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Show Notes
Background
- Group A strep = Streptococcus pyogenes — gram-positive organism that colonizes the pharynx, but also the perianal and genital mucosa (worth remembering when the source isn’t the throat).
- Extremely common. The episode cites an estimated ~289 million cases/yr of strep pharyngitis in children 5–14 (NIH). For a U.S.-specific, verifiable anchor: the CDC estimates strep throat drives ~5.2 million outpatient visits/yr in people <65.
- No true beta-lactam resistance. GAS remains uniformly susceptible to penicillin and amoxicillin. Note this is not true for macrolides/clindamycin — roughly 1 in 3 invasive isolates are now erythromycin/clindamycin resistant.
Pathophysiology — the throughline
- Exotoxins (superantigens) tie the whole spectrum together — they drive scarlet fever, streptococcal toxic shock syndrome (STSS), and are implicated in the Kawasaki overlap discussed below.
- The organism is the same from a sore throat to a life-threat; what changes is host response and toxin burden.
Clinical Presentation
- Core findings: tonsillar inflammation/exudate, tender anterior cervical lymphadenopathy, fever.
- Classic strep tells to hunt for:
- Palatal petechiae
- Strawberry tongue
- Perioral pallor
- Scarlet fever — fine, sandpapery rash, typically starts on the trunk and spreads outward; later desquamation of the fingers and toes.
- Extrapharyngeal clues: kids commonly present with abdominal pain or headache even when the throat looks unimpressive. Low threshold to test with fever + abd pain or fever + headache.
Diagnosis / Workup
Centor / Modified (McIsaac) Score
- Centor Score (Modified/McIsaac) — MDCalc
- One point each: fever, tonsillar exudates, tender anterior cervical lymphadenopathy, absence of cough. The Modified (McIsaac) version adds age.
- Developed and validated in adults (≥16). It is not reliable in young children — don’t lean on it in peds the way you would in an adult.
- For reference, McIsaac culture-positive probabilities: ~2.5% (0 criteria), 6.5% (1), 15% (2), 32% (3), 56% (4).
Testing
- Rapid PCR — high sensitivity and specificity; increasingly the front-line test.
- Rapid antigen detection test (RADT) — highly specific but less sensitive. Per IDSA, a negative RADT in a child/adolescent should be backed up with a throat culture (culture is the more sensitive gold standard). Backup culture is not required in adults.
Who not to test
- Generally don’t test/treat children <3 — acute rheumatic fever is rare in this group.
- Exception: the symptomatic young child with a close contact recently diagnosed with strep.
Management
- First-line: amoxicillin 50 mg/kg once daily, max 1 g/dose. GAS stays beta-lactam susceptible (penicillin and amoxicillin remain treatments of choice per IDSA 2012).
- IM penicillin G / benzathine (bicillin) for kids who can’t tolerate oral meds — one shot, done.
- Return to school: after one full day of treatment (~12–24 h), provided afebrile and feeling well.
- Contact prophylaxis:
- Pharyngitis — routine prophylaxis of asymptomatic contacts is not standard; consider it for households with recurrent infection or a history of rheumatic fever.
- Invasive GAS — more aggressive. Prophylaxis is recommended for household contacts who are immunosuppressed, pregnant, post-recent-surgery, or have an open wound (CDC).
The Bounce-Back / Treatment Failure
The kid who finishes amox and is back a week later. Sort into three buckets:
- Chronic carrier — GAS carriage in children runs 2–20%. Carriers test positive but are asymptomatic, with low risk of transmission or complications. Don’t chase them.
- New infection.
- True treatment failure → ask why:
- The shield effect — the throat is co-colonized with beta-lactamase producers (Staph aureus, H. influenzae, Moraxella) that degrade amoxicillin before it can act, effectively shielding the GAS.
- This is NOT true resistance — the strep is still beta-lactam susceptible; the neighbors are the problem.
- Fix: switch to a beta-lactamase–stable agent — amoxicillin-clavulanate or a first-generation cephalosporin.
Complications
- Suppurative: peritonsillar abscess, sinusitis, meningitis, bacteremia.
- Non-suppurative:
- Acute rheumatic fever — typically 1–5 wks post-infection; Jones criteria (AHA 2015 revision · ACC summary · CDC).
- Post-infectious glomerulonephritis (PIGN) — several weeks out; hematuria / “Coca-Cola” urine. Note strep impetigo can also seed PIGN.
- The pearl: we treat strep to prevent rheumatic fever — but treatment does NOT prevent PIGN.
Invasive Group A Strep (iGAS)
Why it’s on the radar
- Rates have been climbing since 2014, and preliminary 2023 data hit a 20-year high (CDC). A CDC/ABCs analysis flagged a roughly 3-fold pediatric increase in Colorado/Minnesota in late 2022 (MMWR).
- Keep it in mind when a child isn’t following the typical strep course or just looks sicker than expected.
The spectrum
- STSS, necrotizing fasciitis, meningitis, bacteremia, peritonitis.
- Increasingly common and worth highlighting: bone and joint disease — septic arthritis, osteomyelitis — often traveling with pyomyositis.
The trap — nonspecific early presentation
- Symptoms are often nonspecific: fever, “not acting like themselves,” localized pain.
- Septic joint/osteo may show a limp or focal pain — but not always.
- When your gut fires, cast a wide net.
Workup
- Blood cultures, CBC, chemistries, CRP, ESR.
- Imaging — tailor to the suspected site:
- Suspected joint → start with X-ray + ultrasound.
- Worried about osteomyelitis or pyomyositis → MRI (the recommended modality for pyomyositis per IDSA SSTI).
Management
- Broad-spectrum: vancomycin + piperacillin-tazobactam (concordant with IDSA SSTI).
- In shock / STSS: ADD clindamycin or linezolid for toxin suppression — this is on top of vanc/zosyn, not a coverage swap. (IDSA: penicillin plus clindamycin for documented GAS necrotizing infection; consider IVIG in STSS.)
The Kawasaki overlap
- Meaningful overlap between iGAS and Kawasaki disease.
- Proposed mechanism: strep superantigens activate a shared inflammatory (T-cell) pathway that may contribute to KD; some data suggest kids with iGAS may be at higher risk of developing Kawasaki.
- Get rheumatology involved early — they’ll want those inflammatory markers and can help sort KD from mimics.
Take-Home Points
- Adult tools don’t translate to peds. Centor was built for ≥16 and is unreliable in young kids — diagnose on exam, the eponyms, and testing. Low threshold to swab the febrile kid with abdominal pain or headache.
- The bounce-back is a triage problem — carrier (2–20%) vs. new infection vs. true failure. True failure is usually the shield effect (beta-lactamase co-colonizers, not resistance) → switch to amox-clav or a first-gen cephalosporin.
- Treatment prevents rheumatic fever, NOT PIGN — and impetigo can cause PIGN too.
- iGAS is rising and hides behind nonspecific symptoms. When your gut fires, work it up broadly and escalate to MRI for osteo/pyomyositis. Treat with vanc + pip-tazo, and in shock add clindamycin/linezolid for toxin suppression. Keep Kawasaki in the differential and call rheum early.
Links & References
Calculators
Guidelines
- Shulman ST, et al. Clinical Practice Guideline for the Diagnosis and Management of Group A Streptococcal Pharyngitis: 2012 Update. IDSA / Clin Infect Dis. 2012;55(10):e86–e102. — IDSA · Full text
- Stevens DL, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update. IDSA / Clin Infect Dis. 2014;59(2):e10–e52. (necrotizing infection, STSS, clindamycin adjunct, MRI for pyomyositis) — IDSA · Full text
- Gewitz MH, et al. Revision of the Jones Criteria for the Diagnosis of Acute Rheumatic Fever in the Era of Doppler Echocardiography. AHA / Circulation. 2015;131:1806–1818. — Circulation · ACC “10 Points to Remember”
CDC
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