Streptococcus agalactiae—aka Group B Strep (GBS)—is one of those organisms that keeps showing up in Step stems because it ties together obstetrics, neonatology, and microbiology in a super predictable way. If you can quickly recognize who it infects, how it gets transmitted, what it looks like in the lab, and how we prevent it, you’ll pick up easy points on both Step 1 and Step 2.
Where GBS Fits in Gram-Positive Micro (Big Picture)
GBS is a Gram-positive coccus that is:
- Streptococcus (not Staphylococcus)
- Catalase-negative
- Beta-hemolytic on blood agar
- Lancefield group B (cell wall carbohydrate antigen)
- Typically arranged in chains
Quick “ID Card”
| Feature | GBS (Strep agalactiae) |
|---|---|
| Gram stain | Gram-positive cocci in chains |
| Catalase | Negative |
| Hemolysis | Beta-hemolytic |
| Lancefield | Group B |
| Key tests | CAMP positive, hippurate positive |
| Classic population | Neonates, pregnant patients |
| Classic diseases | Neonatal sepsis, pneumonia, meningitis; postpartum endometritis |
First Aid cross-reference: Microbiology → Gram-positive cocci → Streptococci (Group B) (wording/placement varies slightly by edition)
Definition & Epidemiology (Why It’s So Testable)
Strep agalactiae is a common colonizer of the:
- Vagina
- Lower GI tract
The Step-relevant epidemiology
- Many pregnant patients are asymptomatically colonized
- Vertical transmission occurs during labor/delivery
- Major cause of neonatal sepsis and meningitis
Pathophysiology (Mechanisms You Actually Need)
1) Polysaccharide capsule (major virulence factor)
- GBS has a sialic acid–containing polysaccharide capsule
- Functionally:
- Anti-phagocytic
- Helps evade innate immunity (high-yield concept: capsule = immune evasion)
2) Beta-hemolysis
- Supports identification on blood agar (not the key virulence driver, but a classic lab clue)
3) Colonization → ascension/vertical transmission
- Maternal colonization can lead to:
- Chorioamnionitis
- Postpartum endometritis
- Neonate exposure at delivery can lead to:
- Early-onset disease (first week)
- Late-onset disease (weeks later)
First Aid cross-reference: Capsule importance is emphasized across encapsulated bacteria sections; GBS specifically under Strep (Group B).
Clinical Presentation (High-Yield Patterns)
Neonatal disease: Early vs Late
GBS is classically divided into:
Early-onset GBS (0–6 days of life; commonly within 24 hours)
Typically acquired during delivery.
Presentation
- Sepsis
- Pneumonia
- Respiratory distress, apnea, poor feeding, lethargy
Step stem clues
- Newborn with respiratory distress + sepsis shortly after birth
- Maternal history: no prenatal care, or not screened, or no intrapartum prophylaxis
Late-onset GBS (7–89 days)
May be acquired from maternal or environmental sources.
Presentation
- Meningitis is especially high-yield here
- Fever, irritability, poor feeding, bulging fontanelle (if severe)
Step stem clue
- Infant a few weeks old with meningitis; culture grows beta-hemolytic strep; CAMP+
Maternal/pregnancy-associated infections
In pregnant/postpartum patients, GBS can cause:
- Postpartum endometritis
- Chorioamnionitis
- UTIs
Step stem clue
- Postpartum fever + uterine tenderness; culture consistent with GBS risk factors/colonization.
Diagnosis (What They’ll Ask You to Recognize)
Prenatal screening (most testable clinical pearl)
- Screen pregnant patients at 36 0/7 to 37 6/7 weeks gestation (commonly written as 36–37 weeks) with:
- Vaginal + rectal swab culture (or NAAT depending on protocol)
Why it matters: Screening determines whether to give intrapartum prophylaxis.
Lab identification (Step 1 classic)
GBS identification features:
- Beta-hemolytic on blood agar
- CAMP test positive
- Hippurate hydrolysis positive
CAMP test: how to conceptualize it
- GBS produces CAMP factor → enhances hemolysis near Staph aureus streak on blood agar
- “Arrowhead” hemolysis pattern = classic board image description
Differentiate from similar bugs
| Organism | Hemolysis | Key test | Big clinical hook |
|---|---|---|---|
| GBS (S. agalactiae) | Beta | CAMP+, hippurate+ | Neonatal sepsis/meningitis, maternal colonization |
| GAS (S. pyogenes) | Beta | PYR+, bacitracin sensitive | Strep throat, rheumatic fever, PSGN, nec fasc |
| S. pneumoniae | Alpha | Optochin sensitive, bile soluble | Pneumonia, otitis, meningitis in adults/kids |
| Enterococcus | Usually gamma (can vary) | Bile esculin+, grows in 6.5% NaCl | UTI, endocarditis |
First Aid cross-reference: Differentiation tables appear in Gram-positive cocci section; CAMP/hippurate is frequently listed for Group B.
Treatment & Prevention (Step 1 + Step 2 “Do This” Rules)
First-line intrapartum prophylaxis (prevention)
If the mother is GBS positive (or meets criteria), give:
- Penicillin G (classic first-line) or ampicillin
If severe penicillin allergy:
- Alternative depends on susceptibility; common test answers:
- Clindamycin (if susceptible)
- Vancomycin (if resistance or susceptibility unknown)
Testable concept: This is intrapartum prophylaxis (during labor), not just “treat sometime during pregnancy.”
Who gets intrapartum prophylaxis? (High-yield triggers)
You’ll see these in Step 2-style stems:
Give prophylaxis if:
- Positive screening culture at 36–37 weeks
- GBS bacteriuria during current pregnancy (any colony count is treated as a marker of heavy colonization)
- Prior infant with invasive GBS disease
Also give prophylaxis if GBS status unknown and any risk factor present:
- Preterm labor (< 37 weeks)
- ROM ≥ 18 hours
- Intrapartum fever (often ≥ 100.4°F / 38°C)
Treatment of neonatal infection
Empiric neonatal sepsis coverage often includes:
- Ampicillin + gentamicin (classic pairing)
Once GBS confirmed, therapy is generally a beta-lactam (e.g., penicillin/ampicillin), tailored to site (sepsis vs meningitis) and sensitivities.
High-Yield Associations & Board-Style “Buzz Phrases”
The classic USMLE one-liners
- “CAMP positive” and “hippurate positive” = Group B Strep
- Neonatal sepsis + pneumonia = think early-onset GBS
- Late-onset meningitis in infant = think GBS
- Colonizes vagina → vertical transmission during delivery
- Intrapartum penicillin prevents neonatal disease
Rapid-fire mini-questions you should be able to answer
- GBS Gram stain? Gram-positive cocci in chains
- Catalase? Negative
- Hemolysis? Beta
- Where does it live? GI + vagina (colonization)
- Big prevention move? Screen at 36–37 weeks and give intrapartum penicillin if indicated
Step 1 Memory Anchors (Without the Fluff)
“Group B = Baby”
- B for Birth exposure
- B for Beta-hemolytic
- B for Brain (late-onset meningitis)
Two lab tests to lock in
- CAMP+
- Hippurate+
If a question gives you either one plus neonatal infection, you’re basically done.
Common Pitfalls (Where Students Lose Points)
- Confusing GBS with GAS because both are beta-hemolytic
- Remember: GBS = CAMP+, GAS = PYR+ and bacitracin sensitive
- Forgetting rectal swab is part of prenatal screening (it’s not just vaginal)
- Mixing up timing:
- Screen at 36–37 weeks
- Prophylaxis happens during labor
- Assuming prophylaxis is only for positive cultures
- Also for GBS bacteriuria this pregnancy or prior affected infant
Summary Table (Last-Minute Review)
| Category | High-yield takeaways |
|---|---|
| ID | Gram+ cocci in chains, catalase−, beta-hemolytic, Lancefield Group B |
| Key tests | CAMP+, hippurate+ |
| Virulence | Polysaccharide capsule (anti-phagocytic) |
| Colonization | Vaginal/GI tract |
| Neonatal disease | Early: sepsis/pneumonia; Late: meningitis |
| Prevention | Screen 36–37 wks; intrapartum penicillin/ampicillin if indicated |
| Risk-based prophylaxis | Preterm labor, ROM ≥ 18h, intrapartum fever, unknown status + risk factors |