Infective Endocarditis Flashcards
Definition of Endocarditis
Inner layer heart inflammation
Infective Endocarditis
Microbial infection of the endocardium, including the heart valves.
Any area of the endocardium that is subjected to turbulent blood flow can be affected.
Turbulent blood flow can occur around narrow valves or other defects - stenosis
Blood Flow
- Narrowing of the heart valve resulting in turbulent blood flow
- Narrowed valve causes turbulent blood flow, which can damage endocardium
- Exposed tissue causes fibrin and platelets to build up - thrombosis
How do transient bacteria enter the blood stream? How do they cause disease?
Organisms enter blood stream through:
Damaged gums / dental problems - procedures. Wounds. Intravenous drug use - area cleaned (saliva) / not
cleaned prior to injection/ substance not clean.
Transient bacteria usually detected via immune
system: attachment to a thrombus changes this dynamic: attach to tissues/ each other via adhesins. Biofilm formation, vegetation develops and breaks away: septic emboli
What is a biofilm?
■ Extracellular polymeric matrix produced by bacteria.
■ This causes the bacteria to begin to behave like a colony.
■ Specific architecture, creating the ideal environment for the
exchange of genetic material.
■ Biofilms hinder recognition by the immune system.
■ Reduced susceptibility to antimicrobials.
Acute Infective Endocarditis - Causative organism and Clinical pathology
- Main causative organism - Staphylococcus aureus.
Associated with native valves (NVE), can affect healthy and
damaged valves. Forms large vegetations damaging heart valves. IV patients: high risk as S.aureus present on the skin
enters the blood stream at injection site.
Acute IE- Symptoms
■ Fever (High).
■ Chest pain.
■ SOB.
■ Cough.
■ Fatigue.
■ Murmur
Sub Acute Infective Endocarditis - Causative organism and Clinical Pathology
Main causative organism(s) - viridian’s Streptococci e.g. S.mutans, S.mitis etc.
■ Associated with native valves (NVE) and can affect abnormal
valves.
■ Forms small vegetations and the heart valves can recover.
■ Causes non-specific symptoms, persisting for many weeks
prior to diagnosis.
Sub Acute IE- Symptoms
non-specific, persisting for many weeks
prior to diagnosis. Fever (Low). Chills. SOB. Night sweats. Headache. Weight loss. TATT. Splinter haemorrhages and Janeway lesions: thrombus formed on the endocardium undergoing fragmentation (emboli) that form deposits in extremities e.g under finger nails. Jane lesions: Haemorrhage to palms. Interactions between the immune system and the causative organism initiate the formation of antibody / antigen
complexes: form deposits / lodges: inflammation causing: Roth spots (retinal hemorrhages with a white or pale center), Glomerulonephritis (glomeruli inflammation), Oslers nodes (small, tender, raised lesions)
Prosthetic Valve Endocarditis - PVE
Causative organsims: commonly MSSA, Staphylococcus epidermis or enterococcus faecalis
Clinical path: form during placement of prosthetic valve. Organisms form large vegetations on valves.
Right Side vs Left Side IE
Most commonly occurs on left side of the heart - aortic and mitral valves
Cause: Unknown but hypothesised:: Higher pressure, higher oygen content, congenital abnormalities or spontaneous defects. 5% to 10% of IE cases occur on the right side of the heart – tricuspid valve: majority of cases are associated
with IntraVenous patients: Hypothesised causes: changes to valve eptihelium in IVDU, Physiological effects of injected substances, differences in organism and bacterial load
Less common causes of IE- HACEK and BCNE organisms
HACEK organisms – Form part of the oral and upper respiratory
tract microbiome, cause infection if acess to blood stream: H-aemophilus, A-ggregactibacter, C-ardiobacter, E-ikenella, K-ingella. Associated more with previous/ underlying cardiac diseases. Blood culture negative Endocarditis ( previous antibiotic use, slow growing organisms, non-bacterial pathogens, biofilm formation, host factors e.g compromised immune function/immunosupression): Associated with animal contact. Months / years later following initial infection IE can occur. Generally affect patients with IE predisposition, IV use, and/or immunocompromised. Difficult to culture, or cannot be cultured
using conventional methods:16s or 18s RNA sequencing recommended.
Q fever: Coxiella burnetii spp.
■ Bartonella spp.
■ Chlamydia spp.
■ Brucella spp.
■ Fungi / yeast
spp.
■ Tropheryma
whipplei
■ Mycobacteria
spp
IE - Diagnosis
Transthoracic Echocardiogram (External scan / non-invasive) , Transesophageal Echocardiogram (Internal scan /
invasive): visualise heart and detect valve
movement.
Blood cultures : minimum of 3 sets to be taken in 24 hour period. Bacteraemia (bacteria in the blood) constant in IE cases. Standard B/C incubation is 5 days, 10 with IE.
IE - Treatment
Prolonged antibiotics. Surgery. Differs in relation to the type of IE – NVE or PVE.
Preventative methods recommended in high risk groups: If prosthetic valves/transplants/ previous IE: prophylaxis is given prior to dental procedures.
