Biomedical subjects

Viera Lakticová

Publications and source records attributed to Viera Lakticová.

3 recordsLinked to original sources

PubMed2006

Antibiotic-induced enterococcal expansion in the mouse intestine occurs throughout the small bowel and correlates poorly with suppression of competing flora.

To test the hypothesis that establishing gastrointestinal colonization with multiresistant Enterococcus faecium (VRE) C68 results from expansion of the enterococcal population in the upper small bowel, we compared VRE quantities recovered from the proximal, middle, and distal segments of the small bowel from mice treated with different antimicrobial agents. Antibiotics associated with high-level VRE fecal colonization (cefotetan, ceftriaxone, clindamycin, and ticarcillin-clavulanic acid) increased VRE quantities in all small-bowel segments, whereas cefepime and piperacillin-tazobactam did not. Enterococcal expansion did not correlate with reductions in numbers of native gram-negative or anaerobic flora. Green fluorescence protein-expressing E. faecium bacteria were found adjacent to the small bowel epithelial lining in colonized mice. These data indicate that enterococcal bowel colonization begins within the proximal small bowel and does not correlate with inhibition of other cultivable flora. Host or enterococcal factors induced by exposures to certain antibiotics may play a role in facilitating E. faecium colonization of the mammalian gastrointestinal tract.

Animals↗

PubMed2005

Enterococcus faecium low-affinity pbp5 is a transferable determinant.

Using 15 unrelated Enterococcus faecium isolates as donors, we demonstrated that ampicillin resistance was transferable to an E. faecium recipient containing a pbp5 deletion for all but four strains. The transfers occurred at low frequencies (generally ca. 10(-9) transconjugants/recipient CFU), consistent with chromosome-to-chromosome transfer. pbp5 transfer occurred within large genetic regions, and insertion into the recipient genome occurred most commonly into the recipient SmaI restriction fragment that had been created by the previous pbp5 deletion. Restriction mapping of the region upstream of pbp5 revealed a commonality of fragment sizes among the clinical isolates from the United States which differed significantly from those of three strains that were isolated from turkey feces. These data prove conclusively that E. faecium pbp5 is a transferable determinant, even in the absence of a coresiding vancomycin resistance mobile element. They also suggest that the spread of high-level ampicillin resistance among U.S. E. faecium strains is due in part to the transfer of low-affinity pbp5 between clinical isolates.

Conjugation, Genetic↗

PubMed2004

In vitro antienterococcal activity explains associations between exposures to antimicrobial agents and risk of colonization by multiresistant enterococci.

We compared ceftriaxone and piperacillin-tazobactam at doses ranging from 0.1 to 2 times the human equivalent daily dose (HEDD), to determine their impact on gastrointestinal colonization by ampicillin- and vancomycin-resistant Enterococcus faecium C68 in a mouse model. Ceftriaxone failed to promote colonization at doses up to 0.25 times the HEDD, whereas piperacillin-tazobactam promoted colonization at doses up to 0.5 times the HEDD. Ceftriaxone promoted colonization at doses at least 0.5 times the HEDD, whereas piperacillin-tazobactam inhibited colonization at doses at least 0.75 times the HEDD. Both piperacillin-tazobactam and ceftriaxone inhibited colonization by an enterococcal strain devoid of low-affinity penicillin-binding protein-5 (significantly increasing its susceptibility to these agents), at doses that promoted colonization by E. faecium C68. These results support a model in which the impact that different beta -lactam agents have on colonization by VRE is related to the level of the beta -lactam agent's intrinsic antienterococcal activity against the colonizing strain.

Animals↗