Related Experiment Video

Updated: Jul 16, 2026

Antimicrobial Synergy Testing by the Inkjet Printer-assisted Automated Checkerboard Array and the Manual Time-kill Method
12:03

Antimicrobial Synergy Testing by the Inkjet Printer-assisted Automated Checkerboard Array and the Manual Time-kill Method

Published on: April 18, 2019

Time-kill kinetics of Streptococcus pneumoniae with reduced susceptibility to telithromycin

Adnan Al-Lahham1, Ralf René Reinert

  • 1Institute of Medical Microbiology, National Reference Centre for Streptococci, Aachen, Germany.

Chemotherapy
|March 10, 2007
PubMed
Abstract

Insights

Telithromycin resistance in Streptococcus pneumoniae is linked to the ermB genotype. This study found that telithromycin kills resistant pneumococcal strains slowly, with achievable drug concentrations below bactericidal levels.

Area of Science:

  • Microbiology
  • Pharmacology
  • Infectious Diseases

Background:

  • Telithromycin is a widely used ketolide antibiotic.
  • Telithromycin-resistant Streptococcus pneumoniae isolates are rare.
  • Understanding resistance mechanisms is crucial for effective treatment.

Purpose of the Study:

  • To investigate the anti-pneumococcal activity of telithromycin against resistant strains.
  • To characterize the resistance mechanisms in clinical isolates of Streptococcus pneumoniae.

Main Methods:

  • Time-kill methodology was employed to assess telithromycin's activity.
  • Minimum Inhibitory Concentrations (MICs) were determined.
  • Multilocus sequence typing and serotyping were used for strain characterization.

Main Results:

  • Four telithromycin-non-susceptible Streptococcus pneumoniae isolates were identified.
  • All isolates possessed the ermB genotype and a constitutive macrolide-lincosamide-streptogramin B resistance phenotype.
  • Telithromycin demonstrated slow bactericidal activity against resistant strains (MICs 2-8 microg/ml).
  • Three isolates shared serotype 14 and sequence type 143, indicating genetic relatedness.

Conclusions:

  • Telithromycin exhibits slow killing of S. pneumoniae strains with the ermB resistance determinant and telithromycin MIC >= 2 microg/ml.
  • Achievable telithromycin concentrations in vivo are insufficient for rapid bactericidal killing of highly resistant strains.

More Related Videos

A Robust Pneumonia Model in Immunocompetent Rodents to Evaluate Antibacterial Efficacy against S. pneumoniae, H. influenzae, K. pneumoniae, P. aeruginosa or A. baumannii09:17

A Robust Pneumonia Model in Immunocompetent Rodents to Evaluate Antibacterial Efficacy against S. pneumoniae, H. influenzae, K. pneumoniae, P. aeruginosa or A. baumannii

Published on: January 2, 2017

Related Concept Videos

Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Inhibitors of Bacterial Protein Synthesis01:25

Inhibitors of Bacterial Protein Synthesis

Aminoglycosides constitute a highly potent class of bactericidal antibiotics that exert their antimicrobial effects by targeting the bacterial ribosome, specifically disrupting protein synthesis. These polycationic molecules consist of amino-modified sugars linked via glycosidic bonds to an aminocyclitol core such as 2-deoxystreptamine or streptamine. Their strong positive charges facilitate tight binding to the negatively charged phosphate backbone of ribosomal RNA (rRNA), primarily at the 16S...
Pharmacokinetic–Pharmacodynamic Relationship: Influence of Elimination Half-Life on Effect Duration01:23

Pharmacokinetic–Pharmacodynamic Relationship: Influence of Elimination Half-Life on Effect Duration

Drug elimination from the body primarily occurs through metabolic and excretion pathways. Hepatic metabolism transforms lipophilic drugs into hydrophilic forms for excretion, typically via enzymatic processes classified as phase I (modification) and phase II (conjugation). Renal excretion eliminates drugs and metabolites through filtration and secretion in the kidneys. Impairment in liver or kidney function can hinder these processes, delaying drug clearance and extending the drug’s half-life.
Inhibitors of Gram-positive Cell Wall Synthesis01:23

Inhibitors of Gram-positive Cell Wall Synthesis

Bacterial cell walls are typically rigid structures composed mainly of peptidoglycan, a mesh-like polymer that provides mechanical strength and maintains cell shape. The synthesis of peptidoglycan is a crucial process in bacterial growth and serves as a primary target for many antibiotics.Mechanism of Action of Beta-Lactam AntibioticsBeta-lactam antibiotics, such as penicillin, inhibit peptidoglycan synthesis in actively growing cells. These antibiotics share a characteristic four-membered...
Combined Effects of Drugs: Synergism01:27

Combined Effects of Drugs: Synergism

Synergism is a useful mechanism where combining two or more drugs is more effective than each constituent used alone. Such combinations are also called supra-additive interactions. The drugs collectively enhance the final therapeutic effect by acting on different targets. Another advantage is that the low dose of each constituent drug is sufficient to achieve the desired effect. This helps reduce the duration of therapy and lower the adverse effects of these drugs.
Such synergistic combinations...
Atypical Pneumonia01:14

Atypical Pneumonia

Atypical pneumonia, often caused by Mycoplasma pneumoniae, is a form of pulmonary infection that differs from the classical presentation of bacterial pneumonia in both its cause and clinical symptoms. Mycoplasma pneumoniae is a pleomorphic bacterium notable for its lack of a rigid cell wall. This structural characteristic imparts resistance to beta-lactam antibiotics and significantly influences the bacterium’s behavior within the human host.Other pathogens responsible for the disease include...