CV ID

Question 0

What virulence factors allow staph aureus to invade deep tissue? (3)

Answer 0

Hyaluronidase breaks down connective tissue
Staphylokinase lyses formed clots
Lipase breaks down fat

Question 1

Staphylococcus aureus virulence factors and their actions (11)

Answer 1

Biofilm formation, Capsule, Adhesins, pathogenicity islands code methicillin resistance, protein A binds the Fc portion of IgG, Coagulase ->fibrin coat protecting staph from phagocytosis, hemolysins and leukocidins destroy red and white blood cells
Elastin, collagen, & fibronectin (FnbpA) binding proteins

Question 2

Virulence factors of strep species (viridans) (2)

Answer 2

Dextran for glycocalyx formation

Surface adhesion proteins (FimA and GspB)

Question 3

Which organism that causes IE is most frequently found following GU (older men) or OB procedures (younger women)?

Answer 3

Enterococcus (3rd major cause of IE)

Question 4

Virulence factors of enterococcus species

Answer 4

Pili, surface proteins, biofilm formation
Extracellular enzymes (proteases, hyaluronidases)
Usually resistant to penicillin and carbepenems

Question 5

Where is enterococcus usually found?

Answer 5

Lines the GI tract.

Question 6

Strep pyogenes may be a part of normal skin flora. If it causes a localized skin or subcutaneous infection, it presents as ____(3), whereas it can cause ____ or ____ with toxin-mediated infections.

Answer 6

Local: impetigo (pustular lesions and honeycomb crusts)
Sub-q: cellulitis and erysipelas (ery = upper dermis and cutaneous)
Toxic shock syndrome and necrotizing fasciitis

Question 7

What are patients with strep pyogenes cellulitis at risk for?

Answer 7

Glomerulonephritis but not Rheumatic fever (whereas strep pharyngitis can lead to GN and rheumatic heart disease.

Question 8

Strep pyogenes virulence factors

Answer 8

Capsule, streptokinase (converts plasminogen to plasmin), M protein (resists phagocytosis), hyaluronidase (breakdown of conn tissue), DNase, Stretolysin O and S (destroy RBCs and WBCs respectively)
Streptokinase and hyaluronidase from a lysogenized prophage

Question 9

How does TSS happen?

Answer 9

Skin infection –> systemic release of pyrogenic exotoxin A (superantigen) –> polyclonal activation of T cells –> acute fever, shock, multiorgan failure

Question 10

How does strep pyogenes infection lead to necrotizing fasciitis?

Answer 10

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

Question 11

Our body producing an antibody to M protein of strep pyogenes that cross reacts with our own heart tissue is what type of hypersensitivity?

Answer 11

Type II
(I = allergy, II = antibody-dependent autoimmune attack, III = Immune complex disease IgG-antigen complex deposits, IV = delayed type, T cell mediated)

Question 12

Definitive clinical indicator of RHD?

Answer 12

Mitral stenosis following pharyngitis with a rash

- damage due to cross reactive antibodies reacting with meromyosin in heart

Question 13

How does RHD present?

Answer 13

2-4 weeks post strep infection: pain swelling in large joints, fever, weakness, muscle aches, SOB, CP, n/v, hacking cough, circular rash, lumps under skin.
Treat with penicillin-based ab, aspirin, corticosteroids

Question 14

Presentation of myocarditis (3)

Answer 14

CP, heart failure, abnormal heart rhythms possible

Question 15

Major causes of myocarditis. How do they do this?

Answer 15

Coxsackievirus B
Adenovirus (children)
Utilize CAR receptor on heart tissue (coxsackie and adenovirus receptor)

Question 16

Presentation of pericarditis

Answer 16

CP (irritated pericardium layers rubbing) worse swallowing, supine
3 component friction rub, tachycardia
Frequently ECG changes

Question 17

Most likely causative organisms for pericarditis

Answer 17

Viruses are major cause: Coxsackie A & B, echo, influenza, entero
Bacterial: staph aureus, strep pneumoniae, h flu, n meningitidis

Question 18

Artificial valve, pacemaker, defibrillator infections:

• most common cause within 2 weeks
• most common cause within first year
• other culprits

Answer 18

Staph aureus
Staph epidermidis or other coag neg staph
Strep species (viridans) and enterococci species

Question 19

Treatment of RMSF?

Answer 19

Doxycyclin

Question 20

Differentiate between Osler nodes and Janeway lesions

Answer 20

Osler: immunological (though with bacteria found sometimes in early lesions) red-purple, tender, slightly raised lumps usually on fingers and toes.
Janeway: vascular phenom consistent w septic micro-embolism (bacteria inside), usually on palms and soles. Generally non-tender lasting days to weeks

Question 20

What type of hypersensitivity are Osler nodes the result of?

Answer 20

type III (immune complex-mediated)

Question 21

What are MSCRAMMs?

Answer 21

microbial surface components recognizing adhesive matrix molecules
- Broad classification of the various attachment proteins utilized by strep and staph in colony formation

Question 22

Step pneumoniae virulence factors

Answer 22

Capsule

Question 23

Neisseria meningitidis virulence factors

Answer 23

Capsule

Question 24

Staphylococcus epidermidis virulence factors

Answer 24

SD-repeat containing protein-G (SdrG)
Biofilm formation (various proteins)

Question 25

COxsackie A and B + adenovirus virulence factors

Answer 25

CAR binding proteins

Question 26

Rickettsia rickettsii virulence factors

Answer 26

OmpA and OmpB for attachment

Type 4 secretion system (T4SS) for host cell entry