Interactions of methicillin resistant Staphylococcus aureus USA300 and Pseudomonas aeruginosa in polymicrobial wound

Irena Pastar1, Aron G Nusbaum, Joel Gil

  • 1Department of Dermatology and Cutaneous Surgery, Wound Healing and Regenerative Medicine Research Program, University of Miami Miller School of Medicine, Miami, Florida, United States of America.

Plos One
|March 2, 2013
PubMed

Insights

Polymicrobial wound infections with Staphylococcus aureus and Pseudomonas aeruginosa significantly delay healing. Pseudomonas aeruginosa enhances Staphylococcus aureus virulence, increasing infection severity.

Area of Science:

  • Microbiology
  • Wound Healing Research
  • Infectious Diseases

Background:

  • Staphylococcus aureus and Pseudomonas aeruginosa are common causes of difficult-to-heal wound infections.
  • Methicillin-resistant S. aureus USA300 is a significant pathogen in community-associated infections.
  • Polymicrobial infections complicate treatment due to bacterial interactions and resistance.

Purpose of the Study:

  • To investigate the synergistic effects of Staphylococcus aureus USA300 and Pseudomonas aeruginosa in a polymicrobial wound infection model.
  • To understand the impact of these bacteria on wound re-epithelialization and virulence factor expression.

Main Methods:

  • Utilized a porcine partial thickness wound healing model.
  • Studied mixed-species biofilms in vitro and in vivo.
  • Analyzed wound re-epithelialization and bacterial growth.
  • Measured the expression of Staphylococcus aureus virulence factors.

Main Results:

  • Mixed-species biofilms significantly delayed wound re-epithelialization by suppressing keratinocyte growth factor 1.
  • Pseudomonas aeruginosa inhibited Staphylococcus aureus growth in vitro but co-existed in vivo.
  • Pseudomonas aeruginosa induced the expression of Staphylococcus aureus virulence factors Panton-Valentine leukocidin and α-hemolysin.

Conclusions:

  • Bacterial interactions within polymicrobial biofilms in vivo are crucial for wound infection pathology.
  • Pseudomonas aeruginosa contributes to the severity of Staphylococcus aureus wound infections by upregulating virulence factors.
  • Understanding these interactions is key to developing effective treatments for complex wound infections.

Related Concept Videos

Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
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...
Staphylococcal Skin Infections01:29

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...
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...
Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...