoxins. 169 61

The in vitro generation and release of 5-lipoxygenase metabolites of arachidonic acid by bovine peripheral blood neutrophils and alveolar neutrophils elicited with either a heat-killed bacterium, Haemophilus somnus, or platelet-activating factor, were compared. After stimulation with calcium ionophore A23187 for 2.5-60 min, up to 4.5 +/- 0.7 (mean +/- SEM) ng of LTB4 per 10(6) cells was released into the media by circulating neutrophils. LTB4 release by alveolar neutrophils was significantly less (P less than .05) than that of peripheral blood neutrophils from the same animal; 5-HETE release by circulating neutrophils was maximal after 5 min stimulation by ionophore (1.2 +/- 0.1 ng/10(6) cells) but was not identified in cell culture media after 20 min. Alveolar neutrophils released similar amounts of 5-HETE when compared to circulating neutrophils, and release of 5-HETE by alveolar neutrophils was maximal after 5 min of stimulation. However, the 5-HETE released into the culture media persisted throughout the 60 min time period at levels which were maximal (1.5 +/- 0.2 to 1.8 +/- 0.3 ng/10(6) cells). Bacterial killing and the release of superoxide anion were not different between the two cell populations.
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PMID:Characterization of arachidonic acid metabolism, superoxide production, and bacterial killing in bovine circulating neutrophils and elicited alveolar neutrophils. 254 24

Two toxins from Bordetella pertussis, pertussis toxin and Bordetella adenylate cyclase, cause profound disruptions of cAMP metabolism in mammalian cells. While the role of each toxin in the whooping cough syndrome is unknown, it is highly likely that together they confer on the organism an important proliferative advantage. Intact B. pertussis cells express large amounts of adenylate cyclase activity on their exterior surface. In a presently unknown fashion, this enzyme can enter human phagocytes, elevate cellular cAMP and impair host defense. We reasoned that this unusual enzyme might serve to signal the presence of B. pertussis in nasopharyngeal swabs from infected persons. Here we report a series of in vitro experiments which confirm the feasibility of such an approach. We find that calcium alginate swabs containing as few as 100 B. pertussis organisms produce readily detectable amounts of cAMP in our assay. Nasopharyngeal secretions swabbed from healthy volunteers, however produced no detectable cAMP alone and did not affect the production of cAMP by B. pertussis. We have also tested pure cultures of four common bacterial pathogens (Haemophilus influenzae, Streptococcus pyogenes, Staphylococcus aureus, and Escherichia coli) which may be co-isolated in clinical whooping cough and find that none interferes with the detection of B. pertussis. We conclude that the unique adenylate cyclase of B. pertussis might be a valuable diagnostic device.
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PMID:Bordetella adenylate cyclase: host toxicity and diagnostic utility. 287 18

The binding of the outer membrane-disorganizing peptide polymyxin B nonapeptide (PMBN) to gram-negative bacteria was studied by using tritium-labeled PMBN. Smooth Salmonella typhimurium had a binding capacity of ca. 6 nmol of PMBN per mg (dry weight) of bacteria, which corresponds to ca. 1 X 10(6) to 2 X 10(6) molecules of PMBN per single cell. The binding was of relatively high affinity (Kd, 1.3 microM). The isolated outer membrane of S. typhimurium bound ca. 100 nmol of PMBN per mg of outer membrane protein (Kd, 1.1 microM), whereas the cytoplasmic membrane bound 9 to 10 times less. Other bacteria which are susceptible to the action of PMBN (Escherichia coli strains, Pseudomonas aeruginosa, Haemophilus influenzae) also bound large amounts of PMBN. The S. typhimurium pmrA mutant, Neisseria gonorrhoeae, and Proteus mirabilis (all known as resistant to polymyxin and PMBN) bound 3.3, 4, and 12 times less than S. typhimurium, respectively. The binding of PMBN to S. typhimurium was effectively inhibited by low concentrations of polymyxin B, compound EM49 (octapeptin), polylysine, and protamine. Spermine, Ca2+, and Mg2+ also inhibited the PMBN binding although they were ca. 160, 700, and 2,400 times less active (based on molarity) than polymyxin B, respectively. No binding inhibition was found at the tested concentrations of streptomycin, tetralysine, spermidine, or cadaverine.
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PMID:Binding of polymyxin B nonapeptide to gram-negative bacteria. 298 30

The in vitro activity of LY146032, a new peptolide antibiotic, was compared with those of vancomycin, teicoplanin, imipenem, amoxicillin and erythromycin. LY146032 inhibited 90% of Staphylococcus aureus and Staphylococcus epidermidis, including methicillin-resistant isolates at less than or equal to 1 microgram/ml. Its activity was comparable to those of vancomycin and teicoplanin. MIC90s for the beta-hemolytic streptococci varied from 0.25 microgram/ml for group B streptococci to 4 micrograms/ml for some group C and F streptococci. MICs for Streptococcus faecalis were in the range of 0.5 to 8 micrograms/ml, and the MIC90 4 micrograms/ml, compared to 4 micrograms/ml for vancomycin and 1 microgram/ml for teicoplanin. For some viridans streptococci the MICs were 4 micrograms/ml, whereas Streptococcus pneumoniae were inhibited by 0.5 microgram/ml. Corynebacterium JK species were inhibited by 0.5 microgram/ml, similar to vancomycin, and Listeria monocytogenes by 4 micrograms/ml. Neisseria species, Haemophilus species and enteric species were not inhibited. Most MBCs were within two-fold of the respective MICs. After 14 days passage in sub-inhibitory concentrations of LY146032, Staphylococcus aureus, Staphylococcus epidermidis and Streptococcus faecalis showed minimal increase in MICs. The activity of LY146032 was increased by adding Ca2+ and was reduced in an anaerobic environment. Overall, LY146032 is an extremely interesting new agent that inhibits gram-positive species.
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PMID:In vitro activity of LY146032 (daptomycin), a new peptolide. 303 11

Spencer, Hugh T. (The Johns Hopkins University School of Hygiene and Public Health, Baltimore, Md.), and Roger M. Herriott. Development of competence of Haemophilus influenzae. J. Bacteriol. 90:911-920. 1965.-A chemically defined nongrowth medium was developed for the induction of competence of Haemophilus influenzae by a stepdown procedure. Cells grown logarithmically in Heart Infusion Broth became competent after being transferred to a medium which consisted of amino acids, sodium fumarate, and inorganic salts. Chloramphenicol (2 mug/ml) or l-valine (1 mug/ml) in the nongrowth medium inhibited development of competence. The inhibitory action of l-valine was reversed by comparable concentrations of l-isoleucine. Kinetic studies of the development of competence showed a variable capacity of competent cells to take up deoxyribonucleic acid and reaffirmed earlier findings that competence was not transmissible in H. influenzae. Addition of nicotinamide adenine dinucleotide, thiamine, calcium pantothenate, uracil, and hypoxanthine to the medium for competence resulted in a minimal growth medium in which reduced levels of competence were developed.
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PMID:Development of competence of Haemophilus influenzae. 529 17

Production and characterization of Haemophilus pleuropneumoniae hemolysin were investigated by using 5 serotype 2 strains. The hemolysin was produced in chicken meat-infusion broth medium both in stationary and in shaking cultures. In stationary culture, hemolytic activity against horse RBC reached maximum at postincubation day 5 (at the late stage of stationary phase), and the activity was maintained at the same level for 2 days thereafter. The hemolytic activity of shaking culture reached a maximum at postincubation hour 9 (at the early stage of logarithmic-growth phase), gradually decreased, and disappeared at postincubation day 2. The hemolysin was shown to be an extracellular product of the bacterial cells. The RBC of horses, rabbits, and sheep were highly susceptible to the hemolysin, and those of pigs and guinea pigs were less susceptible, whereas RBC of 60-day-old chicks were not susceptible. The hemolysin was not inactivated by autoclaving at 121 C for 2 hours, and by treatments with formalin, trypsin, or pronase. The presence of calcium or magnesium ions did not change the activity, whereas iodoacetic acid significantly reduced the activity.
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PMID:Characterization of the hemolysin produced by haemophilus pleuropneumoniae. 683 24


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