Bacteremia and Infective Endocarditis Flashcards
Transient bacteremia:
Occurs during normal daily activities (toothbrushing, bowel movements).
Intermittent bacteremia:
Occurs with infection and obstruction (pyelonephritis, cholecystitis), and undrained abscesses
Continuous (“high-grade”) bacteremia:
Endovascular infections: endocarditis, infected arterial aneurysms, infected grafts and shunts
Interpretation of blood cultures:
Normal skin flora are usually contaminants: (coagulase-negative staph, Bacillus, proionibacterium acnes, viridans strep)
True pathogens are rarely contaminants:
(gram-negative bacilli, S. aureus, anaerobes, S. pyogenes, S. pneumoniae)
When to suspect that an organism is a contaminant
Clinical course is not suggestive of bacteremia
Primary infection with the same organisms is not found
Predisposing factors are absent
There is no leukocytosis or left shift
Acute endocarditis:
May occur on normal or abnormal valves
Acute onset, hectic pace, early complications
Caused by virulent organisms (S. aureus, beta-hemolytic strep, pneumococcus)
Subacute endocarditis:
Usually occurs on abnormal valves
Subacute onset (months), insidious course
Caused by less virulent organisms (Viridans strep, coagulase-negative staph)
Factors predisposing to native valve IE:
Injection drug use Mitral valve prolapse Degenerative valve disease Rheumatic heart disease Poor dental hygiene Long-term hemodialysis Previous endocarditis
Staph aureus IE:
Nosocomial, IDU
Coagulase-negative staph IE:
Medical interventions
Enterococci IE:
Bladder outlet obstruction
Polymicrobial IE:
IDU
Culture-negative IE:
Due to recent antibiotic treatment or fastidious organisms
Manifestations of SBE:
FEVER (>95%), anorexia, weight loss, malaise, night sweats, MYALGIA, HEART MURMURS (may be pre-existing), embolic stigmata (petechiae), splenomegaly, major emboli, SPLENIC INFARCTS, renal manifestations
Manifestations of ABE:
Abrupt onset, HIGH FEVER, RIGORS, prominent cutaneous manifestations, visceral emboli, CHANGING HEART MURMUR (signifies rapid valve destruction), rapid development of CHF