Search PubMed⌕ Search

Biomedical subjects

R P Novick

Publications and source records attributed to R P Novick.

153 records · Page 9Linked to original sources
PubMed1968

Plasmid-linked resistance to inorganic salts in Staphylococcus aureus.

The penicillinase plasmids, a series of extrachromosomal resistance factors in Staphylococcus aureus, were found to carry determinants of resistance to a series of inorganic ions as well as resistance to penicillin and, in some cases, erythromycin. Most of the ions involved were inhibitory but not lethal to the bacteria; the resistance markers conferred an increase in resistance by comparison with susceptible organisms of between 3- and 100-fold, depending on the ion involved. Separate genetic loci for resistance to arsenate, arsenite, lead, cadmium, mercuric, and bismuth ions were demonstrated. Resistance to antimony and resistance to zinc were also found but were not separated genetically from resistance to arsenite and cadmium, respectively. The ion resistance markers appeared to form a cluster on the plasmid, with no other known marker within it. Naturally occurring plasmids were observed that lacked one or more of these ion resistance markers, as well as penicillinase-negative strains that were resistant to one or more of the ions. The patterns of markers carried by these various strains may provide some understanding of the evolution of a plasmid linkage group.

Arsenic↗
PubMed1967

In vivo transmission of drug resistance factors between strains of Staphylococcus aureus.

1. Multiply resistant strains of Staphylococcus aureus often harbor one or more extrachromosomal drug resistant factors as well as temperate prophages capable of mediating generalized transduction. 2. Spontaneous transduction occurs in mixed cultures of such staphylococcal strains, and the extrachromosomal resistance factors are involved more frequently than are chromosomal genes. 3. Spontaneous transduction of extrachromosomal determinants of erythromycin resistance and of linked penicillin-erythromycin resistance occurs in the kidneys of mice in which mixed infection has been induced.

Animals↗
PubMedDate not supplied

The toxic shock syndrome exotoxin structural gene is not detectably transmitted by a prophage.

Toxic shock syndrome (TSS) is a complex of generalized symptoms caused by a local staphylococcal infection, and a circulating toxin is thought to be involved. Indeed, nearly 100% of TSS isolates produce an exoprotein, TSSE, that is thought to have an aetiological role on the basis of positive animal tests (refs 1,2 and F. Quimby, personal communication) and human serological data. Although the precise role of TSSE in TSS remains unclear (E. Kass, personal communication), no other staphylococcal factor has been implicated. Our preliminary studies of the genetics of TSSE production failed to demonstrate plasmid or phage involvement or linkage with known chromosomal genes (ref. 4 and B.N.K. et al., unpublished data); however, Schutzer et al. have found that most TSS strains harbour prophages with common plating characteristics and suggest that the toxin(s) involved in TSS are transmitted by lysogenic conversion. We show here that TSSE is not demonstrably transferred by lysogeny; moreover, we have cloned the gene and found that the cloned product is serologically and biologically indistinguishable from the native protein, and that the TSSE determinant is associated with a larger DNA segment that is absent or rearranged in TSSE- strains.

Animals↗
PubMedDate not supplied

Analysis of toxic shock syndrome isolates producing staphylococcal enterotoxins B and C1 with use of southern hybridization and immunologic assays.

A study was undertaken to evaluate the production of enterotoxin B (Ent B), EntC1, and toxic shock syndrome toxin 1 (TSST-1) by isolates of Staphylococcus aureus from patients with toxic shock syndrome (TSS) and from a variety of other sources. Levels of toxin in culture supernatants were measured by a quantitative immunodiffusion assay. Most vaginal TSS isolates produced TSST-1, either alone or with EntC1. However, strains that produced EntB or EntC1 but did not express TSST-1 were commonly isolated from patients with nonmenstrual TSS; EntB was usually produced alone or--rarely--with EntC1. These results were confirmed by probing DNA from representative isolates with an internal probe of the EntC1 gene (entC1). Extensive sequence homology between entC1 and entB enabled detection of both genes under conditions of high stringency. The genomic location of entC1 in strains producing both EntC1 and TSST-1 varied little but was dependent on the mammalian host. In contrast, the genomic location of entC1 or entB in strains producing EntC1 or EntB alone was variable. These results suggest that these genes are contained on mobile elements.

Animals↗
PubMedDate not supplied

Toxic shock syndrome toxin 1 is encoded by a variable genetic element.

The primary cause of toxic shock syndrome is toxic shock syndrome toxin 1 (TSST-1), a 22,049-dalton exotoxin. Approximately 20% of Staphylococcus aureus isolates produce TSST-1; the production of this toxin is therefore a variable genetic trait. The TSST-1 gene and its flanking sequences are found on a genetic element that is present in TSST-1-positive isolates and absent in TSST-1-negative isolates. Preliminary sequence data and Southern hybridization experiments with the cloned flanking sequences have provided evidence that the TSST-1 element is 4-7 kilobases in size. Hybridization analysis of whole-cell DNA from two genetically mapped TSST-1-positive strains has demonstrated that the TSST-1 element has at least two chromosomal locations. This finding suggests that the element is mobile. Biotyping of 75 TSST-1-positive isolates showed that the large majority were tryptophan-negative, and Southern hybridization analysis of whole-cell DNA from these isolates revealed a common blotting pattern--an observation suggesting that these strains are clonal.

Animals↗