L25, L27- CVS Infections I, II Flashcards
endocarditis will mostly affect (1) valves; it will often specifically affect (2) valve in (3) patients
1- mitral, aortic
2- tricupid
3- IV drug users
briefly describe the pathogenesis of endocarditis
1) initial damage via mechanical and endothelial injury
2) platelet and fibrin thrombus
3) bacteremia (via some exposure or route of administration)
4) bacterial adhesin
5) biofilm formation (vegetation)
what is a NBTE
nonbacterial thrombotic endocarditis due to inflammation and or microscopic thrombi after some sort of initial damage (mechanical or endothelial injury)
vegetation in endocarditis will often occur at (1) point of the heart because of (2)
low pressure side of valve (atrial side): mitral valve prolapse or something else will cause turbulent blood flow and stasis in atrium allowing vegetation (and or coagulation / thrombus to form)
what are the 3 features of endocarditis that must be considered
1) Etiological Agent: bacteria, fungi
2) Valve Type: native valve (72%) or prosthetic valve (21%- either early/days-wks or late/mos-yrs after surgery)
3) community vs nosocomial (antibiotic resistant, opportunistic) acquired infection
Endocarditis is more likely to occur in (men/women) of the (2) age group.
- (3) cardiac risk factors
- (4) non-cardiac risk factors
1/2- men, >65 y/o
3- previous IE hx, prosthetic valve, cardiac device, congenital / valvular heart disease
4- IV drug use or IV line, immunosuppression (drugs or disease), recent dental or surgical procedure, hemodialysis
the risk factors of endocarditis are related to (1) or (2)
1- direct damage to endothelium
2- introduction of microorganism into blood
IE is diagnosed based on (1), which includes (2), (3), (4)
(infective endocarditis) Duke criteria: -clinical presentation: sxs, risk factors -microbiology: blood cultures -imaging: echocardiogram
List the clinical features of IE (indicate the 2 most common features)
(infective endocarditis)
-fever (80%), heart murmur (85%)
- embolic phenomenon (>50%), petechiae (20-40%), skin manifestations (18-50%), splenomegaly (20-57%)
- Uncommon: osler’s nodes (painful red lesions on hands/feet), janeway lesions (nonpainful nodules of soles/palms), roth spots (white on retina)
describe taking blood cultures in suspected infective endocarditis (IE)
- 2 bottle (aerobic and anaerobic) sets from 3 different locations (=> 96-98% detection)
- note: bacteremia is usually continuous and best to take sample prior to antibiotics
-10% of cases have no growth (blood culture negative endocarditis)
(1) is the first imaging completed in suspected IE
(2) will be complete subsequently if (1) is positive for IE or IE is still suspected
1- transthoracic echocardiogram
2- transesophageal echocardiogram
list the major criteria for IE in Duke Criteria
1) Positive Blood Culture: from 2/3 of samples for most organisms, 3/3 of any organism, or 1/3 for coxiella burnetti
2) evidence of endocardial involvement: echocardiogram shows oscillating intracardic mass on valve, abscess, partial dihiscence of prosthetic valve, or new valvular regurgitation
list the minor criteria for IE in Duke Criteria
- Risk factors: predisposing cardiac condition, IV drug use
- Temp. > 38C, 100.4F
- vascular phenomenon
- immunological phenomenon
- microbiological evident (incomplete blood culture evidence for major parameters otr something else)
- echocardiogram findings not meeting major criteria
Describe Duke Criteria in terms of diagnosing
Definite IE (major - minor): 2 - 0, 1 - 3, 0 - 5
Possible IE: 1 - 1, 0 - 3
Rejected: alternate Dx, resolution <4days with antibiotics, criteria not met
80% of cases of IE are caused by…..
- Staph spp.
- Strep spp.
list the medically relevant Staph. spp. for IE and include the biological features
All: gram+, catalase+, ‘grapelike’ clusters, comensal flora of skin / mucous membranes
Coagulase+: S. aureus
CoNA: S. epidermidis, S. lugdunensis, S. saprophyticus
S. aureus is one of the most common causes of endocarditis in (native/prosthetic) valves. It is a fairly (aggressive/benign) disease and increases the risk for (3).
1- both valve types
2- aggressive
3- embolism, stroke, persistent bacteremia, death
S. aureus bacteria that cause endocarditis usually (do/do not) have polysaccharide capsules. The main surface adhesin is (2) and the critical toxin is (3). The last important virulence factor of S. aureus that is critical to vegetation is (4).
1- do have capsules (90%)
2- Clumping factor A (ClfA)- fibrinogen binding protein
3- α-toxin / α-hemolysin
4- biofilm formation (colonization in layers thru polymer attachment)
The major endocarditis causing CoNS is (1), usually in a (2) setting with (3) patients.
(1) is usually found on (4), therefore introduction into blood is commonly through (5) [note- also a factor for (2)].
1- S. epidermidis
2- hospital-setting (33% of all PVE)
3- prothetic valve patients (major cause of PVE)
4- human skin
5- medical device insertion (via patients or healthcare worker’s skin)
briefly describe the pathogenesis of S. epidermidis causing endocarditis
1) found on skin (patient or healthcare worker) –> picked up by anything inserted / passing through external barrier)
2) rapidly attaches to biomaterial => biofilm
3) inc immunosuppressed and compromised populations and inc use of bioprosthetic devices
(1) is the second most common CoNS causing endocarditis. It is not as frequent as other IEs, but it is usually more (2) and most cases require (3).
1- S. lugdunensis
2- aggressive (>50% => destructive IE)
3- surgery
S. lugdunensis is mostly found on (1). (2) and (3) are its important virulence factors. (4) and (5) are its critical agar / culture distinguishing features.
1- skin, inguinal region
2- adhesion factor (ClfA) binds fibrinogen
3- biofilm formation
4- non-mannitol fermenter
5- β-hemolysis (blood agar, complete hemolysis)
describe how to differentiate S. aureus and S. epidermidis
1) Coagulase Test: + = aureus / - = epidermidis
2) Mannitol agar:
- Selective: 7.5% NaCl only allows Staph. spp. to grow
- Differential: only S. aureus ferments mannitol (+, red –> yellow), S. epidermidis remains red (-)
(1)% of nosocomial S. aureus strains of methicillin resistance and (2)% S. epidemidis are resistant.
1- 40-60% (aureus)
2- 75-90% (epidermidis)
Genes for resistance in Staph. spp. are carried by (1) which encodes for (2) to produce (3). (4) is a special feature of (2) positive organisms.
1- SCCmec (staphlococcal cassette chromosome)
2- mecA
3- altered PBP —–> PBP2a
4- cross-resistance
describe the biological features of Strep. spp.
- Gram+ cocci (catalase-)
- either in pairs, chains, or single
- comensal to mouth and nasopharynx (some spp. on skin)
- contains several human pathogens
Viridans Strep. are mostly responsible for (native/prosthetic) valve endocarditis, particularly after (2) causing (3).
Viridans Strep. are usually found on (4). They are (α/β/γ)-hemolytic on blood agar and are also importantly (5- a distinguishing feature via culturing).
1- both NVE/PVE (>17% of all cases) 2- dental extraction 3- >30% of Pts have transient viridans streptococci bacteremia 4- comsenal oral and URT flora 5- α-hemolytic (incomplete hemolysis) 6- Optochin Resistant
Viridans Strep. spp.:
- (1) most common cause of IE (among Strep. spp.)
- (2) primary agent of dental caries / plaques
- (3), (4), (5) other IE causing Strep. spp.
1- S. sanguinis
2- S. mutans
3/4/5- S. mitis, S. oralis, S. sobrinus
Enterococcus spp. usually cause IE via (community/hospital)-acquired infections, infecting (native/prosthetic) valves. They are often associated with (3) procedures.
1- both, 5-15% of CA and 30% of HA
2- both NVE, PVE
3- GU/GI procedures (arise after)
describe the many biological features of Enterococcus spp. (virulence factors)
- Gram+ cocci as diplococci or in short, medium chains
- catalase-
- mannitol+ (ferments)
- comensal enteric flora
- intrinsic antibiotic resistance
- produces biofilm
(1) is the more common Enterococcus spp, causing IE, (2) is the other popular one. (1) is mostly found (3) type patients.
1- E. faecalis (85-90%)
2- E. faecium (5-10%)
3- ICU Pts, elderly men with comorbidities
list the HACEK organisms
H- haemophilus spp. A- aggregatibacter (actinobacillus) actinomycetemcomitans C- cardiobacterium hominis E- eikenella corrodens K- kingella kingae
list the HACEK organisms (indicate which are most common in causing IE)
H- haemophilus spp. (40% IE among HACEK organisms)
A- aggregatibacter (actinobacillus) actinomycetemcomitans (35%)
C- cardiobacterium hominis
E- eikenella corrodens
K- kingella kingae
HACEK organisms are responsible for (1)% of (CA/HA) (NVE/PVE) patients [of non-IVD users]
1- 5%
2- community acquired
3- native valve endocarditis
HACEK organisms are commensals to (1). They are Gram(+/-), (non-/fastidious), (fast/slow) growers.
1- oropharyngeal tract
2- Gram+
3- fastidious
4- slow growing
HACEK IEs are often associated with _______
- dental disease (periodontitis)
- oral infections / surgeries
- dental procedures
describe the difficulties of testing for HACEK organisms and the complications this causes
Mostly fastidious organisms -mean incubation period 3-5 days, but can go up to 30 days in some species
This causes Dx delays and associated complications can be fatal
give the reasons why there might be culture negative endocarditis and the solution for these situations (indicate possible species.
(2-7% of IE cases)
1) antimicrobial therapy was administered
2) fastidious bacterial or non-bacterial pathogens are difficult to culture
Soln:
- Serology for Coxiella spp., Bartonella spp.
- Molecular testing via PCR
describe the clinical features of myocarditis
-highly variable: ranging from sub-clinical/asymptomatic to HF / shock / SCD
mild chest pain, fever, sweating, chilss, dyspnea, palpitations, syncope, HF, SCD
compare child and adult presentation of myocarditis
Children:
- viral prodrome common
- resting tachycardia, dyspnea, HF sxs
Adult:
- viral prodrome common
- chest pain, palpitations, HF sxs
- DDx: ACS, unstable angina, ventricular tachycardia
(1) are the most common causes of myocarditis in (2)
3) also cause myocarditis, but are mostly seen in (3
1- viruses: enteroviruses (in Coxsackie group of picornavirus family)
2- high income / developed countries
3- bacteria, parasites
4- low income / developing countries
(1) virus in a common cause of primary myocardial disease and is associated with (2) in relation to myocarditis. (1) and other viruses in its family utilize (3) on surface of myocytes to gain entry.
(5% of coxsackie viral infections induces some degree of heart disease)
1- coxsackie B3 virus (picornaviridae family)
2- high mortality
3- coxsackie-adenovirus receptor (CAR)
In viral myocarditis, (1) is a critical piece seen in the patient history. It will usually have a (benign/severe) presentation. It can also be represented by (3) seen in bloodwork.
1- flu-like sxs (fever, arthralgia, malaise), pharyngitis, tonsillitis, or URI 1-2 wks prior
2- subclinical to benign to very severe complications
3- cardiac biomarkers: TnI, TnT, BNP
Fungal myocarditis is usually associated with (1) patients following (2)
1- immuno-compromised/suppressed patients
2- disseminated candidiasis
Parasitic myocarditis usually has a(n) (acute/chronic) clinical presentation. It usually has (2) transmission. Associated risks include (3).
1- chronic presentation
2- vector or zoonotic transmission
3- immune status, geographic location, exposure, etc.
what are the diseases of the pericardium
- acute pericarditis
- pericardial effusion
- cardiac tamponade
- constrictive pericarditis
(1) are the main viral causes of pericarditis. (2) are other possible causes.
1- coxsackievirus A, B (picornaviridae family)
2- CMV, EBV, hepatitis viruses, measles, mumps, HSV6, parvovirus B19, HIV, VZV
(1) bacteria are the main causes of pericarditis, (2) will rarely have this complication
1- gram+/- bacteria
2- M. tuberculosis
fungal pericarditis is usually found in (1) patients due to (2) species
1- immuno-compromised patients
2- blastomyces dermatitidis, candida spp., histoplasma capsulatum
(1) is the most common pericardial disorder, usually due to (2). It will have a (3) duration and presents with the following clinical symptoms: (4).
1- acute pericarditis
2- viral infection
3- 1-3 wk
4- chest pain, pericardial friction rub, serial EKG changes, pericardial effusion
