R Factor. Drug Resistance Plasmid.

1978 ◽  
Vol 88 (6) ◽  
pp. 851
1967 ◽  
Vol 9 (3) ◽  
pp. 283-297 ◽  
Author(s):  
Eugenie Dubnau ◽  
B. A. D. Stocker

An LT2 Hfr strain,his metC gal, was crossed to a multiply marked LT2 F−line. Analysis of recombinant yields, segregation of unselected markers and interrupted matings indicated injection of the Hfr chromosome in the sequenceThe introduction into the Hfr of the colicine factorscolI, colE1andcolE2and the R factorR2had little or no effect on its fertility. All four factors were transmitted at low frequency to the F−population, and to recombinants at higher frequencies (colI5–30%,colE130–80%,colE25–30%,R20–9%). Transfer ofcolE1occurred before 20 min., that ofcolE2andcolIlater than 100 min. Segregation data did not reveal close linkage of any factor to any chromosomal locus, but recombinants with a long stretch of donor chromosome were more likely than others to have acquiredcolE2andcolI. Nearly all recombinants andF−cells which acquiredcolIorcolE2acquired both, andcolE1also. Most cells which acquiredR2acquired one or more colicine factors. These plasmid associations can be formally represented by transfer of plasmids, independently of the chromosome, in the sequencecolE1—(colI, colE2)—R2. Phage P22 grown on the Hfr carrying the four plasmids transduced thetet-rtrait ofR2at very low frequency, and thesul-r str-rcharacters, together, at low frequency. Some of each sort of drug-resistance transductant, but no transductants in respect of chromosomal characters, acquiredcolEl or colE2by co-transduction.


1995 ◽  
Vol 1 (3) ◽  
pp. 203-210 ◽  
Author(s):  
HILDE KRUSE ◽  
HENNING SØRUM ◽  
FRED C. TENOVER ◽  
ØRJAN OLSVIK

1973 ◽  
Vol 71 (1) ◽  
pp. 209-215 ◽  
Author(s):  
D. M. Wells ◽  
O. B. James

SUMMARYThe antibiotic resistance patterns of coliforms in faecal specimens from pigs and their human contacts were studied. The ability of the resistant coliforms to transfer their resistance in vitro to antibiotic-sensitive recipients was examined. The results showed that pigs which had received antibiotics carried more multiply-resistant, R-factor bearing coliforms than pigs which had not been given antibiotics. Human contacts of the antibiotic-treated pigs had a higher incidence of antibiotic-resistant coliforms with R-factors than human contacts of pigs which had not been given antibiotics. It is concluded that antibiotic treatment of farm, animals may lead to acquisition of antibiotic resistance by gut coliforms of man.


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