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)

Three children had osteomyelitis due to Haemophilus influenzae type b. They were seen with signs and symptoms indistinguishable from infection caused by other organisms. One child was initially misdiagnosed as having septic arthritis because of failure to appreciate that Hemophilus may also cause bone infection. In the second patient osteomyelitis and arthritis developed during ampicillin sodium therapy for treatment of Hemophilus meningitis. His initial infection was caused by an ampicillin-sensitive isolate but his orthopedic infection subsequently responded to therapy only after changing to a regimen of chloramphenicol. In the third patient, bone scintigraphy was helpful in diagnosis since serial roentgenograms were not diagnostic of osteomyelitis. The anticapsular antibody responses of these patients were measured by radioimmune assay. The levels found were low but comparable to age-matched control children with H influenzae type b meningitis.
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PMID:Haemophilus influenzae type b osteomyelitis. 30 93

Transposon Tn916 was shown to be capable of direct conjugative transfer in broth and membrane matings between strains of Escherichia coli K12 and between E. coli K12 and Haemophilus influenzae type b. Only Tn916 was transferred, but Tn916 donor ability was not itself inheritable by the recipients and seemed to be associated with the presence of Tn916 on a non-conjugative pBR322-derived vector in the original donor strain. Transfer of Tn916 by conjugation was found to be an efficient method for producing insertion mutations in the chromosome of recipient cells. Although such insertions were unstable when the cells were grown under non-selective conditions, it was possible to show that over 40% of the isolated Tn916 insertions in the chromosome of E. coli K12 were in gene(s) concerned with histidine biosynthesis, implying that there is a partial hot-spot for Tn916 insertion on the E. coli K12 chromosome. When a strain of H. influenzae type b was used as a recipient, out of approximately 1500 transconjugants tested, two mutants were isolated with insertions in genes controlling the expression of iron-regulated transferrin-binding proteins. These mutants constitutively produced major 76 kDa and minor 90 kDa proteins which bound transferrin, even when grown under iron-sufficient conditions. Tn916 insertion mutagenesis, following transfer by conjugation, is a convenient method for isolating mutations in genes concerned with iron acquisition by this important human pathogen.
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PMID:Tn916 insertion mutagenesis in Escherichia coli and Haemophilus influenzae type b following conjugative transfer. 131 5

The mutated gene in JG16, a Haemophilus influenzae strain deficient in competence-induced DNA binding and uptake, was cloned and the wild-type allele was sequenced. The gene was shown by Northern analysis to be constitutively expressed on a 1.7-kilobase transcript. The gene product was identified as a 20.6-kDa protein targeted to the periplasm. The protein contains the sequence Cys-Pro-His-Cys (CPHC) and is highly similar to two other periplasmic CPHC motif-containing proteins: DsbA, an Escherichia coli protein (45% identity, 87% homology) and TcpG, a Vibrio cholerae protein (32% identity, 74% homology). Both DsbA and TcpG promote disulfide bond formation in periplasmic proteins, are required for pilus biogenesis, and, like thioredoxin, are capable of reducing insulin in vitro. The Haemophilus protein was shown to complement an E. coli mutation in DsbA and was named Por (periplasmic oxidoreductase). In JG16 the competence-dependent redistribution of inner membrane proteins did not occur. These findings suggest that Por is required for the correct assembly and/or folding of one or more disulfide-containing cell envelope protein involved either in competence development or in the DNA-binding and -uptake machinery.
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PMID:A periplasmic protein disulfide oxidoreductase is required for transformation of Haemophilus influenzae Rd. 143 13

The phototoxicity of 8-methoxythionepsoralen (8-MOTP) and 6-methylthione coumarin (6-MTC) when activated by UV-A has been investigated using a variety of Escherichia coli strains, Haemophilus influenzae transforming DNA and Escherichia coli pBR322 plasmid DNA. The results demonstrate that 8-MOTP is a strictly oxygen independent photosensitizer that is about 500-fold less efficient in forming lesions leading to equivalent lethality than is the parent compound from which it is derived (8-MOP). As is true for 8-MOP, 8-MOTP is capable of inducing histidine independent mutations in E. coli and inactivating transforming DNA consistent with DNA being a target for lesions induced by this molecule in the presence of UV-A. 6-MTC is a strongly oxygen dependent photosensitizer activated by UV-A when tested with either E. coli cells or transforming DNA in contrast to the parent compound (6-methylcoumarin; 6-MC) which is not phototoxic when treated with UV-A. These results imply that the membrane may be an important target leading to lethality. 6-MTC in the presence of UV-A can inactivate pBR322 plasmid and Haemophilus influenzae transforming DNA activity in vitro suggesting that DNA is a potential target for this molecule when activated by UV-A.
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PMID:The phototoxicity of 8-methoxythionepsoralen and 6-methylthionecoumarin. 143 69

We investigated whether production of histamine by bacteria isolated from sputum of patients with infective lung diseases could be attributed to the presence of histidine decarboxylase (HD). Twenty gram-positive and 20 gram-negative organisms were studied for their ability to decarboxylate 14C-histidine in vitro over the pH range 4.5-7.5. Of the bacteria investigated, lysates from the gram-negative species Haemophilus influenzae, H. parainfluenzae, Moraxella (Branhamella) catarrhalis and Pseudomonas aeruginosa liberated 14CO2 and histamine from 14C-histidine in the presence of the cofactor pyridoxal phosphate. In contrast, results obtained in the absence of cofactor were similar to those of negative (lysate-free) controls suggesting that the HD enzymes of these species resembled those previously described in other gram-negative bacteria. No HD activity was detected over this pH range in lysates from gram-positive species. This finding correlated with earlier observations that these gram-positive organisms did not produce histamine in vitro.
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PMID:Histidine decarboxylases from bacteria that colonise the human respiratory tract. 172 55

alpha-Terthienyl photosensitizes single strand breaks in pBR322 DNA. Almost identical results were observed under oxygen and under argon. In the presence of oxygen, this DNA nicking was enhanced by histidine and was not affected by superoxide dismutase, catalase, or the antioxidant BHT. Although chemical damage to DNA treated with alpha-terthienyl plus near-UV was clearly demonstrated in vitro, transformation in E. coli with this damaged pBR322 DNA still took place. Likewise, Haemophilus influenzae DNA transforming activity was not significantly decreased by photosensitization with alpha-terthienyl.
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PMID:alpha-Terthienyl photosensitizes damage to pBR322 DNA. 185 40

Copper-zinc superoxide dismutase ([Cu,Zn]-SOD) is widely found in eukaryotes but has only rarely been identified in bacteria. Here we describe sodC, encoding [Cu,Zn]-SOD in Haemophilus influenzae and H. parainfluenzae, frequent colonists and pathogens of the human respiratory tract. In capsulate H. influenzae, sodC was found in only one division of the bacterial population, and although the protein it encoded was clearly [Cu,Zn]-SOD from its deduced sequence, it lacked enzymatic activity. In H. parainfluenzae, in contrast, active enzyme was synthesized which appeared to be secreted beyond the cytoplasm when the gene was expressed in Escherichia coli minicells. The origin of gene transcription differed between the Haemophilus species, but protein synthesis from cloned genes in vitro was comparable. A C-T transition was found in the H. influenzae sequence compared with the H. parainfluenzae sequence, leading to a histidine, known to be crucial in eukaryotic [Cu,Zn]-SOD for copper ion coordination and so for enzymatic activity, to be changed to tyrosine. This is speculated to be the cause of inactivity of the H. influenzae enzyme. Secreted SODs have only been described in a few bacterial species, and this is the first identification of [Cu,Zn]-SOD in a common human upper respiratory tract colonist. The role of secreted bacterial SODs is unknown, and we speculate that in Haemophilus species the enzyme may confer survival advantage by accelerating dismutation of superoxide of environmental origin to hydrogen peroxide, disruptive to the normal mucociliary clearance process in the host.
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PMID:Copper-zinc superoxide dismutase of Haemophilus influenzae and H. parainfluenzae. 193 42

Freeze-substitution was performed on strains of Escherichia coli, Pasteurella multocida, Campylobacter fetus, Vibrio cholerae, Pseudomonas aeruginosa, Pseudomonas putida, Aeromonas salmonicida, Proteus mirabilis, Haemophilus pleuropneumoniae, Caulobacter crescentus, and Leptothrix discophora with a substitution medium composed of 2% osmium tetroxide and 2% uranyl acetate in anhydrous acetone. A thick periplasmic gel ranging from 10.6 to 14.3 nm in width was displayed in E. coli K-12, K30, and His 1 (a K-12 derivative containing the K30 capsule genes), P. multocida, C. fetus, P. putida, A. salmonicida, H. pleuropneumoniae, and P. mirabilis. The other bacteria possessed translucent periplasms in which a thinner peptidoglycan layer was seen. Capsular polysaccharide, evident as electron-dense fibers radiating outward perpendicular to the cell surface, was observed on E. coli K30 and His 1 and P. mirabilis cells. A more random arrangement of fibers forming a netlike structure was apparent surrounding cells of H. pleuropneumoniae. For the first time a capsule, distinct from the sheath, was observed on L. discophora. In all instances, capsular polysaccharide was visualized in the absence of stabilizing agents such as homologous antisera or ruthenium red. Other distinct envelope structures were observed external to the outer membrane including the sheath of L. discophora and the S layers of A. salmonicida A450 and C. crescentus CB15A. We believe that the freeze-substitution technique presents a more accurate image of the structural organization of these cells and that it has revealed complex ultrastructural relationships between cell envelope constituents previously difficult to visualize by more conventional means of preparation.
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PMID:Freeze-substitution of gram-negative eubacteria: general cell morphology and envelope profiles. 199 83

We report a case of Burkitt's lymphoma developing in a 7-year-old boy with hyper-IgE syndrome. This is the third reported case of malignancy in the hyper-IgE syndrome. The other two cases were an 18-year-old man with Hodgkin's disease and a 10-year-old girl with histiocytic lymphoma. The patient developed retroperitoneal Burkitt's lymphoma with probable metastasis to the brain. His short life was characterized by recurrent staphylococcal skin, middle ear, and lung infections associated with extremely elevated serum concentrations of IgE. There was also an associated disturbance of bone metabolism with osteoporosis and pathologic fractures and absence of parathormone, findings that have been observed in other patients with hyper-IgE syndrome and other forms of T cell immunodeficiency. At the age of 5 years, inadequate B cell responses to immunization with antigens derived from diphtheria, tetanus, and Haemophilus influenzae type b organisms and with the OX174 bacteriophage were demonstrated in the patient. In his terminal state his in vitro lymphocyte analysis demonstrated findings of anergy. Although the precise immunologic defect in hyper-IgE syndrome is unknown, these cases of associated malignancy stress the role that a completely normal immune system plays in preventing the premature appearance of cancer.
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PMID:Burkitt's lymphoma developing in a 7-year-old boy with hyper-IgE syndrome. 278 97

Fluoranthene, a non-carcinogenic polycyclic aromatic hydrocarbon, inactivates Escherichia coli cells in the presence of near-ultraviolet light (NUV; 300-400 nm). E coli cells carrying defects in the uvrA6 or katF genes are sensitized to inactivation by the simultaneous treatment with fluoranthene and NUV, suggesting that DNA is a target and that hydrogen peroxide is generated. Haemophilus influenzae transforming DNA can be inactivated by the simultaneous treatment with fluoranthene and NUV confirming DNA as a target. Using the photooxidation of imidazole and histidine as probes, fluoranthene was found to generate singlet oxygen in organic and aqueous media. In water, it participated in electron transfer reactions, reducing nitro blue tetrazolium as well as ferricytochrome C. This reduction took place both in the presence of air, where superoxide anion was formed, and under argon. Simultaneous treatment with fluoranthene and NUV was incapable of inducing histidine-independent mutations. Simultaneous treatment with fluoranthene and NUV was incapable of inducing the uvrA gene product as evidenced by the absence of the induction of beta-galactosidase in an E coli operon fusion strain [uvrA215::Mud(Ap,lac)].
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PMID:Phototoxic effects of fluoranthene, a polycyclic aromatic hydrocarbon, on bacterial species. 282 96


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