Group B Streptococcus (GBS), or Streptococcus agalactiae, remains a leading cause of severe infections in newborns, pregnant women, and vulnerable adults. Historically, GBS has been highly susceptible to penicillin, the cornerstone of treatment and prevention strategies, but the landscape of GBS antibiotic resistance is shifting. While penicillin remains largely effective, the increasing frequency of resistance to alternative and other antibiotic classes is a growing public health concern. This evolving resistance profile complicates treatment decisions, especially for patients with severe penicillin allergies.
Penicillin and Beta-Lactam Resistance
For decades, GBS has been considered uniformly susceptible to penicillin and other beta-lactam antibiotics, which include ampicillin and many cephalosporins. This has made penicillin the standard of care for intrapartum antibiotic prophylaxis (IAP) to prevent transmission to newborns. However, while rare, reports of reduced susceptibility or resistance to beta-lactams have emerged in various parts of the world. This reduced susceptibility is often linked to point mutations in penicillin-binding protein (pbp) genes, particularly pbp2x. For instance, a recent study in Ethiopia found a high rate of penicillin resistance in GBS isolates, a trend attributed to the widespread and sometimes unregulated use of beta-lactams. Continued surveillance of penicillin and ampicillin sensitivity is crucial to monitor for potential shifts that could impact treatment efficacy.
Resistance to Alternative Antibiotics
For patients with a penicillin allergy, alternative antibiotics like erythromycin and clindamycin are used. Unfortunately, resistance to these second-line agents is much more common and has been steadily increasing over time. The Centers for Disease Control and Prevention (CDC) notes that clindamycin-resistant GBS strains cause a significant portion of infections, and resistance to erythromycin is even higher. This rise in macrolide and clindamycin resistance is often mediated by the acquisition of specific resistance genes, such as erm genes (causing MLSB resistance) and mef genes (causing M phenotype resistance). High rates of resistance to these alternatives mean that clinicians cannot rely on them empirically without first confirming the GBS isolate's susceptibility.
Emergence of Multidrug and Other Resistance Patterns
In addition to macrolides and clindamycin, GBS has also developed resistance to other antibiotic classes, driven by various genetic mechanisms.
Resistance to Tetracyclines
Tetracycline resistance in GBS is widespread, with some studies reporting very high rates. The resistance is primarily mediated by the tetM gene, often carried on mobile genetic elements, which allows the bacterium to protect its ribosomes from the drug's effects. While tetracyclines are generally not first-line agents for GBS, this resistance highlights the general adaptability of the bacteria.
Resistance to Fluoroquinolones
Increasing resistance to fluoroquinolones, such as levofloxacin, has also been documented. This resistance can occur due to point mutations in genes like gyrA and parC. Trends show a rising prevalence of resistance to these antibiotics over time, particularly in invasive GBS strains.
Resistance to Vancomycin
Vancomycin is considered a last-resort antibiotic for GBS in cases of severe penicillin allergy and confirmed resistance to other alternatives. Vancomycin resistance in GBS is extremely rare, with only a handful of documented cases globally. The emergence of even isolated cases, however, underscores the need for continuous surveillance to protect this critical antibiotic.
Comparative Resistance Patterns in GBS
Here is a comparison of resistance patterns for key antibiotics used in GBS treatment and prophylaxis, based on recent studies:
| Antibiotic Class | Clinical Use | Typical Resistance Rate | Main Resistance Mechanism | Implication for Therapy |
|---|---|---|---|---|
| Penicillins/Ampicillin | First-line IAP and treatment | Low (but emerging) | Mutations in pbp genes | Standard first-line therapy remains reliable, but vigilance is needed for emerging reduced susceptibility. |
| Clindamycin | Alternative for penicillin allergy | High (often >25%) | erm and mef genes | Not a reliable empirical alternative; susceptibility testing is mandatory for allergic patients. |
| Erythromycin | Alternative for penicillin allergy | High (often >35%) | erm and mef genes | Not a reliable empirical alternative; resistance is very common. |
| Tetracyclines | Not typically used for GBS | Very High (often >60%) | tetM gene | Unsuitable for GBS treatment due to high prevalence of resistance. |
| Vancomycin | Alternative for severe penicillin allergy | Extremely Rare | Acquisition of van operon | A reliable option, but reserved for specific, high-risk scenarios to prevent resistance. |
| Fluoroquinolones | Sometimes used for adult infections | Increasing | Mutations in gyrA and parC | Resistance is increasing, particularly in invasive strains; susceptibility testing is important. |
Implications for Clinical Practice
The evolving resistance patterns in GBS have significant implications for managing infections, especially in vulnerable populations. The CDC recommends screening pregnant women for GBS colonization between 35 and 37 weeks of gestation. If a woman tests positive and has a severe penicillin allergy, antibiotic susceptibility testing for alternatives like clindamycin is crucial before administering IAP. Without a confirmed susceptible strain, vancomycin is the recommended alternative. The emergence of even rare beta-lactam resistance necessitates ongoing global and local surveillance and the development of alternative strategies, including vaccines.
The Role of Antibiotic Stewardship
Combating GBS antibiotic resistance requires a multifaceted approach that includes improved surveillance, robust antibiotic stewardship programs, and continuous adaptation of treatment guidelines. Responsible prescribing, based on confirmed susceptibility patterns rather than empirical assumptions, is key to preserving the effectiveness of antibiotics for future generations. The high rates of multidrug resistance seen in some regions emphasize the need for systemic efforts to minimize antibiotic misuse.
Conclusion
Yes, strep B can be resistant to antibiotics, and the prevalence of resistance is a significant and growing problem. While first-line beta-lactams like penicillin and ampicillin remain largely effective, resistance to alternative agents such as macrolides and clindamycin is high and continues to rise. The emergence of rare vancomycin-resistant and beta-lactam-reduced-susceptibility strains highlights the dynamic nature of bacterial adaptation. Ongoing surveillance, informed treatment decisions guided by susceptibility testing, and effective antibiotic stewardship are essential to ensure that life-saving antibiotics remain a viable option for treating and preventing GBS infections. One authoritative source on this topic is the CDC's Antibiotic Resistance Threats Report, which provides comprehensive information on antimicrobial resistance trends.
