Transfer of tetracycline resistance from <i>Escherichia coli</i> to other <i>Enterobacteriaceae in vitro</i>

Macúch, P; Seckárová, A; Parráková, E.; Krčméry, V.; Výmola, F

doi:10.1002/jobm.19670070212

Cited by 6 publications

(6 citation statements)

References 12 publications

(5 reference statements)

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“…Sulfonamide resistance was not estimated nor checked after transfer. (ii) Salmonella typhimurium 5445, isolated from pig feces (8), transfers an R-factor ST at a frequency of about 10-1 to E. coil 2H 1327 and Y 20. (iii) E. coli K-12 185 ST, which received its R factor from 5445, was used to transfer this ST-determinant to E. coli Y 20 and to E. coli ML strains which are lac-.…”

Section: Methodsmentioning

confidence: 99%

Loss of Colicinogeny inEscherichia coliStrains Infected by Certain Resistance Factors

1970

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The original observation that in wild-type colicinogenic Escherichia coli strains the introduction of some R factors abolish their colicin production was studied in certain col+ strains bearing well-defined col factors. Two resistance (R) factors were used and introduced by conjugation in these strains, namely the 222 factor of Watanabe and a Salmonella typhimurium ST factor (coding for resistance to streptomycin and tetracycline only). The introduction of above mentioned R factors abolished the colicin production of col+ strains most probably by elimination of col factors. All col factors, however, were not equally susceptible to elimination by the R factors tested, since colicin production in ML strains was abolished by infection by the 222 factor but not by the R factor of S. typhimurium ST, which is able to eliminate other col factors.During an investigation of the incidence of tetracycline resistance caused by resistancetransfer factors in enterobacteria isolated from swine feces (7), a loss of colicinogeny was observed in a number of Escherichia coli strains after infection with resistance (R) factors carrying resistance to streptomycin (S) and tetracycline (T). We have extended these findings by studying the effect of two different R factors on colicinogeny of other col strains.MATERIALS AND METHODS Strains. Colicinogenic strains were as follows. (i) E. coli 2H 1327, a wild-type strain isolated from swine feces, was used. This strains was found to produce colicin B. As recipient strain for transfer of R factors, we used a nalidixic acid-resistant mutant isolated from this strain. (ii) E. coli Y 20 (Col E 1), a lac-strain which produces colicin E 1, was obtained from S. E. Luria. (iii) The following variants of E. coli ML 35 were tested, which were all found to produce colicin E 1: E. coli ML 35 Nx, a nalidixic acid-resistant mutant isolated from lac--sensitive strain, obtained from H. Rosenkranz; E. coli ML 35 Cl, a S-resistant mutant isolated from a S-dependent strain obtained from H. Rosenkranz, resistant to 1,000 ;&g of S per ml; E. coli ML 35 Cl, ile-try-, a deficient mutant isolated from E. coli ML 35 Cl.R-factor-bearing donor strains were as follows. (i) E. coli CHS-2 (222), resistant to S, T, chloramphenicol (C), and the sulfonamides (Su) was used. This is T. Watanabe's donor strain which usually transfers these resistances as a unit (9). It is sensitive to phages T,, T5, and BF23, which can be used for its identification. The resistance levels of this strain on MacConkey agar are 50 Ag of T per ml, 15 ,ug of S per ml, and 100 pg of chloramphenicol per ml. Sulfonamide resistance was not estimated nor checked after transfer. (ii) Salmonella typhimurium 5445, isolated from pig feces (8), transfers an R-factor ST at a frequency of about 10-1 to E. coil 2H 1327 and Y 20. (iii) E. coli K-12 185 ST, which received its R factor from 5445, was used to transfer this ST-determinant to E. coli Y 20 and to E. coli ML strains which are lac-. It is sensitive to phages T1, Tr, and BF23, whereas none of the col+ st...

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Section: Methodsmentioning

confidence: 99%

Loss of Colicinogeny inEscherichia coliStrains Infected by Certain Resistance Factors

1970

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“…However, due to limitations in human microbial research related to the introduction of antimicrobial resistance plasmids into living hosts, there has been a limit to the understandings available surrounding the factors that participate in regulating the process of plasmid-mediated HGT in and on humans. Many studies have postulated hypothetical host-microbial interactions (HMI) involved in regulating the process of plasmid-mediated HGT in the animal microbiota, but few of these HMI have been experimentally demonstrated in an in vivo environment ( Macuch et al, 1967 ; Dunkley et al, 2007 ; Ziv et al, 2013 ; Gresham and Hong, 2015 ; Card et al, 2017 ; Li et al, 2020 ).…”

Section: Conjugative Elementsmentioning

confidence: 99%

“…Limited in vivo studies have been conducted to determine the roles of factors such as host immunity, antibiotic treatment status, gut environmental conditions, and secretory molecules in the interactions of microbial HGT ( Klimuszko et al, 1989 ; Thomas and Nielsen, 2005 ; Diaz et al, 2012 ; Stecher et al, 2012 ; Huddleston, 2014 ; Machado and Sommer, 2014 ; Getino et al, 2015 ; Zeng and Lin, 2017 ; Devanga Ragupathi et al, 2019 ; Ott et al, 2020 ). While there have been many publications reporting the transfer of AR plasmids in vitro , often in the context of soil or wastewater, there has been a stark lack of experiments that demonstrate the interactions of these bacteria in vivo ( Macuch et al, 1967 ; Rang et al, 1996 ; Gevers et al, 2003 ; Card et al, 2017 ; Benz et al, 2020 ). In this review, we will present the current models for in vitro , in silico , and in vivo HGT experimentation regarding the gut environment, as well as survey of important findings demonstrated in these models.…”

Section: Introductionmentioning

confidence: 99%

Models for Gut-Mediated Horizontal Gene Transfer by Bacterial Plasmid Conjugation

Ott

Mellata

2022

Front. Microbiol.

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Graphical Abstract Models for gut-mediated bacterial conjugation and plasmid transfer. Depiction of conjugative elements (Left, Top), current in silico models (Left, Middle), experimental in vitro models (Left, Bottom), and in vivo animal models (Right) for bacterial conjugation in the gut. Arthropods; spring tails (Folsomia candida), fleas (Alphitobius diaperinus), fruit flies (Drosophila melanogaster), house flies (Musca domestica), beetles (Xenopsylla cheopis); Rhabditidae; nematodes (Caenorhabditis elegans); Phasianidae; chickens (Gallus gallus). Leporidae; rabbits (Oryctolagus cuniculus). Muridae; mice (Mus musculus), rats (Mus rattus).

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“…Over time, however, bacteria developed ways to circumvent these antibiotics and this ended the so‐called golden era of antibiotics (Davies, 2012). Researchers in Japan were the first to report the transfer of multidrug resistance by elements referred to as “R factors” in 1959 (Macuch et al, 1967). Other international studies subsequently confirmed this mechanism (Kruse & Sørum, 1994; Linton et al, 1974).…”

Section: The Discovery Of Antibiotics and Emergence Of Antibiotic Resistancementioning

confidence: 99%

Environmental hotspots for antibiotic resistance genes

et al. 2021

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Bacterial resistance toward broad‐spectrum antibiotics has become a major concern in recent years. The threat posed by the infectious bacteria and the pace with which resistance determinants are transmitted needs to be deciphered. Soil and water contain unique and diverse microbial communities as well as pools of naturally occurring antibiotics resistant genes. Overuse of antibiotics along with poor sanitary practices expose these indigenous microbial communities to antibiotic resistance genes from other bacteria and accelerate the process of acquisition and dissemination. Clinical settings, where most antibiotics are prescribed, are hypothesized to serve as a major hotspot. The predisposition of the surrounding environments to a pool of antibiotic‐resistant bacteria facilitates rapid antibiotic resistance among the indigenous microbiota in the soil, water, and clinical environments via horizontal gene transfer. This provides favorable conditions for the development of more multidrug‐resistant pathogens. Limitations in detecting gene transfer mechanisms have likely left us underestimating the role played by the surrounding environmental hotspots in the emergence of multidrug‐resistant bacteria. This review aims to identify the major drivers responsible for the spread of antibiotic resistance and hotspots responsible for the acquisition of antibiotic resistance genes.

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Transfer of tetracycline resistance from Escherichia coli to other Enterobacteriaceae in vitro

Cited by 6 publications

References 12 publications

Loss of Colicinogeny inEscherichia coliStrains Infected by Certain Resistance Factors

Loss of Colicinogeny inEscherichia coliStrains Infected by Certain Resistance Factors

Models for Gut-Mediated Horizontal Gene Transfer by Bacterial Plasmid Conjugation

Environmental hotspots for antibiotic resistance genes

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