H(2)O(2)-nonproducing Streptococcus pyogenes strains: survival in stationary phase and virulence in chronic

Mitsumasa Saito1, Shouichi Ohga1, Miyoko Endoh2

  • 1Departments of Bacteriology1 and Pediatrics2, Faculty of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.

Insights

Hydrogen peroxide (H2O2) production varies in Streptococcus pyogenes. Non-producing strains are more virulent in mice and pose a threat to patients with chronic granulomatous disease (CGD).

Area of Science:

  • Microbiology
  • Immunology
  • Pathogen Biology

Background:

  • Streptococcus pyogenes causes pharyngitis and severe infections.
  • Hydrogen peroxide (H2O2) production is a phenotype studied in S. pyogenes.
  • The role of H2O2 in S. pyogenes virulence and host interaction is not fully understood.

Purpose of the Study:

  • To investigate H2O2 production in S. pyogenes strains from different infection types.
  • To determine the impact of H2O2 production on S. pyogenes virulence and survival.
  • To assess the susceptibility of H2O2-producing and non-producing strains to phagocyte killing, particularly in the context of chronic granulomatous disease (CGD).

Main Methods:

  • Isolation and characterization of S. pyogenes strains from pharyngitis and severe infections.
  • Culturing strains under specific conditions to measure H2O2 accumulation.
  • Assessing cell viability and the role of H2O2 in lethality using catalase.
  • Evaluating resistance to phagocyte killing from CGD patients.
  • Inoculating CGD mice with different S. pyogenes strains to assess virulence and mortality.

Main Results:

  • 25 out of 46 S. pyogenes strains accumulated H2O2 under glucose-limited, aerobic conditions.
  • H2O2 accumulation correlated with a loss of cell viability, preventable by catalase.
  • H2O2-nonproducing strains showed resistance to CGD phagocyte killing.
  • In CGD mice, H2O2-nonproducing strains caused more severe footpad swelling and higher mortality rates.
  • No correlation was found between H2O2 production and disease type or T type.

Conclusions:

  • H2O2-nonproducing S. pyogenes strains are prevalent and may pose a significant health risk to individuals with CGD.
  • H2O2 production influences S. pyogenes virulence and interaction with the host immune system.
  • Understanding these phenotypes is crucial for managing S. pyogenes infections, especially in immunocompromised individuals.

Related Concept Videos

Streptococcal Pharyngitis01:27

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...
Determinants of Bacterial Pathogenicity and Virulence01:20

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...
Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Pulmonary Tuberculosis II01:28

Pulmonary Tuberculosis II

Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
Viral Replication: Lysogenic Cycle01:16

Viral Replication: Lysogenic Cycle

The lysogenic cycle is a crucial viral replication strategy that allows bacteriophages to persist within host cells without immediately destroying them. This process is primarily observed in temperate phages, such as bacteriophage lambda (λ), which infects Escherichia coli. The cycle allows the viral genome to persist across bacterial generations while keeping host cells viable.Integration of the Viral GenomeUpon infection, bacteriophage lambda attaches to the bacterial surface and injects its...