Introduction
The hallmark of endocarditis is the formation of ‘vegetations’ that bind to valves or mural endocardium. Image reproduced with permission of CDC.
Aberrant flow predisposes to a collection of fibrin, platelets and scant inflammatory cells. This can also happen in hypercoagulable states like SLE, malignancy and anti-phospholipid antibody syndrome.
The action of micro organisms
Micro-organisms that enter blood stream from skin, mucosa or other sites of focal infection bind to the vegetation and cause local infection leading to a pro-coagulant state.
Further fibrin deposition, platelet aggregation and bacterial invasion lead to an infection cascade causing infective endocarditis.
Staphylococcus aureus possesses fibronectin-binding proteins and is capable of binding to intact endothelium and, therefore, can infect previously uninfected endocardium.
Bacterial micro colonies deep within the vegetation are dormant and therefore difficult to eradicate. Superficial bacterial colonies tend to embolise distally causing septic phenomenon as well as reinfection of the vegetation. A constant infection leads to the three hallmarks of the disease:
- Constitutional symptoms which are cytokine mediated
- Local spread of infection causing destruction of myocardium
- Distal blood borne septic embolisation
Constant shedding of bacteria is detected in blood cultures. In laboratories using modern techniques, positive culture rates are in excess of 90%, reaching 98% in people without previous antibiotic exposure.
The traditional role of Streptococcus
Streptococcus has traditionally been considered to be the primary pathogen responsible for endocarditis, however Staphylococcus is actually implicated slightly more in native valve disease, and is overwhelmingly the main pathogen in nosocomial infections and those in intravenous drug users (Table 1)
Recurrent Infection
Recurrence of endocarditis frequently occurs, as damaged valves are prone to further infections; 20% of patients with endocarditis have had previous infection, with this rate going up to 40% in those who inject drugs.
| Causative
Organism |
Native Value | Prosthetic Value | Injection Drug Users | |||
| Community acquired | Nosocomial | Post-op time | ||||
| 0-2 months | 2-12 months | >12 Months | ||||
| Streptococcus | 32 | 7 | 1 | 9 | 31 | 12 |
| Enterococcus | 8 | 16 | 8 | 12 | 11 | 9 |
| Pneumococcus | 1 | 0 | 0 | 0 | 0 | 0 |
| Staph. aureus | 35 | 55 | 22 | 12 | 18 | 57 |
| Coag neg Staph | 4 | 10 | 33 | 32 | 11 | 0 |
| HACEK* | 3 | 0 | 0 | 0 | 6 | 0 |
| Gram negative rods | 3 | 5 | 13 | 3 | 6 | 7 |
| Candida | 1 | 4 | 8 | 12 | 1 | 4 |
| Polymicrobial | 6 | 1 | 3 | 6 | 5 | 7 |
| Diphtheroids | 0 | 0 | 6 | 0 | 3 | 0 |
| Culture negative | 5 | 2 | 5 | 6 | 8 | 3 |
*HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
Endocarditis usually occurs on previously-damaged endocardium, and incidence greatly increases in injecting drug abusers.