May8 M1-Endovascular infection Flashcards
3 types of endovascular infections
- direct infection of blood and its components (blood cells, RBCs, WBCs)
- infection of endovascular device (prosthetic heart valve, PPM, ICD, CVL, LVAD, etc.)
- direct infection of vasculature and structures
acute vs subacute infective endocarditis (IE)
- acute: abrupt toxic course lasting days to weeks
- subacute: indolent protracted (prolonged) course, systemic symptoms, many weeks
characteristic of metal or foreign or plastic objects related to infections
- get biofilm formed on them
- CoNS** very common biofilm forming group of organisms
In IE, what can get infected
- native valve
- prosthetic valve
- endovascular device utilization (IV access, CVAD much more than peripheral IV, implanted devices, surgical material)
- IVDU (IV drug user)
steps for the formation of a nonbacterial thrombotic endocarditis (first step of IE pathogenesis)
- trauma or debris hits tissue (valve for ex) and cell surface markers are exposed
- platelets and fibrin deposit on valve
- get NBTE (initial structure)
how does a NBTE get infected
- transient bacteremia occurs often because our flora (colonizers) express virulence factors and can enter blood
- when body can’t clear it, may go and adhere to the NBTE (initial non sterile vegetation)
what happens when bacteria adhere to NBTE
- microscopic vegetation
- then macroscopic vegetation
- mature vegetation
(imp?) most common sites of IE
#1 mitral valve #2 aortic valve
virulence factors bacteria use to reach NBTE
- dextran (strep spp: S. mutans of caries, S viridans) for adherence to platelet-fibrin matrix
- fibronectin (Staph aureus) to bind normal endothelium and make it apoptose
- bacteria-platelet aggregates using surface Rs and surface Ags (staph spp and strep spp) to use platelets as camouflage (but platelet not infected)
what do prophylactic Abx do in IE (note: given rarely nowadays)
prevent IE by
- reducing expression of adhesion virulent factors
- direct cell killing
3 categories of native valve infections
- community acquired
- nosocomial
- IVDU
(imp?) most common pathogen in native valve IE no matter the category (comm, hosp or IVDU) and special note about comm acquired
- staph aureus (aggressive infections)
* comm acquired = staph aureus AND strep viridans
3 categories of prosthetic valve IE
- early post surgical (<2mo)
- intermediate post surgical (2-12 mo)
- late post-surgical (>12 mo)
(imp?) most common pathogen in prosthetic valve early post surgical IE
CoNS like staph epi (indolent infection)
(imp?) most common pathogen in prosthetic valve intermediate post surgical IE
CoNS like staph epi (indolent infection)
(EXAM) most common pathogen in prosthetic valve in late post surgical IE
#1 staph aureus/strep viridans (so back like native valve comm acquired IE) #2 CoNS (coag negative staph)
4 typical symptoms of IE (non-specific but a 5th symptom will help)
- fever
- chills
- weakness
- dyspnea
(imp?) important physical exam sign that can be very indicative of IE even though it is uncommon
CHANGED murmur or NEW murmur on auscultation
other physical exam signs of IE
- skin manifestations (Janeway, Osler, etc.)
- clubbing
- splenomegaly
- septic complications
- etc
(imp?) main diagnostic test of IE
blood cultures (2 cultures)
(important) two types of echocardiograms (US) to know about for IE investigation AND WHAT DO YOU LOOK FOR
- transthoracic echo (TTE) = over chest
- transesophageal echo (TEE) = more invasive but more sensitive. TEE immediately if prosthetic valve
- looking for vegetations moving with flow and valves*
TTE and TEE in IE are better to investigate what part of the heart
right heart
T-F: you can rule out IE with a negative TTE or TEE
False. can’t rule out endocarditis with negative US
major criteria for IE dx (each point is a criteria)
- positive blood culture for 2 sets with atypical org, many sets with many org or 1 set with coxiella
- positive echo or new/changed murmur
minor criteria for IE dx
- predisposing heart condition or IVDU
- fever over 38
- vascular phenomenon (like petechiae and Janeway lesions on physical)
- immunologic phenomenon (like Osler nodes and Roth spots)
- microbiological evidence that is not major
diagnosis of definite IE definition
- pathologic def: culture or histo or vegetation embolized or intracardiac abscess show microorg
- clinical def: 2 major criteria OR 1 major+3 minor OR 5 minor.
diagnosis of possible IE definition
1 major+1 minor criteria OR 3 minor
heart pathology in IE
- valve vegetations and destruction
- heart tissue infection
- rupture of chordae tendineae, intraventricular septum, papillary muscle
extra cardiac pathology in IE
- embolic phenomenon to kidneys, spleen, coronaries, brain give Abx to reduce this risk
- immune phenomenon (immune complex deposition)
kidney pathology in IE
- abnormal architecture
- abscess
- infarction
- GN
vascular pathology in IE
if strep viridans infection (comm acquired native valve IE or late post surgical prosthetic valve IE), mycotic aneurysm (not fungal)
brain pathology in IE
- cerebral emboli
- ischemic and eventually hemorrhagic stroke
- brain abscess
- edema
- meningitis
Ostringe (or Osler) triad for meningitis in IE
Strep pneumo infection, bacteremia and meningitis (+ IE obviously)
spleen patho in IE
- splenomegaly
- infarction
- abscess
- rupture
lung patho in IE
- septic emboli with infarction
- acute pneumonia
- pleural effusion
- empyema
skin patho in IE
- petechiae
- Osler nodes (IMMUNE mediated). immune complex deposition in blood vessels
- Janeway lesions (VASCULAR event): SEPTIC emboli
eye patho in IE
- conjunctival petechiae (under eyelid)
- conjunctival hemorrhage
- flare hemorrhage (in white of the eye)
- roth spots on retina = lymphocytes infiltration
