Related Experiment Video
Updated: Jul 15, 2026

09:09
High Throughput, Real-time, Dual-readout Testing of Intracellular Antimicrobial Activity and Eukaryotic Cell Cytotoxicity
Published on: November 16, 2016
Antibiotic-induced lysis of enterococci
The Journal of Clinical Investigation
|September 1, 1981
Summary
Enterococci
Area of Science:
- Microbiology
- Bacterial Physiology
Background:
- Enterococci exhibit resistance to penicillin killing.
- Reduced autolytic activity is observed in some penicillin-resistant bacteria.
Purpose of the Study:
- To investigate the relationship between spontaneous and antibiotic-induced lysis in enterococci.
- To explore the role of autolytic activity in enterococcal antibiotic resistance.
Main Methods:
- Examined spontaneous lysis of clinical enterococcal isolates in buffer.
- Compared spontaneous lysis with susceptibility to antibiotic-induced lysis and killing.
- Tested five antibiotics inhibiting cell wall synthesis: penicillin, cephalothin, bacitracin, cycloserine, and vancomycin.
- Assessed enterococcal growth and lysis in human serum.
Main Results:
- Significant correlations were found between spontaneous and antibiotic-induced lysis.
- Strains with rapid lysis by one antibiotic showed rapid lysis by others and higher susceptibility to spontaneous lysis.
- Spontaneous lysis closely correlated with antibiotic-induced lysis in studies with a single strain across different media.
- Human serum demonstrated limited permissiveness for enterococcal growth and antibiotic-induced lysis/killing.
Conclusions:
- A common mechanism, likely the autolytic enzyme system, underlies spontaneous and antibiotic-induced lysis in enterococci.
- Human serum's inhibitory effect on growth and its activation of the autolytic system may contribute to penicillin resistance in enterococcal endocarditis.
Related Concept Videos
Antibiotic Selection
Overview
Development of Antibiotic Resistance
Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
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 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...
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...
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...

