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At least 37 records · Page 2Linked to original sources
PubMed2003

Transcription of the toxin genes present within the Staphylococcal phage phiSa3ms is intimately linked with the phage's life cycle.

phiSa3ms, a lysogenic bacteriophage encoding the staphylococcal enterotoxins SEA, SEG, and SEK and the fibrinolytic enzyme staphylokinase (Sak), was identified in the unannotated genome sequence of the hypervirulent community-acquired Staphylococcus aureus strain 476. We found that mitomycin C induction of phiSa3ms led to increased transcription of all four virulence factors. The increase in sea and sak transcription was a result of read-through transcription from upstream latent phage promoters and an increase in phage copy number. The majority of the seg2 and sek2 transcripts were shown to initiate from the upstream phage cI promoter and hence were regulated by factors influencing cI transcription. The lysogeny module of phiSa3ms was shown to have some lambda-like features with divergent cI and cro genes. Band shift assays were used to identify binding sites for both CI and Cro within the region between these genes, suggesting a mechanism of control for the phiSa3ms lytic-lysogenic switch. Our findings suggest that the production of phage-encoded virulence factors in S. aureus may be regulated by processes that govern lysogeny.

Base Sequence↗
PubMed1986

Colonization of newly arrived house staff by virulent staphylococcal phage types endemic to a hospital environment.

The acquisition of hospital strains of Staphylococcus aureus by new house officers was studied in an 800-bed referral hospital over a 1-year period. S. aureus isolates, including three strains with characteristic phage patterns that had previously been documented to cause disease in patients and colonize hospital personnel, were recovered from the anterior nares of 35 of 54 newly arrived house officers. There was a significant correlation (r = 0.7475; P less than 0.02) between colonization with the dominant hospital strain (S) and exposure to the hospital environment over 12 months. No hospital-wide increase in infections owing to the S strain was seen during this period, which suggests that house staff acquired this strain from reservoirs within the hospital. The finding of colonization with virulent endemic S. aureus strains in house officers working on every ward of the hospital suggests that new strategies for control of S. aureus nosocomial infections must be considered and evaluated.

Bacteriophage Typing↗
PubMed1954

The isolation of a staphylococcal phage variant susceptible to an unusual host control.

A series of phage P(1) variants was isolated from plaques developing on S. aureus WF 145. One in particular, phage 14, was studied in detail because its host range appeared to be dependent on the previous host of production; i.e., it was subject to a host control. When this phage was produced on host K(1) its lysate assayed equally well on both 145 and K(1) cells. When produced on host 145, however, it assayed manyfold higher on 145 than on host K(1). All its particles adsorbed on K(1) cells, but only a small percentage were able to produce plaques. No differences could be found in adsorption rates, latent periods, or burst sizes of the phage on the two hosts. No extracellular inactivating substances could be detected which could account for such changes, nor could the results be explained readily on a mutational basis, since distinct phage strains could not be isolated. The change in virus properties was found to occur in the first burst of singly infected host 145 cells, regardless of the previous host or its prior lytic abilities. Heat inactivation destroyed activity for K(1) cells more rapidly than for 145 cells. This was found to be a property of both the stock phage P(1) and phage 14. Phage 14 could be heated until there remained particles which could multiply only on strain 145. When the plaques of such survivors were examined they were found to contain phage which could multiply on both hosts in a ratio characteristic of the original unheated preparation. The data suggest that the observed changes were caused by a host control over the formation of a phage material(s) necessary for successful infection of host K(1). Such a substance theoretically could be related to the labile material destroyed by heat and required for plaque formation on host K(1).

Adsorption↗
PubMed1983

Structure and properties of the rapidly sedimenting replicating complex of staphylococcal phage K DNA.

Rapidly sedimenting complexes (RSCs) of replicating phage K DNA, isolated by rate zonal centrifugation in sucrose gradients, contain bacterial membrane lipids and protein. During the first half of the latent period the number of DNA molecules in a RSC increased from 1 to about 27. Digestion by Pronase caused the complexes to dissociate and release virion lengths of DNA which sedimented slowly like free mature DNA. RSCs treated with SDS disintegrated and released tangled DNA molecules, each about one virion length in size, but these structures retained their fast sedimentation characteristic. Chloramphenicol (CM) at 100 micrograms/ml did not completely inhibit complex formation or DNA replication, indicating that pre-existing host proteins were involved in these processes. CM reduced DNA replication by 50 to 80%. It is concluded that phage K DNA replicates attached to the cytoplasmic membrane of the host.

Bacterial Proteins↗