Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Haemophilus influenzae is a heme-dependent bacterium. However, little is known of the heme-iron uptake mechanism in this organism. By using a batch ligand affinity chromatography method, a hemin-binding protein of 39,500 molecular weight was isolated from total membranes derived from H. influenzae type b grown under iron-depleted but not under iron-sufficient conditions. Detection of the hemin-binding protein in a whole-cell binding assay demonstrated a surface-exposed location. Competition binding experiments indicated that this hemin-protein interaction was specific, since only hemin or heme-containing proteins, such as human hemoglobin and bovine catalase, but not protoporphyrin IX, iron-loaded human lactoferrin, or transferrin, could abrogate binding. In a limited survey of other H. influenzae strains, an identical hemin-binding protein was isolated, implying that this polypeptide may be structurally and functionally conserved among strains.
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PMID:Isolation of an outer membrane hemin-binding protein of Haemophilus influenzae type b. 154 54

We sought to determine whether chloramphenicol would worsen or mitigate the anemia associated with Haemophilus influenzae type b meningitis if administered in doses which produce 'therapeutic' serum concentrations. Seventy-four cases of H. influenzae meningitis were stratified by chloramphenicol cumulative doses (mg/kg body weight) of less than 300 and greater than 300. There was no significant difference in the decrease in blood hemoglobin concentration or in the increase in the FEP:Heme ratio between the two study groups. Plasma iron and transferrin saturation values indicated iron deficiency at days 1 and 5 of hospitalization; by day 10 mean values were within the normal range. These data suggest that H. influenzae type b meningitis, not chloramphenicol therapy in the presence of monitoring is causing the observed anemia.
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PMID:Anemia during Haemophilus influenzae type b meningitis: lack of an effect of chloramphenicol. 276 22

Brazilian purpuric fever (BPF) is a newly recognized fulminant pediatric infection caused by bacteremia with Hemophilus influenzae biogroup aegyptius (Hae). Following intraperitoneal inoculation, each of five disease isolates caused bacteremia more frequently than control, conjunctival isolates of Hae in complement-depleted 6-d-old rats. Sustained but self-limited bacteremia was observed in normal infant rats after inoculation with a disease strain. These rats developed meningitis and had depressed hemoglobin concentration and platelet counts. Pathologic examination showed meningitis and contiguous otitis. Pretreatment of infant rats with immune adult rat serum raised against disease isolates protected rats from bacteremia. Normal adult rat serum or immune rat serum against control strains failed to protect infant rats. Thus, strains of Hae isolated from patients with BPF are more virulent than control strains. Antibody against antigens unique to disease isolates protects infant rats from bacteremia.
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PMID:An infant rat model of bacteremia with Brazilian purpuric fever isolates of Hemophilus influenzae biogroup aegyptius. Brazilian Purpuric Fever Study Group. 278

There is poor correlation between the MICs and zone sizes obtained for erythromycin against Haemophilus influenzae. The effect of two media, Mueller-Hinton medium supplemented with 3% lysed horse blood and 10 micrograms of NAD per ml (MHA + LYHB) and Mueller-Hinton agar supplemented with 1% bovine hemoglobin and 1% IsoVitaleX (MHA + HGB), on the MICs and zone sizes of erythromycin against H. influenzae was determined. The effect of three different methods for inoculum preparation on the susceptibility of H. influenzae was also determined. The MICs were independent of the method of inoculum preparation, but the zone sizes were smaller if the inoculum was carefully adjusted to contain approximately 10(8) CFU/ml. MICs were higher and zone sizes were smaller when MHA + HGB was used instead of MHA + LYHB. Good correlation was found when MHA + LYHB was used for determining the MIC and MHA + HGB was used for determining susceptibility by the disk method. When the inoculum was adjusted to match a McFarland 0.5 standard, the viable counts had to be approximately 10(8) CFU/ml for good correlation between MICs and zone sizes. A-56268, a new macrolide antibiotic, was tested against H. influenzae, and its MICs and tentative breakpoints against this organism were determined. The MICs obtained by various methods were correlated with in vivo efficacy by using a mouse septicemia model. MICs obtained on MHA + HGB or MHA + LYHB incubated without a 5% CO2 atmosphere showed the best correlation with in vivo efficacy.
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PMID:Susceptibility testing of macrolide antibiotics against Haemophilus influenzae and correlation of in vitro results with in vivo efficacy in a mouse septicemia model. 295 54

The mechanisms for acquisition of iron by Haemophilus influenzae and their role in pathogenesis are not known. Heme and nonheme sources of iron were evaluated for their effect on growth of type b and nontypable strains of H. influenzae in an iron-restricted, defined medium. All 13 strains acquired iron from heme, hemoglobin, hemoglobin-haptoglobin, and heme-hemopexin. Among nonheme sources of protein-bound iron, growth of H. influenzae was enhanced by partially saturated human transferrin but not by lactoferrin or ferritin. Purified ferrienterochelin and ferridesferrioxamine failed to provide iron to H. influenzae, and the supernatants of H. influenzae E1a grown in iron-restricted medium failed to enhance iron-restricted growth of siderophore-dependent strains of Escherichia coli, Salmonella typhimurium, and Arthrobacter terregens. Marked alterations in the profile of outer membrane proteins of H. influenzae were observed when the level of free iron was varied between 1 microM and 1 mM. Catechols were not detected in the supernatants of strain E1a; however, iron-related hydroxamate production was detected by two biochemical assays. We conclude that the sources of iron for H. influenzae are diverse. The significance of hydroxamate production and iron-related outer membrane proteins to H. influenzae iron acquisition is not yet clear.
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PMID:Iron acquisition by Haemophilus influenzae. 296 10

Although Haemophilus influenzae requires heme for growth, the source of heme during invasive infections is not known. We compared heme, lactoperoxidase, catalase, cytochrome c, myoglobin, and hemoglobin as sources of heme for growth in defined media. The minimum concentration of heme permitting unrestricted growth of strain E1a, an H. influenzae type b isolate from cerebrospinal fluid, was 0.02 micrograms/ml. Using molar equivalents of heme as lactoperoxidase, catalase, cytochrome c, myoglobin, and hemoglobin, we determined that myoglobin and hemoglobin permitted unrestricted growth at this concentration. To determine the ability of host defenses to sequester heme from H. influenzae, we used affinity chromatography to purify human haptoglobin and hemopexin, serum proteins which bind hemoglobin and heme. Plate assays revealed that 12 strains of H. influenzae acquired heme from hemoglobin, hemoglobin-haptoglobin, heme-hemopexin, and heme-albumin. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of outer membrane proteins of strain E1a grown in heme-replete and heme-restricted conditions revealed a heme-repressible outer membrane protein with an apparent molecular mass of 38 kilodaltons. These results demonstrated that, unlike Escherichia coli, H. influenzae may acquire heme from hemoglobin-haptoglobin. H. influenzae also may acquire heme from hemopexin and albumin, which have not been previously investigated. The role of outer membrane proteins in the acquisition of heme is not yet clear.
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PMID:Protein sources of heme for Haemophilus influenzae. 302 98

A disseminated and fatal infection was established in C57BL mice, injected intraperitoneally with either Neisseria meningitidis B,2b or Haemophilus influenzae type b bacteria plus enhancement factors. The effects of mucin, hemoglobin, and iron dextran as enhancement of bacterial infectivity in mice were evaluated individually and in combination. A mixture of mucin and hemoglobin was most effective in enhancing the virulence of the pathogens. Inbred mouse lines were more susceptible than outbred ones. Relative virulence of a number of bacterial strains was also compared in one selected mouse line. Neisseria meningitidis B,2b and Haemophilus influenzae type b strains were more virulent than non-B,2b and nontypable strains. Finally, the course of bacteremia for the two infections in mice was followed by quantitative blood cultures. The animals succumbed to the generalized condition within 72 h. In the case of Neisseria meningitidis B,2b, 10 organisms with 4% mucin and 1.6% hemoglobin were sufficient to kill 50% of the animals. For Haemophilus influenzae type b, 300 bacteria with 5% mucin and 2% hemoglobin were necessary to obtain similar effects.
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PMID:Mouse models of infection for Neisseria meningitidis B,2b and Haemophilus influenzae type b diseases. 308 50

In the present study, five non-beta-lactamase- and five beta-lactamase-producing strains of Haemophilus influenzae were used to determine whether three different growth media, Mueller-Hinton broth and agar, brain heart infusion broth and agar, and tryptic soy broth and agar, and their added supplements (0.2% hemin-0.1% IsoVitaleX, 1% hemin-1% IsoVitaleX, 2% sheep blood, 10% Fildes enrichment, 5% Fildes enrichment, 1% supplement B, 5% horse erythrocytes, and 2% hemoglobin-1% IsoVitaleX) would influence the growth rate of this microorganism and the antibacterial activity of eight antibiotics, including ampicillin, tetracycline, chloramphenicol, gentamicin, cefamandole, erythromycin, trimethoprim-sulfamethoxazole (TMP-SMX), and cefoperazone. The growth curve studies were carried out with an initial inoculum of 10(4) bacteria per ml, and MICs were determined with an inoculum of 5 X 10(5) microorganisms. Mueller-Hinton broth, brain heart infusion broth, and tryptic soy broth enriched with 5% Fildes resulted in a maximal growth of more than 10(8) CFU/ml at 24 h. When 10% Fildes or 2% sheep blood was added as enrichment to Mueller-Hinton broth, a considerable reduction in the growth rate of H. influenzae strains resulted (P less than 0.01). Significant variations in MICs (P less than 0.01) were observed with chloramphenicol, TMP-SMX, erythromycin, and cefoperazone when brain heart infusion agar, Mueller-Hinton agar, or tryptic soy agar was used. Chloramphenicol, gentamicin, erythromycin, and TMP-SMX were all affected by the different enrichments added to Mueller-Hinton agar. MICs were in general higher with 5% Fildes enrichment and lower with 1% supplement B. Cefoperazone was the only drug which exhibited a lower MIC in 5% Fildes enrichment for ampicillin-resistant H. influenzae strains.
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PMID:Influence of growth medium and supplement on growth of Haemophilus influenzae and on antibacterial activity of several antibiotics. 349 45

The activity of chloramphenicol against 100 different strains of Haemophilus influenzae was assessed by a macrotube broth dilution technique and by a standardized disk diffusion method using both enriched chocolate agar (CHOC) and Mueller-Hinton agar containing 1.0% hemoglobin and 1.0% IsoVitaleX (BBL Microbiology Systems, Cockeysville, Md.) supplement (CHOC-MHA). Filter disks containing 30 micrograms of chloramphenicol were used with the disk diffusion procedure. The following zone diameter interpretive criteria were defined: CHOC-MHA, less than or equal to 25 mm = resistant [corrected] and greater than or equal to 26 mm = susceptible [corrected]; CHOC, less than or equal to 28 mm = resistant [corrected] and greater than or equal to 29 mm = susceptible [corrected]. all of the H. influenzae strains examined were also characterized by using two rapid assays for chloramphenicol acetyltransferase (CAT) activity: a 1-h tube method (t-CAT) and a 30-min procedure which used commercially available reagent-impregnated disks (d-CAT). The t-CAT procedure was found to be significantly more accurate than the d-CAT procedure as a means for demonstrating production of CAT.
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PMID:In vitro chloramphenicol susceptibility testing of Haemophilus influenzae: disk diffusion procedures and assays for chloramphenicol acetyltransferase. 349 44

A total of 114 strains of Haemophilus influenza were characterized with respect to beta-lactamase production and ampicillin MIC. Of this total, 41 strains produced a TEM-type beta-lactamase, and ampicillin MICs for these strains were greater than or equal to 2.0 microgram/ml. It was found that 54 strains lacked TEM-type beta-lactamase activity, and ampicillin MICs for them were less than or equal to 0.5 microgram/ml. The remaining 19 strains were beta-lactamase negative, but ampicillin MICs were greater than or equal to 2.0 micrograms/ml. Disk diffusion susceptibility tests were performed with two media, i.e., Mueller-Hinton agar containing 1.0% hemoglobin and 1.0% IsoVitaleX supplement (CHOC-MHA) and enriched chocolate agar (CHOC), by using disks containing 10 and 2 micrograms of ampicillin. If strains of H. influenzae for which ampicillin MICs were greater than or equal to 2.0 micrograms/ml were considered resistant, while strains for which MICs were less than or equal to 0.5 microgram/ml were considered susceptible, the following zone diameter interpretive criteria were identified as indicating ampicillin susceptibility: CHOC-MHA (10-micrograms disks), greater than or equal to 20 mm; CHOC-MHA (2-micrograms disks), greater than or equal to 17 mm; CHOC (10-micrograms disks), greater than or equal to 25 mm; and CHOC (2-micrograms disks), greater than or equal to 20 mm. In all cases, zones of inhibition less than those listed above would be interpreted as indicating resistance. Each of these four combinations was found to be essentially equivalent in identifying susceptible and resistant strains of H. influenzae, irrespective of beta-lactamase production.
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PMID:Ampicillin disk diffusion susceptibility testing of Haemophilus influenzae. 349 38


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