Microbio Flashcards
S. aureus virulence factors
biofilm formation, capsule, adhesins, secreted enzymes and hemolysins, and pathogenicity islands which contain information for methicillin resistance., protein A (bind IgG to evade), coagulase (fibrin coat around organism), MSCRAMMS
S. viridans virulence factors
Dextran for glycocalyx formation, surface adhesion proteins that assist colonization (FimA, GspB)
Enterococci virulence factors
pili, surface proteins, extracellular enzymes like proteases and hyaluronidases, biofilm
R. rickettsii virulence factors
OmpA and B for adherence
T4SS for intracellular invasion
Most common cause Acute Endocarditis
Usually S. aureus, sometimes strep pyogenes
Most common cause subacute Endocarditis
Streptococcal species (viridans), Enterococcal species
strep viridans is ____ hemolytic
alpha (thus the green)
strep viridans is common where
normal flora, particularly oral cavity
S. aureus –> ___ valve
tricuspid
S. viridans –> ____ valve
mitral
Duke Criteria, what’s needed for a positive result
2 major criteria, 1 major and 3 minor criteria met, or 5 minor criteria.
Dukes: Major criteria
Positive blood culture (2 separately, all of 3 or majority of 4 taken within an hour, or Coxiella brunetii culture + positive IgG titer)
Evidence of endocardial involvement (intracardiac mass, abscess, or messed up valve)
Dukes: Minor criteria
Predisposition
Fever above 38C (100.4F)
Vascular phenomena (petechiae, Janeway, splinter hemmorhages)
Immunological phenomena (Roth’s spots, Osler nodes, glomerulonephritis, Rh factor)
Microbiological evidence
Enterococci gram status
Gram + Cocci
HACEK organisms
Hard to culture, gram -, sometimes cause infective endocarditis (rare)
Haemophilus Aggregatibacter (Actinobacillus) Cardiobacterium Eikenella Kingella
Tx acute endocarditis
Nafcillin or oxacillin +/- gentamicin or tobramycin
(naf for staph)
OR
Vancomycin + gentamicin
Mechanism Nafcillin, what makes it special, spectrum
Inhibit cross-linking of peptidoglycan by transpeptidase (D-al-D-al spot)
Not susceptible to penicillinase (large R group)
MSSA (staph)
Mechanism gentamicin or tobramycin, class
Aminoglycoside - bactericidal
Bind 30S ribosome to prevent initiation complex, cause misreading of mRNA, and induce early termination (initiation)
Vancomycin mechanism
Bind D-al-D-al of cell wall precursor to inhibit release from bactoprenol carrier, inhibiting peptidoglycan cell wall synthesis – transglycosylase
Why cotreat with aminoglycosides
Hard to get into the cell - use with a cell wall inhibitor = synergy
Tx subacute endocarditis
Ampicillin/sulbactam + gentamicin or tobramycin OR Vancomycin + Ceftriaxone or Gentamycin/tobramycin
Ampicillin mechanism, spectrum, why special
Inhibit cross-linking of peptidoglycan by transpeptidase (D-al-D-al spot)
Gram + and more gram -
More broad spectrum (more water soluble to pass through porin channels in gram -)
Sulbactam mechanism
Beta-lactamase inhibitor, give with beta-lactam drugs susceptible to betalactamases (binds to the enzyme and does not allow it to degrade the abx)
Ceftriaxone mechanism
Cell wall inhibitor, binds to penicillin binding protein
Bind transpeptidase to block crosslinking of peptidoglycan polymers of cell wall formation (same as penicillins)
Tx endocarditis if allergic to penicillins
Cephalosporins (3rd to 5th generation) or carbapenems IF no hx of immediate HS to beta-lactam
Vancomycin
Strep pyogenes vs. Strep viridans
Both Gram + cocci, catalase -
Viridans = alpha hemolytic Pyogenes = beta hemolytic
Myocarditis common cause
Coxsackievirus B
Adenovirus (kids)
Coxsackievirus classifications (genome, segment, capsid, envelope, etc.)
ssRNA(+), Group IV Nonsegmented Icosahedral Nucleocapsid Nonenveloped Picornavirus Enterovirus Cox A & B
Pericarditis common causes
Cox A & B
Echoviruses
Influenza virus
Triad of RMSP
Fever, headache, rash
Tx RMSP
Doxycycline - even in kids
Mechanism doxy
Bacteristatic
Bind 30S to prevent attachment of aminoacyl-tRNA (elongation)
Obligate intracellular organism - think:
Chlamydia, R. rickettsii
Palm and sole rash - think:
RMSF, syphilis, coxsackievirus (also, Kawasaki vasculitis)
Rheumatic Heart disease due to what type of Hypersensitivity
Type II (ab, also some T cell mediated)
Symptoms Rheumatic Fever/HD
Joint swelling, fever, weakness, prior strep infection, muscle aches, SOB, chest pain, N/V, hacking cough, circular rash (EM), lumps under skin
Strep pyogenes virulence factors
Streptokinase (plasminogen → plasmin) M protein (resists phagocytosis) Hyaluronidase (breaks CT) DNase (digests DNA) Streptolysin O (destroys RBCs) Streptolysin S (destroys WBCs)
Endocarditis from Enterococci associated with
GU problems in older men, obstetric procedures in young women
Flu-like illness with chest pain, arrhythmias
Myocarditis
Tachycardia, three-component friction rub, changes in ECG
Pericarditis
Intravascular Catheter related infections - usually
staph aureus
VF that helps bacteria colonize vascular catheter infection
biofilm production
Prosthetic valves causative organisms
First year: Staph epidermidis > Staph aureus
After 1 year: strep viridans
Pacemaker and defibrillators infection causative organisms
Within 2 weeks: Staph aureus
2 weeks - 1 year: Staph epidermidis (coagulase negative staph)
After 1 year: Strep viridans
