Diebel: Intro to CV Infectious Disease Flashcards

1
Q

What are the normal biota of the CVS?

A

NONE

Blood is one of the 3 areas of the body that should never have microorganisms (other two are CNS and lymphatics)

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2
Q

What are the natural host defenses found in the CVS?

A

THOUSANDS of leukocytes, Abs and complement

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3
Q

Blood stream infections are referred to as systemic infections. What is a defense against blood stream infections?

A

Leukocytes!

Thousands/mL

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4
Q

Describe the pathway to infection in the CVS.

A
Exposure to pathogen
adherence to skin
invasion of epithelium
colonization and growth
production of VFs
Toxicity
Tissue damage and release
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5
Q

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

A

Growth of organism: direct cell lysis, apoptosis, autophagy d/t viral/bacterial infection

Toxins produced by microorganism (bacteria)

Immune system collateral damage

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6
Q

What is infectious endocarditis?

A

A BACTERIAL disease associated with SEPSIS and typically an underlying HEART DEFECT, that leads to INFLAMMATION of the inner lining of the heart (endocardium).

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7
Q

How does bacterial disease cause endocarditis?

A

Bacteria cells travel through the bloodstream and lodge on abnormal heart valves (native- mitral, tricuspid or prosthetic) or damaged heart tissue. At these sites bacteria grow and produce vegetations, blocking the valves normal fxn and blood flow. Vegetations encapsulate the bacteria and protect them from the immune response making them hard to treat!

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8
Q

What is a vegetation?

A

Collection of bacterial cells, platelets, fibrin and inflammatory cells

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9
Q

What subgroup of the population are particularly susceptible infectious endocarditis?

A

IV Drug users

Particularly targets the tricuspid valve (80% strep aureus)

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10
Q

What are the portals of entry for pathogens into the bloodstream?

A

Oral cavity
skin
upper respiratory tract

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11
Q

What is indicative of infectious endocarditis in a pt?

A

positive blood cultures–> indicate presence of bacteria in the blood

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12
Q

What are the two types of endocarditis and how do they differ?

A

Acute (103-104) and Subacute (<103)

They have similar sxs, but subacute progresses more slowly and is less pronounced. It is often accompanied by splenomegaly.

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13
Q

What are sxs commonly associated with endocarditis?

A

LOOK ILL

FEVER, CHILLS/SWEATS, HEART MURMUR

low grade fever
night sewats
chills
fatigue
malaise
generalized weakness anorexia
low back pain
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14
Q

What are physical findings associated with endocarditis?

A
cardiac murmur
conjuntival petechiae
Unexplained arterial emboli: (splinter hemorhages in the nails, Roth's spots)
osler nodes
Janeway lesions
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15
Q

What are common laboratory findings associated with infectious endocarditis?

A
Anemia
elevated ESR
elevated CRP
Presence of RF
Circulating Immune complexes
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16
Q

What bacteria are commonly responsible for acute endocarditis?

A
Staph Aureus (Mainly)
Strep pyogenes (sometimes)
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17
Q

Describe the temporal progression of Staph aureus in acute endocarditis?

A

Hectically febrile
Rapidly damages cardiac structures
Seeds infection in distal sites through sepsis
If untreated leads to death in weeks

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18
Q

What bacteria commonly cause subacute endocarditis?

A

Streptococcal species (viridans)

Enterococcal species

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19
Q

Describe the temporal progression of Strep Viridans in Subactue endocarditis?

A

Indolent course of infection
Causes structural damage slowly
rarely seed infection at distal sites
progresses gradually

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20
Q

What does viridis mean in latin? And how does this relate to bacteria?

A

Green

Viridans just refers to “green-growers” on the blood agar plate not a specific species. (alpha hemolytic)

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21
Q

What is the difference between gamma, alpha and beta on a blood agar plate?

A

Gamma- no hemolysis
Alpha- partial deconstruction of blood cells in media–> greenish color
Beta- completely destroys RBCs in the agar so it looks yellow (color of hte agar plate)

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22
Q

How do strep mutans/viridans differ from strep pyogenes on an agar plate?

A

Mutans/viridans are alpha hemolytic.

Pyogenes is beta hemolytic.

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23
Q

What is indicative of a Positive result for endocarditis according to Duke’s Criteris?

A

2 major criteria OR

1 major and 3 minor criteria OR

5 minior

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24
Q

What are the 2 major criteria for endocarditis?

A
  1. Positive blood culture (same organisms, 2 positive cultures separated by time)
  2. Evidence of endocardial involvement (valve issues) –> apparent with echocardiogram
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25
Q

What are the 4 minor criteria for endocarditis?

A
  1. Predisposition (heart condition/drug use)
  2. Fever above 100.3
  3. Vascular phenomena (arterial emboli, janeway lesions)
  4. Immunological phenomena (osler’s nodes, roth’s spots, rheumatoid factor)
  5. Microbiological evidence (positive blood culture, but doesn’t meet criteria)
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26
Q

What is a Janeway lesion?

A

Non-tender, small hemorrhagic lesion on the palms/soles

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27
Q

What are osler’s nodes?

A

Painful, red, raised lesions on the hands and feet (immune complex disposition)

28
Q

What is a rheumatoid factor?

A

autoantibody associated with articular disease

29
Q

What are the most likely causative microorganisms for native valve endocarditis:

community acquired vs. nosocomial?

A

Community acquired:

  1. Strep viridans
  2. Staph aureus

Nosocomial

  1. Staph (methicillin resistance common)
  2. Enterococci
30
Q

Staph aureus is the most common cause of infective endocarditis in what population? What organ does it most commonly effect?

A

IV drug abusers

Skin

31
Q

What is staph aureus?

A

BGCCC- facultative anaerobe
Bacteria, Gram +, Cocci, Catalase +, Coagulase +
Gram +

32
Q

What virulence factors are associated staph aureus?

A

biofilm formation (sticks to valve capsule, avoid immune cells)
adhesins
secreted enzymes/hemolysins
pathogenicity islands (contain info for methicillin resistance)

33
Q

What virulence factors does staph aureus use for deep tissue invasion?

A

hyaluronidase
stapylokinase
lipase

34
Q

What bacteria is the second major cause of infective endocarditis?

A

Streptococcal species (viridans)

35
Q

When is streptococcal viridans most likely to cause an infection?

A

Underlying mitral valve damage (rheumatic fever, etc) which provides the site for bacterial colonization

36
Q

What virulence factors does viridans produce that assist with colonization?

A

Dextran for glycocalyx formation and surface adhesion proteins that assist colonization

37
Q

Which strep species often grows at the gum line? How does this relate to people w/ congenital valve problem undergoing dental procedures?

A

strep viridan

Often get prophylactic doses of antibiotics prior to going to the dentist for a procedure

38
Q

How does strep mutans differ from staph aureus?

A

Catalase -, alpha hemolytic, bacitracin resistant

39
Q

What is the third major cause of infective endocarditis?

A

Enteroccocus species

Preceded by bacteremia

40
Q

When is an enterococcus species likely to cause endocarditis?

A

Following a genitourinary procedure in older men, or an obstetric procedure in younger women

41
Q

What are the VFs for enteroccocus?

A

pili
surface proteins
extracellular enzymes (protease and hyaluronidase)

42
Q

Enterococcus is usually resistant to what two drugs classes?

A

penicillin and carbepenems

43
Q

What bacteria is linked to pharyngitis, glomerular nephritis and rheumatic heart disease?

A

Strep pyogenes

44
Q

What virulence factor of strep pyogenes does our body have the ability to recognize and why is this impt?

A

M protein (resists phagocytosis). Our body has the ability to recognize this protein as a potential antibody target. In some individuals, the antibody response mounted can cross react with heart tissue. When that happens, you can get damage to the heart valves which sets up the conditions for endocarditis later in life. If the immune system makes a cross reactive response. This is a type 2 hypersensitivity reaction. Complement gets attached after the antibody and forms pores in the cells.

45
Q

What is the treatment for infective endocarditis? What do these drugs inhibit?

A

Peptidoglycan synthesis!

Penicillin G
Ceftriaxone
Vanco
Genta
Ampi/Naf/Oxa-cillin
Cefazolin

Impt to culture b/c there are many drug options!

46
Q

Which drugs are bactericidal and why is it important to use a high dose over time?

A

Cell wall inhibitors

It’s important to give a high dose of antibiotics over time b/c it’s difficult to eliminate bacteria in avascular vegetation

47
Q

What is myocarditis?

A

Inflammation of the myocardium (middle layer of the heart wall)

48
Q

What usually causes myocarditis?

A

viral infection

Cox B
Adeno (children)

49
Q

What are the sxs of myocarditis?

A

flu-like illness with chest pain is common, heart failure, abnormal heart rhythyms

Patients may feel like they’re having a heart attack.

50
Q

Why is cox B and NOT A the most likely culprit in myocarditis?

A

Our hearts have a CAR receptor which only group B and subgroup C of the adenoviruses have the appropriate ligand to bind to.

51
Q

What is pericarditis?

A

Inflammation of the pericardium (sac like membrane surrounding the heart)

52
Q

What usually causes pericarditis?

A

Acute viral infection

Cox A and B
Echo
Influenza

53
Q

What does pericarditis usually occur?

A

summer months coinciding with higher incidence of enterovirus infections (fecal-oral)

54
Q

What is a common sx of pericarditis?

A

chest pain associated with the irritated layers of pericardium rubbing together (worse when the pt is swallowing or supine)

Tends to be more acute, severe, have severe fever and tachypnea

55
Q

What is frequently found on physical exam in a pt with pericarditis?

A

tachycardia and a 3 component friction rub

Electrocardiographic changes often found, periocardiocentesis used to establish etiology

56
Q

When does Rheumatic Fever usually occur and to whom?

A

Following strep pyogenes pharyngitis in genetically predisposed individuals.

57
Q

What causes damage to the heart muscle and valve in Rheumatic Fever?

A

Autoantibodies (Abs to bacterial antigens cross-react with meromyosin in the heart)

58
Q

What is a definitive clinical indicator of rheumatic heart disease?

A

Mitral stenosis following pharyngitis with rash

59
Q

What risks are associated with Rheumatic Fever?

A

Strep throat infection (prolonged/untreated)

Prior case of rheumatic fever

5-15 yrs

60
Q

What are sxs of Rheumatic fever?

A
Usually appear 2-4 wks after strep infection
Pain/swelling in large joints
fever
weakness
muscle aches
shortness of breath
chest pain
nausea and vomitting
hacking cough
circular rash
lumps under the skin
61
Q

How do you diagnose rheumatic fever?

A
blood test
throat culture
echocardiogram
chest x-ray
electrocardiogram
62
Q

How do you treat rheumatic fever?

A

penicillin based antibiotics
aspirin
corticosteroids
rest

63
Q

How do you prevent rheumatic fever?

A

Treat strep throat right away with antibiotics.
Prevent infection from developing into rheumatic fever.

People experiencing sore throat/fever should consult a physician after 24 hrs.

64
Q

What bacterium causes RMSF?

A

rickettsia rickettsia

65
Q

What are typical sxs associated with RMSF?

A
RASH, FEVER, HA
abdominal pain
vomiting
muscle pain
Rash- absent first few days, can never develop
66
Q

What is the treatment for RMSF?

A

Doxycycline

67
Q

What is characteristic of the rash for RMSF?

A

maculopapular rash that starts on palms and soles and spreads to the trunk.