Cardiovascular Infectious Disease Flashcards

1
Q

What are the most common cardiovascular infections?

A

Endocarditis
Rheumatic Heart Disease
Myocarditis
Pericarditis
Intravascular Catheter-related Infections
Artificial Valve, Pacemaker and Defibrillator Infections
Rocky Mountain Spotted Fever (Vasculitis)

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2
Q

What are the normal biota of the cardiovascular system?

A

Nothing, it’s a privileged site. You should NOT have any microorganisms in your bloodstream.

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3
Q

What are the natural host defenses found in the cardiovascular system?

A

Leukocytes, billions of them
Complement
Immunoglobulins
Cells of immune system, secreted components
Flow of material helps keep heart cleaned out/makes it hard for bacteria to colonize

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4
Q

Where does the damage (which leads to disease) come from?

A
  • Growth of organism: direct cell lysis, apoptosis, and autophagy due to viral and bacterial infection
  • Toxins produced by microorganism (bacteria)
  • Immune system collateral damage or malfunction
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5
Q

What is infectious endocarditis?

A
  • Inflammation of the inner lining of the heart (endocardium) caused by bacterial infection.
  • Most of the time its an infection of the valves of the heart (usually mitral or aortic valve)
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6
Q

What are the signs of subacute infectious endocarditis?

A
  • Symptoms develop more slowly and are less pronounced
  • Fever anemia and an abnormal heartbeat
  • Abdominal or side pain is sometimes reported
  • Patient may look ill, have petechiae, septic emboli, Roth’s spots, and splinter hemorrhages.
  • Enlarged spleen may develop
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7
Q

-34 yr old, wakes up with reduced vision
-Dizziness after exercise, Roth spots
-Recent dental procedure
-Murmur upon exam, mitral valve regurgitation
What does this man likely have? Organism?

A
  • Infective endocarditis
  • Streptococcus viridans (usually resides in normal mouth flora)
  • Patient started on empiric treatment for endocarditis
  • Pure culture taken of infection to narrow down organism
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8
Q

What two organisms cause most acute endocarditis?

A

Largely Staphylococcus aureus

Sometimes Streptococcus pyogenes

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9
Q

What is the progression of acute endocarditis?

A
  • Hectically febrile (fever that comes and goes)
  • Rapidly damages cardiac structures
  • Seeds infection in distal sites through sepsis
  • If untreated, progresses to death in weeks!
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10
Q

What organisms are usually associated with subacute endocarditis?

A
Streptococcal species (viridians)
Enterococcal species
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11
Q

What is the progression of subacute endocarditis?

A
  • Indolent course of infection
  • Causes structural cardiac damage slowly
  • Rarely seeds infection at distal sites
  • Gradually progressive
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12
Q

What is unique about Streptococcus viridians?

A

Many different species that damage RBC.
Alpha-hemolytic (partial degradation of RBC, turns green on blood agar)
Many oral flora are alpha-hemolytic

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13
Q

Gamma hemolysis

A

No color change

Doesn’t damage RBC at all

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14
Q

Alpha hemolysis

A

Viridans, partial degradation of RBC

Leads to color change/oxidation/turns green

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15
Q

Beta hemolysis

A

Group A strep (streptococcus pyogenes)
Completely destroys RBC
Yellow on blood agar

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16
Q

What are the usual portals of infection for infectious endocarditis?

A

Oral cavity
Skin
Upper respiratory tract

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17
Q

What do most local infections occur in infective endocarditis?

A

Mitral valve
Tricuspid valve (injection drug use)
Prosthetic valves

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18
Q

What group has a high rate of infectious endocarditis?

A

IV drug users

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19
Q

What temperatures are associated with acute vs. subacute infectious endocarditis?

A

Subacute - fever usually lower

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20
Q

How is initial diagnosis made for infective endocarditis?

A

Patient presenting with fever and valvular abnormalities

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21
Q

How is more specific diagnosis made for infective endocarditis?

A

Screening blood cultures for presence of bacteria, unexplained arterial emboli and progressive cardiac valvular incompetence.

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22
Q

What is the Duke Criteria for Infectious Endocarditis?

A

It gives requirements for a positive diagnosis.

+ result = 2 major criteria are met, 1 major and 3 minor are met, or 5 minor criteria are met

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23
Q

What does the Duke Criteria require for possible infectious endocarditis?

A

1 major and 1 minor
OR
3 minor criteria are met

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24
Q

When is the Duke Criteria “trumped”?

A

When alternative diagnosis is established, symptoms resolve and do not recur with less than 5 days of antibiotic therapy, or lack of histological evidence of endocarditis.

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25
Q

What are the two Duke Major Criteria?

A
    • blood culture (many times there can be contamination - brushing teeth, cutting self - all cultures must come back with same microorganism)
  1. Evidence of endocardial involvement
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26
Q

What are the five Duke Minor Criteria?

A
  1. Predisposition (heart condition or injection drug use)
  2. Fever above 38C (100.3F)
  3. Vascular phenomena (arterial emboli, Janeway lesions-non-tender, erythematous lesions on hands and soles, etc.)
  4. Immunological phenomena (Osler node - painful, red raised lesions on hands and feet, Roth’s spots, rheumatic fever, etc.)
  5. Microbiological evidence (positive blood culture, but not meeting major criteria, etc.)
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27
Q

How should you treat acute endocarditis?

A

Gear treatment toward staph infection with concern for MRSA or coat-neg. staph

  1. Nafcillin or Oxacillin +/- gentamicin or tobramycin
  2. Vancomycin + gentamicin
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28
Q

How should you treat subacute endocarditis?

A

Gear treatment toward strep infection.

  1. Ampicillin/sublactam + gentamicin or tobramycin
  2. Vancomycin + ceftriaxone or gentamicin/tobramycin
29
Q

What do you give people with endocarditis and penicillin allergy?

A
  1. Cephalosporins (3rd to 5th generation) or carbepenems

2. Vancomycin

30
Q

What virulence factors are associated with staphylococcus aureus?

A

Biofilm formation, capsule, adhesins, secreted enzymes and hemolysins, and pathogenicity islands which contain information for methicillin resistance.

31
Q

What is the most common cause of infectious endocarditis?

A

Staphylococcus aureus –> majority of infective endocarditis in IV drug users

32
Q

3 things about Staph aureus:

A
  1. Gram +
  2. Facultative anaerobe
  3. Usually preceded by bacteremia
33
Q

What is the bacteria tree for S. aureus?

A

Gram +
Cocci
Catalase +
Coagulase +

34
Q

What is the MOST COMMON infectious agent of the skin? What lesion scan it cause?

A

S. aureus

Superficial boils and abscesses

35
Q

How can staph aureus present on the skin?

A

Localized skin/subcutaneous infection: impetigo, cellulitis, folliculitis, furuncles, carbuncles.

36
Q

What is a common infectious agent of surgical wounds?

A

Staphylococcus aureus

37
Q

How does S. aureus colonize the skin and evade host defenses?

A
  • Protein A (binds Fc portion of IgG)
  • Coagulase (forms fibrin coat around the organism)
  • Hemolysins and leukocidins (destroy RBCs and WBCs)
38
Q

What S. aureus virulence factors help with deep tissue invasion?

A

-Hyaluronidase (breaks down connective tissue)
-Staphylokinase (lyses formed clots)
-Lipase (breaks down fat)
Overwhelming bloodstream colonization can be fatal

39
Q

What is the 2nd major cause of endocarditis?

A
  • Streptococcal species (viridians)-several oral species
  • Usually involves underlying mitral valve damage (rheumatic fever, etc.) which provides the site for bacterial colonization
40
Q

What can Viridans produce?

A

Dextran for glycocalyx formation and surface adhesion proteins that assist colonization

41
Q

What is the bacteria tree for streptococcus mutans?

A
Gram +
Cocci
Catalase -
Alpha-hemolytic
Bacitracin resistant
42
Q

What is the 3rd major cause of endocarditis?

A

Enterococcus species!

43
Q

What type of patients get enterococcus endocarditis?

A
  • Usually preceded by bacteremia

- Most frequently found following genitourinary procedures in older men and obstetric procedures in younger women

44
Q

What virulence factors are associated with enterococcus?

A

Pili, surface proteins, extracellular enzymes (proteases, hyaluronidases)

45
Q

What is enteroccous usually resistant to?

A

Penicillin and Carbepenems

46
Q

What are the usual clinical presentations for Streptococcus pyogenes?

A

Localized skin/subcutaneous infection = impetigo, erysipelas, cellulitis
Toxin mediated = toxic shock syndrome, necrotizing fasciitis

47
Q

What is the pathology associated with strep. pyogenes?

A
  • May be normal skin flora
  • Can colonize skin following trauma –> inflammation –> pustular lesions and honeycomb-like crusts (impetigo) at site of inoculation.
  • Deeper infections lead to erysipelas and cellulitis. Invasion from skin infections can lead to glomerulonephritis but not Rheumatic fever.
48
Q

What is the bacteria tree associated with S. pyogenes?

A
Gram +
Cocci
Catalase -
Beta-hemolytic
Bacitracin sensitive
49
Q

What virulence factors are associated with S. pyogenes?

A

Streptokinase (converts plasminogen to plasmin)
M protein (resists phagocytosis)
Hyaluronidase (breaks down connective tissue)
DNase (digests DNA)
Streptolysin O (destroys RBCs)
Streptolysin S (destroys WBCs)
Streptokinase and hyaluronidase are encoded by a lysogenized prophage.

50
Q

What two main pathologies are associated with strep. pyogenes?

A

Toxic shock syndrome

Necrotizing fasciitis

51
Q

What is the mechanism of TSS?

A
  1. Skin infection (cellulitis)
  2. Systemic release of pyrogenic exotoxins A (super antigen)
  3. Polyclonal activation of T cells
  4. Acute fever, shock, multi-organ failure
52
Q

What is the mechanism of necrotizing fasciitis?

A

Trauma allows for deep seated infection –> release of exotoxin B (protease) –> rapid necrosis along fascial planes with no damage to muscles

53
Q

What is a clinical indicator of rheumatic heart disease?

A

Mitral stenosis following pharyngitis with a RASH

54
Q

How does Rheumatic Heart Disease work?

A
  • Follows Streptococcus pyogenes pharyngitis in genetically predisposed individuals
  • Type II hypersensitivity
  • Damage to heart muscle and valves is attributed to autoantibodies (antibodies to bacterial antigens cross-react with meromyosin in the heart).
55
Q

What risks and symptoms are associated with Rheumatic Heart Disease?

A

Risk:
-Strep throat infection (prolonged/untreated)
-Prior case of rheumatic fever
-Age 5 to 15 years old
Symptoms
-Appear 2-4 weeks after strep infection
-Fever, weakness, muscle aches, pain swelling in large joints, shortness of breath, chest pain, nausea, vomiting, hacking cough, circular rash, lumps under skin

56
Q

What are ways to diagnose Rheumatic Heart Disease?

A
  • Blood tests
  • Throat culture
  • Echocardiogram
  • Chest X-rays
  • Electrocardiogram
57
Q

What are the best treatments for RHD?

A
  • Penicillin based antibiotics
  • Aspirin
  • Corticosteroids
  • Rest
58
Q

How to prevent RHD?

A
  • Treat strep right away with Abx. This prevents the infection from developing into Rheumatic fever.
  • Sore throat + fever for more than 24 hrs should go to Dr.
59
Q

What is myocarditis? What usually causes it? Symptoms?

A

Inflammation of the myocardium (middle heart wall layer).
Usually caused by viral infection (Coxsackievirus B & Adenovirus (children)).
Chest pain, heart failure, and abnormal heart rhythms possible.

60
Q

What is the virus tree for Coxsackievirus A & B?

A
ssRNA (+), Group IV
Nonsegmented
Icosahedral Nucelocapsid
Nonenveloped
Picornaviridae
Enterovirus
Coxsackievirus A & B
61
Q

What is pericarditis?

A

Inflammation of the pericardium (sac-like membrane surrounding the heart).
Typically an acute infection.
Usually caused by a viral infection (Coxsackieviruses A and B, Echoviruses, and influenza virus).

Viral pericarditis usually occurs during the summer months, coinciding with a high incidence of enterovirus infect.

62
Q

What symptom does pericarditis cause?

A

Chest pain - associated with irritated layers of the pericardium rubbing against each other

63
Q

What three picornaviruses cause carditis?

A
  1. Coxsackie A virus
  2. Coxsackie B virus
  3. Echovirus
64
Q

What bacteria causes Rocky Mountain Spotted Fever?

A

Rickettsia Rickettsii

65
Q

What are the symptoms of RMSF?

A

Fever, headache, abdominal pain, vomiting, muscle pain. A rash (petechiae-like red dots) may develop but often absent first few days and sometimes never develops.
-RMSF can be severe or even fatal illness if not treated in first few days of symptoms

66
Q

What is first line treatment for all adults and children with RMSF?

A

Doxycycline

-Most effective if started before fifth day of symptoms

67
Q

How is RMSF diagnosed?

A

Initial diagnosis: clinical signs and symptoms - rash, fever, headache, medical history
Later confirmed: specialized laboratory tests

68
Q

What are the most common areas for RMSF?

A

Lower midwest to the East Coast

69
Q

What is the progression/pathology of RMSF?

A
  1. Carried in dogs, rodents
  2. Bite of dermacentor wood tick or dog tick transmits to humans
  3. Organism infects and proliferates in endothelial cells
  4. Inflammation of endothelial lining of small blood vessels
  5. Maculopapular rash on palms and soles spreading to TRUNK
  6. Widespread vasculitis
  7. Headache and CNS changes, renal damage
  8. May lead to death if untreated!