Dr. Teltscher -- Endovascular Infections Flashcards
3 methods of endovascular infection
- Direct infection of blood and its components
- Infection of endovascular device
- Direct infection of vasculature and structures
4 parasites potentially involved in endovascular infection
- Plasmodium
- Babesia
- Trypanosoma
- Leishmania
3 direct infections of vasculature and structures
- Suppurative thrombophlebitis
- Endarteritis
- Endocarditis
Define acute infective endocarditis
Abrupt toxin couse lasting days to weeks
Define subacute infective endocarditis
Indolent protracted course featuring systemic symptoms often lasting longer than weeks
Sex most commonly affected by endovascular infection
Men
Why is incidence of endovascular infection increasing? (4)
Shifting age distribution:
- Change in nature of underlying heart diseases: rheumatic –> degenerative
- Aging population = aged w/ heart disease survive longer
- Benefiting from prosthetic valve replacement surgeries
- “Healthcare associated” IE due to increased uses of endovascular technologies –> biofilm formation
4 predisposing factors for infective endocarditis
- Native valve (the one’s with which you are born)
- Prosthetic valve
- Endovascular device utilization
- IVDU
4 problems with native valves that can predispose to IE
- Rheumatic heart disease
- Congenital heart disease (some, but not all)
- Degenerative heart disease
- Mitral valve prolapse
- Uncontrolled bacteremia and/or history of endocarditis
Describe the pathogenesis of IE
Distribution of sites affected by iE
- Mitral alone = 28 - 45%
- Aortic alone = 5 - 36%
- Tricuspid = 0 - 6%
- Pulmonic very rare
When does “transient bacteremia” occur?
When heavily colonized mucosal surfaces are traumatized
Typical findings of low grade and transient bacteremia
- ≤ 10 CFUs/ml
- Blood stream sterilized within 30 minutes
- Function of “serum susceptibility” of the organism
Risk of transient bacteremia
Sufficient to infect a NBTE valvular lesion
3 types of virulence factors associated with pathogens involved in IE
- Dextran
- Adhesion to markers of damaged endothelium
- Bacteria-platelet aggregates in circulating blood
What is Dextran
Complex extracellular polysaccharide (glycocalyx)
Dextran function
Promotes adherence to platelet-fibrin matrix (NBTE)
2 pathogens that have dextran as a virulence factor
S. mutans (dental caries)
Prominent among certain *Streptococcus *spp
Marker of damaged endothelium to which bacteria can adhere
Fibronectin
Pathogen with adhesion to fibronectin as virulence factor
*S. aureus *(binding and uptake into “normal” endothelium –> triggered apoptosis)
Bacteria with bacter-platelet-aggregates in circulating blood as virulence factor
- Staphylococcus *spp.
- Streptococcus *spp.
Effect of bacteria-platelet-aggregates in circulating blood
Decreased rate of removal of organism
Increased adherence and aggregation on vegetations
2 ways sub-inhibitory (prophylactic) antibiotics may prevent IE
- Decreasing expression of adhesion virulent factors
- Direct cell killing
Describe the environment within the vegetation
- Minimal phagocyte infiltration
- Protection from circulating immune factors
- Major proliferation (billions CFUs/g of tissue)
- Deeper dormant/inert/planktonic bacterial forms (may rep up to 90% of bacterial burden)
3 pathogens involved in community acquired IE on native valve
- S. aureus
- *Streptococcus *spp.
- Lesser extent *Enterococcus *spp.
2 pathogens involved in nosocomial IE on a native valve
- S. aureus
- Lesser extent *Enterococcus *spp.
Pathogen associated with IVDU IE on native valve
S. aureus (lesser extent other bacteria)
6 pathogens involved in early post surgical (<2 months) IE on prosthetic valve
- Coagulase negative *Staphylococcus *spp. > S. aureus
- Important rate of others:
- Diphtheroids
- Gram negative bacilli
- Candida spp.
- Fungi
4 pathogens involved in intermediate post-surgical (2 - 12 months) IE on prosthetic valve
- Coagulase negative *Staphylococcus *spp. > S. aureus
- Lesser extent *Enterococcus *spp. > *Streptococcus *spp
Pathogens involved in late post-surgical (> 12 months) IE on prosthetic valve
Similar to native valve, but increased rate of CoNS/other
6 organisms that produce culture negative endocarditis
- HACEK
- Gram negative organisms w/ unusual growth characteristics that are not truly “culture negative” using modern techniques
- Coxiella burnetti
- *Bartonella *sp.
- *Mycoplasma *spp. / *Chlamydophila *spp.
- Trophyrema whipplei
- Fungi (i.e. *Candida *spp., Aspergillus spp.)
3 reasons why IE is clinically tricky
- “Protean” manifestation
- Subacute/chronic forms may have multiple B-symptoms
- Systemic symptoms often open differential and may be misleading
4 most common symptoms of IE
- Fever
- Chills
- Weakness
- Dyspnea
Importance of cardiac auscultation in IE diagnosis
- Audible murmur in 85%
- “New murmur” or “changed murmur” = important but uncommon
2 types of IE that do not have audible murmur
- Right-sided IE
- Mural IE
Most important diagnostic test for IE
Blood cultures
Recommended blood culture technique in IE
- 3 sets, only 2 bottles per stick in first 24 hours
- At least 10 mL of blood in each bottle
- May need prolonged incubation
2 electrocradiogram techniques for IE diagnosis
TTE
TEE
Describe the use of TTE in IE
- Utility in all suspected patients
- May be technically inadequate in up to 20% of individuals
- Variable sensitivity
- Negative cannot rule out IE
- Best or right-sided IE
- False postive very rare
Describe the use of TEE in IE
- Invasive
- More sensitive than TTE (65% vs. 95%)
- Consider in suspected cases w/ negative TTE
- Very useful for prosthetic valves
- Negative does not R/O IE
- May repeat in 7 - 10 days
Modified Duke Criteria: Pathologic criteria for definite IE
- Microorganisms: demonstrated by culture or histology in a vegetation OR in a vegetation that has embolized OR in an intracardiac abscess OR
- Pathologic lesions: vegetation or intracardiac abscess present, confirmed by histology showing active endocarditis
Modified Duke Criteria: Clinical criteria for definite IE
- 2 major OR
- 1 major and 3 minor OR
- 5 minor
Modified Duke Criteria: possible IE
- 1 major and 1 minor OR
- 3 minor
Modified Duke Criteria: Rule out IE (4)
- Firm alternative diagnosis OR
- Resolution of manifestation of IE with ABX for 4 days or less OR
- No pathologic evidence of IE at surgery or autopsy, after ABX therapy for 4 days or less
- Does not meet criteria for possible IE
2 major criteria for IE
- Blood culture positive for IE
- Consistent with IE from 2 separate cultures
- Microorganisms consistent with IE from persistently positive blood cultures
- Single postivive blood culture for *Coxiella burnetii *or antiphase I IgG Ab titer >1:800
- Evidence of endocardial involvement
- Echocardiogram positive for IE
- New valvular regurgitation
Define “persistently positive blood cultlures”
- At least 2 positive cultures drawn 12 h apart
- All of 3, or a majority of more than 4 separate cultures with first and last samples at least 1 hour apart
5 minor criteria for IE
- Predisposition (heart condition or injection drug use)
- Fever
- Vascular phenomenon
- Immunologic phenomenon
- Microbiological evidence
6 vascular phenomena that are included in minor criteria for IE
- Major arterial embolu
- Septic pulmonary infarcts
- Mycotic aneurysm
- Intracranial hemorrhage
- Conjunctivital hemorrhages
- Janeway lesions
4 immunologic phenomena that are included in minor criteria for IE
- GN
- Osler nodes
- Roth spots
- Positive RF
Define minor microbiological evidence for IE
Positive blood culture, but does not meet any major criterion as noted above, or serological evidence of active infection with organism consistent with IE
5 pathogens found in blood culture typical for IE in major criteria
- Viridans streptococci
- S. bovis
- HACEK group
- S. aureus
- Community-acquired enterococci, without primary focus
8 Acute IE pathologic heart changes
- Vegetation is larger, softer, more friable
- Associated with more suppuration, more necrosis
- Less healing
- Valve perforation
- Rupture of chordae tendonae, interventricular septum, papillary muscles
- Perivalvular abscess
- Fistula into percardium, myocardium
- Myocarditis, MI, pericarditis
4 organs involved in embolic phenomena due to IE
- Kidney
- Spleen
- Coronaries
- Brain
3 immune phenomena due to pathological changes of IE
- Immune complex deposition
- Complement activation
- Autoimmune process activated by increased circulating antibodies
3 pathologic changes of kidney architecture during IE
ALL biopsies have abnormal architecture
- Abscess
- Infarction
- GN
Vascular pathologic change due to IE
Mycotic aneurysm
Pathogen for which mycotic aneurysm is most common
viridans Streptococcus
3 mechanism of mycotic aneurysm
- Direct invasion of arterial wall, abscess and/or rupture
- (Septic) emboli occluding vasa vasorum
- IC deposition and injury to the vascular wall
NOTE: Tend to occur at bifurcation points
Most common neurologic event in IE
Cerebral emboli (20%)
Leading CNS related cause of death in IE
Hemorrhagic transformation of ischemic event from cerebral emboli
Most common parts involved in cerebral emboli
MCA
Branches
3 CNS pathologic changes due to IE
- Cerebral emboli
- Purulent meningitis
- Microabscesses
Pathogen associated with purulent meningitis due to IE
S. pneumoniae
Pathogen associated with micorabscesses in CNS due to IE
S. aureus
4 pathologic changes of spleen due to IE
- Enlargement
- Infarction (usually clinically silent)
- Abscess
- Surgical indication or percutaneous drainage
- Spontaneous rupture
2 reasons for spleen enlargement in IE
- Immune stimulation
- Follicle engorgement
Type of IE that lung changes are typically associated with
Right-sided
4 pathologic lung changes associated with IE
- PE (septic or “bland”) + infarction
- Acute pneumonia
- Pleural effusion
- Empyema
3 pathologic skin changes due to IE
- Petechiae (20 - 40%)
- Osler nodes (immune mediated)
- Janeway lesions (vascular event)
Cause of Osler nodes
- IC depostiion in blood vessels
- Arteriollar intimal proliferation with extension to venules and capillaries, may be accompanied by thrombosis or necrosis
Describe Osler nodes
Tender lesions at pulp of fingers
Cause of Janeway lesions
Septic emboli
Describe Janeway lesions
- May feature subcutaneous abscesses
- Non-tender
- Palms and soles
3 pathologic eye changes due to IE
- Roth spots
- Conjunctival petechiae/hemorrhage
- Flame hemorrhages
Describe Roth spots
Lymphocytes, edema and hemorrhage in nerve fibre layer of the retina
