DIFFERENTIAL RELEASE OF LIPOTEICHOIC AND TEICHOIC-ACIDS FROM STREPTOCOCCUS-PNEUMONIAE AS A RESULT OF EXPOSURE TO BETA-LACTAM ANTIBIOTICS, RIFAMYCINS, TROVAFLOXACIN, AND QUINUPRISTIN-DALFOPRISTIN

Citation
K. Stuertz et al., DIFFERENTIAL RELEASE OF LIPOTEICHOIC AND TEICHOIC-ACIDS FROM STREPTOCOCCUS-PNEUMONIAE AS A RESULT OF EXPOSURE TO BETA-LACTAM ANTIBIOTICS, RIFAMYCINS, TROVAFLOXACIN, AND QUINUPRISTIN-DALFOPRISTIN, Antimicrobial agents and chemotherapy, 42(2), 1998, pp. 277-281
Citations number
17
Categorie Soggetti
Pharmacology & Pharmacy",Microbiology
ISSN journal
00664804
Volume
42
Issue
2
Year of publication
1998
Pages
277 - 281
Database
ISI
SICI code
0066-4804(1998)42:2<277:DROLAT>2.0.ZU;2-2
Abstract
The release of lipoteichoic acid (LTA) and teichoic acid (TA) from a S treptococcus pneumoniae type 3 strain during exposure to ceftriaxone, meropenem, rifampin, rifabutin, quinupristin-dalfopristin, and trovafl oxacin in tryptic soy broth was monitored by a newly developed enzyme- linked immunosorbent assay, At a concentration of 10 mu g/ml, a rapid and intense release of LTA and TA occurred during exposure to ceftriax one (3,248 +/- 1,688 ng/ml at 3 h and 3,827 +/- 2,133 ng/ml at 12 h) a nd meropenem (2,464 +/- 1,081 ng/ml at 3 h and 2,900 +/- 1,364 ng/ml a t 12 h). Three hours after exposure to rifampin, rifabutin, quinuprist in-dalfopristin, and trovafloxacin, mean LTA and TA concentrations of less than 460 ng/ml were observed (for each group, P < 0.01 versus the concentrations after exposure to ceftriaxone). After 12 h of treatmen t, the LTA and TA concentrations were 463 +/- 126 ng/ml after exposure to rifampin, 669 +/- 303 ng/ml after exposure to rifabutin, and 1,236 +/- 772 ng/ml after exposure to quinupristin-dalfopristin (for each g roup, P < 0.05 versus the concentrations after exposure to ceftriaxone ) and 1,745 +/- 1,185 ng/ml after exposure to trovafloxacin (P = 0.12 versus the concentration after exposure to ceftriaxone). At 10 mu g/ml , bactericidal antibacterial agents that do not primarily affect cell wall synthesis reduced the amount of LTA and TA released during their cidal action against S. pneumoniae in comparison with the amount relea sed after exposure to beta-lactams, Larger quantities of LTA and TA we re released after treatment with low concentrations (1x the MIC and 1x the minimum bactericidal concentration) than after no treatment for a ll antibacterial agents except the rifamycins, This does not support t he concept of using a low first antibiotic dose to prevent the release of proinflammatory cell wall components.