PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Streptococcus Phages”

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.

At least 37 records · Page 2Linked to original sources

Transfection of Streptococcus sanguis by phage deoxyribonucleic acid isolated from Streptococcus mutans.

Streptococcus sanguis ATCC 10556 cells were infected with free phage DNA of S, mutans strain PK 1. Two transformants were isolated which made colonies with large mucoid forms on mitis-salivarius agar. Both transformants had an increased ability to synthesize insoluble glucan and showed an adhesive nature on glass surfaces. These characteristics of the transformants bear a resemblance to S. mutans. These transformants had many physiological characteristics by which they could be recognized as S. sanguis. However, they resembled S. salivarius in forming a large amount of soluble fructan. Furthermore, the transformant cells did not produce ammonia from arginine, whereas their parent cells did.

Bacteriolysis↗

Genome sequence of a serotype M3 strain of group A Streptococcus: phage-encoded toxins, the high-virulence phenotype, and clone emergence.

Genome sequences are available for many bacterial strains, but there has been little progress in using these data to understand the molecular basis of pathogen emergence and differences in strain virulence. Serotype M3 strains of group A Streptococcus (GAS) are a common cause of severe invasive infections with unusually high rates of morbidity and mortality. To gain insight into the molecular basis of this high-virulence phenotype, we sequenced the genome of strain MGAS315, an organism isolated from a patient with streptococcal toxic shock syndrome. The genome is composed of 1,900,521 bp, and it shares approximately 1.7 Mb of related genetic material with genomes of serotype M1 and M18 strains. Phage-like elements account for the great majority of variation in gene content relative to the sequenced M1 and M18 strains. Recombination produces chimeric phages and strains with previously uncharacterized arrays of virulence factor genes. Strain MGAS315 has phage genes that encode proteins likely to contribute to pathogenesis, such as streptococcal pyrogenic exotoxin A (SpeA) and SpeK, streptococcal superantigen (SSA), and a previously uncharacterized phospholipase A(2) (designated Sla). Infected humans had anti-SpeK, -SSA, and -Sla antibodies, indicating that these GAS proteins are made in vivo. SpeK and SSA were pyrogenic and toxic for rabbits. Serotype M3 strains with the phage-encoded speK and sla genes increased dramatically in frequency late in the 20th century, commensurate with the rise in invasive disease caused by M3 organisms. Taken together, the results show that phage-mediated recombination has played a critical role in the emergence of a new, unusually virulent clone of serotype M3 GAS.

Amino Acid Sequence↗

Phage Resistance in a Phage-Insensitive Strain of Streptococcus lactis: Temperature-Dependent Phage Development and Host-Controlled Phage Replication.

Streptococcus lactis ME2 is a dairy starter strain that is insensitive to a variety of phage, including phi18. The efficiency of plating of phi18 on ME2 and N1 could be increased from <1 x 10 to 5.0 x 10 and from 7.6 x 10 to 2.1 x 10, respectively, when the host strains were subcultured at 40 degrees C before plating the phage and the phage assay plates were incubated at 40 degrees C. Host-dependent replication was demonstrated in N1 at 30 degrees C and in N1 and ME2 at 40 degrees C, suggesting the operation of a temperature-sensitive restriction and modification system in ME2 and N1. The increased sensitivity of ME2 and N1 to phi18 at 40 degrees C was also demonstrated by lysis of broth cultures and increased plaque size. ME2 grown at 40 degrees C showed an increased ability to adsorb phi18, indicating a second target for temperature-dependent phage sensitivity in ME2. Challenge of N1 with a phi18 preparation that had been previously modified for growth on N1 indicated that at 40 degrees C phage development was characterized by a shorter latent period and larger burst size than at 30 degrees C. The evidence presented suggests that the high degree of phage insensitivity expressed by ME2 consists of a variety of temperature-sensitive mechanisms, including (i) the prevention of phage adsorption, (ii) host-controlled restriction of phage, and (iii) suppression of phage development. At 30 degrees C these factors appear to act cooperatively to prevent the successful emergence of lytic phage active against S. lactis ME2.

Journal Article↗

Plasmid-mediated reduced phage sensitivity in Streptococcus lactis KR5.

The phage insensitivity of Streptococcus lactis KR5 was evaluated for its possible linkage to plasmid DNA. This strain possessed plasmids of 40, 29, 26, 21, 16.5, 10.5, 7.8, and 1.5 Mdal. Plasmid curing using novobiocin resulted in derivatives with increased sensitivity to prolate-headed phage, suggesting the involvement of plasmid DNA in phage insensitivity. Transformation of S. lactis LM0230 protoplasts with the KR5 plasmid DNA pool produced transformants containing a plasmid of about 27 Mdal. These erythromycin-resistant transformants were lactose-positive phage-sensitive or were lactose-negative and exhibited a reduced sensitivity to phage. Agarose gel electrophoresis and restriction endonuclease digestion analysis showed the 27-Mdal plasmid band to be composed of two distinct plasmids of 26 Mdal (pBF61) and 29 Mdal (pBF62), which coded for reduced phage sensitivity and lactose-positive phenotypes, respectively. The mechanisms of reduced phage sensitivity encoded by pBF61 included a restriction/modification system and a mechanism that resulted in reduced plaque size independent of incubation temperature. These results further support the involvement of plasmid DNA in the mechanisms for reduced phage sensitivity in dairy streptococci.

Bacteriophages↗

Partial characterization of a new C3-type capsule-dissolving phage of Streptococcus cremoris.

A viscous, ropy, sour milk product, called 'viili,' is produced in Finland. Capsule-forming strains of Streptococcus cremoris are the typical starters for this product. Occasionally fermentation fails and results in a non-ropy clot. The reasons for these failures, however, are obscure. In one batch of spoiled 'viili,' a new C3-type bacteriophage, termed KSY1, was isolated. The head of the phage was about 230 nm long and about 50 nm wide and the tail was 35 nm long and carried a complex collar structure. Upon infection of a number of encapsulated cultures of S. cremoris with KSY1, the cocci, though not serving as a host of the phage, lost their capsules. A capsuleless strain, S. cremoris 249, served as a host. The latent period was about 150 min and the average burst size 80. The bouyant density of KSYI1 was 1.436 g/cm3.

Animals↗

Lysin production by phi C2(W), a prolate phage for Streptococcus lactis C2.

A bacteriophage, phi C2(W), which attacked Streptococcus lactis strains C2, ML3 and 712, is described. It had a prolate head and non-contractile tail and produced large haloes around plaques. Infection of eight paired-strain cultures, each containing Str. lactis C2, with phi C2(W) resulted in marked inhibition of acid production for six cultures. Direct phage-nonhomologous "host' contact was not required for inhibition. Lysates of phi C2(W) contained a phage-induced lysin. Evidence is presented that the inhibitory effect of phi C2(W) against paired and multi-strain cultures is due to the lysis of phage-insensitive strains by phage lysin. An isometric phage, phi 712, was shown not to produce such a lysin.

Bacteriophages↗

Type 49 Streptococcus pyogenes: phage subtypes as epidemiological markers in isolates from skin sepsis and acute glomerulonephritis.

Studies of group A, M type 49 streptococci from England, Trinidad and Alaska indicate that isolates of this serotype often differ with respect to phage subtype from one geographical area to another, but are generally homogeneous in one place at one time. The findings support the conclusion that acute glomerulonephritis can be associated with a variety of phage subtypes of M type 49 streptococci. In outbreaks of skin sepsis without nephritis in England, the phage subtypes of M type 49 streptococci isolated from skin lesions of meat handlers were the same as those recovered from skin lesions of non-meat handlers in the same community. The findings on the Trinidad isolates suggest that M type 49 streptococci of one phage subtype may persist in a population for 9 years and may result in a second outbreak of acute glomerulonephritis. In an Alaska Eskimo population in whom acute glomerulonephritis was occurring, most of the M type 49 isolates available for testing were of a single phage subtype. Equally prevalent in this population were group A streptococci that exhibited the same T antigen as the type 49 isolates but differed in their serum opacity reaction and phage subtype. This apparently related strain was not typable with available M antisera but showed functional evidence of M protein and is probably a new M type.

Alaska↗

Nucleotide sequence at the termini of the DNA of Streptococcus pneumoniae phage Cp-1.

The 5' ends of Cp-1 DNA, which have a covalently linked terminal protein, can be partially unblocked by treatment with 1 M NaOH (E. Garcia, A. Gomez, C. Ronda, C. Escarmis, and R. Lopez (1983) Virology 128, 92-104) and labeled with polynucleotide kinase and [gamma-32P]ATP. The sequence of the first 444 and 520 nucleotides at the termini of Cp-1 DNA has been determined. A 236-nucleotide-long inverted terminal repeat was found and, in addition, the 116 nucleotides following the repeat show 93% homology. The first 352 nucleotides at both ends have an adenine plus thymine content of 75%. More than 50% of the nucleotides of the sequenced regions are involved in repeats of a minimum of 8 nucleotides. Three promoter-like sequences were also found at each end of Cp-1 DNA.

Bacteriophages↗

Selection of an immunogenic and protective epitope of the PsaA protein of Streptococcus pneumoniae using a phage display library.

Streptococcus pneumoniae is an important pathogen that causes disease in young and elderly individuals. The currently available polysaccharide vaccines have limited efficacy in those age groups most susceptible to pneumococcal infections. This study focuses on mapping the epitopes of a surface protein of S. pneumoniae by biopanning a 15 mer phage display library using 5 different monoclonal antibodies (MAbs) against the Pneumoccal surface adhesin A (PsaA). PsaA is a component of the bacterial cell wall that is highly species specific and is involved in bacterial adherence and virulence. Biopanning of the phage display library reveals three distinct epitopes on the PsaA protein. The sequence homology of these epitopes ranges from two to six amino acids when compared to the native PsaA protein type 2. Two of these epitopes have been evaluated for their immunogeneicity in mice. The peptide selected by the MAbs 8G12, 6F6, and 1B7 is referred to as the consensus peptide and is immunogenic in mice. Optimal anti-PsaA response is observed in mice immunized with 50microg of the consensus peptide complexed to proteosomes in 1:1 ratio. The anti-PsaA response is significantly lower than the response to the PsaA native protein. The peptide selected by monoclonal antibody 4E9 in its lipidated form is significantly protective in mice challenged with S. pneumoniae serotype 2 when compared to mice immunized with the native protein. These results show that the selected epitopes of PsaA protein are immunogenic and protective in mice. These epitopes need to be evaluated further as alternatives to currently available vaccines.

Adhesins, Bacterial↗

Lack of surface receptors not restriction-modification system determines F4 phage resistance in Streptococcus bovis II/1.

The resistance of Streptococcus bovis strain II/1, the producer of SbvI restriction endonuclease, to F4 phage infection was demonstrated by the double-agar-layer method. Despite the presence of restriction endonuclease SbvI which can cleave F4 phage DNA to numerous fragments in vitro, the evidence that adsorption inhibition is the most important defence mechanism in phage resistance of S. bovis II/1 strain was obtained by adhesion experiments in vivo. Electron microscopy of phage-host mixtures showed many phage particles on the bacterial surface of phage-sensitive S. bovis 47/3 control strain in comparison with no phage particles seen on S. bovis II/1 (phage-resistant) strain surface.

DNA Restriction-Modification Enzymes↗

Characterization of phage receptors in Streptococcus thermophilus using purified cell walls obtained by a simple protocol.

A simple protocol was designed and applied to obtain Streptococcus thermophilus purified cell walls. To identify the structures involved in phage adsorption, the cell walls of two Strep. thermophilus strains were treated with sodium dodecyl sulphate and proteinase K. These treatments did not reduce the adsorption of phages CYM and 0BJ to the cell walls of Strep. thermophilus YSD10 and Strep. thermophilus BJ15, respectively. However, phage binding was reduced when the cell envelopes were treated with mutanolysin or trichloroacetic acid 5%, suggesting that the phage receptor component is part of the peptidoglycan or a polymer closely linked to it. The ability of several saccharides to inactivate both phages was also assayed. These phage inhibition experiments suggested that the phage CYM adsorbed to a component involving glucosamine and rhamnose, while glucosamine and ribose interfered with the adsorption of phage 0BJ.

Adsorption↗

Characterization of Streptococcus thermophilus host range phage mutants.

To investigate phage-host interactions in Streptococcus thermophilus, a phage-resistant derivative (SMQ-301R) was obtained by challenging a Tn917 library of phage-sensitive strain S. thermophilus SMQ-301 with virulent phage DT1. Mutants of phages DT1 and MD2 capable of infecting SMQ-301 and SMQ-301R were isolated at a frequency of 10(-6). Four host range phage mutants were analyzed further and compared to the two wild-type phages. Altogether, three genes (orf15, orf17, and orf18) contained point mutations leading to amino acid substitutions and were responsible for the expanded host range. These three proteins were also identified in both phages by N-terminal sequencing and/or matrix-assisted laser desorption ionization-time-of-flight mass spectrometry. The results suggest that at least three phage structural proteins may be involved in phage-host interactions in S. thermophilus.

Amino Acid Sequence↗

Phage resistance in Streptococcus lactis ssp. diacetylactis transconjugant SLA3.2501 and its derivatives.

Phage 18-16, which was virulent for Streptococcus lactis ssp. diacetylactis SLA3.25 was used to study phage-resistant characteristics of mucoid S. lactis ssp. diacetylactis transconjugant SLA3.2501 obtained through conjugative cotransfer of pSRQ2201 (Lac-plasmid) and pSRQ2202 (Muc-plasmid) to SLA3.25 (15). Interaction of phage 18-16 with SLA3.2501 and its derivatives showed that phage resistance was not related to either the lack of phage adsorption or restriction-modification. Suppression of phage replication in SLA3.2501 and its derivatives was not completely relieved by curing of either pSRQ2201 or pSRQ2202 or both.

Bacteriophages↗