Related Experiment Video

Updated: Jul 9, 2026

Ookluc: A Plasmodium berghei Line for Identifying Transmission-blocking Compounds
07:14

Ookluc: A Plasmodium berghei Line for Identifying Transmission-blocking Compounds

Published on: July 11, 2025

Telithromycin and quinupristin-dalfopristin induce delayed death in Plasmodium falciparum

Diana Barthel1, Martin Schlitzer, Gabriele Pradel

  • 1Research Center for Infectious Diseases, University of Würzburg, Röntgenring 11, 97070 Würzburg, Germany.

Antimicrobial Agents and Chemotherapy
|December 7, 2007
PubMed

Insights

Certain ribosome-blocking antibiotics, like telithromycin and quinupristin-dalfopristin, inhibit malaria parasite growth by affecting apicoplast translation. This leads to a delayed death in the parasite, indicating a potential new therapeutic avenue.

Area of Science:

  • Malariology
  • Microbiology
  • Drug Discovery

Background:

  • Antibacterial agents are explored for malaria treatment due to targeting prokaryotic organelles like mitochondria and apicoplasts.
  • The apicoplast is a key organelle in the malaria parasite Plasmodium falciparum, essential for its survival.

Purpose of the Study:

  • To investigate the efficacy of ribosome-blocking antibiotics against Plasmodium falciparum.
  • To determine if these antibiotics target specific parasite organelles, particularly the apicoplast.

Main Methods:

  • Culturing Plasmodium falciparum in vitro.
  • Treating cultures with specific ribosome-blocking antibiotics: telithromycin, quinupristin-dalfopristin, and linezolid.
  • Observing and quantifying parasite growth inhibition and mortality.

Main Results:

  • Telithromycin and quinupristin-dalfopristin significantly inhibited Plasmodium falciparum growth.
  • Linezolid did not show significant inhibitory effects.
  • Both effective drugs induced a delayed death phenotype in the parasite population.

Conclusions:

  • Ribosome-blocking antibiotics telithromycin and quinupristin-dalfopristin show potential as antimalarial agents.
  • The observed delayed death suggests that these antibiotics impair apicoplast translation processes.
  • Further research into apicoplast-targeted therapies is warranted for malaria treatment.

More Related Videos

In Vitro Assay of Plasmodium-Infected Red Blood Cell Killing by Cytotoxic Lymphocytes08:20

In Vitro Assay of Plasmodium-Infected Red Blood Cell Killing by Cytotoxic Lymphocytes

Published on: August 17, 2022

CRISPR/Cas9 Gene Editing to Make Conditional Mutants of Human Malaria Parasite P. falciparum09:25

CRISPR/Cas9 Gene Editing to Make Conditional Mutants of Human Malaria Parasite P. falciparum

Published on: September 18, 2018

Related Concept Videos

Antiprotozoal Agents01:21

Antiprotozoal Agents

Leishmaniasis is a widespread parasitic disease caused by several Leishmania species. It affects millions of people each year and remains a major public health problem in endemic regions. First-line treatment relies on pentavalent antimonials, including meglumine antimoniate and sodium stibogluconate. Even so, how these drugs work has not been fully clear, especially their interaction with parasite-specific biochemical pathways. One key target is trypanothione reductase (TR), an enzyme that...
Malaria01:29

Malaria

Malaria pathogenesis in humans reflects a delicate interplay between parasite biology and host response. Clinical illness reflects a host’s immune response to the parasite’s asexual replication cycle, which is often asymptomatic in individuals with partial immunity. From the parasite's perspective, transmission between mosquito and human with minimal host pathology is evolutionarily advantageous. Among the six Plasmodium species infecting humans, P. falciparum and P. vivax dominate in global...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...
Anthelminthic Agents01:15

Anthelminthic Agents

Anthelmintic drugs differ significantly from antiparasitic therapies targeting protozoa, primarily due to differences in parasite biology. Whereas most protozoal treatments act on proliferating cells, anthelmintics are typically directed against mature, nonproliferative helminths. The therapeutic approach considers the helminth's reliance on neuromuscular coordination, glucose metabolism, and microtubular integrity for survival, reproduction, and localization within the host. Most anthelmintics...
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 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...