Spread of antibiotic-resistant plasmids from chicken to chicken and from chicken to man

Levy, Stuart B.; Fitzgerald, George; Macone, Ann B.

doi:10.1038/260040a0

Cited by 277 publications

(165 citation statements)

References 11 publications

Supporting

Mentioning

158

Contrasting

Unclassified

Order By: Relevance

“…Several studies have investigated the similarities of UPEC and APEC in their serogroups, virulence genotypes and assignments to phylogenetic groups (Johnson et al, 1998(Johnson et al, , 2001aKaper et al, 2004;Mokady et al, 2005;Johnson et al, 2006a;Moulin-Schouleur et al, 2006). It has been proposed that poultry may be a candidate vehicle for E. coli capable of causing human urinary tract disease, based on research showing transmission of avian E. coli from poultry to humans or similarities between avian E. coli and UPEC (Levy et al, 1976;Linton et al, 1977;Ojeniyi, 1989;van den Bogaard et al, 2002). Although previous studies have compared the content of virulence genes between UPEC and APEC, similarities of expression of the specific virulence genes of UPEC and APEC in the same chicken challenge model and/or murine UTI model have not to our knowledge been reported before.…”

Section: Discussionmentioning

confidence: 99%

Comparison of virulence factors and expression of specific genes between uropathogenic Escherichia coli and avian pathogenic E. coli in a murine urinary tract infection model and a chicken challenge model

et al. 2009

View full text Add to dashboard Cite

Avian pathogenic Escherichia coli (APEC) and uropathogenic E. coli (UPEC) establish infections in extraintestinal habitats of different hosts. As the diversity, epidemiological sources and evolutionary origins of extraintestinal pathogenic E. coli (ExPEC) are so far only partially defined, in the present study,100 APEC isolates and 202 UPEC isolates were compared by their content of virulence genes and phylogenetic groups. The two groups showed substantial overlap in terms of their serogroups, phylogenetic groups and virulence genotypes, including their possession of certain genes associated with large transmissible plasmids of APEC. In a chicken challenge model, both UPEC U17 and APEC E058 had similar LD 50 , demonstrating that UPEC U17 had the potential to cause significant disease in poultry. To gain further information about the similarities between UPEC and APEC, the in vivo expression of 152 specific genes of UPEC U17 and APEC E058 in both a murine urinary tract infection (UTI) model and a chicken challenge model was compared with that of these strains grown statically to exponential phase in rich medium. It was found that in the same model (murine UTI or chicken challenge), various genes of UPEC U17 and APEC E058 showed a similar tendency of expression. Several iron-related genes were upregulated in the UTI model and/or chicken challenge model, indicating that iron acquisition is important for E. coli to survive in blood or the urinary tract. Based on these results, the potential for APEC to act as human UPEC or as a reservoir of virulence genes for UPEC should be considered. Further, this study compared the transcriptional profile of virulence genes among APEC and UPEC in vivo.

show abstract

Section: Discussionmentioning

confidence: 99%

Comparison of virulence factors and expression of specific genes between uropathogenic Escherichia coli and avian pathogenic E. coli in a murine urinary tract infection model and a chicken challenge model

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Antibiotic resistance has also been observed in other Gram-positive bacteria, including an agent of bioterrorism, B. anthracis (44). Widespread use of antibiotics for human therapeutic or food industrial purposes is thought to be the primary selection mechanism for the emergence of drug resistance strains (45). Staphylococcal resistance mechanisms have been reported for all known antibiotics, which necessitates identification of new therapeutic targets and development of new drugs that can be used for the treatment of bacterial infections (46).…”

Section: Discussionmentioning

confidence: 99%

Activation of Inhibitors by Sortase Triggers Irreversible Modification of the Active Site

Maresso

Kern

et al. 2007

Journal of Biological Chemistry

101

106

View full text Add to dashboard Cite

Sortases anchor surface proteins to the cell wall of Gram-positive pathogens through recognition of specific motif sequences. Loss of sortase leads to large reductions in virulence, which identifies sortase as a target for the development of antibacterials. By screening 135,625 small molecules for inhibition, we report here that aryl (␤-amino)ethyl ketones inhibit sortase enzymes from staphylococci and bacilli. Inhibition of sortases occurs through an irreversible, covalent modification of their active site cysteine. Sortases specifically activate this class of molecules via ␤-elimination, generating a reactive olefin intermediate that covalently modifies the cysteine thiol. Analysis of the three-dimensional structure of Bacillus anthracis sortase B with and without inhibitor provides insights into the mechanism of inhibition and reveals binding pockets that can be exploited for drug discovery.The emergence of bacterial strains resistant to antibiotic therapy is a major public health threat (1). Of particular concern is Staphylococcus aureus, because this Gram-positive pathogen is the leading cause of infections in the bloodstream, lower respiratory tract, skin, and soft tissue in the United States (2). S. aureus strains exhibiting resistance against multiple antibiotics, such as methicillin-resistant S. aureus, are isolated in 30 -60% of community and Ͼ80% of hospital infections with this pathogen (3). Vancomycin or other glycopeptides are considered last-resort therapies for methicillin-resistant S. aureus; however, S. aureus strains with intermediate or full resistance to vancomycin can cause infections for which antimicrobial treatment may no longer be effective (4).Surface proteins of Gram-positive bacteria play important roles during pathogenesis (5). Sortases anchor these polypeptides to the bacterial cell wall envelope (6). For example, S. aureus sortase A recognizes proteins destined for the cell surface via an LPXTG motif in their C-terminal sorting signal (7). Following cleavage between the threonine and the glycine residues, an acyl-enzyme intermediate captures cleaved substrate at the active site thiol of sortase (8). Nucleophilic attack of the amino group of the peptidoglycan precursor lipid II (at the thioester intermediate resolves the acyl enzyme and forms an amide bond between the C-terminal threonine of surface protein and pentaglycine crossbridges (9). Lipid II-linked polypeptide is subsequently incorporated into the cell wall envelope of staphylococci (10). The final product of this pathway, protein linked to cell wall pentaglycine cross-bridges, is displayed on the bacterial surface and enables interactions between the pathogen and tissues of its host.Surface protein anchoring to the cell wall envelope is thought to be an essential strategy for bacterial survival during infection, because mutants lacking genes for one or more sortase enzymes are attenuated in virulence (11). Inhibition of sortases by small molecules may therefore function as a therapeutic strategy for bacterial infections. ...

show abstract

“…Moreover, the similarity of the genetic properties of R plasmids between human source and animal source has been reported. Transfer ofdistinguishable E. coli strains with particular R plasmids from calves (Hirsh & Wiger, 1977) and chickens (Levy et al 1976) to humans was demonstrated experimentally. Threlfall et al (1978a) isolated S. typhimurium phage types 204 and 193 carrying particular R plasmids from calves and humans during epidemics of bovine salmonellosis.…”

Section: Genetic Properties Of Conjugative R Plasmids Examinedmentioning

confidence: 99%

“…Most of these drug-resistant enterobacteria carried conjugative R plasmids, and the resistance might be transferred among bacterial genera or from strains colonizing animals to man (Anderson, 1968;Davies & Stewart, 1978;Hirsh & Wigner, 1977;Levy et al 1976).…”

Section: Introductionmentioning

confidence: 99%

Change of drug resistance patterns and genetic properties of R plasmids inSalmonella typhimuriumof bovine origin isolated from 1970 to 1979 in northern Japan

Makino

Ishiguro

Sato

et al. 1981

J. Hyg.

View full text Add to dashboard Cite

SUMMARYA total of 321 Salmonella typhimurium strains of bovine origin obtained in northern Japan during the period [1970][1971][1972][1973][1974][1975][1976][1977][1978][1979] were tested for drug resistance and detection of conjugative R plasmids. Three hundred and eighteen (99-1 %) of these strains were resistant to one or more drugs. The isolation frequency of multiply drug-resistant strains tended to increase year by year. Two hundred and thirtyseven (74'5 %) of these resistant strains carried conjugative R plasmids. A total of 308 R plasmids including 174 (56.5 %) thermosensitive (ts) R plasmids were derived from the 237 drug-resistant strains, indicating that 71 (30'0 %) strains have two different conjugative R plasmids in a single host cell. Of the 308 R plasmids examined for fertility inhibition (fi), 167 ts and 131 non-ts R plasmids were fi-.Of the 60 ts R plasmids examined for incompatibility, 50 were classified into Hi group and 10 into H2 group. Of the 52 non-ts R plasmids examined, 35 were classified into the Ia group and the remaining plasmids were untypable in our tests.Mercury resistance marker was found in about 20 % of Hi R plasmids coding for multiresistance, and all of H2 R plasmids coded for resistance to tellurite. The clonal distribution of an S. typhimurium strain which carried an HI R plasmid coding for resistance to six drugs and mercury was recognized in 1978 and 1979.

show abstract

Spread of antibiotic-resistant plasmids from chicken to chicken and from chicken to man

Cited by 277 publications

References 11 publications

Comparison of virulence factors and expression of specific genes between uropathogenic Escherichia coli and avian pathogenic E. coli in a murine urinary tract infection model and a chicken challenge model

Comparison of virulence factors and expression of specific genes between uropathogenic Escherichia coli and avian pathogenic E. coli in a murine urinary tract infection model and a chicken challenge model

Activation of Inhibitors by Sortase Triggers Irreversible Modification of the Active Site

Change of drug resistance patterns and genetic properties of R plasmids inSalmonella typhimuriumof bovine origin isolated from 1970 to 1979 in northern Japan

Contact Info

Product

Resources

About