Performance, diarrhea incidence, and occurrence of Escherichia coli virulence genes during long-term administration of a probiotic Enterococcus faecium strain to sows and piglets1

2006 ◽  
Vol 84 (3) ◽  
pp. 608-617 ◽  
Author(s):  
D. Taras ◽  
W. Vahjen ◽  
M. Macha ◽  
O. Simon
2015 ◽  
Vol 83 (5) ◽  
pp. 1983-1991 ◽  
Author(s):  
Silvia A. C. Schinner ◽  
Matthew E. Mokszycki ◽  
Jimmy Adediran ◽  
Mary Leatham-Jensen ◽  
Tyrrell Conway ◽  
...  

Escherichia coliMG1655, a K-12 strain, uses glycolytic nutrients exclusively to colonize the intestines of streptomycin-treated mice when it is the onlyE. colistrain present or when it is confronted withE. coliEDL933, an O157:H7 strain. In contrast,E. coliEDL933 uses glycolytic nutrients exclusively when it is the onlyE. colistrain in the intestine but switches in part to gluconeogenic nutrients when it colonizes mice precolonized withE. coliMG1655 (R. L. Miranda et al., Infect Immun 72:1666–1676, 2004,http://dx.doi.org/10.1128/IAI.72.3.1666-1676.2004). Recently, J. W. Njoroge et al. (mBio 3:e00280-12, 2012,http://dx.doi.org/10.1128/mBio.00280-12) reported thatE. coli86-24, an O157:H7 strain, activates the expression of virulence genes under gluconeogenic conditions, suggesting that colonization of the intestine with a probioticE. colistrain that outcompetes O157:H7 strains for gluconeogenic nutrients could render them nonpathogenic. Here we report thatE. coliNissle 1917, a probiotic strain, uses both glycolytic and gluconeogenic nutrients to colonize the mouse intestine between 1 and 5 days postfeeding, appears to stop using gluconeogenic nutrients thereafter in a large, long-term colonization niche, but continues to use them in a smaller niche to compete with invadingE. coliEDL933. Evidence is also presented suggesting that invadingE. coliEDL933 uses both glycolytic and gluconeogenic nutrients and needs the ability to perform gluconeogenesis in order to colonize mice precolonized withE. coliNissle 1917. The data presented here therefore rule out the possibility thatE. coliNissle 1917 can starve the O157:H7E. colistrain EDL933 of gluconeogenic nutrients, even thoughE. coliNissle 1917 uses such nutrients to compete withE. coliEDL933 in the mouse intestine.


2011 ◽  
Vol 80 (2) ◽  
pp. 668-678 ◽  
Author(s):  
Ellaine Salvador ◽  
Florian Wagenlehner ◽  
Christian-Daniel Köhler ◽  
Alexander Mellmann ◽  
Jörg Hacker ◽  
...  

ABSTRACTAsymptomatic bacteriuria (ABU) is a condition where bacteria stably colonize the urinary tract, in a manner closely resembling commensalism at other mucosal sites. The patients carry >105CFU/ml for extended periods of time and rarely develop symptoms. Contrasting the properties of ABU strains to those of uropathogenic isolates causing symptomatic infection is therefore highly relevant to understand mechanisms of bacterial adaptation. The prototype ABU strainEscherichia coli83972 has a smaller genome than uropathogenicE. coli(UPEC) strains with deletions or point mutations in several virulence genes, suggesting that ABU strains undergo a programmed reductive evolution within human hosts. This study addressed if these observations can be generalized. Strains causing ABU in outpatients or hospitalized patients after catheterization or other invasive procedures were compared to commensalE. coliisolates from the intestinal flora of healthy individuals. Notably, clonal complex 73 (CC73) was a prominent phylogenetic lineage dominated by ABU isolates. ABU isolates from outpatients and hospitalized patients had a similar overall virulence gene repertoire, which distinguished them from many commensals, but typical UPEC virulence genes were less frequently attenuated in hospital strains than in outpatient strains or commensals. The decreased virulence potential of outpatient ABU isolates relative to that of ABU strains from hospitalized patients supports the hypothesis that loss of expression or decay of virulence genes facilitates long-term carriage and adaptation to host environments.


2001 ◽  
Vol 120 (5) ◽  
pp. A572-A572
Author(s):  
F JABOLI ◽  
E RODA ◽  
C FABBRI ◽  
S MARCHETTO ◽  
F FERRARA ◽  
...  

2007 ◽  
Vol 87 (2) ◽  
pp. 181 ◽  
Author(s):  
Katia Sivieri ◽  
Veridiana P.S. Cano ◽  
Sandro R. Valentini ◽  
Elizeu A. Rossi

1960 ◽  
Vol XXXIII (IV) ◽  
pp. 630-636
Author(s):  
F.-E. Krusius ◽  
P. Peltola

ABSTRACT The study reported here was performed in order to examine the tap water of Helsinki for its alleged goitrogenous effect. In a short-term, 24-hour experiment with rats, kept on an iodine-poor diet, we noticed no inhibition of the 4-hour 131I uptake, as compared with that of animals receiving physiological saline instead of tap water. Two similar groups of rats receiving 1 and 2 mg of mercazole in redistilled water showed a distinct blockage of the 4-hour uptake, which proved the effect of this substance. In a long-term experiment of 5 weeks' duration there was no detectable difference in the body weight, thyroid weight and the 4-hour 131I uptake when the rats receiving tap water or distilled water to which 0.45 per cent of sodium chloride was added were compared with each other. Replacement of tap water by a 10 mg per cent solution of mercazole in redistilled water enlarged the thyroid to double its normal weight and increased the 131I uptake to approximately five times that of the controls. Thus our experiments failed to demonstrate any goitrogenous effect in the tap water of Helsinki. Changes similar to those produced by a long-term administration of mercazole, i. e. an enlargement of the thyroid and an increased thyroidal iodine uptake, have been shown to be due to milk collected from goitrous areas. The observations here reported confirm the importance of milk in the genesis of the goitre endemia of Helsinki. Attention is further called to the fact that a thyroidal enlargement combined with an increased thyroidal iodine uptake cannot always be taken as a sign of iodine deficiency because similar changes may be produced by the administration of goitrogens.


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