Microbiology of Heart Disease Hersh DSA Flashcards
serous pericarditis
produced by noninfectious infl diseases (rheumatic fever, SLE, scleroderma), tumors, uremia
fibrinous and serofibrinous pericarditis- composed of? causes?
- most frequent types of pericarditis!
- serous fluid mixed with fibrinous exudate
- acute MI
- postinfarction (Dressler) syndrome (autoimmune response days/wks after MI)
- uremia
- chest radiation
- rheumatic fever, SLE
fibrinous and serofibrinous pericarditis- symptoms
- pain (sharp, pleuritic, position dependent) and fever!!
- loud pericardial friction rub- most striking finding!!!
purulent or suppurative pericarditis- caused by? outcome?
- active infection caused by microbial invasion of pericardial space (via direct extension, blood, lymph, cardiotomy)
- serosal surfaces are reddened, granular, coated with exudate
- outcome- scarring- frequently produces constrictive pericarditis?
hemorrhagic pericarditis- composed of? caused by?
- exudate of blood mixed with fibrinous or suppurative effusion
- caused by malignant neoplasm spread to pericardial space
- also found in bacterial infections, in pts with bleeding diathesis and tb
caseous pericarditis- caused by?
- tb!! and fungal infections
- spread from tb foci within tracheobronchial nodes
- common antecedent of disabling, fibrocalcific, chronic constrictive pericarditis
chronic or healed pericarditis
- plaque-like fibrosis thickenings of serosal membranes
- thin, delicate lesions
- adhesive pericarditis- fibrosis in mesh-like stringy adhesions-obliterates the pericardial sac
adhesive mediastinopericarditis- after? effects?
- after infectious pericarditis, cardiac surgery, or mediastinal irradiation
- obliterated pericardial sac- adherence of external aspect of parietal layer to surround structures- strains cardiac fxn!!
- hearts pulls against parietal pericardium and surround structures
- systolic retraction of rib cage and diaphragm- pulsus paradoxus
- cardiac hypertrophy and dilatoin
constrictive pericarditis- effects? signs?
- heart encases in a dense, fibrous or fibrocalcific scar that limits diastolic expansion and CO
- fibrous scar obliterates the pericardial space and sometimes calcifying- if extreme resembles a plaster mold (concretio cordis)
- dense enclosing scar- cardiac hypertrophy cannot occur
- CO reduced at rest- heart cannot inc its output in response to inc demands
- signs- muffled heart sounds, elevated jugular venous P, peripheral edema
acute pericarditis- diagnosis
- anterior pleuritic chest pain, worse supine
- pericardial rub
- fever common
- erythrocyte sedimentation rate usually elevated
- ECG- diffuse ST-segment elevation, PR depression
pericarditis- treatment?
- NSAIDs
- colchicine- helps prevent recurrences
- ibuprofen (600-800 mg 3x daily for 1-2 wks) or indomethacin (50 mg 3x daily)
post-MI pericarditis- treatment
- aspirin and colchicine (instead of NSAIDs)
- aspirin (650-1000 mg 3x daily for 1-2 wks)
- colchicine (3 months)
pericarditis treatment- if colchicine therapy fails?
-immunosuppression (cyclophosphamide or methotrexate)
Picornaviridae- 2 subtypes
1- Enteroviridae (infect intestinal epit and lymphoid cells- excreted in feces and spread fecal-oral route): -poliovirus -coxsackie A and B -echovirus 2- Rhinoviridae (common cold)
Coxsackie B- causes?
- pleurodynia (resp infection)
- myocarditis/pericarditis (50% of cases!!)- self-limited chest pain or serious arrhythmias, cardiomyopathy, HF
Mycobacterium tb- morphology
- 40% of total cell dry weight is lipid
- mycolic acids
- thin rods
- non-motile
Mycobacterium tb- metabolism
- aerobic
- catalase-positive
- slow growth rate
Mycobacterium tb- virulence
- mycosides- cord factor, sulfatides, wax D
- iron siderophore
- facultative intracellular growth
Mycobacterium tb- clinical
- primary- asymptomatic, overt disease involving lungs or other organs
- reactivation/secondary- pulm, pleural or pericardial, LN, kidney, skeletal joints, CNS
Mycobacterium tb- diagnositcs
- acid-fast stain
- RAPID CULTURE
- PPD skin test
- IGRA (interferon gamma release assay)
- chest xray
- Gene Xpert MT/Rif
mycobacterium endocarditis- treatment
- isoniazid
- rifampin
- pyrazinamide
- ethambutol
- streptomycin
infective endocarditis
-microbial infection of heart valves- leads formation of vegetations composed of thrombotic debris and organisms, often assoc with destruction of underlying cardiac tissues
acute infective endocarditis- caused by?
- prev normal heart valve by a highly virulent organism (staph aureus)- rapidly produces necrotizing lesions
- difficult to cure with antibiotics; need surgery
- death can occur within days/wks
subacute infective endocarditis- caused by?
- organisms with lower virulences (viridans streptococci)- infections of deformed valves with less destruction
- course days/wks; cured with antibiotics
risks of developing infective endocarditis
- rheumatic heart disease with valvular scarring
- mitral vavle prolapse
- degenerative calcific valvular stenosis
- bicuspid aortic valve
- artifiial valves
endocarditis of prev damaged/abnormal valves- caused by?
streptococcus viridans (50%)
endocarditis of healthy valves- caused by??
-S aureus (20-30%)- major in IV drug abusers
endocarditis- other bacterial causes
- Haemophilus
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella
prosthetic valve endocarditis- caused by?
S epidermidis (coagulase-neg)
IE- morphology
- vegetations on heart valves!- friable, bulky, destructive lesions containing fibrin, infl cells, bacteria
- aortic and mitral valves most common
- prone to embolization
acute endocarditis- clinical features
- fevers, chills, weakness, lassitude
- fever- most consistent sign!!
- murmurs- 90% of pts with left-sided IE
acute endocarditis- complications
- GN (glomerular ag-ab complex deposition)
- microthromboemboli
- erythematous or hemorrhagic nontender lesions on palms/soles (Janeway lesions)
- subcutaneous nodules in pulp of digits (Osler nodes)
- retinal hemorrhages in eyes (Roth spots)
4 major forms of vegetative endocarditis- morphology
- RHD- small, warty vegetations along closure lines of valve leaflets
- IE- large, irregular masses on valve cusps that extend onto chordae
- NBTE (nonbacterial thrombotic endocarditis)- small,bland vegetations attached at line of closure
- LSE (libman-sacks endocarditis)- medium vegetations on either/both sides of valve leaflets
Duke criteria- pathologic
- microorganisms by culture or histologic examination in a vegetation, embolus, or intracardiac abscess
- histologic confirmation of active endocarditis in vegetation or intracardiac abscess
Duke criteria- clinical- major
- 2 blood cultures + for characteristic organism or persistently + for an unusual organism
- echocardiographic ID of valve-related or implant-related mass or abscess
- new valvular regurgitation
Duke criteria- clinical- minor
- predisposing heart lesion or IV drug use
- fever
- vascular lesions
- immunological phenomena (GN, osler nodes, roth spots)
- microbiologic evidence- culture positive for unusual organism
- echocardiographic findings- consistent with but not diagnostic of endocarditis- worsening/changing of preexistent murmur
Viridans Group Streptococci- 3 main types of infection
- dental infections (streptococci mutans)
- endocarditis (viridans streptococcus- slowly/subacute; staph aureus- fast/acute)
- abscesses (streptococcus intermedius)
Viridans Group Streptococci- virulence, treatment, diagnostics
- normal oral flora and GI tract
- extracellular dextran- helps bind to heart valves
- penicillin G
- gram stain, culture, resistant to optochin
Group D streptococci- 2 subtypes
- Enterococci (faecalis, faecium)
- non-enterococci
Enterococci
(faecalis, faecium)
- normal bowel flora
- subacute bacterial endocarditis
- 2/3rd most common cause of hospital acquired infection- prosthetic valve endocarditis!!
- resistant to ampicillin, vancomycin!
staphylococcus aureus- causes? morphology? treatment?
- acute endocarditis- high fever, chills, myalgias- no history of valvular disease; grow rapidly
- catalase-positive; coagulase-positive!!
- most are penicillin resistant- use nafcillin, dicloxacillin
- cephalosporins- cefazolin, cephalexin
- clindamycin
staphylococcus epidermis- morphology, treatment, infects?
- catalase-positive; coagulase neg!!
- vancomycin
- lives in our skin- compromised hospital pts withI lines
- infections of prosthetic valves!!- most frequent organism from infected prosthetic devices!!
HACEK organisms- characteristic
- fastidious, very slow growing
- cause endocarditis!!
- Haemophilus
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella
myocarditis- pathogenesis- most common cause?
- viral infections- most common cause!!
- Coxsackie viruses A and B- most cases
- CMV, HIV, influenza- other cases
- infl cytokines can cause myocardial dysfxn
myocarditis- other causes
- nonviral agents- mostly Trypanosoma cruzi (Chagas disease)
- Trichinosis (Trichinella spiralis)- most common helminthic disease
- Lyme disease (Borrelia burgdorferi)
- Diphtheritic myocarditis (Corynebacterium diphtheriae)
active myocarditis- morphology
- interstitial infl infiltrate assoc with focal myocyte necrosis
- diffuse, mononuclear, predominantly lymphocyte infiltrate
infective endocarditis- essentials of diagnosis
- fever
- preexisting organic heart lesion
- positive blood cultures
- evidence of vegetation on echocardiography
- new or changing heart murmur
- evidence of systemic emboli
native valve endocarditis- caused by?
- viridans streptococci
- Group D streptococci
- S aureus
- enterococci
- HACEK group
endocarditis- symptoms/signs
- fever!
- duration- few days/wks
- nonspecific symptoms
- peripheral lesions- petechiae, subungual (splinter) hemorrhages, osler nodes, Janeway lesions, Roth spots
endocarditis- diagnostic studies
- blood cultures
- modified Duke criteria
endocarditis- blood cultures
-3 sets at least 1 hr apart before starting antibiotics
endocarditis- treatment?
- agents against staphylococci, streptococci, enterococci
- vancomycin (1 gm every 12 hrs) plus ceftriaxone (2 gm every 12 hrs)!!!!
enterococci- treatment
- penicillin
- streptomycin or gentamicin
