From the Guidelines
Strep A and Strep B are distinct types of streptococcal bacteria with different infection sites, target populations, and treatment approaches, emphasizing the need for accurate identification and management to prevent morbidity and mortality. The primary difference between Strep A (Group A Streptococcus or Streptococcus pyogenes) and Strep B (Group B Streptococcus or Streptococcus agalactiae) lies in their typical infection sites and the populations they affect. Strep A commonly causes throat infections (strep throat), skin infections like impetigo, and can lead to complications such as scarlet fever, rheumatic fever, or post-streptococcal glomerulonephritis 1. It is usually treated with penicillin or amoxicillin, with alternatives like clindamycin or macrolides for penicillin-allergic patients. On the other hand, Strep B colonizes the genital and gastrointestinal tracts without symptoms but can cause serious infections in newborns, pregnant women, elderly people, and those with chronic conditions 1.
Key Differences and Considerations
- Strep A typically affects the general population, causing acute symptomatic infections, whereas Strep B more often affects specific vulnerable groups.
- Pregnant women are screened for Strep B at 35-37 weeks, and if positive, receive intravenous antibiotics during labor to prevent early-onset GBS disease in newborns.
- The approach to treatment and prevention differs significantly between Strep A and Strep B, highlighting the importance of accurate diagnosis and targeted management strategies. Given the potential for severe outcomes, especially in vulnerable populations, it is crucial to prioritize the prevention of Strep B infections in newborns through universal screening and intrapartum antibiotic prophylaxis 1. This approach has been endorsed by major health organizations and has significantly reduced the incidence of early-onset GBS disease.
From the Research
Differences between Strep A and Strep B
- Strep A, also known as Group A β-hemolytic Streptococcus (GAS), and Strep B, also known as Group B streptococcus (GBS), are two common pathogens that cause various diseases in children 2.
- GBS tends to affect younger infants compared to GAS, with a median age of 0.13 years versus 5.47 years for GAS 2.
- Cerebrospinal fluids are more likely to be positive in GBS infections than in GAS infections 2.
- Both GAS and GBS are sensitive to penicillin, but GBS is more resistant to clindamycin and erythromycin compared to GAS 2.
- Co-infections are common in both GAS and GBS, but viruses are only isolated with GAS 2.
Pathogenesis and Vaccine Development
- GAS poses a significant global disease burden, with manifestations ranging from pharyngitis and skin infection to severe diseases like necrotizing fasciitis and streptococcal toxic shock syndrome 3.
- Developing a safe and effective vaccine against GAS is crucial to address GAS-related diseases, but it has been challenging due to the wide genetic heterogeneity of GAS and diverse autoimmune responses 3.
- GBS, on the other hand, has been less studied in terms of vaccine development, but it is known to cause severe infections, especially in infants 2.
Antimicrobial Resistance
- Both GAS and GBS have shown resistance to antibiotics, including penicillin, macrolides, and lincosamides 4.
- The mechanisms of resistance include mutations in genes encoding penicillin-binding proteins, ribosomal target modifications, and active efflux pumps 4.
- The spread of antibiotic resistance is a significant concern, and monitoring and precautionary measures are necessary to prevent the spread of resistant mutant strains 4.
Membrane Phospholipid Remodeling
- GAS, GBS, and Streptococcus pneumoniae can remodel their membrane phospholipids in response to human serum 5.
- The three streptococcal species can synthesize phosphatidylcholine, a zwitterionic phospholipid commonly found in eukaryotes, when grown in human serum-supplemented medium 5.
- GBS possesses unique membrane biochemical or biophysical properties, as evidenced by the presence of plasmanyl-PC in its membrane during growth with human serum 5.