MI3.1-4 | Infective Endocarditis & Rheumatic Fever — Summary & Reflection

REFLECT

Think about a common scenario in your clinical placement: a patient with a known heart murmur (possibly from childhood rheumatic fever) undergoes a dental extraction. Three weeks later, they present with fever and malaise.

• Which organisms are most likely responsible?
• What would you tell the dentist about antibiotic prophylaxis for high-risk patients?
• If blood cultures grow Streptococcus mutans, which Duke's criterion does this satisfy?
• How does molecular mimicry explain why the child's strep throat decades earlier led to this valve damage?

Link these events as a single biological narrative — from pharyngeal GABHS to mitral stenosis to IE vegetation.

KEY TAKEAWAYS

Rheumatic Fever:
- Caused exclusively by pharyngeal GABHS; latent period 2–4 weeks
- Mechanism: molecular mimicry — M-protein antibodies cross-react with cardiac, joint, neural antigens
- Diagnose with Jones criteria (2 major, or 1 major + 2 minor) + evidence of GABHS (ASO titre, anti-DNase B)
- Aschoff body = pathognomonic histological lesion
- Secondary prophylaxis with monthly benzathine penicillin prevents recurrence and progression to RHD

Infective Endocarditis:
- Acute: S. aureus (destroys normal valves); Subacute: viridans strep (on damaged valves)
- Pathogenesis: endothelial damage → NBTE → bacteraemia → vegetation
- Diagnose with Duke's criteria (major: blood culture + echo; minor: fever, vascular/immune phenomena)
- Blood cultures: 3 sets from 3 sites, continuous bacteraemia — no need to time to fever spike
- Blood culture-negative IE: prior antibiotics, Coxiella, Bartonella, Brucella — use serology/PCR
- Sepsis risk: organ dysfunction from dysregulated host response — prompt diagnosis is life-saving