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