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At least 73 records · Page 4Linked to original sources
PubMed2000

Characterization of the distal tail fiber locus and determination of the receptor for phage AR1, which specifically infects Escherichia coli O157:H7.

Phage AR1 is similar to phage T4 in several essential genes but differs in host range. AR1 infects various isolates of Escherichia coli O157:H7 but does not infect K-12 strains that are commonly infected by T4. We report here the determinants that confer this infection specificity. In T-even phages, gp37 and gp38 are components of the tail fiber that are critical for phage-host interaction. The counterparts in AR1 may be similarly important and, therefore, were characterized. The AR1 gp37 has a sequence that differs totally from those of T2 and T4, except for a short stretch at the N terminus. The gp38 sequence, however, has some conservation between AR1 and T2 but not between AR1 and T4. The sequences that are most closely related to the AR1 gp37 and gp38 are those of phage Ac3 in the T2 family. To identify the AR1-specific receptor, E. coli O157:H7 was mutated by Tn10 insertion and selected for an AR1-resistant phenotype. A mutant so obtained has an insertion occurring at ompC that encodes an outer membrane porin. To confirm the role of OmpC in the AR1 infection, homologous replacement was used to create an ompC disruption mutant (RM). When RM was complemented with OmpC originated from an O157:H7 strain, but not from K-12, its AR1 susceptibility was fully restored. Our results suggest that the host specificity of AR1 is mediated at least in part through the OmpC molecule.

Bacteriophages↗
PubMed2002

Febrile urinary tract infection: Escherichia coli susceptibility to oral antimicrobials.

Empirical treatment is indicated for young children with febrile urinary tract infection (UTI). In this clinical setting, oral antibiotics are as safe and effective as intravenous therapy. The aim of this study was to investigate in children with febrile UTI whether there were longitudinal changes in the prevalence of bacteria and in the pattern of Escherichia coli susceptibility to oral antimicrobial agents. Two hundred and eighty-seven positive urine cultures from children (1 month to 12 years) with febrile UTI collected over three periods (1986-1989, 1990-1991, and 1997) were studied. E. coli was the most-prevalent microorganism in all three study-periods ( n=228). The susceptibility pattern of E. coli to nitrofurantoin (92%, 95%, 94%) and nalidixic acid (85%, 92%, 95%) did not present any statistically significant differences ( P>0.05) over time. There was a significant increase ( P<0.05) in E. coli susceptibility to cephalexin (65%, 54%, 81%). The E. coli susceptibility to trimethoprim-sulfamethoxazole (40%, 85%, 40%) behaved differently. Initially there was a significant rise ( P<0.05), followed by a significant decrease ( P<0.05). Empirical oral treatment with nitrofurantoin or nalidixic acid can safely be started in children with febrile UTI seen in the Emergency Department, Hospital de Clínicas de Porto Alegre, Brazil.

Administration, Oral↗
PubMed1975

The regulation of transcription in bacteriophage T5-infected Escherichia coli.

The expression of bacteriophage T5-specific RNA and protein in infected cells is temporally separated into three classes: class I (preearly), class II (early), and class III (late). By immunoprecipitation techniques we have shown that T5 infection of cells leads to the synthesis of one class I polypeptide (11,000 daltons) and two class II polypeptides (90,000 and 15,000 daltons) capable of binding to the RNA polymerase of the host Escherichia coli cell. One of the class II polypeptides (90,000 daltons) is the product of gene C2, which is an essential gene product required for the initiation of class III RNA synthesis. The colicinogenic factor, ColIb, is a plasmid which prevents the normal synthesis of class II and the III bacteriophage T5-specific RNA in infected colicinogenic (ColIb+) cells. In T5-infected colicinogenic cells, only the T5 class I polypeptide is found associated with the RNA polymerase. Mutants of T5, designated T5h minus, are capable of growth on both noncolicinogenic and ColIb+ hosts. Extracts of T5h minus infected ColIb+ cells were shown to lack a small class I polypeptide (12,000 daltons) as compared to T5-infected cells. The h minus mutation, however, has no effect on the levels of the class I T5 polypeptide of similar molecular weight which is bound to the RNA polymerase. One effect of the h minus mutation is to enhance the quantities of the two class II polypeptides bound to the enzyme.

Bacterial Proteins↗
PubMed1978

Release of a special fraction of the outer membrane from both growing and phage T4-infected Escherichia coli B.

Growing Escherichia coli release envelope material into the medium. Upon infection with T4 phage increased amounts of this material are released and at a greater rate. In order to determine whether both inner and outer membranes are present in this material, and whether the material released by growing cells differs from that released by infected cells, we have examined the protein composition of envelope released by growing and T4-infected E. coli B. Our results show: (a) the protein composition of envelope released from growing or infected cells is similar, (b) the proteins present are representative of the outer membrane, (c) the major outer membrane protein of E. coli B, protein II, is deficient in the released material. We therefore conclude that the envelope material released from growing or infected E. coli represents a special fraction of the outer membrane. This finding is discussed in relation to outer membrane structure and function. In addition, data are presented on the differing outer membrane protein composition of substrains of E. coli B obtained from different laboratories.

Bacterial Proteins↗
PubMed1991

[Ultrastructural changes in rectal mucosa cells in experimental Escherichia infection].

Ultrastructural changes of rectum epitheliocytes and cells of lamina propria were studied at the period from 15 minutes to 2 days after inoculation using the model of experimental escherichiosis. The results obtained allow to determine the correlation of ultrastructural changes and the data of morphometric analysis. Ultrastructural peculiarities were determined of the rectum cells and the different cell populations were studied during infection's process.

Acute Disease↗
PubMed1985

Lethal microbial synergism in intra-abdominal infections. Escherichia coli and Bacteroides fragilis.

The ability of Bacteroides fragilis and Escherichia coli to produce synergistic mortality when mixed into intraperitoneal (IP) fibrin clots was tested in rats. The addition of B fragilis (2 X 10(9) colony-forming units/clot) to E coli (2 X 10(8) colony-forming units/clot) in the clot significantly enhanced both early and late mortality rates when compared to either E coli or B fragilis alone. Multiple washings of B fragilis prior to mixing with E coli in the clot delayed the enhancement of lethality from 24 to 48 hours. By seven days, washed B fragilis was as synergistic with E coli as unwashed B fragilis plus E coli. Furthermore, unwashed killed B fragilis was as synergistic when mixed with E coli in the fibrin clot as unwashed living B fragilis. However, washed dead B fragilis plus E coli produced no greater mortality than E coli alone. The lethality of an IP clot containing E coli was significantly increased when B fragilis was mixed with it in the same clot, injected free IP, and or implanted into a separate IP clot. Intraperitoneal E coli-fibrin clot lethality was not increased by subcutaneous B fragilis and was only slightly enhanced by intravenous B fragilis inoculation. The strain of B fragilis used in these studies did not produce fibrinolysins at any concentration. The data support the idea that synergistic mortality between E coli and B fragilis in this model is caused by a heat-stable surface factor produced by B fragilis, which acts to increase the lethal effects of E coli.

Abscess↗
PubMed1979

RNA-linked nascent DNA pieces in phage T7-infected Escherichia coli. III. Detection of intact primer RNA.

RNA-linked DNA fragments of T7-infected Escherichiacoli were labeled with [(32)P]orthophosphate invivo. The RNA segments of the labeled fragments were isolated by degrading the DNA portion with the 3'--> 5' exonuclease intrinsic to bacteriophage T4 DNA polymerase and fractionated according to net charge by a DEAE-Sephadex A-25 column chromatography in the presence of 7 M urea. Tri-, tetra- and pentanucleotides were obtained which have ATP residues at their 5' ends. Most of the pentanucleotides had a single deoxynucleotide at the 3' end but a minor portion was totally an oligoribonucleotide. In the light of prior results, the former is a cooligomer of an intact tetraribonucleotide primer and a monodeoxynucleotide and the latter is an intact pentaribonucleotide primer. Tri- and tetraribonucleotides with ATP at the 5' ends had no deoxynucleotide at the 3' ends, therefore it is not clear if intact triribonucleotide primers are present. The 5'-terminal dinucleotides of the tetra- and pentanucleotides were mostly pppApC and a trace amount of pppApA was present.Images

Base Sequence↗
PubMed1992

[Submicroscopic features of cecal cells in experimental Escherichia infection].

Ultrastructural changes of the caecum cells were studied for the period from 15 minutes to 2 weeks after inoculation using the model of experimental escherichiosis. Evolution processes in relation to different caecum cell populations were followed up submicroscopically. Ultrastructural changes observed evidence derangement of protein and water-salt cell metabolism, immune trends of experimental escherichiosis.

Animals↗
PubMed1990

[Ultrastructure of the epithelial cells of the duodenum at the early stages of experimental Escherichia infection].

Ultrastructural changes of duodenal epitheliocytes were studied at the period from 15 minutes to 24 hours after inoculation using the model of experimental esherichiosis. The results obtained allow to determine the succession of ultrastructural changes and dynamics of adenylate cyclase activity of epithelial cells, involvement of endocrine cells in the pathological process. Combination of the certain morphological and cytochemical reactions and their dynamics allowed to make conclusions about typical ultrastructural changes in epitheliocytes at the early stages of experimental esherichiosis.

Adenylyl Cyclases↗
PubMed1982

Demonstration of pyrimidine dimer-DNA glycosylase activity in vivo: bacteriophage T4-infected Escherichia coli as a model system.

An approach to the detection of pyrimidine dimer-DNA glycosylase activity in living cells is presented. Mutants of Escherichia coli defective in uvr functions required for incision of UV-irradiated DNA were infected with phage T4 denV+ or denV- (defective in the T4 pyrimidine dimer-DNA glycosylase activity). In the former case the denV gene product catalyzed the incision of UV-irradiated host DNA, facilitating the subsequent excision of thymine-containing pyrimidine dimers. Isolation of these dimers from the acid-soluble fraction of infected cells was achieved by a multistep thin-layer chromatographic system. Exposure of the dimers to irradiation that monomerizes pyrimidine dimers (direct photoreversal) resulted in the stoichiometric formation of free thymine. Thus, in vivo incision of UV-irradiated DNA dependent on a pyrimidine dimer-DNA glycosylase can be demonstrated.

Cell-Free System↗
PubMed1983

Transcription in bacteriophage f1-infected Escherichia coli: very large RNA species are synthesized on the phage DNA.

Fractionation of pulse-labeled RNA extracted from E. coli cells infected with phage f1 and hybridization of this RNA to f1 DNA reveals that very large species are synthesized on the phage genome. Hybridization of the RNA to specific fragments of f1 DNA shows that, in the infected cell, at least one mRNA is present into which the sequences of genes III, VI, and I are all transcribed together. This result fully explains the polar effect shown by gene III mutants on the expression of genes VI and I (Pratt et al. 1966).

Coliphages↗
PubMed1985

Host transfer RNA cleavage and reunion in T4-infected Escherichia coli CTr5x.

T4 mutants lacking polynucleotide kinase (pnk-) or RNA ligase (rli-) do not grow on E. coli CTr5x. During the abortive infections there accumulate host tRNA fragments that match into two species severed 3' to the anticodon. The CTr5x-specific fragments appear only transiently with wt phage, implicating the affected enzymes in phosphoryl group rearrangement and religation [David et al. (1982) Virol. 123, 480]. In a search for the vulnerable host tRNAs and putative religation products, tRNA ensembles from uninfected E. coli CTr5x or cells infected with various phage strains were fractionated and compared. A tRNA species absent from rli- infected cells but present in uninfected cells or late in wt infection was thus detected. RNase T1 finger prints of this species, isolated before or after wt infection, were compared with that of an in vitro ligated pair of CTr5x-specific fragments. The results indicated that this tRNA is cleaved upon infection and later on restored to it's original or to a very similar form, by polynucleotide kinase and RNA ligase reactions. It is suggested that depletion of such vulnerable host tRNA species underlies the restriction of pnk- or rli- phage on E. coli CTr5x.

Anticodon↗
PubMed1973

Accumulation of guanosine tetraphosphate in T7 bacteriophage-infected Escherichia coli.

Accumulation of guanosine tetraphosphate (ppGpp) in Escherichia coli strain AS19 valS, carrying a temperature-sensitive valyl-transfer ribonucleic acid synthetase and infected with bacteriophage T7, was studied. Valine starvation was achieved by culturing this strain at 42 C. Addition of rifampin to an uninfected culture at the nonpermissive temperature resulted in loss of accumulated ppGpp; however, cultures infected with phage T7, treated with rifampin, and then shifted to the nonpermissive temperature maintained the ability to accumulate ppGpp. Moreover, treatment of the T7-infected culture with rubidomycin, an antibiotic which inhibits transcription, did not reduce the amount of ppGpp accumulated following shift to the nonpermissive temperature. Measurements of the instantaneous rate of T7 transcription showed that it is not under stringent control of amino acids. ppGpp synthesized in T7-infected E. coli appears to be more stable than its counterpart in an uninfected culture. These results are interpreted to mean that ppGpp production is not directly dependent on transcription and arises instead from inhibition of another reaction, most likely some aspect of translation.

Adenine↗