Smoking Promotes Vancomycin-Resistant Enterococci in Peritonsillar Abscess: A Growing Public Health Concern
Introduction
Peritonsillar abscess (PTA) is a common deep neck infection characterized by pus accumulation near the tonsils. While Streptococcus pyogenes and Staphylococcus aureus are typical pathogens, recent studies highlight the increasing prevalence of vancomycin-resistant enterococci (VRE) in PTA cases. Alarmingly, smoking has been identified as a significant risk factor for VRE colonization and infection. This article explores the relationship between smoking and VRE in PTA, discussing mechanisms, clinical implications, and preventive strategies.
Vancomycin-Resistant Enterococci (VRE) in Peritonsillar Abscess
VRE, particularly Enterococcus faecium and Enterococcus faecalis, are Gram-positive bacteria resistant to vancomycin, a last-resort antibiotic. Their emergence in PTA complicates treatment, as standard antibiotics may fail, leading to prolonged infections, systemic spread, and higher mortality rates.
Risk Factors for VRE in PTA
- Antibiotic Overuse – Prior exposure to vancomycin or broad-spectrum antibiotics promotes VRE selection.
- Hospitalization – Nosocomial transmission increases VRE colonization risk.
- Smoking – Disrupts mucosal immunity and alters oral microbiota, facilitating VRE persistence.
How Smoking Promotes VRE Colonization and Infection
1. Impaired Mucosal Immunity
Smoking damages the respiratory and oropharyngeal mucosa, reducing:
- Ciliary function – Impairs bacterial clearance.
- Neutrophil activity – Weakens innate immune responses.
- Secretory IgA levels – Decreases mucosal defense against pathogens.
This compromised immunity allows VRE to colonize and invade peritonsillar tissues more easily.
2. Altered Oral Microbiome
Tobacco smoke disrupts the balance of commensal bacteria, promoting dysbiosis. Studies show smokers have:
- Higher Enterococcus colonization – Due to reduced competition from beneficial flora.
- Increased biofilm formation – VRE adheres better to damaged epithelial surfaces.
3. Enhanced Antibiotic Resistance
Smoking induces oxidative stress, which may accelerate bacterial mutations and resistance gene acquisition. Additionally, nicotine has been shown to:
- Upregulate efflux pumps – Enhancing bacterial antibiotic expulsion.
- Promote horizontal gene transfer – Facilitating resistance gene spread among bacteria.
Clinical Implications of VRE-Positive PTA
Diagnostic Challenges
- Delayed identification – Routine cultures may miss VRE without specific testing.
- Misdiagnosis risk – Symptoms mimic typical PTA, leading to inappropriate initial therapy.
Treatment Difficulties
- Limited antibiotic options – Linezolid, daptomycin, or tigecycline may be required.
- Higher recurrence rates – Due to persistent colonization in smokers.
- Increased complications – Sepsis, mediastinitis, or Lemierre’s syndrome.
Preventive and Management Strategies
1. Smoking Cessation Programs
- Counseling and nicotine replacement therapy – Reduces VRE colonization risk.
- Public health campaigns – Highlighting the link between smoking and resistant infections.
2. Antimicrobial Stewardship
- Avoid unnecessary vancomycin use – Prevents VRE selection pressure.
- Culture-guided therapy – Ensures appropriate antibiotic selection.
3. Enhanced Infection Control
- Screening high-risk patients – Smokers, immunocompromised individuals.
- Strict hygiene protocols – To limit nosocomial VRE transmission.
Conclusion
The rise of VRE in peritonsillar abscesses poses a serious clinical challenge, particularly among smokers. By impairing immunity, altering microbiota, and promoting resistance, tobacco use significantly increases VRE risk. Addressing this issue requires a multidisciplinary approach, including smoking cessation, prudent antibiotic use, and rigorous infection control. Future research should further explore molecular mechanisms and targeted therapies to mitigate this emerging threat.
