TY  - JOUR
A1  - Hetzer, Benjamin
A1  - Orth-Höller, Dorothea
A1  - Würzner, Reinhard
A1  - Kreidl, Peter
A1  - Lackner, Michaela
A1  - Müller, Thomas
A1  - Knabl, Ludwig
A1  - Geisler-Moroder, Daniel Rudolf
A1  - Mellmann, Alexander
A1  - Sesli, Özcan
A1  - Holzknecht, Jeanett
A1  - Noce, Damia
A1  - Akarathum, Noppadon
A1  - Chotinaruemol, Somporn
A1  - Prelog, Martina
A1  - Oberdorfer, Peninnah
T1  - “Enhanced acquisition of antibiotic-resistant intestinal E. coli during the first year of life assessed in a prospective cohort study”
JF  - Antimicrobial Resistance & Infection Control
N2  - Background
Increasing bacterial resistance to antibiotics is a serious problem worldwide. We sought to record the acquisition of antibiotic-resistant Escherichia coli (E. coli) in healthy infants in Northern Thailand and investigated potential determinants.

Methods
Stool samples from 142 infants after birth, at ages 2wk, 2mo, 4 to 6mo, and 1y, and parent stool samples were screened for E. coli resistance to tetracycline, ampicillin, co-trimoxazole, and cefazoline by culture, and isolates were further investigated for multiresistance by disc diffusion method. Pulsed-field gel electrophoresis was performed to identify persistent and transmitted strains. Genetic comparison of resistant and transmitted strains was done by multilocus sequence typing (MLST) and strains were further investigated for extra- and intra-intestinal virulence factors by multiplex PCR.

Results
Forty-seven (33%) neonatal meconium samples contained resistant E. coli. Prevalence increased continuously: After 1y, resistance proportion (tetracycline 80%, ampicillin 72%, co-trimoxazole 66%, cefazoline 35%) almost matched those in parents. In 8 infants (6%), identical E. coli strains were found in at least 3 sampling time points (suggesting persistence). Transmission of resistant E. coli from parents to child was observed in only 8 families. MLST showed high diversity. We could not identify any virulence genes or factors associated with persistence, or transmission of resistant E. coli. Full-term, vaginal birth and birth in rural hospital were identified as risk factors for early childhood colonization with resistant E. coli.

Conclusion
One third of healthy Thai neonates harboured antibiotic-resistant E. coli in meconium. The proportion of resistant E. coli increased during the first year of life almost reaching the value in adults. We hypothesize that enhancement of infection control measures and cautious use of antibiotics may help to control further increase of resistance.
KW  - Escherichia coli
KW  - antibiotic resistance
KW  - multiresistance
KW  - transmission
KW  - persistence
KW  - children
KW  - neonates
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-320284
VL  - 8
ER  - 
TY  - JOUR
A1  - Bielaszewska, Martina
A1  - Schiller, Roswitha
A1  - Lammers, Lydia
A1  - Bauwens, Andreas
A1  - Fruth, Angelika
A1  - Middendorf, Barbara
A1  - Schmidt, M. Alexander
A1  - Tarr, Phillip I.
A1  - Dobrindt, Ulrich
A1  - Karch, Helge
A1  - Mellmann, Alexander
T1  - Heteropathogenic virulence and phylogeny reveal phased pathogenic metamorphosis in Escherichia coli O2:H6
JF  - EMBO Molecular Medicine
N2  - Extraintestinal pathogenic and intestinal pathogenic (diarrheagenic) Escherichia coli differ phylogenetically and by virulence profiles. Classic theory teaches simple linear descent in this species, where non-pathogens acquire virulence traits and emerge as pathogens. However, diarrheagenic Shiga toxin-producing E.coli (STEC) O2:H6 not only possess and express virulence factors associated with diarrheagenic and uropathogenic E.coli but also cause diarrhea and urinary tract infections. These organisms are phylogenetically positioned between members of an intestinal pathogenic group (STEC) and extraintestinal pathogenic E.coli. STEC O2:H6 is, therefore, a 'heteropathogen,' and the first such hybrid virulent E.coli identified. The phylogeny of these E.coli and the repertoire of virulence traits they possess compel consideration of an alternate view of pathogen emergence, whereby one pathogroup of E.coli undergoes phased metamorphosis into another. By understanding the evolutionary mechanisms of bacterial pathogens, rational strategies for counteracting their detrimental effects on humans can be developed.
KW  - phased metamorphosis
KW  - phylogeny
KW  - heteropathogenicity
KW  - Shiga toxin-producing Escherichia coli
KW  - hemolytic-uremic syndrome
KW  - urinary-tract-infection
KW  - cytolethal distending toxin
KW  - shiga toxin
KW  - Crohns-disease
KW  - outbreak
KW  - genes
KW  - island
KW  - strains
KW  - parallel evolution
KW  - uropathogenic Escherichia coli
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-117254
SN  - 1757-4684
VL  - 6
IS  - 3
ER  -