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Antimicrobial Agents and Chemotherapy, February 1998, p. 277-281, Vol. 42, No. 2
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

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,1 H. Schmidt,1 H. Eiffert,2 P. Schwartz,3 M. Mäder,1 and R. Nau1,*

Departments of Neurology,1 Medical Microbiology,2 and Morphology,3 University of Göttingen, Göttingen, Germany

Received 11 April 1997/Returned for modification 14 October 1997/Accepted 15 November 1997

The release of lipoteichoic acid (LTA) and teichoic acid (TA) from a Streptococcus pneumoniae type 3 strain during exposure to ceftriaxone, meropenem, rifampin, rifabutin, quinupristin-dalfopristin, and trovafloxacin in tryptic soy broth was monitored by a newly developed enzyme-linked immunosorbent assay. At a concentration of 10 µg/ml, a rapid and intense release of LTA and TA occurred during exposure to ceftriaxone (3,248 ± 1,688 ng/ml at 3 h and 3,827 ± 2,133 ng/ml at 12 h) and meropenem (2,464 ± 1,081 ng/ml at 3 h and 2,900 ± 1,364 ng/ml at 12 h). Three hours after exposure to rifampin, rifabutin, quinupristin-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 treatment, 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 group, 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 µg/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 released after exposure to beta -lactams. Larger quantities of LTA and TA were released after treatment with low concentrations (1× the MIC and 1× the minimum bactericidal concentration) than after no treatment for all antibacterial agents except the rifamycins. This does not support the concept of using a low first antibiotic dose to prevent the release of proinflammatory cell wall components.

* Corresponding author. Mailing address: Department of Neurology, University of Göttingen, Robert-Koch-Str. 40, D-37075 Göttingen, Germany. Phone: 49-551-398455 or 49-551-396684. Fax: 49-551-398405. E-mail: rnau{at}gwdg.de.

Antimicrobial Agents and Chemotherapy, February 1998, p. 277-281, Vol. 42, No. 2
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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