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Introductory Microbiology > Cardiovascular System Infections > Flashcards

Cardiovascular System Infections Flashcards

1
Q

What is bacteremia?

A

Presence of bacteria in the bloodstream; may or may not be clinically significant

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2
Q

What is transient bacteremia?

A
  • generally not clinically significant
  • self-resolving in clients with no underlying illness, immune deficiency, or turbulent cardiac blood flow
  • can occur from minor cut (we are frequently bacteremic)
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3
Q

What is primary bacteremia?

A
  • direct inoculation of the blood stream

- can be nosocomial or due to IV drug use

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4
Q

What is secondary bacteremia?

A
  • opportunistic
  • microorganisms causing infection at another site (e.g. pneumonia) invade the blood stream and disseminate via the circulation to other body areas (hematogenous spread
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5
Q

What is sepsis?

A
  • life-threatening organ dysfunction due to a dysregulated host response to infection
  • arises when the body’s response to an infection injures its own tissues and organs
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6
Q

What are the two characteristics of sepsis?

A
  • infection (suspected or confirmed)

- acute, life-threatening organ dysfunction as defined as 2 or more points of SOFA

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7
Q

What is SOFA?

A
  • sepsis-related organ dysfunction assessment

- measures respiratory, hepatic, cardiovascular, renal, central nervous system, and platelet dysfunction

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8
Q

What is septic shock?

A
  • subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality
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9
Q

What is the clinical criteria for septic shock?

A

1) Sepsis
2) Hypotension requiring vasopressors to maintain mean arterial pressure (MAP) ≥ 65 mm Hg despite fluid resuscitation
3) Lactate ≥ to 2 mmol/L

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10
Q

How is sepsis managed?

A
  • elimination of the original site of infection
    via surgical removal of abscesses and biofilms, drainage
  • intravenous antimicrobial therapy
    -fluid replacement
  • vasopressors and intotropes (norepinephrine, dobutamine)
  • supportive therapy for organ dysfunction (dialysis, mechanical ventilation)
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11
Q

What are the three layers of the heart?

A

1) Endocardium - thin lining inside the chambers of the heart (typically bacterial infections)
2) Myocardium - muscle tissue of the heart (typically viral infections)
3) Pericardium - thin double-layered sac that encloses the heart (typically viral infections)

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12
Q

How are strep throat and cardiac turbulent blood flow related?

A
  • turbulent blood flow in heart makes infection more likely; allows group A strep to cause rheumatic fever
  • rheumatic fever can cause rheumatic heart valve, which is associated with increased risk of bacteremia-related complications
  • this increased risk is associated with the turbulent blood flow at the site of the damaged valve
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13
Q

What is rheumatic fever?

A
  • a rare complication of streptococcal pharyngitis (strep throat) infections
  • caused by streptococcus pyogenes aka Group A streptococcus (GAS)
  • most commonly observed in children (5 – 15 years of age) and adults in developing countries
  • autoimmune reaction, lasting approximately 3 months
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14
Q

What are the characteristics of rheumatic fever?

A
  • carditis – inflammation of heart valves, no active infection
  • polyarthritis – large joints, lasting approximately 2 – 4 weeks
  • erythema marginatum – red rings on skin, rarely observed in adults
    Chorea – jerky involuntary movements, observed in children
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15
Q

How is rheumatic fever treated?

A
  • treat with anti-inflammatories, diuretics to decrease cardiac workload, and bed rest
  • prevent further attacks with antibiotics
  • no residual heart disease: Penicillin (IM), once monthly for a minimum of 10 years or until 25 years old
  • residual heart disease: Penicillin (IM), once monthly until 40-45 years old, but often continued for life
  • residual heart disease includes rheumatic valve, heart failure valve replacement may be required
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16
Q

Why does turbulent blood flow result from damaged rheumatic heart valves? How does this increase the risk for bacteremia-related complications?

A
  • minor fibrin and platelet deposition can occur on the low pressure side of the damaged valve causing non-bacterial thrombotic endocarditis (NBTE)
  • congenital heart defects and damaged/prosthetic valves are similarly predisposed
  • transient cases of bacteremia become problematic – microbe now has a place to adhere, increasing the risk of infective endocarditis
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17
Q

What is a cardiac vegetation?

A
  • accumulation of bacteria, fibrin and platelets in the heart
  • parts can break off and obstruct blood vessels
18
Q

What is endocarditis?

A

Infection and inflammation of the endocardium; commonly affects heart valves - mitral and aortic

19
Q

What are the symptoms and signs of subacute endocarditis?

A
  • symptoms develop slowly; fatigue, malaise, fever, chills, anorexia, weight loss, back pain
  • signs; new or changing heart murmur, peripheral manifestations
  • associated with relatively non-virulent bacteria (ie: viridans streptococci)
  • occurs in those predisposed to developing nonbacterial vegetations
20
Q

What are the symptoms and signs of acute endocarditis?

A
  • symptoms develop quickly; intense fever, shaking, chills, exhaustion
  • signs; new or changing heart murmur, peripheral manifestations, sepsis
  • associated with highly virulent bacteria (ie: Staphylococcus aureus)

21
Q

What are peripheral manifestations of endocarditis?

A
  • splinter hemorrhages
  • Osler’s nodes
  • conjunctival petechiae
  • Roth’s spots
  • Janeway lesions (septic emboli)
22
Q

What are risk factors of endocarditis?

A
  • injection drug users and central IVs can cause bacteremia; normal and abnormal valves
  • abnormal valves including prosthetics, rheumatic valve, mitral valve prolapse, congenitally abnormal valve; associated mainly with subacute infective endocarditis
23
Q

What are complications of endocarditis?

A

1) Persistent bacteremia and risk of seeding distant sites; risk of secondary infections/abscesses, sepsis
2) Tissue destruction; damage to heart valve, heart failure
3) Fragmentation of the vegetation; CNS emboli, MI, stroke, vascular insufficiency (Janeway lesions), and necrosis
4) Stimulation of antibodies; combine with bacterial antigens and form circulating immune complexes that deposit in kidneys or skin (Osler’s nodes), impaired perfusion of tissues

24
Q

What is Duke Criteria for infective endocarditis?

A
  • 2 major criteria, 1 major and 3 minor criteria, 5 minor criteria
  • any of the above denotes diagnosis of infective endocarditis
25
Q

What is the major criteria for diagnosing endocarditis?

A
  • 1) Two separate, positive blood cultures with “typical” organisms; 95% of patients with IE have positive cultures - collect samples before initiating treatment
    2) Evidence of a compatible cardiac lesion; new murmur, vegetation by echocardiogram, myocardial abscess, detachment of prosthetic valve
26
Q

How many blood cultures are taken for IE?

A

3 blood cultures

27
Q

What is the minor criteria for diagnosing endocarditis?

A

1) Predisposition (e.g. IV drug use, valve abnormality)
2) Clinical symptoms (e.g. Fever > 38 °C)
3) Vascular phenomena (e.g., Janeway lesions, stroke, splenic infarct)
4) Immunologic phenomena (e.g. Osler’s node, Roth’s spots, glomerulonephritis)
5) Positive blood cultures not meeting major criteria (e.g. one culture)
6) Minor echocardiographic finding (e.g. valve thickening without definite vegetation)

28
Q

How is infective endocarditis treated?

A
  • appropriate antimicrobial therapy (bactericidal) administered parenterally (long duration, e.g. 4 – 6 weeks)
  • valve replacement surgery in cases of severe AROs, severe valve dysfunction, recurrent embolism, or in cases of fungal endocarditis
  • there is a risk of repeat endocarditis
29
Q

How is infective endocarditis prevented?

A
  • patients at high risk of IE who undergo procedures that are associated with transient bacteremia should receive antibiotic prophylaxis
30
Q

What is myocarditis?

A
  • also called inflammatory cardiomyopathy
  • most often associated with a viral infection of the myocardium and infiltration by T-lympocytes
  • non-infectious causes should be considered
  • pediatric cases more common
31
Q

What viruses cause myocarditis?

A
  • enteroviruses (coxsackievirus B), adenovirus, herpes viruses, influenza, HIV
32
Q

What are symptoms of myocarditis?

A
  • history of recent (within 1-2 weeks) flu-like syndrome of fever, malaise, pharyngitis, tonsillitis, or upper respiratory tract infection
  • symptoms of mild heart failure (fatigue, weakness, shortness of breath, edema, palpitations), and arrhythmias
  • pain reported in those with concomitant pericarditis
33
Q

How does myocarditis differ based on age?

A
  • acute symptoms in pediatric patients; cardiogenic shock & acute heart failure, sudden death
  • in adults, progresses slowly; progressive HF & dilated cardiomyopathy
34
Q

What is the CAR portal of entry?

A
  • coxsackie-adenoviral receptor
  • expressed in myocytes; higher concentrations in children that adults
  • explains increased risk of coxsackieviral myocarditis infections in newborns and young children, and risk for more acute disease
  • viral replication in myocytes leads to autoimmune injury, then dilated cardiomyopathy
35
Q

How is myocarditis treated?

A
  • same as for heart failure (ACE inhibitors, diuretics, beta blockers)
  • avoid NSAIDs – increase risk of mortality from heart failure (induce fluid retention due to vasoconstriction of blood vessels in the kidney and resulting retention of sodium and potassium)
  • antimicrobials (but mostly viral causes)
36
Q

What are complications of myocarditis?

A
  • if early resolution of of symptoms (<2 weeks); generally complete recovery
  • prolonged symptoms (> 2 weeks to months) can result in dilated cardiomyopathy, heart attack & stroke
  • worsening heart failure, death (or cardiac transplantation)
37
Q

What is pericarditis?

A
  • inflammation of the pericardium; may co-exist with myocarditis
  • usually caused by viruses such as enteroviruses (coxsackievirus, echovirus), influenza, HIV
  • appears 2-3 weeks post “flu-like” illness
  • non-infectious causes should be considered
38
Q

What are the symptoms of pericarditis?

A
  • sharp, stabbing chest pain caused by rubbing of two layers of the pericardium
  • pain worsens when laying down, with deep breaths, swallowing and coughing
  • pain improves with sitting upright or forward
39
Q

What are the diagnostic findings of pericarditis?

A
  • abnormal heart sounds, “pericardial rub”
  • abnormal ECG
  • echocardiogram – appearance of fluid surrounding heart
40
Q

How is pericarditis treated?

A
  • analgesics & anti-inflammatory drugs (NSAIDS or steroids); assess for concomitant myocarditis
  • antibiotics for bacterial causes (more severe illness)
  • in cases of pericardial tamponade (tachycardia, SOB, increased RR & prominent neck veins) - pericardiocentesis; drainage of pericardial fluid
  • in cases of constrictive pericarditis – pericardiectomy; surgical removal of pericardium

Introductory Microbiology (11 decks)

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