Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Determinants of Bacterial Pathogenicity and Virulence

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...

Streptococcal Pharyngitis

Streptococcal Pharyngitis

Streptococcal pharyngitis, commonly known as “strep throat,” is an acute infection of the oropharyngeal tissues caused by the Gram‑positive Group A Streptococcus (Streptococcus pyogenes). Transmission occurs primarily through respiratory droplets expelled during coughing, sneezing, or talking.Mechanisms of Host Entry and Immune EvasionUpon entering the host, S. pyogenes adheres to the mucosal epithelial cells of the pharynx via surface proteins, notably lipoteichoic acid and the antiphagocytic...

Colonisation of Pathogens

Colonisation of Pathogens

Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...

Staphylococcal Skin Infections

Staphylococcal Skin Infections

Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Intussusception; a comparison of the infant and adult types.

The Southern surgeon·2014

Same author

The chemotherapeutic properties of Win 5047, (mantomide); a new synthetic amebacide.

Antibiotics & chemotherapy (Northfield, Ill.)·2014

Same author

Relation between arterial pressure and blood flow in the foot.

The American journal of medicine·2010

Same author

EXPERIMENTAL GRANULOPENIA, DUE TO BACTERIAL TOXINS ELABORATED IN VIVO.

The Journal of experimental medicine·2009

Same author

Aortocoronary bypass with saphenous vein graft. Seven-year follow-up. 1973.

JAMA·1996

Same author

Fatal hepatic necrosis in association with the use of hycanthone.

South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde·1978

Search research articles

Related Experiment Video

Updated: Jun 19, 2026

Invasion of Human Cells by a Bacterial Pathogen

Invasion of Human Cells by a Bacterial Pathogen

Published on: March 21, 2011

A STUDY ON THE MECHANISM OF INVASIVENESS OF STREPTOCOCCI.

E W Dennis¹, D Berberian

¹Department of Bacteriology, School of Medicine, American University of Beirut, Beirut, Lebanon.

The Journal of Experimental Medicine

|October 30, 2009

Summary

Streptococcus haemolyticus produces fibrinolytic and antifibrinogenic substances that prevent clot formation, aiding bacterial spread. These factors are thermostable, antigenic, and correlate with streptococcal invasiveness.

More Related Videos

A Murine Model of Group B Streptococcus Vaginal Colonization

A Murine Model of Group B Streptococcus Vaginal Colonization

Published on: November 16, 2016

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells

Published on: August 19, 2016

Related Experiment Videos

Last Updated: Jun 19, 2026

Invasion of Human Cells by a Bacterial Pathogen

Invasion of Human Cells by a Bacterial Pathogen

Published on: March 21, 2011

A Murine Model of Group B Streptococcus Vaginal Colonization

A Murine Model of Group B Streptococcus Vaginal Colonization

Published on: November 16, 2016

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells

Published on: August 19, 2016

Area of Science:

Microbiology
Immunology
Pathology

Background:

Inflammatory fixation is crucial for limiting pathogen spread.
Streptococcus haemolyticus infections can overcome this defense mechanism.

Purpose of the Study:

To confirm Menkin's findings on the failure of inflammatory fixation in Streptococcus haemolyticus infections.
To investigate the mechanisms by which streptococci evade inflammatory responses.

Main Methods:

Confirmation of previous observations regarding inflammatory fixation.
Analysis of bacterial products responsible for interfering with fibrin barrier formation.
Assessment of the thermostability and antigenicity of these substances.
Correlation studies between substance production and bacterial invasiveness.

Main Results:

The failure of inflammatory fixation is confirmed in acute Streptococcus haemolyticus infections.
Streptococci produce fibrinolytic and antifibrinogenic substances that prevent fibrin barrier formation.
These substances maintain lymphatic and capillary patency, facilitating bacterial dissemination.
The production of these substances correlates with the invasiveness of Streptococcus strains.
Both substances are relatively thermostable and appear to be antigenic with type specificity.

Conclusions:

Fibrinolytic and antifibrinogenic substances produced by Streptococcus haemolyticus are key factors in its invasiveness.
These bacterial products disrupt the host's inflammatory response by preventing fibrin clot formation.
Understanding these mechanisms can inform strategies to combat streptococcal infections.